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首页> 外文期刊>Cellular immunology >Cilomilast counteracts the effects of cigarette smoke in airway epithelial cells.
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Cilomilast counteracts the effects of cigarette smoke in airway epithelial cells.

机译：Cilomilast可抵消香烟烟雾对气道上皮细胞的影响。

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摘要

Cigarette smoke extracts (CSE) alter TLR4 expression and activation in bronchial epithelial cells. Cilomilast, a phosphodiesterase-4 inhibitor, inhibits cigarette smoke-induced neutrophilia. This study was aimed to explore whether cilomilast, in a human bronchial epithelial cell line (16-HBE), counteracted CSE effects. In particular, TLR4 expression, IP-10 and IL-8 release, lymphocyte and neutrophil chemotactic activity and ERK and IkBa phosphorylation in CSE and LPS-stimulated 16-HBE were assessed. CSE increased TLR4 expression, reduced IP-10 release and lymphocyte chemotactic activity and increased IL-8 release and neutrophil chemotactic activity. Cilomilast reduced TLR4 expression, IL-8 release and neutrophil chemotactic activity as well as it increased IP-10 release and lymphocyte chemotactic activity. All these cilomilast mediated effects were associated with a reduced ERK1/2 and with an increased IkBa phosphorylation. In conclusion, the present study provides compelling evidences that cilomilast may be considered a possible valid therapeutic option in controlling inflammatory processes present in smokers.
机译：香烟烟雾提取物（CSE）会改变支气管上皮细胞中TLR4的表达和激活。 Cilomilast，一种磷酸二酯酶4抑制剂，可抑制香烟烟雾引起的中性粒细胞增多。这项研究旨在探讨在人支气管上皮细胞系（16-HBE）中cilomilast是否能抵消CSE的作用。特别是，评估了CSE和LPS刺激的16-HBE中的TLR4表达，IP-10和IL-8释放，淋巴细胞和嗜中性粒细胞趋化活性以及ERK和IkBa磷酸化。 CSE增加TLR4表达，减少IP-10释放和淋巴细胞趋化活性，并增加IL-8释放和中性粒细胞趋化活性。 Cilomilast降低TLR4表达，IL-8释放和中性粒细胞趋化活性，并增加IP-10释放和淋巴细胞趋化活性。所有这些cilomilast介导的作用均与ERK1 / 2减少和IkBa磷酸化增加有关。总之，本研究提供了令人信服的证据，表明西洛司特可以被认为是控制吸烟者发炎过程的一种可能的有效治疗选择。

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