PDF(Pubmed)
Abstract：
We previously found that the respiratory epithelial cells could eliminate the invaded group A streptococcus (GAS) through autophagy induced by binding a fibronectin (Fn) binding protein (FnBp) expressed on the surface of GAS to plasma protein Fn and its receptor integrin α5β1 of epithelial cells. Is autophagy initiated by FnBp+ bacteria via FnBp-Fn-Integrin α5β1 axis a common event in respiratory epithelial cells?
We chose Staphylococcus aureus (S. aureus/S. a) and Listeria monocytogenes (L. monocytogenes/L. m) as representatives of extracellular and intracellular FnBp+ bacteria, respectively. The FnBp of them was purified and the protein function was confirmed by western blot, viable bacteria count, confocal and pull-down. The key molecule downstream of the action axis was detected by IP, mass spectrometry and bio-informatics analysis.
We found that different FnBp from both S. aureus and L. monocytogenes could initiate autophagy through FnBp-Fn-integrin α5β1 axis and this could be considered a universal event, by which host tries to remove invading bacteria from epithelial cells. Importantly, we firstly reported that S100A8, as a key molecule downstream of integrin β1 chain, is highly expressed upon activation of integrin α5β1, which in turn up-regulates autophagy.
Various FnBp from FnBp+ bacteria have the ability to initiate autophagy via FnBp-Fn-Integrin α5β1 axis to promote the removal of invading bacteria from epithelial cells in the presence of fewer invaders. S100A8 is a key molecule downstream of Integrin α5β1 in this autophagy pathway.
We chose Staphylococcus aureus (S. aureus/S. a) and Listeria monocytogenes (L. monocytogenes/L. m) as representatives of extracellular and intracellular FnBp+ bacteria, respectively. The FnBp of them was purified and the protein function was confirmed by western blot, viable bacteria count, confocal and pull-down. The key molecule downstream of the action axis was detected by IP, mass spectrometry and bio-informatics analysis.
We found that different FnBp from both S. aureus and L. monocytogenes could initiate autophagy through FnBp-Fn-integrin α5β1 axis and this could be considered a universal event, by which host tries to remove invading bacteria from epithelial cells. Importantly, we firstly reported that S100A8, as a key molecule downstream of integrin β1 chain, is highly expressed upon activation of integrin α5β1, which in turn up-regulates autophagy.
Various FnBp from FnBp+ bacteria have the ability to initiate autophagy via FnBp-Fn-Integrin α5β1 axis to promote the removal of invading bacteria from epithelial cells in the presence of fewer invaders. S100A8 is a key molecule downstream of Integrin α5β1 in this autophagy pathway.
摘要：
■我们先前发现，呼吸道上皮细胞可以通过将表达在GAS表面的纤连蛋白（Fn）结合蛋白（FnBp）与血浆蛋白Fn结合而诱导的自噬来消除侵袭的A族链球菌（GAS）及其受体整合素α5β1。FnBp+细菌通过FnBp-Fn-整合素α5β1轴启动的自噬是否是呼吸道上皮细胞的常见事件？
■我们选择了金黄色葡萄球菌(S.金黄色葡萄球菌/S.a)和单核细胞增生李斯特菌(L.单核细胞增多症/L.M)作为细胞外和细胞内FnBp+细菌的代表，分别。对它们的FnBp进行纯化,并通过蛋白质印迹确认蛋白功能,活细菌计数，共聚焦和下拉。通过IP检测到作用轴下游的关键分子，质谱和生物信息学分析。
■我们发现来自金黄色葡萄球菌和单核细胞增生李斯特菌的不同FnBp可以通过FnBp-Fn-整合素α5β1轴启动自噬，这可以被认为是一个普遍事件，宿主试图从上皮细胞中清除入侵的细菌。重要的是,我们首先报道了S100A8作为整合素β1链下游的关键分子，在整合素α5β1激活后高度表达，从而上调自噬。
■来自FnBp+细菌的各种FnBp具有通过FnBp-Fn-整合素α5β1轴启动自噬的能力，以促进在较少的入侵者存在下从上皮细胞中去除入侵细菌。S100A8是自噬途径中整合素α5β1下游的关键分子。
■我们选择了金黄色葡萄球菌(S.金黄色葡萄球菌/S.a)和单核细胞增生李斯特菌(L.单核细胞增多症/L.M)作为细胞外和细胞内FnBp+细菌的代表，分别。对它们的FnBp进行纯化,并通过蛋白质印迹确认蛋白功能,活细菌计数，共聚焦和下拉。通过IP检测到作用轴下游的关键分子，质谱和生物信息学分析。
■我们发现来自金黄色葡萄球菌和单核细胞增生李斯特菌的不同FnBp可以通过FnBp-Fn-整合素α5β1轴启动自噬，这可以被认为是一个普遍事件，宿主试图从上皮细胞中清除入侵的细菌。重要的是,我们首先报道了S100A8作为整合素β1链下游的关键分子，在整合素α5β1激活后高度表达，从而上调自噬。
■来自FnBp+细菌的各种FnBp具有通过FnBp-Fn-整合素α5β1轴启动自噬的能力，以促进在较少的入侵者存在下从上皮细胞中去除入侵细菌。S100A8是自噬途径中整合素α5β1下游的关键分子。
