PepO通过上调腹腔巨噬细胞中MircroRNA-155的表达来抑制IL-6的产生

发布时间：2018-01-19 08:49

本文关键词： PepO MircroRNA- MyD IL-　出处：《基因组学与应用生物学》2016年05期 　论文类型：期刊论文

【摘要】：探索microRNA-155在细胞炎症反应调控中的作用机制。采用重组PepO蛋白刺激小鼠腹腔巨噬细胞(PEMs)诱导的microRNA-155(miR-155)及其对IL-6的调节。PepO刺激腹腔巨噬细胞诱导miRNA-155呈剂量和时间依赖性表达;Mimic和inhibitor转染实验显示过表达mi R-155可抑制IL-6及My D88的表达;IL-6及MyD88与PepO也呈剂量依赖性;且IL-6与MyD88存在PepO处理时间的相关性。这些结果提示,PepO刺激腹腔巨噬细胞诱导miRNA-155可能通过靶向myD88通路信号从而抑制IL-6的表达,避免宿主不至于过度炎症反应导致炎症损伤。
[Abstract]:To explore the role of microRNA-155 in the regulation of cellular inflammatory response. The recombinant PepO protein was used to stimulate mouse peritoneal macrophages (PEMs). MicroRNA-155 miR-155) and its regulation on IL-6. PepO stimulated the expression of miRNA-155 in a dose-and time-dependent manner in peritoneal macrophages. Mimic and inhibitor transfection experiments showed that overexpression of mi R-155 could inhibit the expression of IL-6 and my D88. IL-6, MyD88 and PepO were also dose-dependent. There was a correlation between IL-6 and MyD88 in PepO processing time. PepO stimulates peritoneal macrophages to induce miRNA-155 to inhibit the expression of IL-6 by targeting the myD88 pathway signal to prevent the host from causing inflammatory damage without excessive inflammatory reaction.
【作者单位】：重庆医科大学临床检验诊断学教育部重点实验室;
【基金】：国家自然科学基金(No.83171778) 教育部科技项目(No.21303A)共同资助
【分类号】：R392
【正文快照】： 巨噬细胞能够快速识别人侵病原体、导致自身活化、触发天然免疫和获得性免疫反应、对细菌毒素因子产生信号,分泌炎性介质,诱发炎症反应(Murrayand Wynn,2011;Brüne et al.,2013;Campbell et al.,2015)。在呼吸道感染和肺部炎症建立过程中,细菌毒力因子与肺部定居的巨噬细胞相

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