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首页> 外文期刊>Physiological Reports >Cigarette smoke represses the innate immune response to asbestos
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Cigarette smoke represses the innate immune response to asbestos

机译：香烟烟雾抑制对石棉的天然免疫反应

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AbstractBoth cigarette smoke (CS) and asbestos cause lung inflammation and lung cancer, and at high asbestos exposure levels, populations exposed to both of these carcinogens display a synergistic increase in the development of lung cancer. The mechanisms through which these two toxic agents interact to promote lung tumorigenesis are poorly understood. Here, we begin to dissect the inflammatory signals induced by asbestos in combination with CS using a rodent inhalation model and in vitro cell culture. Wild-type C57BL/6 mice were exposed to room air as a control, CS, and/or asbestos (4 days per week to CS and 1 day per week to asbestos for 5 weeks). Bronchoalveolar lavage (BAL) fluid was collected following exposure and analyzed for inflammatory mediators. Asbestos-exposed mice displayed an increased innate immune response consistent with NLRP3 inflammasome activation. Compared to mice exposed only to asbestos, animals coexposed to CS + asbestos displayed attenuated levels of innate immune mediators and altered inflammatory cell recruitment. Histopathological changes in CS + asbestos-exposed mice correlated with attenuated fibroproliferative lesion development relative to their counterparts exposed only to asbestos. In vitro experiments using a human monocyte cell line (THP-1 cells) supported the in vivo results in that coexposure to cigarette smoke extract repressed NLRP3 inflammasome markers in cells treated with asbestos. These observations indicate that CS represses central components of the innate immune response to inhaled asbestos.
机译：摘要香烟烟雾（CS）和石棉都会引起肺部炎症和肺癌，在高石棉暴露水平下，接触这两种致癌物的人群在肺癌的发展中具有协同增效作用。这两种毒性剂相互作用以促进肺肿瘤发生的机制了解甚少。在这里，我们开始使用啮齿动物吸入模型和体外细胞培养物来分析石棉与CS结合诱导的炎症信号。将野生型C57BL / 6小鼠作为对照，CS和/或石棉暴露于室内空气中（每周4天暴露于CS，每周1天暴露于石棉，持续5周）。暴露后收集支气管肺泡灌洗液（BAL），并分析其炎症介质。接触石棉的小鼠显示出与NLRP3炎症小体激活一致的先天免疫应答增加。与仅接触石棉的小鼠相比，与CS +石棉同时暴露的动物表现出先天免疫介质水平降低和炎性细胞募集改变。与仅接触石棉的小鼠相比，接触CS +石棉的小鼠的组织病理学变化与纤维增生性病变的发展相关。使用人单核细胞系（THP-1细胞）的体外实验支持体内结果，即与烟熏提取物共同暴露会抑制用石棉处理的细胞中的NLRP3炎性标记。这些观察结果表明，CS抑制了对吸入石棉的先天免疫应答的中枢成分。

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