Mostarica Stojković, Marija

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  • Mostarica Stojković, Marija (7)
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Author's Bibliography

Complete Freund's adjuvant-free experimental autoimmune encephalomyelitis in Dark Agouti rats is a valuable tool for multiple sclerosis studies.

Lazarević, Milica; Nikolovski, Neda; Stanisavljević, Suzana; Dimitrijević, Mirjana; Stegnjaić, Goran; Krishnamoorthy, Gurumoorthy; Mostarica Stojković, Marija; Miljković, Đorđe; Jevtić, Bojan

(Elsevier BV, 2021)

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/123456789/4200
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 . .
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Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats.

Nikolovski, Neda; Jevtić, Bojan; Mansilla, M. José; Petković, Filip; Blaževski, Jana; Timotijević, Gordana; Navarro-Barriuso, Juan; Martinez-Caceres, Eva; Mostarica Stojković, Marija; Miljković, Đorđe

(2019)

TY  - JOUR
AU  - Nikolovski, Neda
AU  - Jevtić, Bojan
AU  - Mansilla, M. José
AU  - Petković, Filip
AU  - Blaževski, Jana
AU  - Timotijević, Gordana
AU  - Navarro-Barriuso, Juan
AU  - Martinez-Caceres, Eva
AU  - Mostarica Stojković, Marija
AU  - Miljković, Đorđe
PY  - 2019
UR  - https://www.sciencedirect.com/science/article/pii/S0171298518302201?via%3Dihub
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3265
AB  - Dendritic cells (DC) are responsible for the initiation and shaping of the adaptive immune response and are in the focus of autoimmunity research. We were interested in comparison of DC obtained from autoimmunity-prone Dark Agouti (DA) rats and autoimmunity-resistant Albino Oxford (AO) rats. DC were generated from bone marrow precursors and matured (mDC) by lipopolysaccharide. Tolerogenic DC (tolDC) obtained by vitamin D3 treatment were studied in parallel. Profile of cytokine production was different in AO and DA mDC and tolDC. Expression of MHC class II molecules and CD86 were higher in DA DC, while vitamin D3 reduced their expression in dendritic cells of both strains. Allogeneic proliferation of CD4+ T cells was reduced by AO tolDC, but not with DA tolDC in comparison to respective mDC. Finally, expression of various genes identified as differentially expressed in human mDC and tolDC was also analyzed in AO and DA DC. Again, AO and DA DC differed in the expression of the analyzed genes. To conclude, AO and DA DC differ in production of cytokines, expression of antigen presentation-related molecules and in regulation of CD4+ T proliferation. The difference is valuable for understanding the divergence of the strains in their susceptibility to autoimmunity.
T2  - Immunobiology
T1  - Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats.
DO  - 10.1016/j.imbio.2019.01.001
ER  - 
@article{
author = "Nikolovski, Neda and Jevtić, Bojan and Mansilla, M. José and Petković, Filip and Blaževski, Jana and Timotijević, Gordana and Navarro-Barriuso, Juan and Martinez-Caceres, Eva and Mostarica Stojković, Marija and Miljković, Đorđe",
year = "2019",
abstract = "Dendritic cells (DC) are responsible for the initiation and shaping of the adaptive immune response and are in the focus of autoimmunity research. We were interested in comparison of DC obtained from autoimmunity-prone Dark Agouti (DA) rats and autoimmunity-resistant Albino Oxford (AO) rats. DC were generated from bone marrow precursors and matured (mDC) by lipopolysaccharide. Tolerogenic DC (tolDC) obtained by vitamin D3 treatment were studied in parallel. Profile of cytokine production was different in AO and DA mDC and tolDC. Expression of MHC class II molecules and CD86 were higher in DA DC, while vitamin D3 reduced their expression in dendritic cells of both strains. Allogeneic proliferation of CD4+ T cells was reduced by AO tolDC, but not with DA tolDC in comparison to respective mDC. Finally, expression of various genes identified as differentially expressed in human mDC and tolDC was also analyzed in AO and DA DC. Again, AO and DA DC differed in the expression of the analyzed genes. To conclude, AO and DA DC differ in production of cytokines, expression of antigen presentation-related molecules and in regulation of CD4+ T proliferation. The difference is valuable for understanding the divergence of the strains in their susceptibility to autoimmunity.",
journal = "Immunobiology",
title = "Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats.",
doi = "10.1016/j.imbio.2019.01.001"
}
Nikolovski, N., Jevtić, B., Mansilla, M. J., Petković, F., Blaževski, J., Timotijević, G., Navarro-Barriuso, J., Martinez-Caceres, E., Mostarica Stojković, M.,& Miljković, Đ.. (2019). Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats.. in Immunobiology.
https://doi.org/10.1016/j.imbio.2019.01.001
Nikolovski N, Jevtić B, Mansilla MJ, Petković F, Blaževski J, Timotijević G, Navarro-Barriuso J, Martinez-Caceres E, Mostarica Stojković M, Miljković Đ. Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats.. in Immunobiology. 2019;.
doi:10.1016/j.imbio.2019.01.001 .
Nikolovski, Neda, Jevtić, Bojan, Mansilla, M. José, Petković, Filip, Blaževski, Jana, Timotijević, Gordana, Navarro-Barriuso, Juan, Martinez-Caceres, Eva, Mostarica Stojković, Marija, Miljković, Đorđe, "Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats." in Immunobiology (2019),
https://doi.org/10.1016/j.imbio.2019.01.001 . .
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Oral neonatal antibiotic treatment perturbs gut microbiota and aggravates central nervous system autoimmunity in Dark Agouti rats.

