Research progress of  actin polymerization triggered by pathogenic <I>E.coli</I>

Enteropathogenic IE. coli/I (EPEC) and enterohemorrhagic IE. coli/I (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.