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人类重要的肠道致病菌,肠致病性大肠埃希菌(EPEC)和肠出血性大肠埃希菌(EHEC),在细菌黏附细胞周围形成肌动蛋白聚集的杯垫样结构来黏附并定植到肠道黏膜上,完成侵入宿主细胞的第一步。同时,被感染的肠道黏膜上皮细胞刷状缘脱落并失去微绒毛,这种特殊的病理损伤过程,称为黏附抹平效应(A/E效应)。通过细胞培养感染模型对典型菌株的研究显示,尽管EHEC和EPEC都能激活下游N-WASP蛋白,Arp2/3蛋白,最终引起有效肌动蛋白的聚集,但是它们却采取了不同的途径引起肌动蛋白的聚集。EPEC运用Tir-Nck途径,而EHEC运用是Tir-TccP途径来激活N-WASP蛋白。最近通过细胞培养感染模型研究发现,EHEC和EPEC菌株存在一种既不依赖TccP也不依赖Nck但能引起微弱肌动蛋白聚集的途径。在体内实验(in vivo)和体外组织实验(ex vivo)中,黏膜组织感染也显示不依赖TccP或Nck同样能产生典型的A/E损伤。
Human gut pathogens, enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic Escherichia coli (EHEC), form actin-aggregated coleoptile-like structures around bacterial adherent cells to adhere Colonization to the intestinal mucosa to complete the invasion of host cells in the first step. At the same time, the infected gut mucosal epithelial cells shed the brush edge and lose the microvilli, this special pathological damage process, called the adhesion effect (A / E effect). Studies of typical strains by the cell culture infection model showed that although EHEC and EPEC both activate the downstream N-WASP and Arp2 / 3 proteins and eventually cause the accumulation of actin, they act in different ways Aggregation of proteins. EPEC utilizes the Tir-Nck pathway, whereas EHEC utilizes the Tir-TccP pathway to activate N-WASP protein. Recent studies in cell culture infection models found that EHEC and EPEC strains have a pathway that is independent of TccP and not dependent on Nck but causes weak actin to aggregate. In in vivo and ex vivo, mucosal tissue infections also showed that typical A / E lesions were also produced without TccP or Nck.