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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Cigarette smoke increases Toll-like receptor 4 and modifies lipopolysaccharide-mediated responses in airway epithelial cells.
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Cigarette smoke increases Toll-like receptor 4 and modifies lipopolysaccharide-mediated responses in airway epithelial cells.

机译：香烟烟雾会增加Toll样受体4并修饰气道上皮细胞中脂多糖介导的反应。

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摘要

Airway epithelium is emerging as a regulator of innate immune responses to a variety of insults including cigarette smoke. The main goal of this study was to explore the effects of cigarette smoke extracts (CSE) on Toll-like receptor (TLR) expression and activation in a human bronchial epithelial cell line (16-HBE). The CSE increased the expression of TLR4 and the lipopolysaccharide (LPS) binding, the nuclear factor-kappaB (NF-kappaB) activation, the release of interleukin-8 (IL-8) and the chemotactic activity toward neutrophils. It did not induce TLR2 expression or extracellular signal-regulated signal kinase 1/2 (ERK1/2) activation. The LPS increased the expression of TLR4 and induced both NF-kappaB and ERK1/2 activation. The combined exposure of 16-HBE to CSE and LPS was associated with ERK activation rather than NF-kappaB activation and with a further increase of IL-8 release and of chemotactic activity toward neutrophils. Furthermore, CSE decreased the constitutive interferon-inducible protein-10 (IP-10) release and counteracted the effect of LPS in inducing both the IP-10 release and the chemotactic activity toward lymphocytes. In conclusion, cigarette smoke, by altering the expression and the activation of TLR4 via the preferential release of IL-8, may contribute to the accumulation of neutrophils within the airways of smokers.
机译：气道上皮正逐渐成为对包括香烟烟雾在内的各种损伤的先天免疫反应的调节剂。这项研究的主要目的是探讨香烟烟雾提取物（CSE）对人支气管上皮细胞系（16-HBE）中Toll样受体（TLR）表达和激活的影响。 CSE增加了TLR4的表达和脂多糖（LPS）的结合，核因子-κB（NF-kappaB）的激活，白介素8（IL-8）的释放以及对嗜中性白细胞的趋化活性。它不诱导TLR2表达或细胞外信号调节信号激酶1/2（ERK1 / 2）激活。 LPS增加TLR4的表达，并诱导NF-κB和ERK1 / 2激活。 16-HBE对CSE和LPS的联合暴露与ERK活化而不是NF-κB活化有关，并且与IL-8释放和对嗜中性粒细胞的趋化活性进一步增加有关。此外，CSE减少了组成型干扰素诱导性蛋白10（IP-10）的释放，并抵消了LPS在诱导IP-10释放和对淋巴细胞的趋化活性中的作用。总之，香烟烟雾通过IL-8的优先释放来改变TLR4的表达和激活，可能有助于中性粒细胞在吸烟者气道中的积累。

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