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首页> 外文期刊>Toxicology and Applied Pharmacology >Arsenic alters transcriptional responses to Pseudomonas aeruginosa infection and decreases antimicrobial defense of human airway epithelial cells
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Arsenic alters transcriptional responses to Pseudomonas aeruginosa infection and decreases antimicrobial defense of human airway epithelial cells

机译：砷改变对铜绿假单胞菌感染的转录反应，降低人气道上皮细胞的抗微生物防御

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摘要

Arsenic contamination of drinking water and food threatens the health of hundreds of millions of people worldwide by increasing the risk of numerous diseases. Arsenic exposure has been associated with infectious lung disease in epidemiological studies, but it is not yet understood how ingestion of low levels of arsenic increases susceptibility to bacterial infection. Accordingly, the goal of this study was to examine the effect of arsenic on gene expression in primary human bronchial epithelial (HBE) cells and to determine if arsenic altered epithelial cell responses to Pseudomonas aeruginosa, an opportunistic pathogen. Bronchial epithelial cells line the airway surface, providing a physical barrier and serving critical roles in antimicrobial defense and signaling to professional immune cells. We used RNA-seq to define the transcriptional response of HBE cells to Pseudomonas aeruginosa, and investigated how arsenic affected HBE gene networks in the presence and absence of the bacterial challenge. Environmentally relevant levels of arsenic significantly changed the expression of genes involved in cellular redox homeostasis and host defense to bacterial infection, and decreased genes that code for secreted antimicrobial factors such as lysozyme. Using pathway analysis, we identified Sox4 and Nrf2-regulated gene networks that are predicted to mediate the arsenic-induced decrease in lysozyme secretion. In addition, we demonstrated that arsenic decreased lysozyme in the airway surface liquid, resulting in reduced lysis of Microccocus luteus. Thus, arsenic alters the expression of genes and proteins in innate host defense pathways, thereby decreasing the ability of the lung epithelium to fight bacterial infection. (C) 2017 Elsevier Inc. All rights reserved.
机译：饮用水和食品中的砷污染增加了许多疾病的风险，威胁着全世界数亿人的健康。在流行病学研究中，砷暴露与传染性肺病有关，但目前尚不清楚摄入低水平砷如何增加细菌感染的易感性。因此，本研究的目的是检测砷对原代人支气管上皮（HBE）细胞基因表达的影响，并确定砷是否改变了上皮细胞对铜绿假单胞菌（一种机会性病原体）的反应。支气管上皮细胞排列在气道表面，提供物理屏障，在抗菌防御和向专业免疫细胞发送信号方面发挥关键作用。我们使用RNA-seq来定义HBE细胞对铜绿假单胞菌的转录反应，并研究在存在和不存在细菌挑战的情况下，砷如何影响HBE基因网络。与环境相关的砷水平显著改变了细胞氧化还原稳态和宿主对细菌感染防御相关基因的表达，并减少了编码溶菌酶等分泌性抗菌因子的基因。通过通路分析，我们确定了Sox4和Nrf2调控的基因网络，这些基因网络被预测介导砷诱导的溶菌酶分泌减少。此外，我们还证明，砷降低了气道表面液体中的溶菌酶，从而减少了黄微球菌的溶解。因此，砷会改变先天性宿主防御途径中基因和蛋白质的表达，从而降低肺上皮抵抗细菌感染的能力。（C） 2017爱思唯尔公司版权所有。

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