TY  - CONF
AU  - Stegnjaić, Goran
AU  - Lazarević, Milica
AU  - Jevtić, Bojan
AU  - Stanisavljević, Suzana
AU  - Nikolovski, Neda
AU  - Momčilović, Miljana
AU  - Mostarica Stojković, Marija
AU  - Miljković, Đorđe
AU  - Dimitrijević, Mirjana
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6363
AB  - Experimental autoimmune encephalomyelitis (EAE) in inbred rodents commonly shows different clinical courses, so that the diseased animals can be clustered into four groups: mild. moderate, severe and lethal. Our aim was to determine biomolecular markers in the preclinical phase of EAE that allow the prediction of clinical course. 
Methods: Female Dark Agouti rats were immunized with spinal cord homogenate without adjuvant and examined for four weeks for clinical signs of EAE. Cells and sera from blood collected on days 0, 3, and 7 after immunization were processed for detection of proinflammatory cytokines (IL-1, IL-6, TNF, and IFN) by "real-time" RT-PCR and ELISA, respectively. 
Results: Induction of EAE resulted in the downregulation of IFN and TNF in the preclinical phase of disease, whereas IL-1 and IL-6 expression levels were unaffected. However, there was no correlation between the relative expression of IFN or TNF and the cumulative clinical score (sum of daily clinical scores), suggesting that they are not predictive markers of EAE severity. Our preliminary results that suggest a negative correlation between IL-1 expression level before EAE induction and cumulative score require further justification. 
Conclusion: The proinflammatory cytokines investigated so far in our study cannot be considered as good biomarkers of EAE severity. However, the downregulation of IFN and TNF in the blood cells during the asymptomatic phase of EAE suggests that they enter the central nervous system early from the bloodstream, which argues for the study of chemokine and/or chemokine receptors expression as potential biomarkers for the clinical courses of EAE.
PB  - Belgrade: Institute of Molecular Genetics and Genetic Engineering, University of Belgrade
C3  - Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia
T1  - Molecular biomarkers as a prognostic tool for clinical courses of experimental autoimmune encephalomyelitis in rats immunized with spinal cord homogenate
SP  - 89
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6363
ER  - 

@conference{
author = "Stegnjaić, Goran and Lazarević, Milica and Jevtić, Bojan and Stanisavljević, Suzana and Nikolovski, Neda and Momčilović, Miljana and Mostarica Stojković, Marija and Miljković, Đorđe and Dimitrijević, Mirjana",
year = "2023",
abstract = "Experimental autoimmune encephalomyelitis (EAE) in inbred rodents commonly shows different clinical courses, so that the diseased animals can be clustered into four groups: mild. moderate, severe and lethal. Our aim was to determine biomolecular markers in the preclinical phase of EAE that allow the prediction of clinical course. 
Methods: Female Dark Agouti rats were immunized with spinal cord homogenate without adjuvant and examined for four weeks for clinical signs of EAE. Cells and sera from blood collected on days 0, 3, and 7 after immunization were processed for detection of proinflammatory cytokines (IL-1, IL-6, TNF, and IFN) by "real-time" RT-PCR and ELISA, respectively. 
Results: Induction of EAE resulted in the downregulation of IFN and TNF in the preclinical phase of disease, whereas IL-1 and IL-6 expression levels were unaffected. However, there was no correlation between the relative expression of IFN or TNF and the cumulative clinical score (sum of daily clinical scores), suggesting that they are not predictive markers of EAE severity. Our preliminary results that suggest a negative correlation between IL-1 expression level before EAE induction and cumulative score require further justification. 
Conclusion: The proinflammatory cytokines investigated so far in our study cannot be considered as good biomarkers of EAE severity. However, the downregulation of IFN and TNF in the blood cells during the asymptomatic phase of EAE suggests that they enter the central nervous system early from the bloodstream, which argues for the study of chemokine and/or chemokine receptors expression as potential biomarkers for the clinical courses of EAE.",
publisher = "Belgrade: Institute of Molecular Genetics and Genetic Engineering, University of Belgrade",
journal = "Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia",
title = "Molecular biomarkers as a prognostic tool for clinical courses of experimental autoimmune encephalomyelitis in rats immunized with spinal cord homogenate",
pages = "89",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6363"
}

Stegnjaić, G., Lazarević, M., Jevtić, B., Stanisavljević, S., Nikolovski, N., Momčilović, M., Mostarica Stojković, M., Miljković, Đ.,& Dimitrijević, M.. (2023). Molecular biomarkers as a prognostic tool for clinical courses of experimental autoimmune encephalomyelitis in rats immunized with spinal cord homogenate. in Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia
Belgrade: Institute of Molecular Genetics and Genetic Engineering, University of Belgrade., 89.
https://hdl.handle.net/21.15107/rcub_ibiss_6363

Stegnjaić G, Lazarević M, Jevtić B, Stanisavljević S, Nikolovski N, Momčilović M, Mostarica Stojković M, Miljković Đ, Dimitrijević M. Molecular biomarkers as a prognostic tool for clinical courses of experimental autoimmune encephalomyelitis in rats immunized with spinal cord homogenate. in Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia. 2023;:89.
https://hdl.handle.net/21.15107/rcub_ibiss_6363 .

Stegnjaić, Goran, Lazarević, Milica, Jevtić, Bojan, Stanisavljević, Suzana, Nikolovski, Neda, Momčilović, Miljana, Mostarica Stojković, Marija, Miljković, Đorđe, Dimitrijević, Mirjana, "Molecular biomarkers as a prognostic tool for clinical courses of experimental autoimmune encephalomyelitis in rats immunized with spinal cord homogenate" in Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia (2023):89,
https://hdl.handle.net/21.15107/rcub_ibiss_6363 .

TY  - JOUR
AU  - Lazarević, Milica
AU  - Nikolovski, Neda
AU  - Stanisavljević, Suzana
AU  - Dimitrijević, Mirjana
AU  - Stegnjaić, Goran
AU  - Krishnamoorthy, Gurumoorthy
AU  - Mostarica Stojković, Marija
AU  - Miljković, Đorđe
AU  - Jevtić, Bojan
PY  - 2021
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4193
AB  - Experimental autoimmune encephalomyelitis (EAE) is classically induced with complete Freund's adjuvant (CFA). The immune response against CFA has a confounding influence on the translational capacity of EAE as a multiple sclerosis model. Here, we compare clinical, cellular and molecular properties between syngeneic spinal cord homogenate (SCH)- and SCH + CFA-immunized Dark Agouti rats. EAE signs were observed earlier and the cumulative clinical score was higher without CFA. Also, a higher number of immune cells infiltrates in the spinal cords was noticed at the peak of EAE without CFA. High spinal cord abundance of CD8+CD11bc+MHC class II+ cells was detected in SCH-immunized rats. Myelin basic protein -specific response can be elicited in the cells from the lymph nodes draining the site of SCH immunization. This CFA-free EAE is a reliable multiple sclerosis model.
PB  - Elsevier BV
T2  - Journal of Neuroimmunology
T1  - Complete Freund's adjuvant-free experimental autoimmune encephalomyelitis in Dark Agouti rats is a valuable tool for multiple sclerosis studies.
VL  - 354
DO  - 10.1016/j.jneuroim.2021.577547
SP  - 577547
ER  - 

@article{
author = "Lazarević, Milica and Nikolovski, Neda and Stanisavljević, Suzana and Dimitrijević, Mirjana and Stegnjaić, Goran and Krishnamoorthy, Gurumoorthy and Mostarica Stojković, Marija and Miljković, Đorđe and Jevtić, Bojan",
year = "2021",
abstract = "Experimental autoimmune encephalomyelitis (EAE) is classically induced with complete Freund's adjuvant (CFA). The immune response against CFA has a confounding influence on the translational capacity of EAE as a multiple sclerosis model. Here, we compare clinical, cellular and molecular properties between syngeneic spinal cord homogenate (SCH)- and SCH + CFA-immunized Dark Agouti rats. EAE signs were observed earlier and the cumulative clinical score was higher without CFA. Also, a higher number of immune cells infiltrates in the spinal cords was noticed at the peak of EAE without CFA. High spinal cord abundance of CD8+CD11bc+MHC class II+ cells was detected in SCH-immunized rats. Myelin basic protein -specific response can be elicited in the cells from the lymph nodes draining the site of SCH immunization. This CFA-free EAE is a reliable multiple sclerosis model.",
publisher = "Elsevier BV",
journal = "Journal of Neuroimmunology",
title = "Complete Freund's adjuvant-free experimental autoimmune encephalomyelitis in Dark Agouti rats is a valuable tool for multiple sclerosis studies.",
volume = "354",
doi = "10.1016/j.jneuroim.2021.577547",
pages = "577547"
}

Lazarević, M., Nikolovski, N., Stanisavljević, S., Dimitrijević, M., Stegnjaić, G., Krishnamoorthy, G., Mostarica Stojković, M., Miljković, Đ.,& Jevtić, B.. (2021). Complete Freund's adjuvant-free experimental autoimmune encephalomyelitis in Dark Agouti rats is a valuable tool for multiple sclerosis studies.. in Journal of Neuroimmunology
Elsevier BV., 354, 577547.
https://doi.org/10.1016/j.jneuroim.2021.577547

Lazarević M, Nikolovski N, Stanisavljević S, Dimitrijević M, Stegnjaić G, Krishnamoorthy G, Mostarica Stojković M, Miljković Đ, Jevtić B. Complete Freund's adjuvant-free experimental autoimmune encephalomyelitis in Dark Agouti rats is a valuable tool for multiple sclerosis studies.. in Journal of Neuroimmunology. 2021;354:577547.
doi:10.1016/j.jneuroim.2021.577547 .

Lazarević, Milica, Nikolovski, Neda, Stanisavljević, Suzana, Dimitrijević, Mirjana, Stegnjaić, Goran, Krishnamoorthy, Gurumoorthy, Mostarica Stojković, Marija, Miljković, Đorđe, Jevtić, Bojan, "Complete Freund's adjuvant-free experimental autoimmune encephalomyelitis in Dark Agouti rats is a valuable tool for multiple sclerosis studies." in Journal of Neuroimmunology, 354 (2021):577547,
https://doi.org/10.1016/j.jneuroim.2021.577547 . .

TY  - JOUR
AU  - Stanisavljević, Suzana
AU  - Lukić, Jovanka
AU  - Momčilović, Miljana
AU  - Miljković, Marija
AU  - Jevtić, Bojan
AU  - Kojić, Milan
AU  - Golić, Nataša
AU  - Mostarica Stojković, Marija
AU  - Miljković, Đorđe
PY  - 2016
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6049
AB  - Gut microbiota and gut-associated lymphoid tissue have been increasingly appreciated as important players in pathogenesis of various autoimmune diseases, including multiple sclerosis. Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis that can be induced with an injection of spinal cord homogenate emulsified in complete Freund's adjuvant in Dark Agouti (DA) rats, but not in Albino Oxford (AO) rats. In this study, mesenteric lymph nodes (MLN), Peyer's patches (PP) and gut microbiota were analysed in these two rat strains. There was higher proportion of CD4(+) T cells and regulatory T cells in non-immunised DA rats in comparison to AO rats. Also, DA rat MLN and PP cells were higher producers of pro-inflammatory cytokines interferon-γ and interleukin-17. Finally, microbial analyses showed that uncultivated species of Turicibacter and Atopostipes genus were exclusively present in AO rats, in faeces and intestinal tissue, respectively. Thus, it is clear that in comparison of an EAE-susceptible with an EAE-resistant strain of rats, various discrepancies at the level of gut associated lymphoid tissue, as well as at the level of gut microbiota can be observed. Future studies should determine if the differences have functional significance for EAE pathogenesis.
PB  - Wageningen Academic Publishers
T2  - Beneficial Microbes
T1  - Gut-associated lymphoid tissue, gut microbes and susceptibility to experimental autoimmune encephalomyelitis
IS  - 3
VL  - 7
DO  - 10.3920/BM2015.0159
SP  - 363
EP  - 373
ER  - 

@article{
author = "Stanisavljević, Suzana and Lukić, Jovanka and Momčilović, Miljana and Miljković, Marija and Jevtić, Bojan and Kojić, Milan and Golić, Nataša and Mostarica Stojković, Marija and Miljković, Đorđe",
year = "2016",
abstract = "Gut microbiota and gut-associated lymphoid tissue have been increasingly appreciated as important players in pathogenesis of various autoimmune diseases, including multiple sclerosis. Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis that can be induced with an injection of spinal cord homogenate emulsified in complete Freund's adjuvant in Dark Agouti (DA) rats, but not in Albino Oxford (AO) rats. In this study, mesenteric lymph nodes (MLN), Peyer's patches (PP) and gut microbiota were analysed in these two rat strains. There was higher proportion of CD4(+) T cells and regulatory T cells in non-immunised DA rats in comparison to AO rats. Also, DA rat MLN and PP cells were higher producers of pro-inflammatory cytokines interferon-γ and interleukin-17. Finally, microbial analyses showed that uncultivated species of Turicibacter and Atopostipes genus were exclusively present in AO rats, in faeces and intestinal tissue, respectively. Thus, it is clear that in comparison of an EAE-susceptible with an EAE-resistant strain of rats, various discrepancies at the level of gut associated lymphoid tissue, as well as at the level of gut microbiota can be observed. Future studies should determine if the differences have functional significance for EAE pathogenesis.",
publisher = "Wageningen Academic Publishers",
journal = "Beneficial Microbes",
title = "Gut-associated lymphoid tissue, gut microbes and susceptibility to experimental autoimmune encephalomyelitis",
number = "3",
volume = "7",
doi = "10.3920/BM2015.0159",
pages = "363-373"
}

Stanisavljević, S., Lukić, J., Momčilović, M., Miljković, M., Jevtić, B., Kojić, M., Golić, N., Mostarica Stojković, M.,& Miljković, Đ.. (2016). Gut-associated lymphoid tissue, gut microbes and susceptibility to experimental autoimmune encephalomyelitis. in Beneficial Microbes
Wageningen Academic Publishers., 7(3), 363-373.
https://doi.org/10.3920/BM2015.0159

Stanisavljević S, Lukić J, Momčilović M, Miljković M, Jevtić B, Kojić M, Golić N, Mostarica Stojković M, Miljković Đ. Gut-associated lymphoid tissue, gut microbes and susceptibility to experimental autoimmune encephalomyelitis. in Beneficial Microbes. 2016;7(3):363-373.
doi:10.3920/BM2015.0159 .

