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Interleukin-17 stimulates inducible nitric oxide synthase activation in rodent astrocytes.

Abstract：

:The 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-gamma-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-gamma-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-gamma-pretreated astrocytes was abolished by antagonists of nuclear factor-kappaB (NF-kappaB) 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-1beta 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-1beta and TNF-alpha 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.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Trajkovic V,Stosic-Grujicic S,Samardzic T,Markovic M,Miljkovic D,Ramic Z,Mostarica Stojkovic M

doi

10.1016/s0165-5728(01)00391-5

subject

Has Abstract

pub_date

2001-10-01 00:00:00

pages

183-91

issue

2

eissn

0165-5728

issn

1872-8421

pii

S0165572801003915

journal_volume

119

pub_type

杂志文章

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