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 .