Stanisavljević, Suzana, Lukić, Jovanka, Momčilović, Miljana, Miljković, Marija, Jevtić, Bojan, Kojić, Milan, Golić, Nataša, Mostarica Stojković, Marija, Miljković, Đorđe, "Gut-associated lymphoid tissue, gut microbes and susceptibility to experimental autoimmune encephalomyelitis" in Beneficial Microbes, 7, no. 3 (2016):363-373,
https://doi.org/10.3920/BM2015.0159 . .

TY  - JOUR
AU  - Timotijević, Gordana S
AU  - Petković, Filip
AU  - Blaževski, Jana
AU  - Momčilović, Miljana
AU  - Mostarica-Stojković, Marija B
AU  - Miljković, Đorđe
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/996
AB  - CXCL12 plays a protective role in CNS autoimmunity. Expression of CXCL12-gamma, which has distinct structural and functional properties than the other isoforms of CXCL12, was determined in spinal cords of rats immunized to develop experimental autoimmune encephalomyelitis (EAE). CNS expression of CXCL12-gamma was markedly lower in EAE-prone Dark Agouti rats than in EAE-resistant Albino Oxford rats, both in spinal cord homogenates and micro-blood vessels isolated from spinal cords. Inhibition of nitric oxide (NO) synthesis in DA rats upregulated, while donation of NO in AO rats downregulated CNS expression of CXCL12-gamma. NO inhibited CXCL12-gamma expression in astrocytes in vitro. A splice variant of CXCL12-gamma which migrates into nucleolus was not detected in spinal cord or astrocytes. Thus, CXCL12-gamma is expressed in the CNS after EAE induction, but its expression is markedly suppressed in spinal cord affected with full blown inflammation. NO is an important regulator of CXCL12-gamma expression in neuroinflammation. (C) 2013 Elsevier B.V. All rights reserved.
PB  - Amsterdam: Elsevier
T2  - Brain Research
T1  - CXCL12-γ expression is inhibited in neuroinflammation
VL  - 1519
DO  - 10.1016/j.brainres.2013.04.056
SP  - 120
EP  - 126
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_996
ER  - 

@article{
author = "Timotijević, Gordana S and Petković, Filip and Blaževski, Jana and Momčilović, Miljana and Mostarica-Stojković, Marija B and Miljković, Đorđe",
year = "2013",
abstract = "CXCL12 plays a protective role in CNS autoimmunity. Expression of CXCL12-gamma, which has distinct structural and functional properties than the other isoforms of CXCL12, was determined in spinal cords of rats immunized to develop experimental autoimmune encephalomyelitis (EAE). CNS expression of CXCL12-gamma was markedly lower in EAE-prone Dark Agouti rats than in EAE-resistant Albino Oxford rats, both in spinal cord homogenates and micro-blood vessels isolated from spinal cords. Inhibition of nitric oxide (NO) synthesis in DA rats upregulated, while donation of NO in AO rats downregulated CNS expression of CXCL12-gamma. NO inhibited CXCL12-gamma expression in astrocytes in vitro. A splice variant of CXCL12-gamma which migrates into nucleolus was not detected in spinal cord or astrocytes. Thus, CXCL12-gamma is expressed in the CNS after EAE induction, but its expression is markedly suppressed in spinal cord affected with full blown inflammation. NO is an important regulator of CXCL12-gamma expression in neuroinflammation. (C) 2013 Elsevier B.V. All rights reserved.",
publisher = "Amsterdam: Elsevier",
journal = "Brain Research",
title = "CXCL12-γ expression is inhibited in neuroinflammation",
volume = "1519",
doi = "10.1016/j.brainres.2013.04.056",
pages = "120-126",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_996"
}

Timotijević, G. S., Petković, F., Blaževski, J., Momčilović, M., Mostarica-Stojković, M. B.,& Miljković, Đ.. (2013). CXCL12-γ expression is inhibited in neuroinflammation. in Brain Research
Amsterdam: Elsevier., 1519, 120-126.
https://doi.org/10.1016/j.brainres.2013.04.056
https://hdl.handle.net/21.15107/rcub_ibiss_996

Timotijević GS, Petković F, Blaževski J, Momčilović M, Mostarica-Stojković MB, Miljković Đ. CXCL12-γ expression is inhibited in neuroinflammation. in Brain Research. 2013;1519:120-126.
doi:10.1016/j.brainres.2013.04.056
https://hdl.handle.net/21.15107/rcub_ibiss_996 .

Timotijević, Gordana S, Petković, Filip, Blaževski, Jana, Momčilović, Miljana, Mostarica-Stojković, Marija B, Miljković, Đorđe, "CXCL12-γ expression is inhibited in neuroinflammation" in Brain Research, 1519 (2013):120-126,
https://doi.org/10.1016/j.brainres.2013.04.056 .,
https://hdl.handle.net/21.15107/rcub_ibiss_996 .

TY  - JOUR
AU  - Blaževski, Jana
AU  - Petković, Filip
AU  - Momčilović, Miljana
AU  - Jevtić, Bojan
AU  - Miljković, Đorđe
AU  - Mostarica-Stojković, Marija B
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/974
AB  - Dark Agouti (DA) rats are highly susceptible to induction of experimental autoimmune encephalomyelitis (EAE), still they completely recover from the disease. Here, we were interested to determine contribution of major anti-inflammatory cytokines transforming growth factor (TGF)-beta and interleukin (IL)-10 to the recovery of DA rats from EAE. To that extent we determined CNS expression of these cytokines in DA rats at different phases of EAE and compared data to those obtained in EAE-resistant Albino Oxford (AO) rats. Higher expression of TGF-beta was persistently observed in the CNS of AO rats, even if rats were not immunized. This implied that high TGF-beta within the CNS is important for resistance of AO rats to EAE induction. On the contrary, IL-10 expression was consistently higher in DA than in AO rats and it culminated at the peak of EAE. Methylprednisolone suppressed EAE and expression of IL-10 in spinal cord homogenates, while IL-10 was increased in CNS-infiltrating immune cells. This implied that IL-10 might have a significant role in recovery of DA rats from the disease. Thus, we next explored effects of IL-10 on astrocytes, glial cells that largely contribute to control of CNS inflammation. IL-10 stimulated astrocytic expression of an important regulator of neuroinflammation, CXCL12. Thus, IL-10 might contribute to recovery of DA rats from EAE through induction of CXCL12 expression in astrocytes. (C) 2013 Elsevier GmbH. All rights reserved.
T2  - Immunobiology
T1  - High interleukin-10 expression within the central nervous system may be important for initiation of recovery of Dark Agouti rats from experimental autoimmune encephalomyelitis
IS  - 9
VL  - 218
SP  - 301
EP  - 1199
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_974
ER  - 

@article{
author = "Blaževski, Jana and Petković, Filip and Momčilović, Miljana and Jevtić, Bojan and Miljković, Đorđe and Mostarica-Stojković, Marija B",
year = "2013",
abstract = "Dark Agouti (DA) rats are highly susceptible to induction of experimental autoimmune encephalomyelitis (EAE), still they completely recover from the disease. Here, we were interested to determine contribution of major anti-inflammatory cytokines transforming growth factor (TGF)-beta and interleukin (IL)-10 to the recovery of DA rats from EAE. To that extent we determined CNS expression of these cytokines in DA rats at different phases of EAE and compared data to those obtained in EAE-resistant Albino Oxford (AO) rats. Higher expression of TGF-beta was persistently observed in the CNS of AO rats, even if rats were not immunized. This implied that high TGF-beta within the CNS is important for resistance of AO rats to EAE induction. On the contrary, IL-10 expression was consistently higher in DA than in AO rats and it culminated at the peak of EAE. Methylprednisolone suppressed EAE and expression of IL-10 in spinal cord homogenates, while IL-10 was increased in CNS-infiltrating immune cells. This implied that IL-10 might have a significant role in recovery of DA rats from the disease. Thus, we next explored effects of IL-10 on astrocytes, glial cells that largely contribute to control of CNS inflammation. IL-10 stimulated astrocytic expression of an important regulator of neuroinflammation, CXCL12. Thus, IL-10 might contribute to recovery of DA rats from EAE through induction of CXCL12 expression in astrocytes. (C) 2013 Elsevier GmbH. All rights reserved.",
journal = "Immunobiology",
title = "High interleukin-10 expression within the central nervous system may be important for initiation of recovery of Dark Agouti rats from experimental autoimmune encephalomyelitis",
number = "9",
volume = "218",
pages = "301-1199",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_974"
}

Blaževski, J., Petković, F., Momčilović, M., Jevtić, B., Miljković, Đ.,& Mostarica-Stojković, M. B.. (2013). High interleukin-10 expression within the central nervous system may be important for initiation of recovery of Dark Agouti rats from experimental autoimmune encephalomyelitis. in Immunobiology, 218(9), 301-1199.
https://hdl.handle.net/21.15107/rcub_ibiss_974

Blaževski J, Petković F, Momčilović M, Jevtić B, Miljković Đ, Mostarica-Stojković MB. High interleukin-10 expression within the central nervous system may be important for initiation of recovery of Dark Agouti rats from experimental autoimmune encephalomyelitis. in Immunobiology. 2013;218(9):301-1199.
https://hdl.handle.net/21.15107/rcub_ibiss_974 .

Blaževski, Jana, Petković, Filip, Momčilović, Miljana, Jevtić, Bojan, Miljković, Đorđe, Mostarica-Stojković, Marija B, "High interleukin-10 expression within the central nervous system may be important for initiation of recovery of Dark Agouti rats from experimental autoimmune encephalomyelitis" in Immunobiology, 218, no. 9 (2013):301-1199,
https://hdl.handle.net/21.15107/rcub_ibiss_974 .

TY  - JOUR
AU  - Blaževski, Jana
AU  - Petković, Filip
AU  - Momčilović, Miljana
AU  - Paschke, Reinhard
AU  - Kaluđerović, Goran N.
AU  - Mostarica-Stojković, Marija B
AU  - Miljković, Đorđe
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1037
AB  - Aim: To investigate the influences of betulinic acid (BA), a triterpenoid isolated from birch bark, on neuroinflammatory mediators involved in the pathogenesis of multiple sclerosis and experimental autoimmune encephalomyelitis in vitro. Methods: Encephalitogenic T cells were prepared from draining lymph nodes and spinal cords of Dark Agouti rats 8 to 10 d after immunization with myelin basic protein (MBP) and complete Freund's adjuvant. Macrophages were isolated from the peritoneal cavity of adult untreated rats. Astrocytes were isolated from neonatal rat brains. The cells were cultured and then treated with different agents. IFN-gamma, IL-17, iNOS and CXCL12 mRNA levels in the cells were analyzed with RT-PCR. iNOS and CXCL12 protein levels were detected using immunoblot. NO and ROS generation was measured using Griess reaction and flow cytometry, respectively. Results: In encephalitogenic T cells stimulated with MBP (10 mu g/mL), addition of BA inhibited IL-17 and IFN-gamma production in a dose-dependent manner. The estimated IC50 values for IL-17 and IFN gamma were 11.2 and 63.8 mu mol/L, respectively. When the macrophages were stimulated with LPS (10 ng/mL), addition of BA (50 mu mol/L) significantly increased ROS generation, and suppressed NO generation. The astrocytes were stimulated with ConASn containing numerous inflammatory mediators, which mimicked the inflammatory milieu within CNS; addition of BA (50 mu mol/L) significantly increased ROS generation, and blocked ConASn-induced increases in iNOS and CXCL12 mRNA levels, but did not affect iNOS and CXCL12 protein levels. Importantly, in both the macrophages and astrocytes, addition of BA (50 mu mol/L) inhibited lipid peroxidation. Conclusion: Besides inhibiting encephalitogenic T cell cytokines and reducing NO generation, BA induces tissue-damaging ROS generation within CNS.
T2  - Acta Pharmacologica Sinica
T1  - Betulinic acid regulates generation of neuroinflammatory mediators responsible for tissue destruction in multiple sclerosis in vitro
IS  - 3
VL  - 34
SP  - 51
EP  - 431
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1037
ER  - 

