期刊
EXPERIMENTAL LUNG RESEARCH
卷 29, 期 6, 页码 401-412出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/01902140303756
关键词
acute lung injury; alveolar macrophage; lipopolysaccharide; proinflammatory cytokine; toll-like receptor
The authors investigated the regulation of toll-like receptor (TLR) TLR2 and TLR4 gene expression in alveolar macrophage (AM) in response to lipopolysaccharide (LPS) or proinflammatory cytokines in vitro. Treatment of a murine AM cell line, MH-S, with LPS, tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta significantly increased TLR2 mRNA expression, whereas TLR4 mRNA expression remained constant. LPS-mediated TLR2 mRNA up-regulation was attenuated by inhibition of p38 kinase (with SB203580) or nuclear factor (NF)-kappaB (with sulfasalazine or SN-50), but not by inhibition of extracellular signal-regulated kinase (with PD98059) or c-Jun N-terminal kinase (with SP600125), suggesting that LPS may induce TLR2 mRNA expression through p38 kinase and NF-kappaB activation. These results indicate that TLR2 expression up-regulated in AM in response to bacterial respiratory infections may render AM responsive to TLR2 ligands, which may accelerate the innate immunity against pathogens in the lung.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据