TY  - JOUR
AU  - Miletić, Tatjana
AU  - Kovačević-Jovanović, Vesna
AU  - Vujić, Vesna
AU  - Stanojević, Stanislava
AU  - Mitić, Katarina
AU  - Lazarević-Macanović, Miriana
AU  - Dimitrijević, Mirjana
PY  - 2007
UR  - http://intor.torlakinstitut.com/handle/123456789/229
AB  - There is extensive evidence for the critical role of reactive oxygen species (ROS) and nitric oxide (NO) produced by phagocytes in development of inflammatory processes and pathogenesis of numerous diseases, including rheumatoid arthritis (RA). Apart from their function as mediators of inflammation and tissue damage, recent research supports their role as signaling and regulatory molecules. In the present study we have investigated the production of ROS and NO over the course of adjuvant arthritis (AA) and oil-induced arthritis (OIA), by resident peritoneal macrophages of two rat strains: Dark Agouti (DA), susceptible, and Albino Oxford (AO), resistant to induction of AA and OIA. We have compared levels of ROS and NO produced by susceptible vs. resistant rat strain, and investigated their relevancy for arthritis development and severity. In addition, we have stimulated macrophages in vitro with Mycobacterium bovis BCG, and two heat shock proteins (HSP): endogenous HSP47 and mycobacterial HSP71 (rnHSP71). Our results suggest a possible contribution of increased ROS production to arthritis resistance of AO rats. The ROS production in AO rats is potentiated by endogenous HSP47, but not with mycobacterial cell and mHSP71, suggesting HSP47 participates in AA control. We have found no fundamental relationship between the magnitude of NO production and AA and OIA susceptibility and severity, suggesting that NO has no effector role in AA and OIA. Our results advocate a regulatory type action of NO molecule aught be more significant in arthritis development. (c) 2006 Elsevier GmbH. All rights reserved.
PB  - Elsevier Gmbh, Munich
T2  - Immunobiology
T1  - Reactive oxygen species (ROS), but not nitric oxide (NO), contribute to strain differences in the susceptibility to experimental arthritis in rats
EP  - 105
IS  - 2
SP  - 95
VL  - 212
DO  - 10.1016/j.imbio.2006.11.012
ER  - 

@article{
author = "Miletić, Tatjana and Kovačević-Jovanović, Vesna and Vujić, Vesna and Stanojević, Stanislava and Mitić, Katarina and Lazarević-Macanović, Miriana and Dimitrijević, Mirjana",
year = "2007",
abstract = "There is extensive evidence for the critical role of reactive oxygen species (ROS) and nitric oxide (NO) produced by phagocytes in development of inflammatory processes and pathogenesis of numerous diseases, including rheumatoid arthritis (RA). Apart from their function as mediators of inflammation and tissue damage, recent research supports their role as signaling and regulatory molecules. In the present study we have investigated the production of ROS and NO over the course of adjuvant arthritis (AA) and oil-induced arthritis (OIA), by resident peritoneal macrophages of two rat strains: Dark Agouti (DA), susceptible, and Albino Oxford (AO), resistant to induction of AA and OIA. We have compared levels of ROS and NO produced by susceptible vs. resistant rat strain, and investigated their relevancy for arthritis development and severity. In addition, we have stimulated macrophages in vitro with Mycobacterium bovis BCG, and two heat shock proteins (HSP): endogenous HSP47 and mycobacterial HSP71 (rnHSP71). Our results suggest a possible contribution of increased ROS production to arthritis resistance of AO rats. The ROS production in AO rats is potentiated by endogenous HSP47, but not with mycobacterial cell and mHSP71, suggesting HSP47 participates in AA control. We have found no fundamental relationship between the magnitude of NO production and AA and OIA susceptibility and severity, suggesting that NO has no effector role in AA and OIA. Our results advocate a regulatory type action of NO molecule aught be more significant in arthritis development. (c) 2006 Elsevier GmbH. All rights reserved.",
publisher = "Elsevier Gmbh, Munich",
journal = "Immunobiology",
title = "Reactive oxygen species (ROS), but not nitric oxide (NO), contribute to strain differences in the susceptibility to experimental arthritis in rats",
pages = "105-95",
number = "2",
volume = "212",
doi = "10.1016/j.imbio.2006.11.012"
}

Miletić, T., Kovačević-Jovanović, V., Vujić, V., Stanojević, S., Mitić, K., Lazarević-Macanović, M.,& Dimitrijević, M.. (2007). Reactive oxygen species (ROS), but not nitric oxide (NO), contribute to strain differences in the susceptibility to experimental arthritis in rats. in Immunobiology
Elsevier Gmbh, Munich., 212(2), 95-105.
https://doi.org/10.1016/j.imbio.2006.11.012

Miletić T, Kovačević-Jovanović V, Vujić V, Stanojević S, Mitić K, Lazarević-Macanović M, Dimitrijević M. Reactive oxygen species (ROS), but not nitric oxide (NO), contribute to strain differences in the susceptibility to experimental arthritis in rats. in Immunobiology. 2007;212(2):95-105.
doi:10.1016/j.imbio.2006.11.012 .

Miletić, Tatjana, Kovačević-Jovanović, Vesna, Vujić, Vesna, Stanojević, Stanislava, Mitić, Katarina, Lazarević-Macanović, Miriana, Dimitrijević, Mirjana, "Reactive oxygen species (ROS), but not nitric oxide (NO), contribute to strain differences in the susceptibility to experimental arthritis in rats" in Immunobiology, 212, no. 2 (2007):95-105,
https://doi.org/10.1016/j.imbio.2006.11.012 . .