@article{
author = "Blaževski, Jana and Petković, Filip and Momčilović, Miljana and Paschke, Reinhard and Kaluđerović, Goran N. and Mostarica-Stojković, Marija B and Miljković, Đorđe",
year = "2013",
abstract = "Aim: To investigate the influences of betulinic acid (BA), a triterpenoid isolated from birch bark, on neuroinflammatory mediators involved in the pathogenesis of multiple sclerosis and experimental autoimmune encephalomyelitis in vitro. Methods: Encephalitogenic T cells were prepared from draining lymph nodes and spinal cords of Dark Agouti rats 8 to 10 d after immunization with myelin basic protein (MBP) and complete Freund's adjuvant. Macrophages were isolated from the peritoneal cavity of adult untreated rats. Astrocytes were isolated from neonatal rat brains. The cells were cultured and then treated with different agents. IFN-gamma, IL-17, iNOS and CXCL12 mRNA levels in the cells were analyzed with RT-PCR. iNOS and CXCL12 protein levels were detected using immunoblot. NO and ROS generation was measured using Griess reaction and flow cytometry, respectively. Results: In encephalitogenic T cells stimulated with MBP (10 mu g/mL), addition of BA inhibited IL-17 and IFN-gamma production in a dose-dependent manner. The estimated IC50 values for IL-17 and IFN gamma were 11.2 and 63.8 mu mol/L, respectively. When the macrophages were stimulated with LPS (10 ng/mL), addition of BA (50 mu mol/L) significantly increased ROS generation, and suppressed NO generation. The astrocytes were stimulated with ConASn containing numerous inflammatory mediators, which mimicked the inflammatory milieu within CNS; addition of BA (50 mu mol/L) significantly increased ROS generation, and blocked ConASn-induced increases in iNOS and CXCL12 mRNA levels, but did not affect iNOS and CXCL12 protein levels. Importantly, in both the macrophages and astrocytes, addition of BA (50 mu mol/L) inhibited lipid peroxidation. Conclusion: Besides inhibiting encephalitogenic T cell cytokines and reducing NO generation, BA induces tissue-damaging ROS generation within CNS.",
journal = "Acta Pharmacologica Sinica",
title = "Betulinic acid regulates generation of neuroinflammatory mediators responsible for tissue destruction in multiple sclerosis in vitro",
number = "3",
volume = "34",
pages = "51-431",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1037"
}

Blaževski, J., Petković, F., Momčilović, M., Paschke, R., Kaluđerović, G. N., Mostarica-Stojković, M. B.,& Miljković, Đ.. (2013). Betulinic acid regulates generation of neuroinflammatory mediators responsible for tissue destruction in multiple sclerosis in vitro. in Acta Pharmacologica Sinica, 34(3), 51-431.
https://hdl.handle.net/21.15107/rcub_ibiss_1037

Blaževski J, Petković F, Momčilović M, Paschke R, Kaluđerović GN, Mostarica-Stojković MB, Miljković Đ. Betulinic acid regulates generation of neuroinflammatory mediators responsible for tissue destruction in multiple sclerosis in vitro. in Acta Pharmacologica Sinica. 2013;34(3):51-431.
https://hdl.handle.net/21.15107/rcub_ibiss_1037 .

Blaževski, Jana, Petković, Filip, Momčilović, Miljana, Paschke, Reinhard, Kaluđerović, Goran N., Mostarica-Stojković, Marija B, Miljković, Đorđe, "Betulinic acid regulates generation of neuroinflammatory mediators responsible for tissue destruction in multiple sclerosis in vitro" in Acta Pharmacologica Sinica, 34, no. 3 (2013):51-431,
https://hdl.handle.net/21.15107/rcub_ibiss_1037 .

TY  - CONF
AU  - Petković, Filip
AU  - Blaževski, Jana
AU  - Momčilović, Miljana
AU  - Mostarica-Stojković, Marija B
AU  - Miljković, Đorđe
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/650
C3  - Glia
T1  - Opposing Roles of Nitric Oxide and Interleukin-10 on Cxcl12 Gene Expression in Astrocytes
IS  - null
VL  - 61
SP  - 109
EP  - S166
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_650
ER  - 

@conference{
author = "Petković, Filip and Blaževski, Jana and Momčilović, Miljana and Mostarica-Stojković, Marija B and Miljković, Đorđe",
year = "2013",
journal = "Glia",
title = "Opposing Roles of Nitric Oxide and Interleukin-10 on Cxcl12 Gene Expression in Astrocytes",
number = "null",
volume = "61",
pages = "109-S166",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_650"
}

Petković, F., Blaževski, J., Momčilović, M., Mostarica-Stojković, M. B.,& Miljković, Đ.. (2013). Opposing Roles of Nitric Oxide and Interleukin-10 on Cxcl12 Gene Expression in Astrocytes. in Glia, 61(null), 109-S166.
https://hdl.handle.net/21.15107/rcub_ibiss_650

Petković F, Blaževski J, Momčilović M, Mostarica-Stojković MB, Miljković Đ. Opposing Roles of Nitric Oxide and Interleukin-10 on Cxcl12 Gene Expression in Astrocytes. in Glia. 2013;61(null):109-S166.
https://hdl.handle.net/21.15107/rcub_ibiss_650 .

Petković, Filip, Blaževski, Jana, Momčilović, Miljana, Mostarica-Stojković, Marija B, Miljković, Đorđe, "Opposing Roles of Nitric Oxide and Interleukin-10 on Cxcl12 Gene Expression in Astrocytes" in Glia, 61, no. null (2013):109-S166,
https://hdl.handle.net/21.15107/rcub_ibiss_650 .

TY  - JOUR
AU  - Petković, Filip
AU  - Blaževski, Jana
AU  - Momčilović, Miljana
AU  - Mostarica-Stojković, Marija B
AU  - Miljković, Đorđe
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/648
AB  - Chemokine CXCL12 (C-X-C motif chemokine ligand 12) restricts immune cell invasion of the central nervous system (CNS) and limits neuroinflammation in experimental autoimmune encephalomyelitis (EAE), an animal model of inflammatory and demyelinating disease of the CNS, multiple sclerosis (MS). Nitric oxide (NO), by contrast, predominantly contributes to CNS tissue destruction in MS and EAE. Thus, the influence of NO on CXCL12 in the inflamed CNS was investigated. Excess expression of inducible NO synthase was inversely correlated to CXCL12 gene expression in spinal cord homogenates of rats immunized to develop EAE. NO inhibited gene expression of CXCL12 in astrocytes and endothelial cells in vitro. The inhibition was paralleled with reduction of p38 mitogen-activated protein kinase (MAPK) phosphorylation and it was mimicked with inhibitors of p38 MAPK activation in astrocytes. In vivo suppression of nitric generation recovered CXCL12 expression in the CNS and attenuated EAE in Dark Agouti rats. On the contrary, in vivo NO donation decreased CXCL12 expression in the CNS of EAE-resistant Albino Oxford (AO) rats. However, the effect was not paralleled with induction of EAE in AO rats. It is suggested that NO acting through suppression of p38 MAPK inhibits CXCL12 expression in neuroinflammation. These results imply that downregulation of NO release and protection of CXCL12 expression within the CNS might present the potential approaches in MS therapy.
T2  - Immunology and Cell Biology
T1  - Nitric oxide inhibits CXCL12 expression in neuroinflammation
IS  - 6
VL  - 91
SP  - 89
EP  - 434
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_648
ER  - 

@article{
author = "Petković, Filip and Blaževski, Jana and Momčilović, Miljana and Mostarica-Stojković, Marija B and Miljković, Đorđe",
year = "2013",
abstract = "Chemokine CXCL12 (C-X-C motif chemokine ligand 12) restricts immune cell invasion of the central nervous system (CNS) and limits neuroinflammation in experimental autoimmune encephalomyelitis (EAE), an animal model of inflammatory and demyelinating disease of the CNS, multiple sclerosis (MS). Nitric oxide (NO), by contrast, predominantly contributes to CNS tissue destruction in MS and EAE. Thus, the influence of NO on CXCL12 in the inflamed CNS was investigated. Excess expression of inducible NO synthase was inversely correlated to CXCL12 gene expression in spinal cord homogenates of rats immunized to develop EAE. NO inhibited gene expression of CXCL12 in astrocytes and endothelial cells in vitro. The inhibition was paralleled with reduction of p38 mitogen-activated protein kinase (MAPK) phosphorylation and it was mimicked with inhibitors of p38 MAPK activation in astrocytes. In vivo suppression of nitric generation recovered CXCL12 expression in the CNS and attenuated EAE in Dark Agouti rats. On the contrary, in vivo NO donation decreased CXCL12 expression in the CNS of EAE-resistant Albino Oxford (AO) rats. However, the effect was not paralleled with induction of EAE in AO rats. It is suggested that NO acting through suppression of p38 MAPK inhibits CXCL12 expression in neuroinflammation. These results imply that downregulation of NO release and protection of CXCL12 expression within the CNS might present the potential approaches in MS therapy.",
journal = "Immunology and Cell Biology",
title = "Nitric oxide inhibits CXCL12 expression in neuroinflammation",
number = "6",
volume = "91",
pages = "89-434",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_648"
}

Petković, F., Blaževski, J., Momčilović, M., Mostarica-Stojković, M. B.,& Miljković, Đ.. (2013). Nitric oxide inhibits CXCL12 expression in neuroinflammation. in Immunology and Cell Biology, 91(6), 89-434.
https://hdl.handle.net/21.15107/rcub_ibiss_648

Petković F, Blaževski J, Momčilović M, Mostarica-Stojković MB, Miljković Đ. Nitric oxide inhibits CXCL12 expression in neuroinflammation. in Immunology and Cell Biology. 2013;91(6):89-434.
https://hdl.handle.net/21.15107/rcub_ibiss_648 .

Petković, Filip, Blaževski, Jana, Momčilović, Miljana, Mostarica-Stojković, Marija B, Miljković, Đorđe, "Nitric oxide inhibits CXCL12 expression in neuroinflammation" in Immunology and Cell Biology, 91, no. 6 (2013):89-434,
https://hdl.handle.net/21.15107/rcub_ibiss_648 .

TY  - CONF
AU  - Momčilović, Miljana
AU  - Blaževski, Jana
AU  - Petković, Filip
AU  - Mostarica-Stojković, Marija B
AU  - Miljković, Đorđe
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1114
C3  - Immunology
T1  - High MMP-2, MMP-9 and low TIMP-1 expression in the spinal cord of rats correlate to CNS autoimmunity resistance
IS  - null
VL  - 137
SP  - 1
EP  - 491
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1114
ER  - 

@conference{
author = "Momčilović, Miljana and Blaževski, Jana and Petković, Filip and Mostarica-Stojković, Marija B and Miljković, Đorđe",
year = "2012",
journal = "Immunology",
title = "High MMP-2, MMP-9 and low TIMP-1 expression in the spinal cord of rats correlate to CNS autoimmunity resistance",
number = "null",
volume = "137",
pages = "1-491",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1114"
}

Momčilović, M., Blaževski, J., Petković, F., Mostarica-Stojković, M. B.,& Miljković, Đ.. (2012). High MMP-2, MMP-9 and low TIMP-1 expression in the spinal cord of rats correlate to CNS autoimmunity resistance. in Immunology, 137(null), 1-491.
https://hdl.handle.net/21.15107/rcub_ibiss_1114

Momčilović M, Blaževski J, Petković F, Mostarica-Stojković MB, Miljković Đ. High MMP-2, MMP-9 and low TIMP-1 expression in the spinal cord of rats correlate to CNS autoimmunity resistance. in Immunology. 2012;137(null):1-491.
https://hdl.handle.net/21.15107/rcub_ibiss_1114 .

Momčilović, Miljana, Blaževski, Jana, Petković, Filip, Mostarica-Stojković, Marija B, Miljković, Đorđe, "High MMP-2, MMP-9 and low TIMP-1 expression in the spinal cord of rats correlate to CNS autoimmunity resistance" in Immunology, 137, no. null (2012):1-491,
https://hdl.handle.net/21.15107/rcub_ibiss_1114 .

TY  - CONF
AU  - Petković, Filip
AU  - Blaževski, Jana
AU  - Momčilović, Miljana
AU  - Mostarica-Stojković, Marija B
AU  - Miljković, Đorđe
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1112
C3  - Immunology
T1  - Nitric oxide downregulates CXCL12 gene expression in neuroinflammation
IS  - null
VL  - 137
SP  - 331
EP  - 19
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1112
ER  - 

@conference{
author = "Petković, Filip and Blaževski, Jana and Momčilović, Miljana and Mostarica-Stojković, Marija B and Miljković, Đorđe",
year = "2012",
journal = "Immunology",
title = "Nitric oxide downregulates CXCL12 gene expression in neuroinflammation",
number = "null",
volume = "137",
pages = "331-19",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1112"
}

Petković, F., Blaževski, J., Momčilović, M., Mostarica-Stojković, M. B.,& Miljković, Đ.. (2012). Nitric oxide downregulates CXCL12 gene expression in neuroinflammation. in Immunology, 137(null), 331-19.
https://hdl.handle.net/21.15107/rcub_ibiss_1112

Petković F, Blaževski J, Momčilović M, Mostarica-Stojković MB, Miljković Đ. Nitric oxide downregulates CXCL12 gene expression in neuroinflammation. in Immunology. 2012;137(null):331-19.
https://hdl.handle.net/21.15107/rcub_ibiss_1112 .

Petković, Filip, Blaževski, Jana, Momčilović, Miljana, Mostarica-Stojković, Marija B, Miljković, Đorđe, "Nitric oxide downregulates CXCL12 gene expression in neuroinflammation" in Immunology, 137, no. null (2012):331-19,
https://hdl.handle.net/21.15107/rcub_ibiss_1112 .

