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首页> 外文期刊>American Journal of Physiology >Diesel exhaust enhances virus- and poly(I:C)-induced Toll-like receptor 3 expression and signaling in respiratory epithelial cells.
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Diesel exhaust enhances virus- and poly(I:C)-induced Toll-like receptor 3 expression and signaling in respiratory epithelial cells.

机译：柴油机排气增强了呼吸道上皮细胞中病毒和聚（I：C）诱导的Toll样受体3的表达和信号传导。

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摘要

Prior exposure of respiratory epithelial cells to an aqueous-trapped solution of diesel exhaust (DE(as)) enhances the susceptibility to influenza infections. Here, we examined the effect of DE(as) on the Toll-like receptor 3 (TLR3) pathway, which is responsible for the recognition of and response to viruses and double-stranded RNA. Flow cytometric and confocal microscopy analyses showed that TLR3 is predominantly expressed in the cytoplasm of respiratory epithelial cells. To examine the effect of DE on TLR3 expression and function, differentiated human bronchial or nasal epithelial cells as well as A549 cells were exposed to DE(as) and then infected with influenza A or treated with polyriboinosinic acid-polyribocytidylic acid [poly(I:C)], a synthetic form of double-stranded RNA. Exposure to DE(as) before infection with influenza or stimulation with poly(I:C) significantly upregulated the expression of TLR3. Additionally, preexposure to DE(as) significantly increased the poly(I:C)-induced expression of IL-6. Overexpression of a dominant-negative mutant form of TNF receptor-associated factor 6 reversed the effects of DE(as) on poly(I:C)-induced IL-6 expression, suggesting that the response was TLR3 dependent. Similarly, preexposure to DE(as) significantly increased nuclear levels of interferon regulatory factor 3 and the expression of IFN-beta in response to poly(I:C). Pretreatment with wortmannin, a specific inhibitor of phosphatidylinositol 3-kinase, was able to abate the effect of DE(as) on poly(I:C)-induced IFN-beta expression. Together, these results indicate that exposure of respiratory epithelial cells to DE(as) could potentially alter the response to viral infections by increasing the expression and function of TLR3.
机译：呼吸道上皮细胞事先暴露于水汽捕集的柴油机废气（DE（as））溶液中会增强对流感感染的敏感性。在这里，我们检查了DE（as）对Toll样受体3（TLR3）途径的影响，该途径负责识别和响应病毒和双链RNA。流式细胞术和共聚焦显微镜分析表明，TLR3主要在呼吸道上皮细胞的细胞质中表达。为了检查DE对TLR3表达和功能的影响，将分化的人支气管或鼻上皮细胞以及A549细胞暴露于DE（as），然后感染甲型流感或用聚核糖苷酸-多核糖核酸[poly（I： C）]，双链RNA的合成形式。在感染流感或用聚（I：C）刺激之前暴露于DE（as）会显着上调TLR3的表达。此外，预先暴露于DE（as）会显着增加poly（I：C）诱导的IL-6表达。 TNF受体相关因子6的显性负突变体形式的过表达逆转了DE（as）对poly（I：C）诱导的IL-6表达的影响，表明该反应是TLR3依赖性的。同样，对DE（as）的预接触显着增加了干扰素调节因子3的核水平，并响应于poly（I：C）增强了IFN-β的表达。用渥曼青霉素（一种磷脂酰肌醇3-激酶的特异性抑制剂）进行预处理能够减轻DE（as）对聚（I：C）诱导的IFN-β表达的影响。总之，这些结果表明呼吸道上皮细胞暴露于DE（as）可能通过增加TLR3的表达和功能来改变对病毒感染的反应。

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