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Sendai virus C protein inhibits lipopolysaccharide-induced nitric oxide production through impairing interferon-β signaling.
- Source :
-
International Immunopharmacology . Nov2014, Vol. 23 Issue 1, p267-272. 6p. - Publication Year :
- 2014
-
Abstract
- The effect of Sendai virus (SeV) C protein on lipopolysaccharide (LPS)-induced nitric oxide (NO) production was examined using RAW 264.7 macrophage cells. Infection of SeV inhibited LPS-induced NO production via downregulating the expression of an inducible NO synthase protein (iNOS). On the other hand, C gene-knockout 4C(−) SeV inhibited neither NO production nor iNOS expression. Wild type and 4C(−) SeV did not affect LPS-induced production of tumor necrosis factor-α and interleukin-6, and further LPS-induced activation of nuclear factor (NF)-κB and mitogen-activated protein kinases. Although wild type and 4C(−) SeV did not inhibit LPS-induced interferon (IFN)-β production, wild type SeV but not 4C(−) SeV inhibited the activation of STAT1/2 in the IFN-β signaling. SeV C protein inhibited LPS-induced iNOS expression and NO production. C protein inhibited the promotor activation of IFN-β and IFN-sensitive response element (ISRE) in response to LPS whereas the C mutant protein C F170S , which lacks the ability to block the STAT activation, did not inhibit it. Taken together, SeV C protein was suggested to inhibit LPS-induced NO production through impairing IFN-β signaling. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 15675769
- Volume :
- 23
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- International Immunopharmacology
- Publication Type :
- Academic Journal
- Accession number :
- 99512358
- Full Text :
- https://doi.org/10.1016/j.intimp.2014.09.012