TY  - JOUR
AU  - Momčilović, Miljana
AU  - Mostarica-Stojković, Marija B
AU  - Miljković, Đorđe
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1190
AB  - Inflammation within the central nervous system (CNS) is strictly controlled and if possible prevented. Such a tight control is necessary due to high sensitivity of nervous tissue to mechanical and biochemical consequences of inflammation. Still, neuroinflammation is a typical feature of a chronic, inflammatory, demyelinating disease multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). It is assumed that mechanisms that should prevent activation of immune cells at the periphery, in the lymphoid tissues, and/or inflammation within the CNS are inadequately efficient in MS patients. Here, some recent data about the importance of CXCL12 for regulation of neuroinflammation and contribution of its deviant expression within the CNS to EAE and MS pathogenesis are presented.
T2  - Immunologic Research
T1  - CXCL12 in control of neuroinflammation
IS  - 1-2
VL  - 52
EP  - 63
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1190
ER  - 

@article{
author = "Momčilović, Miljana and Mostarica-Stojković, Marija B and Miljković, Đorđe",
year = "2012",
abstract = "Inflammation within the central nervous system (CNS) is strictly controlled and if possible prevented. Such a tight control is necessary due to high sensitivity of nervous tissue to mechanical and biochemical consequences of inflammation. Still, neuroinflammation is a typical feature of a chronic, inflammatory, demyelinating disease multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). It is assumed that mechanisms that should prevent activation of immune cells at the periphery, in the lymphoid tissues, and/or inflammation within the CNS are inadequately efficient in MS patients. Here, some recent data about the importance of CXCL12 for regulation of neuroinflammation and contribution of its deviant expression within the CNS to EAE and MS pathogenesis are presented.",
journal = "Immunologic Research",
title = "CXCL12 in control of neuroinflammation",
number = "1-2",
volume = "52",
pages = "63",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1190"
}

Momčilović, M., Mostarica-Stojković, M. B.,& Miljković, Đ.. (2012). CXCL12 in control of neuroinflammation. in Immunologic Research, 52(1-2).
https://hdl.handle.net/21.15107/rcub_ibiss_1190

Momčilović M, Mostarica-Stojković MB, Miljković Đ. CXCL12 in control of neuroinflammation. in Immunologic Research. 2012;52(1-2):null-63.
https://hdl.handle.net/21.15107/rcub_ibiss_1190 .

Momčilović, Miljana, Mostarica-Stojković, Marija B, Miljković, Đorđe, "CXCL12 in control of neuroinflammation" in Immunologic Research, 52, no. 1-2 (2012),
https://hdl.handle.net/21.15107/rcub_ibiss_1190 .

TY  - JOUR
AU  - Timotijević, Gordana S
AU  - Mostarica-Stojković, Marija B
AU  - Miljković, Đorđe
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1179
AB  - CxCL12, also known as SDF-1 (stromal cell derived factor-1) is a small protein that belongs to the chemokine family, whose members have a crucial role in directing cell migration. CXCL12 has an essential role in neural and vascular development, hematopoiesis and in immunity. It acts through two receptors. CXCR4 and CXCR7. While the former is a classic G protein-coupled transmembrane chemokine receptor, the latter primarily function as a scavenger of CXCL12. CXCL12 has been considered as a standard proinflammatory molecule for a long time, as it attracts leukocytes to inflammatory sites and contributes to their activation. However, recent findings indicate that this chemokine has the opposite role in neuroinflammation. In this review, basic data about molecular and functional properties of CXCL12 are presented, while its role in CNS autoimmunity is addressed in details. (C) 2012 Elsevier Ltd. All rights reserved.
T2  - International Journal of Biochemistry & Cell Biology
T1  - CXCL12: Role in neuroinflammation
IS  - 6
VL  - 44
EP  - 841
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1179
ER  - 

@article{
author = "Timotijević, Gordana S and Mostarica-Stojković, Marija B and Miljković, Đorđe",
year = "2012",
abstract = "CxCL12, also known as SDF-1 (stromal cell derived factor-1) is a small protein that belongs to the chemokine family, whose members have a crucial role in directing cell migration. CXCL12 has an essential role in neural and vascular development, hematopoiesis and in immunity. It acts through two receptors. CXCR4 and CXCR7. While the former is a classic G protein-coupled transmembrane chemokine receptor, the latter primarily function as a scavenger of CXCL12. CXCL12 has been considered as a standard proinflammatory molecule for a long time, as it attracts leukocytes to inflammatory sites and contributes to their activation. However, recent findings indicate that this chemokine has the opposite role in neuroinflammation. In this review, basic data about molecular and functional properties of CXCL12 are presented, while its role in CNS autoimmunity is addressed in details. (C) 2012 Elsevier Ltd. All rights reserved.",
journal = "International Journal of Biochemistry & Cell Biology",
title = "CXCL12: Role in neuroinflammation",
number = "6",
volume = "44",
pages = "841",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1179"
}

Timotijević, G. S., Mostarica-Stojković, M. B.,& Miljković, Đ.. (2012). CXCL12: Role in neuroinflammation. in International Journal of Biochemistry & Cell Biology, 44(6).
https://hdl.handle.net/21.15107/rcub_ibiss_1179

Timotijević GS, Mostarica-Stojković MB, Miljković Đ. CXCL12: Role in neuroinflammation. in International Journal of Biochemistry & Cell Biology. 2012;44(6):null-841.
https://hdl.handle.net/21.15107/rcub_ibiss_1179 .

Timotijević, Gordana S, Mostarica-Stojković, Marija B, Miljković, Đorđe, "CXCL12: Role in neuroinflammation" in International Journal of Biochemistry & Cell Biology, 44, no. 6 (2012),
https://hdl.handle.net/21.15107/rcub_ibiss_1179 .

TY  - JOUR
AU  - Miljković, Đorđe
AU  - Momčilović, Miljana
AU  - Stanojević, Zeljka S
AU  - Rasić, Dejan M
AU  - Mostarica-Stojković, Marija B
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1279
AB  - Experimental autoimmune encephalomyelitis (EAE) is a model of multiple sclerosis. Dark Agouti rats immunized with spinal cord homogenate (SCH) and carbonyl iron (CI), as an adjuvant, develop severe hyperacute form of EAE. They succumb to EAE earlier and have higher clinical scores and lethality rate in comparison to counterparts immunized with SCH + complete Freund's adjuvant. There is no difference in the number of cells or in histological presentation of the CNS infiltrates of rats immunized with the two adjuvants. However, there are more granulocytes, NK and NKT cells, and less CD4(+) T cells in the spinal cord infiltrates of SCH + CI-immunized animals. Nitric oxide (NO)-generating enzyme inducible NO synthase have higher expression in spinal cord of SCH + CI-immunized rats, and this corresponds to more intensive nitrotyrosine formation in the CNS tissue of these rats. Abundant infiltration of granulocytes and NK cells into the CNS and excessive generation of peroxynitrite within the CNS of SCH + CI-immunized rats might account for the severe neurological deficits induced by immunization with CI. These factors should be closely examined in the fulminant forms of multiple sclerosis and acute disseminated encephalomyelitis, as they could represent a promising targets for therapy.
T2  - Journal of Neurochemistry
T1  - It is still not for the old iron: adjuvant effects of carbonyl iron in experimental autoimmune encephalomyelitis induction
IS  - 2
VL  - 118
EP  - 214
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1279
ER  - 

@article{
author = "Miljković, Đorđe and Momčilović, Miljana and Stanojević, Zeljka S and Rasić, Dejan M and Mostarica-Stojković, Marija B",
year = "2011",
abstract = "Experimental autoimmune encephalomyelitis (EAE) is a model of multiple sclerosis. Dark Agouti rats immunized with spinal cord homogenate (SCH) and carbonyl iron (CI), as an adjuvant, develop severe hyperacute form of EAE. They succumb to EAE earlier and have higher clinical scores and lethality rate in comparison to counterparts immunized with SCH + complete Freund's adjuvant. There is no difference in the number of cells or in histological presentation of the CNS infiltrates of rats immunized with the two adjuvants. However, there are more granulocytes, NK and NKT cells, and less CD4(+) T cells in the spinal cord infiltrates of SCH + CI-immunized animals. Nitric oxide (NO)-generating enzyme inducible NO synthase have higher expression in spinal cord of SCH + CI-immunized rats, and this corresponds to more intensive nitrotyrosine formation in the CNS tissue of these rats. Abundant infiltration of granulocytes and NK cells into the CNS and excessive generation of peroxynitrite within the CNS of SCH + CI-immunized rats might account for the severe neurological deficits induced by immunization with CI. These factors should be closely examined in the fulminant forms of multiple sclerosis and acute disseminated encephalomyelitis, as they could represent a promising targets for therapy.",
journal = "Journal of Neurochemistry",
title = "It is still not for the old iron: adjuvant effects of carbonyl iron in experimental autoimmune encephalomyelitis induction",
number = "2",
volume = "118",
pages = "214",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1279"
}

Miljković, Đ., Momčilović, M., Stanojević, Z. S., Rasić, D. M.,& Mostarica-Stojković, M. B.. (2011). It is still not for the old iron: adjuvant effects of carbonyl iron in experimental autoimmune encephalomyelitis induction. in Journal of Neurochemistry, 118(2).
https://hdl.handle.net/21.15107/rcub_ibiss_1279

Miljković Đ, Momčilović M, Stanojević ZS, Rasić DM, Mostarica-Stojković MB. It is still not for the old iron: adjuvant effects of carbonyl iron in experimental autoimmune encephalomyelitis induction. in Journal of Neurochemistry. 2011;118(2):null-214.
https://hdl.handle.net/21.15107/rcub_ibiss_1279 .

Miljković, Đorđe, Momčilović, Miljana, Stanojević, Zeljka S, Rasić, Dejan M, Mostarica-Stojković, Marija B, "It is still not for the old iron: adjuvant effects of carbonyl iron in experimental autoimmune encephalomyelitis induction" in Journal of Neurochemistry, 118, no. 2 (2011),
https://hdl.handle.net/21.15107/rcub_ibiss_1279 .

TY  - JOUR
AU  - Miljković, Đorđe
AU  - Stanojević, Zeljka S
AU  - Momčilović, Miljana
AU  - Odoardi, Francesca
AU  - Fluegel, Alexander
AU  - Mostarica-Stojković, Marija B
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1267
AB  - Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis, a chronic inflammatory and demyelinating disease of the CNS. Albino Oxford (AO) rats are resistant to the induction of EAE, while the disease can be readily induced in Dark Agouti (DA) rats. Here we investigated a potential contribution of the CNS milieu in the limitation of the encephalitogenic autoimmune response. EAE was induced by immunization of the respective rat strains with spinal cord homogenate emulsified in complete Freund's adjuvant. AO rats did not exhibit clinical signs after immunization while DA rats developed severe neurologic deficits. Infiltration of immune cells into spinal cords (SC) was evident in both strains 12-14 days after the immunization. EAE lesions of AO rats contained substantially lower numbers of CD4+ T cells and CD11b+ cells compared to those in DA rats. This went together with lower levels of interferon (IFN)-gamma and interleukin (IL)-17 in the cells isolated from SC. We found a dramatic increase of CXCL12 expression in SC tissue and microvessels of AO rats, whereas DA rats markedly decreased the expression of this chemokine within their CNS. Administration of the CXCL12 antagonist AMD3100 to a substrain of AO rats that developed a weak EAE led to earlier onset and exacerbation of the disease. These results suggest a role of CXCL12 in down-regulating autoimmune processes in AO rats during EAE. Therapeutic modulation of CXCL12 could be a promising strategy for the treatment of CNS autoimmunity. (C) 2011 Elsevier GmbH. All rights reserved.
T2  - Immunobiology
T1  - CXCL12 expression within the CNS contributes to the resistance against experimental autoimmune encephalomyelitis in Albino Oxford rats
IS  - 9
VL  - 216
EP  - 987
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1267
ER  - 

@article{
author = "Miljković, Đorđe and Stanojević, Zeljka S and Momčilović, Miljana and Odoardi, Francesca and Fluegel, Alexander and Mostarica-Stojković, Marija B",
year = "2011",
abstract = "Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis, a chronic inflammatory and demyelinating disease of the CNS. Albino Oxford (AO) rats are resistant to the induction of EAE, while the disease can be readily induced in Dark Agouti (DA) rats. Here we investigated a potential contribution of the CNS milieu in the limitation of the encephalitogenic autoimmune response. EAE was induced by immunization of the respective rat strains with spinal cord homogenate emulsified in complete Freund's adjuvant. AO rats did not exhibit clinical signs after immunization while DA rats developed severe neurologic deficits. Infiltration of immune cells into spinal cords (SC) was evident in both strains 12-14 days after the immunization. EAE lesions of AO rats contained substantially lower numbers of CD4+ T cells and CD11b+ cells compared to those in DA rats. This went together with lower levels of interferon (IFN)-gamma and interleukin (IL)-17 in the cells isolated from SC. We found a dramatic increase of CXCL12 expression in SC tissue and microvessels of AO rats, whereas DA rats markedly decreased the expression of this chemokine within their CNS. Administration of the CXCL12 antagonist AMD3100 to a substrain of AO rats that developed a weak EAE led to earlier onset and exacerbation of the disease. These results suggest a role of CXCL12 in down-regulating autoimmune processes in AO rats during EAE. Therapeutic modulation of CXCL12 could be a promising strategy for the treatment of CNS autoimmunity. (C) 2011 Elsevier GmbH. All rights reserved.",
journal = "Immunobiology",
title = "CXCL12 expression within the CNS contributes to the resistance against experimental autoimmune encephalomyelitis in Albino Oxford rats",
number = "9",
volume = "216",
pages = "987",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1267"
}

Miljković, Đ., Stanojević, Z. S., Momčilović, M., Odoardi, F., Fluegel, A.,& Mostarica-Stojković, M. B.. (2011). CXCL12 expression within the CNS contributes to the resistance against experimental autoimmune encephalomyelitis in Albino Oxford rats. in Immunobiology, 216(9).
https://hdl.handle.net/21.15107/rcub_ibiss_1267

Miljković Đ, Stanojević ZS, Momčilović M, Odoardi F, Fluegel A, Mostarica-Stojković MB. CXCL12 expression within the CNS contributes to the resistance against experimental autoimmune encephalomyelitis in Albino Oxford rats. in Immunobiology. 2011;216(9):null-987.
https://hdl.handle.net/21.15107/rcub_ibiss_1267 .