Stanisavljević, Suzana; Čepić, Aleksa; Bojić, Svetlana; Veljović, Katarina; Mihajlović, Sanja; Nikolovski, Neda; Jevtić, Bojan; Momčilović, Miljana; Lazarević, Milica; Mostarica Stojković, Marija; Miljković, Đorđe; Golić, Nataša

(2019)

TY  - JOUR
AU  - Stanisavljević, Suzana
AU  - Čepić, Aleksa
AU  - Bojić, Svetlana
AU  - Veljović, Katarina
AU  - Mihajlović, Sanja
AU  - Nikolovski, Neda
AU  - Jevtić, Bojan
AU  - Momčilović, Miljana
AU  - Lazarević, Milica
AU  - Mostarica Stojković, Marija
AU  - Miljković, Đorđe
AU  - Golić, Nataša
PY  - 2019
UR  - http://www.nature.com/articles/s41598-018-37505-7
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC6351648
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3264
AB  - Gut microbiota dysbiosis has been considered the essential element in the pathogenesis of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). Antibiotics were administered orally to Dark Agouti (DA) rats early in their life with the aim of perturbing gut microbiota and investigating the effects of such intervention on the course of EAE. As a result, the diversity of the gut microbiota was reduced under the influence of antibiotics. Mainly, Firmicutes and Actinobacteria were replaced by Proteobacteria and Bacteroidetes, while decreased proportions of Clostridia and Bacilli classes were accompanied by an increase in Gamma-Proteobacteria in antibiotic-treated animals. Interestingly, a notable decrease in the Helicobacteraceae, Spirochaetaceae and Turicibacteriaceae was scored in antibiotic-treated groups. Also, levels of short chain fatty acids were reduced in the faeces of antibiotic-treated rats. Consequently, aggravation of EAE, paralleled with stronger immune response in lymph nodes draining the site of immunization, and increased inflammation within the CNS, were observed in antibiotic-treated DA rats. Thus, the alteration of gut microbiota leads to an escalation of CNS-directed autoimmunity in DA rats. The results of this study indicate that antibiotic use in early life may have subsequent unfavourable effects on the regulation of the immune system.
T2  - Scientific Reports
T1  - Oral neonatal antibiotic treatment perturbs gut microbiota and aggravates central nervous system autoimmunity in Dark Agouti rats.
IS  - 1
VL  - 9
DO  - 10.1038/s41598-018-37505-7
SP  - 918
ER  - 
@article{
author = "Stanisavljević, Suzana and Čepić, Aleksa and Bojić, Svetlana and Veljović, Katarina and Mihajlović, Sanja and Nikolovski, Neda and Jevtić, Bojan and Momčilović, Miljana and Lazarević, Milica and Mostarica Stojković, Marija and Miljković, Đorđe and Golić, Nataša",
year = "2019",
abstract = "Gut microbiota dysbiosis has been considered the essential element in the pathogenesis of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). Antibiotics were administered orally to Dark Agouti (DA) rats early in their life with the aim of perturbing gut microbiota and investigating the effects of such intervention on the course of EAE. As a result, the diversity of the gut microbiota was reduced under the influence of antibiotics. Mainly, Firmicutes and Actinobacteria were replaced by Proteobacteria and Bacteroidetes, while decreased proportions of Clostridia and Bacilli classes were accompanied by an increase in Gamma-Proteobacteria in antibiotic-treated animals. Interestingly, a notable decrease in the Helicobacteraceae, Spirochaetaceae and Turicibacteriaceae was scored in antibiotic-treated groups. Also, levels of short chain fatty acids were reduced in the faeces of antibiotic-treated rats. Consequently, aggravation of EAE, paralleled with stronger immune response in lymph nodes draining the site of immunization, and increased inflammation within the CNS, were observed in antibiotic-treated DA rats. Thus, the alteration of gut microbiota leads to an escalation of CNS-directed autoimmunity in DA rats. The results of this study indicate that antibiotic use in early life may have subsequent unfavourable effects on the regulation of the immune system.",
journal = "Scientific Reports",
title = "Oral neonatal antibiotic treatment perturbs gut microbiota and aggravates central nervous system autoimmunity in Dark Agouti rats.",
number = "1",
volume = "9",
doi = "10.1038/s41598-018-37505-7",
pages = "918"
}
Stanisavljević, S., Čepić, A., Bojić, S., Veljović, K., Mihajlović, S., Nikolovski, N., Jevtić, B., Momčilović, M., Lazarević, M., Mostarica Stojković, M., Miljković, Đ.,& Golić, N.. (2019). Oral neonatal antibiotic treatment perturbs gut microbiota and aggravates central nervous system autoimmunity in Dark Agouti rats.. in Scientific Reports, 9(1), 918.
https://doi.org/10.1038/s41598-018-37505-7
Stanisavljević S, Čepić A, Bojić S, Veljović K, Mihajlović S, Nikolovski N, Jevtić B, Momčilović M, Lazarević M, Mostarica Stojković M, Miljković Đ, Golić N. Oral neonatal antibiotic treatment perturbs gut microbiota and aggravates central nervous system autoimmunity in Dark Agouti rats.. in Scientific Reports. 2019;9(1):918.
doi:10.1038/s41598-018-37505-7 .
Stanisavljević, Suzana, Čepić, Aleksa, Bojić, Svetlana, Veljović, Katarina, Mihajlović, Sanja, Nikolovski, Neda, Jevtić, Bojan, Momčilović, Miljana, Lazarević, Milica, Mostarica Stojković, Marija, Miljković, Đorđe, Golić, Nataša, "Oral neonatal antibiotic treatment perturbs gut microbiota and aggravates central nervous system autoimmunity in Dark Agouti rats." in Scientific Reports, 9, no. 1 (2019):918,
https://doi.org/10.1038/s41598-018-37505-7 . .
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Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis.

