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IL-8 and IP-10 expression from human bronchial epithelial cells BEAS-2B are promoted by Streptococcus pneumoniae endopeptidase O (PepO)

机译:肺炎链球菌内肽酶O(PepO)促进人支气管上皮细胞BEAS-2B的IL-8和IP-10表达

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摘要

BackgroundThe bronchial epithelium serves as the first defendant line of host against respiratory inhaled pathogens, mainly through releasing chemokines (e.g. interleukin-8 (IL-8), interferon-induced protein 10 (IP-10) etc.) responsible for neutrophil or lymphocyte recruitment to promote the clearance of inhaled pathogens including Streptococcus pneumoniae (S. pneumoniae). Previous studies have shown that IL-8 expression is induced by pneumococcal virulence factors (e.g. pneumolysin, peptidoglycan-polysaccharides, pneumococcal surface protein A (PspA) etc.), which contributes to the pathogenesis of pneumonia. Whether other pneumococcal virulence factors are involved in inducing chemokines expression in epithelium is still unknown.
机译:背景支气管上皮细胞是抵抗呼吸道吸入病原体的第一道宿主防御系,主要通过释放负责中性粒细胞或淋巴细胞募集的趋化因子(例如白介素8(IL-8),干扰素诱导的蛋白10(IP-10)等)释放。促进清除包括肺炎链球菌(S. pneumoniae)在内的吸入病原体。先前的研究表明,IL-8表达是由肺炎球菌毒力因子(例如,肺炎球菌溶血素,肽聚糖多糖,肺炎球菌表面蛋白A(PspA)等)诱导的,这有助于肺炎的发病。尚无其他肺炎球菌致病因子参与上皮细胞趋化因子表达的诱导。

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