Miljković, Đorđe, Stanojević, Zeljka S, Momčilović, Miljana, Odoardi, Francesca, Fluegel, Alexander, Mostarica-Stojković, Marija B, "CXCL12 expression within the CNS contributes to the resistance against experimental autoimmune encephalomyelitis in Albino Oxford rats" in Immunobiology, 216, no. 9 (2011),
https://hdl.handle.net/21.15107/rcub_ibiss_1267 .

TY  - JOUR
AU  - Miljković, Đorđe
AU  - Timotijević, Gordana S
AU  - Mostarica-Stojković, Marija B
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1240
AB  - Astrocytes are the most abundant cell population within the CNS of mammals. Their glial role is perfectly performed in the healthy CNS as they support functions of neurons. The omnipresence of astrocytes throughout the white and grey matter and their intimate relation with blood vessels of the CNS, as well as numerous immunity-related actions that these cells are capable of, imply that astrocytes should have a prominent role in neuroinflammatory disorders, such as multiple sclerosis (MS). The role of astrocytes in MS is rather ambiguous, as they have the capacity to both stimulate and restrain neuroinflammation and tissue destruction. In this paper we present some of the proved and the proposed functions of astrocytes in neuroinflammation and discuss the effect of MS therapeutics on astrocytes. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
T2  - Febs Letters
T1  - Astrocytes in the tempest of multiple sclerosis
IS  - 23
VL  - 585
EP  - 3788
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1240
ER  - 

@article{
author = "Miljković, Đorđe and Timotijević, Gordana S and Mostarica-Stojković, Marija B",
year = "2011",
abstract = "Astrocytes are the most abundant cell population within the CNS of mammals. Their glial role is perfectly performed in the healthy CNS as they support functions of neurons. The omnipresence of astrocytes throughout the white and grey matter and their intimate relation with blood vessels of the CNS, as well as numerous immunity-related actions that these cells are capable of, imply that astrocytes should have a prominent role in neuroinflammatory disorders, such as multiple sclerosis (MS). The role of astrocytes in MS is rather ambiguous, as they have the capacity to both stimulate and restrain neuroinflammation and tissue destruction. In this paper we present some of the proved and the proposed functions of astrocytes in neuroinflammation and discuss the effect of MS therapeutics on astrocytes. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.",
journal = "Febs Letters",
title = "Astrocytes in the tempest of multiple sclerosis",
number = "23",
volume = "585",
pages = "3788",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1240"
}

Miljković, Đ., Timotijević, G. S.,& Mostarica-Stojković, M. B.. (2011). Astrocytes in the tempest of multiple sclerosis. in Febs Letters, 585(23).
https://hdl.handle.net/21.15107/rcub_ibiss_1240

Miljković Đ, Timotijević GS, Mostarica-Stojković MB. Astrocytes in the tempest of multiple sclerosis. in Febs Letters. 2011;585(23):null-3788.
https://hdl.handle.net/21.15107/rcub_ibiss_1240 .

Miljković, Đorđe, Timotijević, Gordana S, Mostarica-Stojković, Marija B, "Astrocytes in the tempest of multiple sclerosis" in Febs Letters, 585, no. 23 (2011),
https://hdl.handle.net/21.15107/rcub_ibiss_1240 .

TY  - JOUR
AU  - Stošić-Grujičić, Stanislava
AU  - Gruden-Movsesijan, Alisa
AU  - Radulović, Nataša
AU  - Mostarica-Stojković, Marija B
AU  - Milić, M
AU  - Sofronić-Milosavljević, Ljiljana
PY  - 2010
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1373
AB  - P>Trichinella spiralis is a helminth that provokes Th2 and anti-inflammatory type responses in an infected host. Our previous studies using Dark Agouti (DA) rats indicated that T. spiralis infection reduced experimental autoimmune encephalomyelitis (EAE) severity in rats. The aim of this study was to analyse the mechanisms underlying EAE suppression driven by T. spiralis infection. Reduced clinical and histological manifestations of the disease were accompanied by increased IL-4 and IL-10 production and decreased IFN-gamma and IL-17 production in draining lymph node cells. This indicates that T. spiralis infection successfully maintains a Th2 cytokine bias regardless of EAE induction. High IL-10 signifies parasite-induced anti-inflammatory and/or regulatory cell responses. Transfer of splenic T cell-enriched population of cells from T. spiralis-infected rats into EAE immunized rats caused amelioration of EAE and in some cases protection from disease development. This population of cells contained higher proportion of CD4+ CD25+ Foxp3+ regulatory cells and produced high level of IL-10 when compared with uninfected rats.
T2  - Parasite Immunology
T1  - Mechanisms of modulation of experimental autoimmune encephalomyelitis by chronic Trichinella spiralis infection in Dark Agouti rats
IS  - 6
VL  - 32
EP  - 459
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1373
ER  - 

@article{
author = "Stošić-Grujičić, Stanislava and Gruden-Movsesijan, Alisa and Radulović, Nataša and Mostarica-Stojković, Marija B and Milić, M and Sofronić-Milosavljević, Ljiljana",
year = "2010",
abstract = "P>Trichinella spiralis is a helminth that provokes Th2 and anti-inflammatory type responses in an infected host. Our previous studies using Dark Agouti (DA) rats indicated that T. spiralis infection reduced experimental autoimmune encephalomyelitis (EAE) severity in rats. The aim of this study was to analyse the mechanisms underlying EAE suppression driven by T. spiralis infection. Reduced clinical and histological manifestations of the disease were accompanied by increased IL-4 and IL-10 production and decreased IFN-gamma and IL-17 production in draining lymph node cells. This indicates that T. spiralis infection successfully maintains a Th2 cytokine bias regardless of EAE induction. High IL-10 signifies parasite-induced anti-inflammatory and/or regulatory cell responses. Transfer of splenic T cell-enriched population of cells from T. spiralis-infected rats into EAE immunized rats caused amelioration of EAE and in some cases protection from disease development. This population of cells contained higher proportion of CD4+ CD25+ Foxp3+ regulatory cells and produced high level of IL-10 when compared with uninfected rats.",
journal = "Parasite Immunology",
title = "Mechanisms of modulation of experimental autoimmune encephalomyelitis by chronic Trichinella spiralis infection in Dark Agouti rats",
number = "6",
volume = "32",
pages = "459",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1373"
}

Stošić-Grujičić, S., Gruden-Movsesijan, A., Radulović, N., Mostarica-Stojković, M. B., Milić, M.,& Sofronić-Milosavljević, L.. (2010). Mechanisms of modulation of experimental autoimmune encephalomyelitis by chronic Trichinella spiralis infection in Dark Agouti rats. in Parasite Immunology, 32(6).
https://hdl.handle.net/21.15107/rcub_ibiss_1373

Stošić-Grujičić S, Gruden-Movsesijan A, Radulović N, Mostarica-Stojković MB, Milić M, Sofronić-Milosavljević L. Mechanisms of modulation of experimental autoimmune encephalomyelitis by chronic Trichinella spiralis infection in Dark Agouti rats. in Parasite Immunology. 2010;32(6):null-459.
https://hdl.handle.net/21.15107/rcub_ibiss_1373 .

Stošić-Grujičić, Stanislava, Gruden-Movsesijan, Alisa, Radulović, Nataša, Mostarica-Stojković, Marija B, Milić, M, Sofronić-Milosavljević, Ljiljana, "Mechanisms of modulation of experimental autoimmune encephalomyelitis by chronic Trichinella spiralis infection in Dark Agouti rats" in Parasite Immunology, 32, no. 6 (2010),
https://hdl.handle.net/21.15107/rcub_ibiss_1373 .

TY  - JOUR
AU  - Lavrnja, Irena
AU  - Nedeljković, Nadezda N
AU  - Bjelobaba, Ivana
AU  - Savić, Danijela
AU  - Dačić, Sanja
AU  - Peković, Sanja
AU  - Rakić, Ljubisav
AU  - Mostarica-Stojković, Marija B
AU  - Stošić-Grujičić, Stanislava
AU  - Stojiljković, Mirjana B
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1474
AB  - The role of extracellular purines and purinoreceptors in the pathophysiology of different neurological disorders is the focus of rapidly expanding area of research. Ectonucleotidases are the enzymes with multiple roles in extracellular nucleotides metabolism and regulation of nucleotide-based intercellular signaling. The aim of present study was to investigate the changes in the ATP, ADP and AMP hydrolyzing activities after ribavirin treatment in spinal cord during experimental autoimmune encephalomyelitis (EAE). Our results demonstrate that ribavirin itself had no significant effect on ectoenzyme activities, when tested in vitro and in vivo on spinal cord crude membrane preparation of intact animals. We observed significant increase in ATP, ADP and AMP hydrolyzing activity in the spinal cord crude membrane preparation in EAE animals at 15 days post immunization compared to control animals. The increase was registered at 28 days post immunization, as well. At same time points, ribavirin treatment decreased ATP, ADP and AMP hydrolyzing activity compared to EAE animals. In addition, no significant changes 8 days post immunization was observed between EAE-induced and ribavirin- treated EAE animals and these levels were similar to control level. Thus, we suppose that ribavirin-induced alteration in ectonucleotidase activities is rather due to its suppression of inflammation, than to its direct action on ATP, ADP and AMP hydrolysis.
T2  - General Physiology and Biophysics
T1  - Ribavirin administration alters ectonudeotidase activities in experimental autoimmune encephalomyelitis
IS  - null
VL  - 28
EP  - 76
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1474
ER  - 

@article{
author = "Lavrnja, Irena and Nedeljković, Nadezda N and Bjelobaba, Ivana and Savić, Danijela and Dačić, Sanja and Peković, Sanja and Rakić, Ljubisav and Mostarica-Stojković, Marija B and Stošić-Grujičić, Stanislava and Stojiljković, Mirjana B",
year = "2009",
abstract = "The role of extracellular purines and purinoreceptors in the pathophysiology of different neurological disorders is the focus of rapidly expanding area of research. Ectonucleotidases are the enzymes with multiple roles in extracellular nucleotides metabolism and regulation of nucleotide-based intercellular signaling. The aim of present study was to investigate the changes in the ATP, ADP and AMP hydrolyzing activities after ribavirin treatment in spinal cord during experimental autoimmune encephalomyelitis (EAE). Our results demonstrate that ribavirin itself had no significant effect on ectoenzyme activities, when tested in vitro and in vivo on spinal cord crude membrane preparation of intact animals. We observed significant increase in ATP, ADP and AMP hydrolyzing activity in the spinal cord crude membrane preparation in EAE animals at 15 days post immunization compared to control animals. The increase was registered at 28 days post immunization, as well. At same time points, ribavirin treatment decreased ATP, ADP and AMP hydrolyzing activity compared to EAE animals. In addition, no significant changes 8 days post immunization was observed between EAE-induced and ribavirin- treated EAE animals and these levels were similar to control level. Thus, we suppose that ribavirin-induced alteration in ectonucleotidase activities is rather due to its suppression of inflammation, than to its direct action on ATP, ADP and AMP hydrolysis.",
journal = "General Physiology and Biophysics",
title = "Ribavirin administration alters ectonudeotidase activities in experimental autoimmune encephalomyelitis",
number = "null",
volume = "28",
pages = "76",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1474"
}

Lavrnja, I., Nedeljković, N. N., Bjelobaba, I., Savić, D., Dačić, S., Peković, S., Rakić, L., Mostarica-Stojković, M. B., Stošić-Grujičić, S.,& Stojiljković, M. B.. (2009). Ribavirin administration alters ectonudeotidase activities in experimental autoimmune encephalomyelitis. in General Physiology and Biophysics, 28(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1474

Lavrnja I, Nedeljković NN, Bjelobaba I, Savić D, Dačić S, Peković S, Rakić L, Mostarica-Stojković MB, Stošić-Grujičić S, Stojiljković MB. Ribavirin administration alters ectonudeotidase activities in experimental autoimmune encephalomyelitis. in General Physiology and Biophysics. 2009;28(null):null-76.
https://hdl.handle.net/21.15107/rcub_ibiss_1474 .

Lavrnja, Irena, Nedeljković, Nadezda N, Bjelobaba, Ivana, Savić, Danijela, Dačić, Sanja, Peković, Sanja, Rakić, Ljubisav, Mostarica-Stojković, Marija B, Stošić-Grujičić, Stanislava, Stojiljković, Mirjana B, "Ribavirin administration alters ectonudeotidase activities in experimental autoimmune encephalomyelitis" in General Physiology and Biophysics, 28, no. null (2009),
https://hdl.handle.net/21.15107/rcub_ibiss_1474 .