Stanisavljević, Suzana; Dinić, Miroslav; Jevtić, Bojan; Nikolovski, Neda; Momčilović, Miljana; Đokić, Jelena; Golić, Nataša; Mostarica Stojković, Marija; Miljković, Đorđe

(2018)

TY  - JOUR
AU  - Stanisavljević, Suzana
AU  - Dinić, Miroslav
AU  - Jevtić, Bojan
AU  - Nikolovski, Neda
AU  - Momčilović, Miljana
AU  - Đokić, Jelena
AU  - Golić, Nataša
AU  - Mostarica Stojković, Marija
AU  - Miljković, Đorđe
PY  - 2018
UR  - http://journal.frontiersin.org/article/10.3389/fimmu.2018.00942/full
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC5942155
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3056
AB  - Albino Oxford (AO) rats are extremely resistant to induction of experimental autoimmune encephalomyelitis (EAE). EAE is an animal model of multiple sclerosis, a chronic inflammatory disease of the central nervous system (CNS), with established autoimmune pathogenesis. The autoimmune response against the antigens of the CNS is initiated in the peripheral lymphoid tissues after immunization of AO rats with CNS antigens. Subsequently, limited infiltration of the CNS occurs, yet without clinical sequels. It has recently become increasingly appreciated that gut-associated lymphoid tissues (GALT) and gut microbiota play an important role in regulation and propagation of encephalitogenic immune response. Therefore, modulation of AO gut microbiota by antibiotics was performed in this study. The treatment altered composition of gut microbiota in AO rats and led to a reduction in the proportion of regulatory T cells in Peyer's patches, mesenteric lymph nodes, and in lymph nodes draining the site of immunization. Upregulation of interferon-γ and interleukin (IL)-17 production was observed in the draining lymph nodes. The treatment led to clinically manifested EAE in AO rats with more numerous infiltrates and higher production of IL-17 observed in the CNS. Importantly, transfer of AO gut microbiota into EAE-prone Dark Agouti rats ameliorated the disease. These results clearly imply that gut microbiota is an important factor in AO rat resistance to EAE and that gut microbiota transfer is an efficacious way to treat CNS autoimmunity. These findings also support the idea that gut microbiota modulation has a potential as a future treatment of multiple sclerosis.
T2  - Frontiers in Immunology
T1  - Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis.
VL  - 9
DO  - 10.3389/fimmu.2018.00942
SP  - 942
ER  - 
@article{
author = "Stanisavljević, Suzana and Dinić, Miroslav and Jevtić, Bojan and Nikolovski, Neda and Momčilović, Miljana and Đokić, Jelena and Golić, Nataša and Mostarica Stojković, Marija and Miljković, Đorđe",
year = "2018",
abstract = "Albino Oxford (AO) rats are extremely resistant to induction of experimental autoimmune encephalomyelitis (EAE). EAE is an animal model of multiple sclerosis, a chronic inflammatory disease of the central nervous system (CNS), with established autoimmune pathogenesis. The autoimmune response against the antigens of the CNS is initiated in the peripheral lymphoid tissues after immunization of AO rats with CNS antigens. Subsequently, limited infiltration of the CNS occurs, yet without clinical sequels. It has recently become increasingly appreciated that gut-associated lymphoid tissues (GALT) and gut microbiota play an important role in regulation and propagation of encephalitogenic immune response. Therefore, modulation of AO gut microbiota by antibiotics was performed in this study. The treatment altered composition of gut microbiota in AO rats and led to a reduction in the proportion of regulatory T cells in Peyer's patches, mesenteric lymph nodes, and in lymph nodes draining the site of immunization. Upregulation of interferon-γ and interleukin (IL)-17 production was observed in the draining lymph nodes. The treatment led to clinically manifested EAE in AO rats with more numerous infiltrates and higher production of IL-17 observed in the CNS. Importantly, transfer of AO gut microbiota into EAE-prone Dark Agouti rats ameliorated the disease. These results clearly imply that gut microbiota is an important factor in AO rat resistance to EAE and that gut microbiota transfer is an efficacious way to treat CNS autoimmunity. These findings also support the idea that gut microbiota modulation has a potential as a future treatment of multiple sclerosis.",
journal = "Frontiers in Immunology",
title = "Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis.",
volume = "9",
doi = "10.3389/fimmu.2018.00942",
pages = "942"
}
Stanisavljević, S., Dinić, M., Jevtić, B., Nikolovski, N., Momčilović, M., Đokić, J., Golić, N., Mostarica Stojković, M.,& Miljković, Đ.. (2018). Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis.. in Frontiers in Immunology, 9, 942.
https://doi.org/10.3389/fimmu.2018.00942
Stanisavljević S, Dinić M, Jevtić B, Nikolovski N, Momčilović M, Đokić J, Golić N, Mostarica Stojković M, Miljković Đ. Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis.. in Frontiers in Immunology. 2018;9:942.
doi:10.3389/fimmu.2018.00942 .
Stanisavljević, Suzana, Dinić, Miroslav, Jevtić, Bojan, Nikolovski, Neda, Momčilović, Miljana, Đokić, Jelena, Golić, Nataša, Mostarica Stojković, Marija, Miljković, Đorđe, "Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis." in Frontiers in Immunology, 9 (2018):942,
https://doi.org/10.3389/fimmu.2018.00942 . .
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25

