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首页> 外文期刊>Molecular medicine reports >Respiratory syncytial virus infection modulates interleukin-8 production in respiratory epithelial cells through a transcription factor-activator protein-1 signaling pathway
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Respiratory syncytial virus infection modulates interleukin-8 production in respiratory epithelial cells through a transcription factor-activator protein-1 signaling pathway

机译：呼吸道合胞病毒感染通过转录因子激活蛋白1信号通路调节呼吸道上皮细胞中白介素8的产生

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摘要

Respiratory syncytial virus (RSV) is a leading cause of respiratory duct infection that can result in severe clinical symptoms, particularly among children under 3 years of age. In the current study, the effect of RSV on airway epithelial cell function and the potential signaling pathways involved were investigated. A549 human airway epithelial cells were infected with RSV at a multiplicity of infection of 1. After 24 h, interleukin (IL)-8 secretion in the cell supernatant was analyzed. A microarray assay of RSV-infected A549 cells was conducted in order to identify any potential pathways involved, and quantitative polymerase chain reaction was performed to examine mRNA expression levels in these pathways. Electrophoretic mobility shift assays of nuclear transcription factors were conducted for further verification. IL-8 levels increased significantly in the supernatant of RSV-infected A549 cells compared with levels in non-infected cells. Microarray data suggested the involvement of the Toll-like receptor 4 (TLR4) pathway, and mRNA expression levels of genes (MYD88, TRAM and TRIF) involved in this pathway were higher in infected cells. Enhanced synthesis of activator protein-1 (AP-1) was observed. RSV infection of A549 cells may promote IL-8 secretion. In conclusion, the results of the present study indicate that the TLR4 signaling pathway, in conjunction with MYD88, TRAM, TRIF and the transcription factor AP-1, may activate immune responses to RSV infection in airway epithelial cells.
机译：呼吸道合胞病毒（RSV）是呼吸道感染的主要原因，可能导致严重的临床症状，尤其是在3岁以下的儿童中。在当前的研究中，研究了RSV对气道上皮细胞功能的影响以及潜在的信号通路。用感染复数为1的RSV感染A549人气道上皮细胞。24小时后，分析细胞上清液中的白介素（IL）-8分泌。进行了RSV感染的A549细胞的微阵列分析，以鉴定涉及的任何潜在途径，并进行定量聚合酶链反应以检查这些途径中的mRNA表达水平。进行了核转录因子的电泳迁移率迁移分析，以进一步验证。与未感染的细胞相比，RSV感染的A549细胞的上清液中的IL-8水平显着增加。微阵列数据表明Toll样受体4（TLR4）途径的参与，并且该途径中涉及的基因（MYD88，TRAM和TRIF）的mRNA表达水平在感染细胞中更高。观察到激活蛋白1（AP-1）的合成得到增强。 RS549感染A549细胞可能会促进IL-8分泌。总之，本研究的结果表明，TLR4信号通路与MYD88，TRAM，TRIF和转录因子AP-1结合，可以激活对气道上皮细胞中RSV感染的免疫反应。

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