TY  - JOUR
AU  - Momčilović, Miljana
AU  - Miljković, Đorđe
AU  - Mostarica-Stojković, Marija B
PY  - 2009
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/216
AB  - Brain endothelial cells (BEC) are the major constituents of the blood-brain barrier (BBB), the structure that controls entrance of immune cells into CNS parenchyma. Our aim was to investigate the influence of BEC on production of IL-17 and IFN-γ-cytokines that are important for CNS inflammation. To that end, co-cultivations of the bEnd.3 brain endothelial cell line and lymph node cells (LNC) were performed, and gene expression and production of IL-17 and IFN-γ were determined. It was found that bEnd.3 cells inhibited expression and production of IFN-γ, but not of IL-17. Additionally, bEnd.3 cells also reduced production of the major IFN-γ-promoting cytokine - IL-12 - in LNC. The observed variation in modulation of pro-inflammatory cytokines by BEC could be of importance for the understanding of CNS inflammation.
AB  - Ćelije moždanog endotela su osnovni elementi građe krvno moždane barijere, strukture koja kontroliše ulazak ćelija imunskog sistema u parenhim CNS. Naš cilj je bio da se ispita uticaj ovih ćelija na produkciju interferona-gama i interleukina 17, kao ključnih proinflamatornih citokina u neuroinflamaciji. Zbog toga smo vršili ko-kultivaciju bEnd.3 linije moždanog endotela i ćelija limfnog čvora, i to u prisustvu ili odsustvu direktnog kontakta među navedenim populacijama, i određivali ekspresiju gena i produkciju navedenih citokina. Pokazalo se da bEnd.3 ćelije potentno inhibiraju produkciju interferona-gama, ali ne i interleukina-17. Takođe, merili smo i produkciju interleukina-12, glavnog stimulatornog citokina za produkciju interferona-gama, i pokazali da je i njegova produkcija smanjena u ko-kultivaciji bEnd.3 ćelija i ćelija limfnog čvora. Zapažena različitost u delovanju ćelija moždanog Endotela na dva osnovna proinflamatorna citokina je od Značaja za razumevanje kompleksnog procesa regulacije inflamacije u CNS.
T2  - Archives of Biological Sciences
T1  - Ćelije mišjeg moždanog endotela ostvaruju različit uticaj na produkciju interferona-γ i interleukina-17 in vitro
T1  - Murine brain endothelial cells differently modulate interferon-γ and interleukin-17 production in vitro
IS  - 1
VL  - 61
DO  - 10.2298/ABS0901029M
SP  - 29
EP  - 36
ER  - 

@article{
author = "Momčilović, Miljana and Miljković, Đorđe and Mostarica-Stojković, Marija B",
year = "2009, 2009",
abstract = "Brain endothelial cells (BEC) are the major constituents of the blood-brain barrier (BBB), the structure that controls entrance of immune cells into CNS parenchyma. Our aim was to investigate the influence of BEC on production of IL-17 and IFN-γ-cytokines that are important for CNS inflammation. To that end, co-cultivations of the bEnd.3 brain endothelial cell line and lymph node cells (LNC) were performed, and gene expression and production of IL-17 and IFN-γ were determined. It was found that bEnd.3 cells inhibited expression and production of IFN-γ, but not of IL-17. Additionally, bEnd.3 cells also reduced production of the major IFN-γ-promoting cytokine - IL-12 - in LNC. The observed variation in modulation of pro-inflammatory cytokines by BEC could be of importance for the understanding of CNS inflammation., Ćelije moždanog endotela su osnovni elementi građe krvno moždane barijere, strukture koja kontroliše ulazak ćelija imunskog sistema u parenhim CNS. Naš cilj je bio da se ispita uticaj ovih ćelija na produkciju interferona-gama i interleukina 17, kao ključnih proinflamatornih citokina u neuroinflamaciji. Zbog toga smo vršili ko-kultivaciju bEnd.3 linije moždanog endotela i ćelija limfnog čvora, i to u prisustvu ili odsustvu direktnog kontakta među navedenim populacijama, i određivali ekspresiju gena i produkciju navedenih citokina. Pokazalo se da bEnd.3 ćelije potentno inhibiraju produkciju interferona-gama, ali ne i interleukina-17. Takođe, merili smo i produkciju interleukina-12, glavnog stimulatornog citokina za produkciju interferona-gama, i pokazali da je i njegova produkcija smanjena u ko-kultivaciji bEnd.3 ćelija i ćelija limfnog čvora. Zapažena različitost u delovanju ćelija moždanog Endotela na dva osnovna proinflamatorna citokina je od Značaja za razumevanje kompleksnog procesa regulacije inflamacije u CNS.",
journal = "Archives of Biological Sciences",
title = "Ćelije mišjeg moždanog endotela ostvaruju različit uticaj na produkciju interferona-γ i interleukina-17 in vitro, Murine brain endothelial cells differently modulate interferon-γ and interleukin-17 production in vitro",
number = "1",
volume = "61",
doi = "10.2298/ABS0901029M",
pages = "29-36"
}

Momčilović, M., Miljković, Đ.,& Mostarica-Stojković, M. B.. (2009). Ćelije mišjeg moždanog endotela ostvaruju različit uticaj na produkciju interferona-γ i interleukina-17 in vitro. in Archives of Biological Sciences, 61(1), 29-36.
https://doi.org/10.2298/ABS0901029M

Momčilović M, Miljković Đ, Mostarica-Stojković MB. Ćelije mišjeg moždanog endotela ostvaruju različit uticaj na produkciju interferona-γ i interleukina-17 in vitro. in Archives of Biological Sciences. 2009;61(1):29-36.
doi:10.2298/ABS0901029M .

Momčilović, Miljana, Miljković, Đorđe, Mostarica-Stojković, Marija B, "Ćelije mišjeg moždanog endotela ostvaruju različit uticaj na produkciju interferona-γ i interleukina-17 in vitro" in Archives of Biological Sciences, 61, no. 1 (2009):29-36,
https://doi.org/10.2298/ABS0901029M . .

TY  - JOUR
AU  - Đukanović, Ljubica D
AU  - Lezaić, Visnja D
AU  - Miljković, Đorđe
AU  - Momčilović, Miljana
AU  - Bukvić, Danica
AU  - Marić, Ivko
AU  - Miljković, Zeljka
AU  - Marinković, Jelena M
AU  - Mostarica-Stojković, Marija B
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1485
AB  - Background/Aim: The aim of this study was to compare plasma and urine transforming growth factor-beta(1) (TGF-beta(1)) levels in patients with different stages of Balkan endemic nephropathy (BEN) with those in patients with primary glomerulonephritis (GN) and healthy controls. Methods: The study involved 47 patients with BEN (30 with manifest BEN and 17 in the early stage of BEN), 12 patients with GN and 10 healthy controls. Plasma and urine TGF-beta(1) was assayed by enzyme-linked immunosorbent assay. Results: The median plasma TGF-beta(1) levels differed nonsignificantly between the groups (4,908-6,442 pg/ml), but individual plasma TGF-beta(1) levels in BEN patients exhibited the highest dispersion. Median urinary TGF-beta(1) excretion (pg/mg creatinine) was significantly higher in patient groups (manifest BEN: 203, early-stage BEN: 341, GN: 775) than in healthy controls (42). No correlation was found between plasma and urine TGF-beta(1) levels or between plasma TGF-beta(1) levels and creatinine clearance for any of the examined groups. Conclusion: Plasma TGF-beta(1) levels in BEN patients extended over the widest range, but no significant differences were found between the median values for the groups. Median urinary TGF-beta(1) excretion was significantly higher in patients with BEN and GN than in healthy controls. Copyright (C) 2009 S. Karger AG, Basel
T2  - Nephron Clinical Practice
T1  - Transforming Growth Factor-beta(1) in Balkan Endemic Nephropathy
IS  - 2
VL  - 111
EP  - C132
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1485
ER  - 

@article{
author = "Đukanović, Ljubica D and Lezaić, Visnja D and Miljković, Đorđe and Momčilović, Miljana and Bukvić, Danica and Marić, Ivko and Miljković, Zeljka and Marinković, Jelena M and Mostarica-Stojković, Marija B",
year = "2009",
abstract = "Background/Aim: The aim of this study was to compare plasma and urine transforming growth factor-beta(1) (TGF-beta(1)) levels in patients with different stages of Balkan endemic nephropathy (BEN) with those in patients with primary glomerulonephritis (GN) and healthy controls. Methods: The study involved 47 patients with BEN (30 with manifest BEN and 17 in the early stage of BEN), 12 patients with GN and 10 healthy controls. Plasma and urine TGF-beta(1) was assayed by enzyme-linked immunosorbent assay. Results: The median plasma TGF-beta(1) levels differed nonsignificantly between the groups (4,908-6,442 pg/ml), but individual plasma TGF-beta(1) levels in BEN patients exhibited the highest dispersion. Median urinary TGF-beta(1) excretion (pg/mg creatinine) was significantly higher in patient groups (manifest BEN: 203, early-stage BEN: 341, GN: 775) than in healthy controls (42). No correlation was found between plasma and urine TGF-beta(1) levels or between plasma TGF-beta(1) levels and creatinine clearance for any of the examined groups. Conclusion: Plasma TGF-beta(1) levels in BEN patients extended over the widest range, but no significant differences were found between the median values for the groups. Median urinary TGF-beta(1) excretion was significantly higher in patients with BEN and GN than in healthy controls. Copyright (C) 2009 S. Karger AG, Basel",
journal = "Nephron Clinical Practice",
title = "Transforming Growth Factor-beta(1) in Balkan Endemic Nephropathy",
number = "2",
volume = "111",
pages = "C132",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1485"
}

Đukanović, L. D., Lezaić, V. D., Miljković, Đ., Momčilović, M., Bukvić, D., Marić, I., Miljković, Z., Marinković, J. M.,& Mostarica-Stojković, M. B.. (2009). Transforming Growth Factor-beta(1) in Balkan Endemic Nephropathy. in Nephron Clinical Practice, 111(2).
https://hdl.handle.net/21.15107/rcub_ibiss_1485

Đukanović LD, Lezaić VD, Miljković Đ, Momčilović M, Bukvić D, Marić I, Miljković Z, Marinković JM, Mostarica-Stojković MB. Transforming Growth Factor-beta(1) in Balkan Endemic Nephropathy. in Nephron Clinical Practice. 2009;111(2):null-C132.
https://hdl.handle.net/21.15107/rcub_ibiss_1485 .

Đukanović, Ljubica D, Lezaić, Visnja D, Miljković, Đorđe, Momčilović, Miljana, Bukvić, Danica, Marić, Ivko, Miljković, Zeljka, Marinković, Jelena M, Mostarica-Stojković, Marija B, "Transforming Growth Factor-beta(1) in Balkan Endemic Nephropathy" in Nephron Clinical Practice, 111, no. 2 (2009),
https://hdl.handle.net/21.15107/rcub_ibiss_1485 .

TY  - JOUR
AU  - Miljković, Đorđe
AU  - Dekanski, Dragana P.
AU  - Miljković, Zeljka
AU  - Momčilović, Miljana
AU  - Mostarica-Stojković, Marija B
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1447
AB  - Background & aims: Experimental autoimmune encephalomyelitis (EAE) is an animal model of CNS inflammatory and demyelinating disease multiple sclerosis. Mediterranean diet, rich in olive products is associated with lower incidence of multiple sclerosis in South European population. Therefore, the influence of dry olive leaf extract (DOLE) on EAE course was investigated. Methods: Spinal cord homogenate and complete Freund's adjuvant were used for the induction of EAE in Dark Agouti rats. DOLE was applied intragastrically once per day, starting from the day of the immunization. Real time PCR and ELISA were used for the determination of IFN-gamma and IL-17 gene expression and production, respectively. Results: DOLE reduced various parameters of EAE severity in DA rats, including cumulative disease index, maximal clinical score and disease duration. Also, DOLE decreased cellularity of the draining lymph nodes and production of IFN-gamma and IL-17 by the cells infiltrating spinal cord of EAE rats. Conclusions: The results presented in this paper strongly suggest that DOLE-enriched diet has a beneficial effect in EAE in rats. Further studies in humans are required in order to investigate if DOLE could be a useful supplementary dietetic for the patients suffering from multiple sclerosis and other neuroinflammatory disorders. (C) 2009 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.
T2  - Clinical Nutrition
T1  - Dry olive leaf extract ameliorates experimental autoimmune encephalomyelitis
IS  - 3
VL  - 28
EP  - 350
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1447
ER  - 

@article{
author = "Miljković, Đorđe and Dekanski, Dragana P. and Miljković, Zeljka and Momčilović, Miljana and Mostarica-Stojković, Marija B",
year = "2009",
abstract = "Background & aims: Experimental autoimmune encephalomyelitis (EAE) is an animal model of CNS inflammatory and demyelinating disease multiple sclerosis. Mediterranean diet, rich in olive products is associated with lower incidence of multiple sclerosis in South European population. Therefore, the influence of dry olive leaf extract (DOLE) on EAE course was investigated. Methods: Spinal cord homogenate and complete Freund's adjuvant were used for the induction of EAE in Dark Agouti rats. DOLE was applied intragastrically once per day, starting from the day of the immunization. Real time PCR and ELISA were used for the determination of IFN-gamma and IL-17 gene expression and production, respectively. Results: DOLE reduced various parameters of EAE severity in DA rats, including cumulative disease index, maximal clinical score and disease duration. Also, DOLE decreased cellularity of the draining lymph nodes and production of IFN-gamma and IL-17 by the cells infiltrating spinal cord of EAE rats. Conclusions: The results presented in this paper strongly suggest that DOLE-enriched diet has a beneficial effect in EAE in rats. Further studies in humans are required in order to investigate if DOLE could be a useful supplementary dietetic for the patients suffering from multiple sclerosis and other neuroinflammatory disorders. (C) 2009 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.",
journal = "Clinical Nutrition",
title = "Dry olive leaf extract ameliorates experimental autoimmune encephalomyelitis",
number = "3",
volume = "28",
pages = "350",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1447"
}

Miljković, Đ., Dekanski, D. P., Miljković, Z., Momčilović, M.,& Mostarica-Stojković, M. B.. (2009). Dry olive leaf extract ameliorates experimental autoimmune encephalomyelitis. in Clinical Nutrition, 28(3).
https://hdl.handle.net/21.15107/rcub_ibiss_1447

Miljković Đ, Dekanski DP, Miljković Z, Momčilović M, Mostarica-Stojković MB. Dry olive leaf extract ameliorates experimental autoimmune encephalomyelitis. in Clinical Nutrition. 2009;28(3):null-350.
https://hdl.handle.net/21.15107/rcub_ibiss_1447 .