Protective effects of carbonyl iron against multiple low-dose streptozotocin-induced diabetes in rodents.

Vujičić, Milica; Saksida, Tamara; Mostarica Stojković, Marija; Nikolovski, Neda; Stojanović, Ivana D.; Stošić-Grujičić, Stanislava

(2018)

TY  - JOUR
AU  - Vujičić, Milica
AU  - Saksida, Tamara
AU  - Mostarica Stojković, Marija
AU  - Nikolovski, Neda
AU  - Stojanović, Ivana D.
AU  - Stošić-Grujičić, Stanislava
PY  - 2018
UR  - http://doi.wiley.com/10.1002/jcp.26338
UR  - http://www.ncbi.nlm.nih.gov/pubmed/29215791
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2959
AB  - Particulate adjuvants have shown increasing promise as effective, safe, and durable agents for the stimulation of immunity, or alternatively, the suppression of autoimmunity. Here we examined the potential of the adjuvant carbonyl iron (CI) for the modulation of organ-specific autoimmune disease-type 1 diabetes (T1D). T1D was induced by multiple low doses of streptozotocin (MLDS) that initiates beta cell death and triggers immune cell infiltration into the pancreatic islets. The results of this study indicate that the single in vivo application of CI to MLDS-treated DA rats, CBA/H mice, or C57BL/6 mice successfully counteracted the development of insulitis and hyperglycemia. The protective action was obtained either when CI was applied 7 days before, simultaneously with the first dose of streptozotocin, or 1 day after MLDS treatment. Ex vivo cell analysis of C57BL/6 mice showed that CI treatment reduced the proportion of proinflammatory F4/80+ CD40+ M1 macrophages and activated T lymphocytes in the spleen. Moreover, the treatment down-regulated the number of inflammatory CD4+ IFN-γ+ cells in pancreatic lymph nodes, Peyer's patches, and pancreas-infiltrating mononuclear cells, while simultaneously potentiating proportion of CD4+ IL17+ cells. The regulatory arm of the immune system represented by CD3+ NK1.1+ (NKT) and CD4+ CD25+ FoxP3+ regulatory T cells was potentiated after CI treatment. In vitro analysis showed that CI down-regulated CD40 and CD80 expression on dendritic cells thus probably interfering with their antigen-presenting ability. In conclusion, particulate adjuvant CI seems to suppress the activation of the innate immune response, which further affects the adaptive immune response directed toward pancreatic beta cells.
T2  - Journal of Cellular Physiology
T1  - Protective effects of carbonyl iron against multiple low-dose streptozotocin-induced diabetes in rodents.
IS  - 6
VL  - 233
DO  - 10.1002/jcp.26338
SP  - 4990
EP  - 5001
ER  - 
@article{
author = "Vujičić, Milica and Saksida, Tamara and Mostarica Stojković, Marija and Nikolovski, Neda and Stojanović, Ivana D. and Stošić-Grujičić, Stanislava",
year = "2018",
abstract = "Particulate adjuvants have shown increasing promise as effective, safe, and durable agents for the stimulation of immunity, or alternatively, the suppression of autoimmunity. Here we examined the potential of the adjuvant carbonyl iron (CI) for the modulation of organ-specific autoimmune disease-type 1 diabetes (T1D). T1D was induced by multiple low doses of streptozotocin (MLDS) that initiates beta cell death and triggers immune cell infiltration into the pancreatic islets. The results of this study indicate that the single in vivo application of CI to MLDS-treated DA rats, CBA/H mice, or C57BL/6 mice successfully counteracted the development of insulitis and hyperglycemia. The protective action was obtained either when CI was applied 7 days before, simultaneously with the first dose of streptozotocin, or 1 day after MLDS treatment. Ex vivo cell analysis of C57BL/6 mice showed that CI treatment reduced the proportion of proinflammatory F4/80+ CD40+ M1 macrophages and activated T lymphocytes in the spleen. Moreover, the treatment down-regulated the number of inflammatory CD4+ IFN-γ+ cells in pancreatic lymph nodes, Peyer's patches, and pancreas-infiltrating mononuclear cells, while simultaneously potentiating proportion of CD4+ IL17+ cells. The regulatory arm of the immune system represented by CD3+ NK1.1+ (NKT) and CD4+ CD25+ FoxP3+ regulatory T cells was potentiated after CI treatment. In vitro analysis showed that CI down-regulated CD40 and CD80 expression on dendritic cells thus probably interfering with their antigen-presenting ability. In conclusion, particulate adjuvant CI seems to suppress the activation of the innate immune response, which further affects the adaptive immune response directed toward pancreatic beta cells.",
journal = "Journal of Cellular Physiology",
title = "Protective effects of carbonyl iron against multiple low-dose streptozotocin-induced diabetes in rodents.",
number = "6",
volume = "233",
doi = "10.1002/jcp.26338",
pages = "4990-5001"
}
Vujičić, M., Saksida, T., Mostarica Stojković, M., Nikolovski, N., Stojanović, I. D.,& Stošić-Grujičić, S.. (2018). Protective effects of carbonyl iron against multiple low-dose streptozotocin-induced diabetes in rodents.. in Journal of Cellular Physiology, 233(6), 4990-5001.
https://doi.org/10.1002/jcp.26338
Vujičić M, Saksida T, Mostarica Stojković M, Nikolovski N, Stojanović ID, Stošić-Grujičić S. Protective effects of carbonyl iron against multiple low-dose streptozotocin-induced diabetes in rodents.. in Journal of Cellular Physiology. 2018;233(6):4990-5001.
doi:10.1002/jcp.26338 .
Vujičić, Milica, Saksida, Tamara, Mostarica Stojković, Marija, Nikolovski, Neda, Stojanović, Ivana D., Stošić-Grujičić, Stanislava, "Protective effects of carbonyl iron against multiple low-dose streptozotocin-induced diabetes in rodents." in Journal of Cellular Physiology, 233, no. 6 (2018):4990-5001,
https://doi.org/10.1002/jcp.26338 . .
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2

