Nicotine inhibits the production of proinflammatory mediators in human monocytes by suppression of I‐κB phosphorylation and nuclear factor‐κB transcriptional activity through nicotinic acetylcholine receptor α7
作者： H. Yoshikawa , M. Kurokawa , N. Ozaki , K. Nara , K. Atou
DOI: 10.1111/J.1365-2249.2006.03169.X
关键词:
摘要: Macrophages/monocytes and the proinflammatory mediators, such as tumour necrosis factor (TNF)-alpha, prostaglandin E(2) (PGE(2)), macrophage inflammatory protein (MIP)-1alpha MIP-1alpha, play a critical role in progression of immunological disorders including rheumatoid arthritis, Behcet's disease Crohn's disease. In addition, nicotinic acetylcholine receptor-alpha7 (alpha7nAChR) subunit is an essential regulator inflammation. this study, we evaluated expression alpha7nAChR on human peripheral monocytes effect nicotine production these mediators by activated monocytes. Fluorescein isothiocyanate (FITC)-labelled alpha-bungarotoxin demonstrated cell surface alpha7nAchR subunit. Pretreatment with low-dose caused inhibition TNF-alpha, PGE(2), MIP-1alpha production, mRNA COX-2 lipopolysaccharide (LPS)-activated These suppressive effects were at transcriptional level mediated through alpha7nAChR. Nicotine suppressed phosphorylation I-kappaB, then inhibited activity nuclear factor-kappaB. immunosuppressive may contribute to regulation some immune diseases.
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