Miljković, Đorđe, Dekanski, Dragana P., Miljković, Zeljka, Momčilović, Miljana, Mostarica-Stojković, Marija B, "Dry olive leaf extract ameliorates experimental autoimmune encephalomyelitis" in Clinical Nutrition, 28, no. 3 (2009),
https://hdl.handle.net/21.15107/rcub_ibiss_1447 .

TY  - JOUR
AU  - Marković, Milos
AU  - Miljković, Đorđe
AU  - Momčilović, Miljana
AU  - Popadić, Dusan M
AU  - Miljković, Zeljka
AU  - Savić, Emina
AU  - Ramić, Zorica D.
AU  - Mostarica-Stojković, Marija B
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1129
AB  - Albino Oxford (AO) rats are resistant to induction of experimental autoimmune encephalomyelitis (EAE), in contrast to susceptible Dark Agouti (DA) rats. We have previously shown that draining lymph node cells (DLNC) obtained from immunized DA rats before the onset of the clinical disease produced more interferon (IFN)-gamma and interleukin (IL)-17 (signature cytokines of T(H)1 and T(H)17 responses, respectively) compared to DLNC from AO rats. In this study, we extend our analysis to entire induction phase of EAE with the emphasis on the T(H)1 and T(H)17-inducing cytokines. As a result, we show that throughout the inductive phase of the disease DLNC of DA rats, not only expressed higher levels of IFN-gamma and IL-17, but also of T(H)1-inducing cytokine-IL-12. As for T(H)17-inducing cytokines, DLNC of DA rats expressed more mRNA for p19, specific subunit of IL-23, but the expression of transforming growth factor (TGF)-beta in both strains was similar. Interestingly, the analysis of IL-6 expression revealed striking difference: while all DA DLNC were positive for IL-6 mRNA, cells from none of AO rats expressed detectable levels of mRNA for this cytokine. Taken together, our data suggest that the differential regulation of production of T(H)1 and T(H)17 cytokines, and IL-6 in particular, during the induction phase of disease could be responsible for the discrepancy in susceptibility to EAE between these two rat strains. (C) 2009 Elsevier Ltd. All rights reserved.
T2  - Molecular Immunology
T1  - Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles
IS  - 1
VL  - 47
SP  - 243
EP  - 146
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1129
ER  - 

@article{
author = "Marković, Milos and Miljković, Đorđe and Momčilović, Miljana and Popadić, Dusan M and Miljković, Zeljka and Savić, Emina and Ramić, Zorica D. and Mostarica-Stojković, Marija B",
year = "2009",
abstract = "Albino Oxford (AO) rats are resistant to induction of experimental autoimmune encephalomyelitis (EAE), in contrast to susceptible Dark Agouti (DA) rats. We have previously shown that draining lymph node cells (DLNC) obtained from immunized DA rats before the onset of the clinical disease produced more interferon (IFN)-gamma and interleukin (IL)-17 (signature cytokines of T(H)1 and T(H)17 responses, respectively) compared to DLNC from AO rats. In this study, we extend our analysis to entire induction phase of EAE with the emphasis on the T(H)1 and T(H)17-inducing cytokines. As a result, we show that throughout the inductive phase of the disease DLNC of DA rats, not only expressed higher levels of IFN-gamma and IL-17, but also of T(H)1-inducing cytokine-IL-12. As for T(H)17-inducing cytokines, DLNC of DA rats expressed more mRNA for p19, specific subunit of IL-23, but the expression of transforming growth factor (TGF)-beta in both strains was similar. Interestingly, the analysis of IL-6 expression revealed striking difference: while all DA DLNC were positive for IL-6 mRNA, cells from none of AO rats expressed detectable levels of mRNA for this cytokine. Taken together, our data suggest that the differential regulation of production of T(H)1 and T(H)17 cytokines, and IL-6 in particular, during the induction phase of disease could be responsible for the discrepancy in susceptibility to EAE between these two rat strains. (C) 2009 Elsevier Ltd. All rights reserved.",
journal = "Molecular Immunology",
title = "Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles",
number = "1",
volume = "47",
pages = "243-146",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1129"
}

Marković, M., Miljković, Đ., Momčilović, M., Popadić, D. M., Miljković, Z., Savić, E., Ramić, Z. D.,& Mostarica-Stojković, M. B.. (2009). Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles. in Molecular Immunology, 47(1), 243-146.
https://hdl.handle.net/21.15107/rcub_ibiss_1129

Marković M, Miljković Đ, Momčilović M, Popadić DM, Miljković Z, Savić E, Ramić ZD, Mostarica-Stojković MB. Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles. in Molecular Immunology. 2009;47(1):243-146.
https://hdl.handle.net/21.15107/rcub_ibiss_1129 .

Marković, Milos, Miljković, Đorđe, Momčilović, Miljana, Popadić, Dusan M, Miljković, Zeljka, Savić, Emina, Ramić, Zorica D., Mostarica-Stojković, Marija B, "Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles" in Molecular Immunology, 47, no. 1 (2009):243-146,
https://hdl.handle.net/21.15107/rcub_ibiss_1129 .

TY  - JOUR
AU  - Miljković, Zeljka
AU  - Momčilović, Miljana
AU  - Miljković, Đorđe
AU  - Mostarica-Stojković, Marija B
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1417
AB  - Background: Glucocorticoids have been shown to be effective in the treatment of autoimmune diseases of the CNS such as multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). However, the mechanisms and the site of glucocorticoids' actions are still not completely defined. The aim of this study was to investigate the in vivo effect of the synthetic glucocorticoid methylprednisolone (MP) on the expression and production of proinflammatory cytokines interferon (IFN)-gamma and interleukin (IL)-17 by cells infiltrating CNS tissue. Methods: Experimental autoimmune encephalomyelitis was induced in Dark Agouti (DA) rats by immunization with rat spinal cord homogenate mixed with adjuvants. Commencing on the day when the first EAE signs appeared, DA rats were injected daily for 3 days with MP and/or RU486, an antagonist of glucocorticoid receptor. Cytokine production and gene expression in CNS-infiltrating cells and lymph node cells were measured using ELISA and real time PCR, respectively. Results: Treatment of rats with MP ameliorated EAE, and the animals recovered without relapses. Further, MP inhibited IFN-gamma and IL-17 expression and production in cells isolated from the CNS of DA rats with EAE after the last injection of MP. The observed effect of MP in vivo treatment was not mediated through depletion of CD4(+) T cells among CNS infiltrating cells, or through induction of their apoptosis within the CNS. Finally, the glucocorticoid receptor-antagonist RU486 prevented the inhibitory effect of MP on IFN-gamma and IL-17 production both in vitro and in vivo, thus indicating that the observed effects of MP were mediated through glucocorticoid receptor-dependent mechanisms. Conclusion: Taken together, these results demonstrate that amelioration of EAE by exogenous glucocorticoids might be, at least partly, ascribed to the limitation of effector cell functions in the target tissue.
T2  - Journal of Neuroinflammation
T1  - Methylprednisolone inhibits IFN-gamma and IL-17 expression and production by cells infiltrating central nervous system in experimental autoimmune encephalomyelitis
IS  - null
VL  - 6
EP  - na
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1417
ER  - 

@article{
author = "Miljković, Zeljka and Momčilović, Miljana and Miljković, Đorđe and Mostarica-Stojković, Marija B",
year = "2009",
abstract = "Background: Glucocorticoids have been shown to be effective in the treatment of autoimmune diseases of the CNS such as multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). However, the mechanisms and the site of glucocorticoids' actions are still not completely defined. The aim of this study was to investigate the in vivo effect of the synthetic glucocorticoid methylprednisolone (MP) on the expression and production of proinflammatory cytokines interferon (IFN)-gamma and interleukin (IL)-17 by cells infiltrating CNS tissue. Methods: Experimental autoimmune encephalomyelitis was induced in Dark Agouti (DA) rats by immunization with rat spinal cord homogenate mixed with adjuvants. Commencing on the day when the first EAE signs appeared, DA rats were injected daily for 3 days with MP and/or RU486, an antagonist of glucocorticoid receptor. Cytokine production and gene expression in CNS-infiltrating cells and lymph node cells were measured using ELISA and real time PCR, respectively. Results: Treatment of rats with MP ameliorated EAE, and the animals recovered without relapses. Further, MP inhibited IFN-gamma and IL-17 expression and production in cells isolated from the CNS of DA rats with EAE after the last injection of MP. The observed effect of MP in vivo treatment was not mediated through depletion of CD4(+) T cells among CNS infiltrating cells, or through induction of their apoptosis within the CNS. Finally, the glucocorticoid receptor-antagonist RU486 prevented the inhibitory effect of MP on IFN-gamma and IL-17 production both in vitro and in vivo, thus indicating that the observed effects of MP were mediated through glucocorticoid receptor-dependent mechanisms. Conclusion: Taken together, these results demonstrate that amelioration of EAE by exogenous glucocorticoids might be, at least partly, ascribed to the limitation of effector cell functions in the target tissue.",
journal = "Journal of Neuroinflammation",
title = "Methylprednisolone inhibits IFN-gamma and IL-17 expression and production by cells infiltrating central nervous system in experimental autoimmune encephalomyelitis",
number = "null",
volume = "6",
pages = "na",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1417"
}

Miljković, Z., Momčilović, M., Miljković, Đ.,& Mostarica-Stojković, M. B.. (2009). Methylprednisolone inhibits IFN-gamma and IL-17 expression and production by cells infiltrating central nervous system in experimental autoimmune encephalomyelitis. in Journal of Neuroinflammation, 6(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1417

Miljković Z, Momčilović M, Miljković Đ, Mostarica-Stojković MB. Methylprednisolone inhibits IFN-gamma and IL-17 expression and production by cells infiltrating central nervous system in experimental autoimmune encephalomyelitis. in Journal of Neuroinflammation. 2009;6(null):null-na.
https://hdl.handle.net/21.15107/rcub_ibiss_1417 .

Miljković, Zeljka, Momčilović, Miljana, Miljković, Đorđe, Mostarica-Stojković, Marija B, "Methylprednisolone inhibits IFN-gamma and IL-17 expression and production by cells infiltrating central nervous system in experimental autoimmune encephalomyelitis" in Journal of Neuroinflammation, 6, no. null (2009),
https://hdl.handle.net/21.15107/rcub_ibiss_1417 .

TY  - JOUR
AU  - Dujmović, Irena
AU  - Pekmezović, Tatjana D
AU  - Obrenović, Radmila Z
AU  - Nikolić, Aleksandra L.
AU  - Spasić, Mihajlo
AU  - Mostarica-Stojković, Marija B
AU  - Drulović, Jelena S
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1442
AB  - Background: Peroxynitrite was hypothesized to be involved in the pathogenesis of multiple sclerosis (MS) through its various neurotoxic effects. Uric acid (UA) was shown to be a strong peroxynitrite scavenger. Methods: We analyzed cerebrospinal fluid (CSF) and serum UA concentrations in 30 MS patients and 20 controls with non-inflammatory neurological diseases (NIND) and correlated these findings with demographic and clinical characteristics of MS patients. Disease activity was assessed by brain magnetic resonance imaging (MRI) and the CSF/serum albumin quotient as an indicator of the state of blood-brain-barrier (BBB). Results: Serum UA concentrations were found to be significantly lower in MS patients compared with controls (p=0.019). CSF UA concentrations were lower in MS patients as compared to controls, as well as in patients with active MS (clinical and/or MRI activity) in comparison to patients with inactive MS or controls, but these differences were not statistically significant. Significant correlation was found between CSF and serum UA concentrations (p=0.016) in MS patients, but not in controls; and between CSF UA concentrations and the CSF/serum albumin quotient in MS patients (p=0.043), but not in controls. Conclusions: Our results support the significance of UA in the pathogenesis of MS. Decreased serum UA concentrations in MS patients might be due to both intrinsically reduced antioxidant capacity and increased UA consumption in MS. CSF UA concentrations may not be a reliable marker of disease activity in MS since its concentration is dependent on leakage of UA molecules from serum through the damaged BBB and the balance between consumption/production within the central nervous system (CNS). Clin Chem Lab Med 2009; 47: 848-53.
T2  - Clinical Chemistry and Laboratory Medicine
T1  - Cerebrospinal fluid and serum uric acid levels in patients with multiple sclerosis
IS  - 7
VL  - 47
EP  - 853
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1442
ER  - 