Correlation of Gut Microbiota Composition with Resistance to Experimental Autoimmune Encephalomyelitis in Rats

Stanisavljević, Suzana; Lukić, Jovanka; Soković, Svetlana; Mihajlović, Sanja; Mostarica Stojković, Marija; Miljković, Đorđe; Golić, Nataša

(2016)

TY  - JOUR
AU  - Stanisavljević, Suzana
AU  - Lukić, Jovanka
AU  - Soković, Svetlana
AU  - Mihajlović, Sanja
AU  - Mostarica Stojković, Marija
AU  - Miljković, Đorđe
AU  - Golić, Nataša
PY  - 2016
UR  - http://journal.frontiersin.org/article/10.3389/fmicb.2016.02005/full
UR  - https://www.scopus.com/record/display.uri?eid=2-s2.0-85008932586&origin=SingleRecordEmailAlert&dgcid=scalert_sc_search_email&txGid=4EB499CE54E80575D67A4CAC3995163A.wsnAw8kcdt7IPYLO0V48gA%3A1
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2513
AB  - Multiple sclerosis is a chronic inflammatory disease of the central nervous system (CNS). It is widely accepted that autoimmune response against the antigens of the CNS is the essential pathogenic force in the disease. It has recently become increasingly appreciated that activated encephalitogenic cells tend to migrate toward gut associated lymphoid tissues (GALTs) and that interrupted balance between regulatory and inflammatory immunity within the GALT might have decisive role in the initiation and propagation of the CNS autoimmunity. Gut microbiota composition and function has the major impact on the balance in the GALT. Thus, our aim was to perform analyses of gut microbiota in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. Albino Oxford (AO) rats that are highly resistant to EAE induction and Dark Agouti (DA) rats that develop EAE after mild immunization were compared for gut microbiota composition in different phases after EAE induction. Microbial analyses of the genus Lactobacillus and related lactic acid bacteria showed higher diversity of Lactobacillus spp. in EAE-resistant AO rats, while some members of Firmicutes and Proteobacteria (Undibacterium oligocarboniphilum) were detected only in feces of DA rats at the peak of the disease (between 13 and 16 days after induction). Interestingly, in contrast to our previous study where Turicibacter sp. was found exclusively in non-immunized AO, but not in DA rats, in this study it was detected in DA rats that remained healthy 16 days after induction, as well as in four of 12 DA rats at the peak of the disease. Similar observation was obtained for the members of Lachnospiraceae. Further, production of a typical regulatory cytokine interleukin-10 was compared in GALT cells of AO and DA rats, and higher production was observed in DA rats. Our data contribute to the idea that gut microbiota and GALT considerably influence multiple sclerosis pathogenesis.
T2  - Frontiers in Microbiology
T1  - Correlation of Gut Microbiota Composition with Resistance to Experimental Autoimmune Encephalomyelitis in Rats
VL  - 7
DO  - 10.3389/fmicb.2016.02005
SP  - 2005
EP  - 2005
ER  - 
@article{
author = "Stanisavljević, Suzana and Lukić, Jovanka and Soković, Svetlana and Mihajlović, Sanja and Mostarica Stojković, Marija and Miljković, Đorđe and Golić, Nataša",
year = "2016",
