کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10941035 | 1095548 | 2013 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
IL-27 promotes nitric oxide production induced by LPS through STAT1, NF-κB and MAPKs
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کلمات کلیدی
NF-κBNG-monomethyl L-arginineL-NMMAT helperIRFIL-27TLRiNOSERKOSMLPSJnknatural killer - (سلول های) کشنده طبیعیc-Jun N-terminal kinase - C-Jun N-terminal kinaseMAPK - MAPKinducible NO synthase - NO سنتاز القاء شدهSTAT - آمارoncostatin M - اوکتواستاتین مinterferon - اینترفرونIFN - اینترفرون هاinterleukin - اینترلوکینToll-like receptor - تیالآرnuclear factor κB - فاکتور هسته ای κBlipopolysaccharide - لیپوپلی ساکاریدMacrophages - ماکروفاژها،درشت خوارهاSignal transducer and activator of transcription - مبدل سیگنال و فعال کننده رونویسیNitric oxide - نیتریک اکسیدmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیReceptor - گیرنده
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
Interleukin (IL)-27, a member of the IL-6/IL-12 heterodimeric cytokine family, induces pro-inflammatory responses including early T helper (Th)1 differentiation and generation of cytotoxic T lymphocytes, and also anti-inflammatory responses including the differentiation to IL-10-producing regulatory T cells, inhibition of Th2 and Th17 differentiation, and suppression of pro-inflammatory cytokine production. Nitric oxide (NO) is a potent source of reactive nitrogen species that play an important role in killing intracellular pathogens and forms a crucial component of host defense. Inducible NO synthase (iNOS), which catalyzes the production of NO, is induced by a range of stimuli including cytokines and microbes. Recently, IL-27 was reported to play an anti-inflammatory role in microglia by blocking oncostatin M-induced iNOS expression and neuronal toxicity. In the present study, we investigated the effects of IL-27 on NO production in thioglycollate-elicited peritoneal macrophages. IL-27 together with lipopolysaccharide (LPS) induced morphological change into more spread and elongated cells and synergistically enhanced NO production. The combined stimulation also enhanced iNOS mRNA expression and the NO production was abrogated by an iNOS inhibitor, NG-monomethyl l-arginine. The synergistic NO production could be attributed to the augmented Toll-like receptor (TLR)4 mRNA expression by the combination. Signal transducer and activator of transcription (STAT)1 was indispensable for the morphological change and NO production. The combination induced nuclear factor κB (NF-κB) translocation into nuclear and phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), and their inhibitors suppressed NO production. These results suggest that in contrast to the anti-proinflammatory role in microglia, IL-27 exerts a pro-inflammatory role by enhancing NO production in peritoneal macrophages stimulated with LPS through activation of STAT1, NF-κB and MAPKs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunobiology - Volume 218, Issue 4, April 2013, Pages 628-634
Journal: Immunobiology - Volume 218, Issue 4, April 2013, Pages 628-634
نویسندگان
Motomu Shimizu, Kiyoshi Ogura, Izuru Mizoguchi, Yukino Chiba, Kaname Higuchi, Hiromi Ohtsuka, Junichiro Mizuguchi, Takayuki Yoshimoto,