@article{
author = "Dujmović, Irena and Pekmezović, Tatjana D and Obrenović, Radmila Z and Nikolić, Aleksandra L. and Spasić, Mihajlo and Mostarica-Stojković, Marija B and Drulović, Jelena S",
year = "2009",
abstract = "Background: Peroxynitrite was hypothesized to be involved in the pathogenesis of multiple sclerosis (MS) through its various neurotoxic effects. Uric acid (UA) was shown to be a strong peroxynitrite scavenger. Methods: We analyzed cerebrospinal fluid (CSF) and serum UA concentrations in 30 MS patients and 20 controls with non-inflammatory neurological diseases (NIND) and correlated these findings with demographic and clinical characteristics of MS patients. Disease activity was assessed by brain magnetic resonance imaging (MRI) and the CSF/serum albumin quotient as an indicator of the state of blood-brain-barrier (BBB). Results: Serum UA concentrations were found to be significantly lower in MS patients compared with controls (p=0.019). CSF UA concentrations were lower in MS patients as compared to controls, as well as in patients with active MS (clinical and/or MRI activity) in comparison to patients with inactive MS or controls, but these differences were not statistically significant. Significant correlation was found between CSF and serum UA concentrations (p=0.016) in MS patients, but not in controls; and between CSF UA concentrations and the CSF/serum albumin quotient in MS patients (p=0.043), but not in controls. Conclusions: Our results support the significance of UA in the pathogenesis of MS. Decreased serum UA concentrations in MS patients might be due to both intrinsically reduced antioxidant capacity and increased UA consumption in MS. CSF UA concentrations may not be a reliable marker of disease activity in MS since its concentration is dependent on leakage of UA molecules from serum through the damaged BBB and the balance between consumption/production within the central nervous system (CNS). Clin Chem Lab Med 2009; 47: 848-53.",
journal = "Clinical Chemistry and Laboratory Medicine",
title = "Cerebrospinal fluid and serum uric acid levels in patients with multiple sclerosis",
number = "7",
volume = "47",
pages = "853",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1442"
}

Dujmović, I., Pekmezović, T. D., Obrenović, R. Z., Nikolić, A. L., Spasić, M., Mostarica-Stojković, M. B.,& Drulović, J. S.. (2009). Cerebrospinal fluid and serum uric acid levels in patients with multiple sclerosis. in Clinical Chemistry and Laboratory Medicine, 47(7).
https://hdl.handle.net/21.15107/rcub_ibiss_1442

Dujmović I, Pekmezović TD, Obrenović RZ, Nikolić AL, Spasić M, Mostarica-Stojković MB, Drulović JS. Cerebrospinal fluid and serum uric acid levels in patients with multiple sclerosis. in Clinical Chemistry and Laboratory Medicine. 2009;47(7):null-853.
https://hdl.handle.net/21.15107/rcub_ibiss_1442 .

Dujmović, Irena, Pekmezović, Tatjana D, Obrenović, Radmila Z, Nikolić, Aleksandra L., Spasić, Mihajlo, Mostarica-Stojković, Marija B, Drulović, Jelena S, "Cerebrospinal fluid and serum uric acid levels in patients with multiple sclerosis" in Clinical Chemistry and Laboratory Medicine, 47, no. 7 (2009),
https://hdl.handle.net/21.15107/rcub_ibiss_1442 .

TY  - JOUR
AU  - Lavrnja, Irena
AU  - Bjelobaba, Ivana
AU  - Stojiljković, Mirjana B
AU  - Peković, Sanja
AU  - Mostarica-Stojković, Marija B
AU  - Stošić-Grujičić, Stanislava
AU  - Nedeljković, Nadezda N
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1436
AB  - The aim of the present study was to analyze the activities of extracellular purine metabolizing enzymes, CD39 (apyrase, EC 3.6.1.5) and CD73 (ecto-5' nucleotidase, EC 3.1.3.5) in experimental autoimmune encephalomyelitis (EAE). The levels of ATP, ADP and AMP hydrolysis were analyzed in the blood serum and in the rat spinal cord plasma membrane preparation 8, 15 and 25 days after induction of EAE. The animals were divided in three groups: control (saline), CFA (adjuvant-only) and EAE (CFA and homogenate of spinal cords). Eight days after immunization, ATP, ADP and AMP hydrolysis in the blood serum and spinal cord membrane preparations were unaffected in EAE compared to both, control and CFA group. In the peak of disease, ATP, ADP and AMP hydrolysis in EAE group showed significant decrease in the blood serum and prominent increase in the spinal cord membrane preparation compared to CFA and control group. At the end of illness, as judged by disappearance of clinical manifestation of EAE, ATP, ADP and AMP hydrolysis, although closer to CFA levels, were still significantly different in respect to the CFA group. Modulation of ATP, ADP and AMP hydrolysis suggests that they operate during EAE and might represent the basis of novel therapeutic strategies in immune-mediated diseases, such as MS. (C) 2009 Elsevier Ltd. All rights reserved.
T2  - Neurochemistry International
T1  - Time-course changes in ectonucleotidase activities during experimental autoimmune encephalomyelitis
IS  - 4
VL  - 55
EP  - 198
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1436
ER  - 

@article{
author = "Lavrnja, Irena and Bjelobaba, Ivana and Stojiljković, Mirjana B and Peković, Sanja and Mostarica-Stojković, Marija B and Stošić-Grujičić, Stanislava and Nedeljković, Nadezda N",
year = "2009",
abstract = "The aim of the present study was to analyze the activities of extracellular purine metabolizing enzymes, CD39 (apyrase, EC 3.6.1.5) and CD73 (ecto-5' nucleotidase, EC 3.1.3.5) in experimental autoimmune encephalomyelitis (EAE). The levels of ATP, ADP and AMP hydrolysis were analyzed in the blood serum and in the rat spinal cord plasma membrane preparation 8, 15 and 25 days after induction of EAE. The animals were divided in three groups: control (saline), CFA (adjuvant-only) and EAE (CFA and homogenate of spinal cords). Eight days after immunization, ATP, ADP and AMP hydrolysis in the blood serum and spinal cord membrane preparations were unaffected in EAE compared to both, control and CFA group. In the peak of disease, ATP, ADP and AMP hydrolysis in EAE group showed significant decrease in the blood serum and prominent increase in the spinal cord membrane preparation compared to CFA and control group. At the end of illness, as judged by disappearance of clinical manifestation of EAE, ATP, ADP and AMP hydrolysis, although closer to CFA levels, were still significantly different in respect to the CFA group. Modulation of ATP, ADP and AMP hydrolysis suggests that they operate during EAE and might represent the basis of novel therapeutic strategies in immune-mediated diseases, such as MS. (C) 2009 Elsevier Ltd. All rights reserved.",
journal = "Neurochemistry International",
title = "Time-course changes in ectonucleotidase activities during experimental autoimmune encephalomyelitis",
number = "4",
volume = "55",
pages = "198",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1436"
}

Lavrnja, I., Bjelobaba, I., Stojiljković, M. B., Peković, S., Mostarica-Stojković, M. B., Stošić-Grujičić, S.,& Nedeljković, N. N.. (2009). Time-course changes in ectonucleotidase activities during experimental autoimmune encephalomyelitis. in Neurochemistry International, 55(4).
https://hdl.handle.net/21.15107/rcub_ibiss_1436

Lavrnja I, Bjelobaba I, Stojiljković MB, Peković S, Mostarica-Stojković MB, Stošić-Grujičić S, Nedeljković NN. Time-course changes in ectonucleotidase activities during experimental autoimmune encephalomyelitis. in Neurochemistry International. 2009;55(4):null-198.
https://hdl.handle.net/21.15107/rcub_ibiss_1436 .

Lavrnja, Irena, Bjelobaba, Ivana, Stojiljković, Mirjana B, Peković, Sanja, Mostarica-Stojković, Marija B, Stošić-Grujičić, Stanislava, Nedeljković, Nadezda N, "Time-course changes in ectonucleotidase activities during experimental autoimmune encephalomyelitis" in Neurochemistry International, 55, no. 4 (2009),
https://hdl.handle.net/21.15107/rcub_ibiss_1436 .

TY  - JOUR
AU  - Harhaji-Trajković, Ljubica
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - Stojanović, Ivana D.
AU  - Momčilović, Miljana
AU  - Maksimović, Vuk M.
AU  - Tufegdžić, Srđan J.
AU  - Marjanović, Zaklina S.
AU  - Mostarica-Stojković, Marija B.
AU  - Vučinić, Zeljko B.
AU  - Stošić-Grujičić, Stanislava
PY  - 2008
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1531
AB  - Numerous studies have shown immunostimulatory and anti-tumor effects of water and standardized aqueous ethanol extracts derived from the medicinal mushroom, Coriolus versicolor, but the biological activity of methanol extracts has not been examined so far. In the present study we investigated the anti-tumor effect of C versicolor methanol extract (which contains terpenoids and poly-phenols) on B16 mouse melanoma cells both in vitro and in vivo. In vitro treatment of the cells with the methanol extract (25-1600 mu g/ml) reduced melanoma cell viability in it dose-dependent manner. Furthermore, in the presence of the methanol extract (200 mu g/ml, concentration IC50) the proliferation of B16 cells was arrested in the G(0)/G(1) phase of the cell cycle, followed by both apoptotic and secondary necrotic cell death. In vivo methanol extract treatment (i.p. 50 mg/kg, for 14 days) inhibited tumor growth in C57BL/6 mice inoculated with syngeneic B16 tumor cells. Moreover, peritoneal macrophages collected 21 days after tumor implantation from methanol extract-treated animals exerted stronger tumoristatic activity ex vivo than macrophages from control melanoma-bearing rnice. Taken together, our results demonstrate that C. versicolor methanol extract exerts pronounced anti-melanoma activity, both directly through antiproliferative and cytotoxic effects on tumor cells and indirectly through promotion of macrophage anti-tumor activity. (c) 2008 Elsevier Ltd. All rights reserved.
PB  - Elsevier
T2  - Food and Chemical Toxicology
T1  - Anti-tumor effect of Coriolus versicolor methanol extract against mouse B16 melanoma cells: In vitro and in vivo study
IS  - 5
VL  - 46
DO  - 10.1016/j.fct.2008.01.027
SP  - 1825
EP  - 1833
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1531
ER  - 

@article{
author = "Harhaji-Trajković, Ljubica and Mijatović, Sanja and Maksimović-Ivanić, Danijela and Stojanović, Ivana D. and Momčilović, Miljana and Maksimović, Vuk M. and Tufegdžić, Srđan J. and Marjanović, Zaklina S. and Mostarica-Stojković, Marija B. and Vučinić, Zeljko B. and Stošić-Grujičić, Stanislava",
year = "2008",
abstract = "Numerous studies have shown immunostimulatory and anti-tumor effects of water and standardized aqueous ethanol extracts derived from the medicinal mushroom, Coriolus versicolor, but the biological activity of methanol extracts has not been examined so far. In the present study we investigated the anti-tumor effect of C versicolor methanol extract (which contains terpenoids and poly-phenols) on B16 mouse melanoma cells both in vitro and in vivo. In vitro treatment of the cells with the methanol extract (25-1600 mu g/ml) reduced melanoma cell viability in it dose-dependent manner. Furthermore, in the presence of the methanol extract (200 mu g/ml, concentration IC50) the proliferation of B16 cells was arrested in the G(0)/G(1) phase of the cell cycle, followed by both apoptotic and secondary necrotic cell death. In vivo methanol extract treatment (i.p. 50 mg/kg, for 14 days) inhibited tumor growth in C57BL/6 mice inoculated with syngeneic B16 tumor cells. Moreover, peritoneal macrophages collected 21 days after tumor implantation from methanol extract-treated animals exerted stronger tumoristatic activity ex vivo than macrophages from control melanoma-bearing rnice. Taken together, our results demonstrate that C. versicolor methanol extract exerts pronounced anti-melanoma activity, both directly through antiproliferative and cytotoxic effects on tumor cells and indirectly through promotion of macrophage anti-tumor activity. (c) 2008 Elsevier Ltd. All rights reserved.",
publisher = "Elsevier",
journal = "Food and Chemical Toxicology",
title = "Anti-tumor effect of Coriolus versicolor methanol extract against mouse B16 melanoma cells: In vitro and in vivo study",
number = "5",
volume = "46",
doi = "10.1016/j.fct.2008.01.027",
pages = "1825-1833",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1531"
}

Harhaji-Trajković, L., Mijatović, S., Maksimović-Ivanić, D., Stojanović, I. D., Momčilović, M., Maksimović, V. M., Tufegdžić, S. J., Marjanović, Z. S., Mostarica-Stojković, M. B., Vučinić, Z. B.,& Stošić-Grujičić, S.. (2008). Anti-tumor effect of Coriolus versicolor methanol extract against mouse B16 melanoma cells: In vitro and in vivo study. in Food and Chemical Toxicology
Elsevier., 46(5), 1825-1833.
https://doi.org/10.1016/j.fct.2008.01.027
https://hdl.handle.net/21.15107/rcub_ibiss_1531

Harhaji-Trajković L, Mijatović S, Maksimović-Ivanić D, Stojanović ID, Momčilović M, Maksimović VM, Tufegdžić SJ, Marjanović ZS, Mostarica-Stojković MB, Vučinić ZB, Stošić-Grujičić S. Anti-tumor effect of Coriolus versicolor methanol extract against mouse B16 melanoma cells: In vitro and in vivo study. in Food and Chemical Toxicology. 2008;46(5):1825-1833.
doi:10.1016/j.fct.2008.01.027
https://hdl.handle.net/21.15107/rcub_ibiss_1531 .

Harhaji-Trajković, Ljubica, Mijatović, Sanja, Maksimović-Ivanić, Danijela, Stojanović, Ivana D., Momčilović, Miljana, Maksimović, Vuk M., Tufegdžić, Srđan J., Marjanović, Zaklina S., Mostarica-Stojković, Marija B., Vučinić, Zeljko B., Stošić-Grujičić, Stanislava, "Anti-tumor effect of Coriolus versicolor methanol extract against mouse B16 melanoma cells: In vitro and in vivo study" in Food and Chemical Toxicology, 46, no. 5 (2008):1825-1833,
https://doi.org/10.1016/j.fct.2008.01.027 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1531 .