abstract = "Multiple sclerosis is a chronic inflammatory disease of the central nervous system (CNS). It is widely accepted that autoimmune response against the antigens of the CNS is the essential pathogenic force in the disease. It has recently become increasingly appreciated that activated encephalitogenic cells tend to migrate toward gut associated lymphoid tissues (GALTs) and that interrupted balance between regulatory and inflammatory immunity within the GALT might have decisive role in the initiation and propagation of the CNS autoimmunity. Gut microbiota composition and function has the major impact on the balance in the GALT. Thus, our aim was to perform analyses of gut microbiota in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. Albino Oxford (AO) rats that are highly resistant to EAE induction and Dark Agouti (DA) rats that develop EAE after mild immunization were compared for gut microbiota composition in different phases after EAE induction. Microbial analyses of the genus Lactobacillus and related lactic acid bacteria showed higher diversity of Lactobacillus spp. in EAE-resistant AO rats, while some members of Firmicutes and Proteobacteria (Undibacterium oligocarboniphilum) were detected only in feces of DA rats at the peak of the disease (between 13 and 16 days after induction). Interestingly, in contrast to our previous study where Turicibacter sp. was found exclusively in non-immunized AO, but not in DA rats, in this study it was detected in DA rats that remained healthy 16 days after induction, as well as in four of 12 DA rats at the peak of the disease. Similar observation was obtained for the members of Lachnospiraceae. Further, production of a typical regulatory cytokine interleukin-10 was compared in GALT cells of AO and DA rats, and higher production was observed in DA rats. Our data contribute to the idea that gut microbiota and GALT considerably influence multiple sclerosis pathogenesis.",
journal = "Frontiers in Microbiology",
title = "Correlation of Gut Microbiota Composition with Resistance to Experimental Autoimmune Encephalomyelitis in Rats",
volume = "7",
doi = "10.3389/fmicb.2016.02005",
pages = "2005-2005"
}
Stanisavljević, S., Lukić, J., Soković, S., Mihajlović, S., Mostarica Stojković, M., Miljković, Đ.,& Golić, N.. (2016). Correlation of Gut Microbiota Composition with Resistance to Experimental Autoimmune Encephalomyelitis in Rats. in Frontiers in Microbiology, 7, 2005-2005.
https://doi.org/10.3389/fmicb.2016.02005
Stanisavljević S, Lukić J, Soković S, Mihajlović S, Mostarica Stojković M, Miljković Đ, Golić N. Correlation of Gut Microbiota Composition with Resistance to Experimental Autoimmune Encephalomyelitis in Rats. in Frontiers in Microbiology. 2016;7:2005-2005.
doi:10.3389/fmicb.2016.02005 .
Stanisavljević, Suzana, Lukić, Jovanka, Soković, Svetlana, Mihajlović, Sanja, Mostarica Stojković, Marija, Miljković, Đorđe, Golić, Nataša, "Correlation of Gut Microbiota Composition with Resistance to Experimental Autoimmune Encephalomyelitis in Rats" in Frontiers in Microbiology, 7 (2016):2005-2005,
https://doi.org/10.3389/fmicb.2016.02005 . .
14
36
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35

Astrocyte-induced regulatory T cells mitigate CNS autoimmunity

Trajković, Vladimir S; Vucković, Olivera; Stošić-Grujičić, Stanislava; Miljković, Đorđe; Popadić, Dušan M.; Marković, Miloš; Bumbaširević, Vesna D; Backović, Aleksandar; Stojanović, Ivana D.; Harhaji-Trajković, Ljubica; Ramić, Zorica D.; Mostarica-Stojković, Marija

(2004)

