致泻性大肠埃希菌诱发细胞肌动蛋白聚集的研究

Research progress of actin polymerization triggered by pathogenic E.coli

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。

Enteropathogenic E.coli（EPEC） and enterohemorrhagic E.coli（EHEC）,the important human enteric pathogenic bacterium,can colonize on gut mucosa by the formation of pedestal-shaped structure of actin polymerization,which is the first step to aggress host cell,then the epithelial cell brush border and microvilli of gut mucosa affected are effaced.This pathogenic process is called as attaching and effacing lesions.Study of prototypical strains by cell culture model indicated that although EHEC and EPEC could activate N-WASP and Arp2/3 to mediate actin polymerization,the pathways to do so were different,EPEC used Tir-Nck pathway,EHEC used Tir-TccP pathway.Recent cell culture model study revealed that both EHEC and EPEC strains had a pathway to induce inefficient actin polymerization which was neither TccP dependable nor Nck dependable.In vivo and ex vivo study indicated that mucosa tissue could develop efficient attaching and effacing lesions without the dependence of TccP or Nck.This review covers the related proteins of EPEC and EHEC strains to mediate actin polymerization in cell culture model study,the classical pathway or alternative pathway of actin polymerization.The difference found recently between in vitro and in vivo studies indicate that the pedestal formation is not the key event during the A/E lesions.