Trajkovic, Vladimir (7004516866)Vladimir (7004516866)TrajkovicStosic-Grujicic, Stanislava (7004253020)Stanislava (7004253020)Stosic-GrujicicSamardzic, Tatjana (6602855000)Tatjana (6602855000)SamardzicMarkovic, Milos (7101935774)Milos (7101935774)MarkovicMiljkovic, Djordje (7006524033)Djordje (7006524033)MiljkovicRamic, Zorica (6603943950)Zorica (6603943950)RamicStojkovic, Marija Mostarica (6701741422)Marija Mostarica (6701741422)Stojkovic2025-07-022025-07-022001https://doi.org/10.1016/S0165-5728(01)00391-5https://www.scopus.com/inward/record.uri?eid=2-s2.0-0035479119&doi=10.1016%2fS0165-5728%2801%2900391-5&partnerID=40&md5=85af621c3e1300f36355b1f5df5b6d75https://remedy.med.bg.ac.rs/handle/123456789/14466The effect of interleukin-17 (IL-17) on production of nitric oxide (NO) in rodent astrocytes was investigated. While IL-17 by itself did not induce NO production, it caused a dose-dependent enhancement of IFN-γ-triggered NO synthesis in both mouse and rat primary astrocytes. In contrast, IL-17 was unable to stimulate NO synthesis in either murine or rat macrophages. IFN-γ-triggered expression of mRNA for iNOS, but not for its transcription factor interferon regulatory factor-1 (IRF-1), was markedly elevated in IL-17-treated astrocytes. The induction of iNOS mRNA by IL-17 in IFN-γ-pretreated astrocytes was abolished by antagonists of nuclear factor-κB (NF-κB) activation - a proteasome inhibitor MG132 and an antioxidant agent PDTC, as well as with specific p38 MAP kinase inhibitor SB203580. While IL-17 stimulated both IL-1β and IL-6 production in astrocytes, only IL-1 was partly responsible for IL-17-induced NO release. Finally, IL-17 synergized with exogenous IL-1β and TNF-α for astrocyte NO production. Having in mind a well-known neurotoxic action of NO, these results suggest a possible role for IL-17 in the inflammatory diseases of the CNS. © 2001 Elsevier Science B.V. All rights reserved.AstrocyteIL-17iNOSNitric oxide