TY  - JOUR
AU  - Trajković, Vladimir S
AU  - Vucković, Olivera
AU  - Stošić-Grujičić, Stanislava
AU  - Miljković, Đorđe
AU  - Popadić, Dušan M.
AU  - Marković, Miloš
AU  - Bumbaširević, Vesna D
AU  - Backović, Aleksandar
AU  - Stojanović, Ivana D.
AU  - Harhaji-Trajković, Ljubica
AU  - Ramić, Zorica D.
AU  - Mostarica-Stojković, Marija
PY  - 2004
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1682
AB  - Although astrocytes presumably participate in maintaining the immune privilege of the central nervous system (CNS), the mechanisms behind their immunoregulatory properties are still largely undefined. In this study, we describe the development of regulatory T cells upon contact with astrocytes. Rat T cells pre-incubated with astrocytes completely lost the ability to proliferate in response to mitogenic stimuli. The cells were blocked in G0/G1 phase of the cell cycle, expressed less IL-2R, and produced significantly lower amounts of interferon-gamma (IFN-gamma), but not interleukin-2 (IL-2), IL-10, or tumor necrosis factor (TNF). These anergic cells completely prevented mitogen-induced growth of normal T lymphocytes, as well as CNS antigen-driven proliferation of autoreactive T cells. The suppressive activity resided in both CD4(+) and CD8(+) T-cell compartments. Heat-sensitive soluble T-cell factors, not including transforming growth factor-beta (TGF-beta) or IL-10, were solely responsible for the observed suppression, as well as for the transfer of suppressive activity to normal T cells. The administration of astrocyte-induced regulatory T cells markedly alleviated CNS inflammation and clinical symptoms of CNS autoimmunity in rats with experimental allergic encephalomyelitis. Finally, the cells with suppressive properties were readily generated from human lymphocytes after contact with astrocytes. Taken together, these data indicate that astrocyte-induced regulatory T cells might represent an important mechanism for self-limitation of excessive inflammation in the brain. (C) 2004 Wiley-Liss, Inc.
T2  - Glia
T1  - Astrocyte-induced regulatory T cells mitigate CNS autoimmunity
IS  - 2
VL  - 47
DO  - 10.1002/glia.20046
SP  - 168
EP  - 179
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1682
ER  - 
@article{
author = "Trajković, Vladimir S and Vucković, Olivera and Stošić-Grujičić, Stanislava and Miljković, Đorđe and Popadić, Dušan M. and Marković, Miloš and Bumbaširević, Vesna D and Backović, Aleksandar and Stojanović, Ivana D. and Harhaji-Trajković, Ljubica and Ramić, Zorica D. and Mostarica-Stojković, Marija",
year = "2004",
abstract = "Although astrocytes presumably participate in maintaining the immune privilege of the central nervous system (CNS), the mechanisms behind their immunoregulatory properties are still largely undefined. In this study, we describe the development of regulatory T cells upon contact with astrocytes. Rat T cells pre-incubated with astrocytes completely lost the ability to proliferate in response to mitogenic stimuli. The cells were blocked in G0/G1 phase of the cell cycle, expressed less IL-2R, and produced significantly lower amounts of interferon-gamma (IFN-gamma), but not interleukin-2 (IL-2), IL-10, or tumor necrosis factor (TNF). These anergic cells completely prevented mitogen-induced growth of normal T lymphocytes, as well as CNS antigen-driven proliferation of autoreactive T cells. The suppressive activity resided in both CD4(+) and CD8(+) T-cell compartments. Heat-sensitive soluble T-cell factors, not including transforming growth factor-beta (TGF-beta) or IL-10, were solely responsible for the observed suppression, as well as for the transfer of suppressive activity to normal T cells. The administration of astrocyte-induced regulatory T cells markedly alleviated CNS inflammation and clinical symptoms of CNS autoimmunity in rats with experimental allergic encephalomyelitis. Finally, the cells with suppressive properties were readily generated from human lymphocytes after contact with astrocytes. Taken together, these data indicate that astrocyte-induced regulatory T cells might represent an important mechanism for self-limitation of excessive inflammation in the brain. (C) 2004 Wiley-Liss, Inc.",
journal = "Glia",
title = "Astrocyte-induced regulatory T cells mitigate CNS autoimmunity",
number = "2",
volume = "47",
doi = "10.1002/glia.20046",
pages = "168-179",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1682"
}
Trajković, V. S., Vucković, O., Stošić-Grujičić, S., Miljković, Đ., Popadić, D. M., Marković, M., Bumbaširević, V. D., Backović, A., Stojanović, I. D., Harhaji-Trajković, L., Ramić, Z. D.,& Mostarica-Stojković, M.. (2004). Astrocyte-induced regulatory T cells mitigate CNS autoimmunity. in Glia, 47(2), 168-179.
https://doi.org/10.1002/glia.20046
https://hdl.handle.net/21.15107/rcub_ibiss_1682
Trajković VS, Vucković O, Stošić-Grujičić S, Miljković Đ, Popadić DM, Marković M, Bumbaširević VD, Backović A, Stojanović ID, Harhaji-Trajković L, Ramić ZD, Mostarica-Stojković M. Astrocyte-induced regulatory T cells mitigate CNS autoimmunity. in Glia. 2004;47(2):168-179.
doi:10.1002/glia.20046
https://hdl.handle.net/21.15107/rcub_ibiss_1682 .
Trajković, Vladimir S, Vucković, Olivera, Stošić-Grujičić, Stanislava, Miljković, Đorđe, Popadić, Dušan M., Marković, Miloš, Bumbaširević, Vesna D, Backović, Aleksandar, Stojanović, Ivana D., Harhaji-Trajković, Ljubica, Ramić, Zorica D., Mostarica-Stojković, Marija, "Astrocyte-induced regulatory T cells mitigate CNS autoimmunity" in Glia, 47, no. 2 (2004):168-179,
https://doi.org/10.1002/glia.20046 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1682 .
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60
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Uric acid levels in sera from patients with multiple sclerosis

Drulović, Jelena; Dujmović, Irena; Stojsavljević, Nebojša; Mesaroš, Šarlota; Anđelković, Slobodanka; Miljković, Đorđe; Perić, Vesna; Dragutinović, Gradimir; Marinković, Jelena; Lević, Zvonimir; Mostarica Stojković, Marija

