【摘要】 金黄色葡萄球菌（S.aureus）是导致哺乳动物感染性疾病的重要革兰氏阳性病原菌，其侵入宿主机体后能够在短时间内激活天然免疫系统，诱导炎症反应的发生。论文探究了细菌菌体成分对免疫细胞炎性反应的诱导作用。通过实时荧光定量PCR、Western blot和ELISA方法，分析了S.aureus脂蛋白在诱导小鼠巨噬细胞模式识别受体TLR2表达、炎性细胞因子（TNF-α、IL-1β和IL-6）和趋化因子（RANTES）分泌、炎性信号通路激活、前列腺素E₂（PGE₂）分泌中的作用。结果表明，与S.aureus SA113野生株和脂蛋白表达回补株相比，S.aureus脂蛋白表达缺失株诱导巨噬细胞TLR2表达的能力处于较低水平（P<0.05）。同时，细菌脂蛋白是S.aureus感染过程中诱导巨噬细胞炎性信号通路激活，进而导致炎性细胞因子、趋化因子和炎症介质PGE₂分泌的重要免疫活性物质。此外，细胞脂蛋白对S.aureus在巨噬细胞中的存活发挥了重要作用。表明细菌脂蛋白对S.aureus诱导巨噬细胞炎性反应具有重要作用，可能是参与S.aureus感染性疾病进程发展的关键菌体成分。更多还原

【Abstract】 Staphylococcus aureus is a significant Gram-positive pathogen responsible for infectious diseases in mammals.Upon invading the host,it promptly activates the innate immune system,triggering inflammation.In this study,we investigated the induction effect of bacterial components on the inflammatory response of immune cells.The real-time PCR,Western blot and ELISA were used to analyze the roles of S.aureus lipoproteins in eliciting the expression of the pattern recognition receptor TLR2,secretion of inflammatory cytokines（TNF-α,IL-1β,and IL-6）,chemokines（RANTES）,activation of inflammatory signaling pathways,and secretion of prostaglandin E₂（PGE₂） in mouse macrophages.The findings demonstrated that the S.aureus lipoprotein expression-deficient strain exhibited a diminished ability to induce TLR2expression in macrophages compared to the wild-type S.aureus SA113 strain and its lipoprotein expression complement strain（P<0.05）.Bacterial lipoproteins emerged as crucial immunoreactive compounds,driving the activation of macrophage inflammatory signaling pathways during S.aureus infection.This activation resulted in the secretion of inflammatory cytokines,chemokines,and the inflammatory mediator PGE₂.Additionally,lipoproteins played a pivotal role in the survival of S.aureus within macrophages.These results signify the essential role of bacterial lipoproteins in macrophage-induced inflammatory responses to S.aureus.These lipoproteins may serve as key components influencing the development of S.aureus infectious diseases.更多还原