(Heidelberg: Springer, 2001)

TY  - JOUR
AU  - Drulović, Jelena
AU  - Dujmović, Irena
AU  - Stojsavljević, Nebojša
AU  - Mesaroš, Šarlota
AU  - Anđelković, Slobodanka
AU  - Miljković, Đorđe
AU  - Perić, Vesna
AU  - Dragutinović, Gradimir
AU  - Marinković, Jelena
AU  - Lević, Zvonimir
AU  - Mostarica Stojković, Marija
PY  - 2001
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5995
AB  - The levels of uric acid (UA), a natural peroxynitrite scavenger, were measured in sera from 240 patients with multiple sclerosis (MS) and 104 sex- and age-matched control patients with other neurological diseases (OND). The mean serum UA concentration was lower in the MS than in the OND group, but the difference did not reach the level of statistical significance (P = 0.068). However, the mean serum UA level from patients with active MS (202.6 + 67.1 mumol/l) was significantly lower than that in inactive MS patients (226.5 + 78.6 mumol/l; P = 0.046) and OND controls (P = 0.007). We found a significant inverse correlation of serum UA concentration with female gender (P = 0.0001), disease activity (P = 0.012) and duration (P = 0.017), and a trend towards an inverse correlation with disability as assessed by EDSS score, which did not reach statistical significance (P = 0.067). Finally, multivariate linear regression analyses showed that UA concentration was independently correlated with gender (P = 0.0001), disease activity (P = 0.014) and duration of the disease (P = 0.043) in MS patients. These findings suggest that serum UA might serve as a possible marker of disease activity in MS. They also provide support to the potential beneficial therapeutic effect of radical-scavenging substances in MS.
PB  - Heidelberg: Springer
T2  - Journal of Neurology
T1  - Uric acid levels in sera from patients with multiple sclerosis
IS  - 2
VL  - 248
DO  - 10.1007/s004150170246
SP  - 121
EP  - 126
ER  - 
@article{
author = "Drulović, Jelena and Dujmović, Irena and Stojsavljević, Nebojša and Mesaroš, Šarlota and Anđelković, Slobodanka and Miljković, Đorđe and Perić, Vesna and Dragutinović, Gradimir and Marinković, Jelena and Lević, Zvonimir and Mostarica Stojković, Marija",
year = "2001",
abstract = "The levels of uric acid (UA), a natural peroxynitrite scavenger, were measured in sera from 240 patients with multiple sclerosis (MS) and 104 sex- and age-matched control patients with other neurological diseases (OND). The mean serum UA concentration was lower in the MS than in the OND group, but the difference did not reach the level of statistical significance (P = 0.068). However, the mean serum UA level from patients with active MS (202.6 + 67.1 mumol/l) was significantly lower than that in inactive MS patients (226.5 + 78.6 mumol/l; P = 0.046) and OND controls (P = 0.007). We found a significant inverse correlation of serum UA concentration with female gender (P = 0.0001), disease activity (P = 0.012) and duration (P = 0.017), and a trend towards an inverse correlation with disability as assessed by EDSS score, which did not reach statistical significance (P = 0.067). Finally, multivariate linear regression analyses showed that UA concentration was independently correlated with gender (P = 0.0001), disease activity (P = 0.014) and duration of the disease (P = 0.043) in MS patients. These findings suggest that serum UA might serve as a possible marker of disease activity in MS. They also provide support to the potential beneficial therapeutic effect of radical-scavenging substances in MS.",
publisher = "Heidelberg: Springer",
journal = "Journal of Neurology",
title = "Uric acid levels in sera from patients with multiple sclerosis",
number = "2",
volume = "248",
doi = "10.1007/s004150170246",
pages = "121-126"
}
Drulović, J., Dujmović, I., Stojsavljević, N., Mesaroš, Š., Anđelković, S., Miljković, Đ., Perić, V., Dragutinović, G., Marinković, J., Lević, Z.,& Mostarica Stojković, M.. (2001). Uric acid levels in sera from patients with multiple sclerosis. in Journal of Neurology
Heidelberg: Springer., 248(2), 121-126.
https://doi.org/10.1007/s004150170246
Drulović J, Dujmović I, Stojsavljević N, Mesaroš Š, Anđelković S, Miljković Đ, Perić V, Dragutinović G, Marinković J, Lević Z, Mostarica Stojković M. Uric acid levels in sera from patients with multiple sclerosis. in Journal of Neurology. 2001;248(2):121-126.
doi:10.1007/s004150170246 .
Drulović, Jelena, Dujmović, Irena, Stojsavljević, Nebojša, Mesaroš, Šarlota, Anđelković, Slobodanka, Miljković, Đorđe, Perić, Vesna, Dragutinović, Gradimir, Marinković, Jelena, Lević, Zvonimir, Mostarica Stojković, Marija, "Uric acid levels in sera from patients with multiple sclerosis" in Journal of Neurology, 248, no. 2 (2001):121-126,
https://doi.org/10.1007/s004150170246 . .
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