| Enterohemorrhagic Escherichia coli (EHEC) O157, an emerging pathogen, causes severe hemorrhagic colitis and the life-threatening extraintestinal complication of hemolytic uremic syndrome (HUS). E. coli O157 produce Shiga toxin 1 or 2 (Stx1 or Stx2, respectively), or both. The major source of E. coli O157 are contaminated food or drinking water .Treatment of E. coli O157 infection is difficult because antibiotics do not change the course of its and may increase the incidence of HUS caused by the pathogen .This untoward effect has been proposed to be mediated by antibiotic-induced bacteriolysis such as vaccines and antibody. It is very significant to this disease.The interplay between bacterium and ruminant host probably has its main role in promoting infection and pathopoiesis. The adherence of EHEC on intestinal epithelial cells is believed to be the first step for developing these diseases. The adhesion is mainly mediated through the type III secretion system. The translocon apparatus is initially an extended structure primarily made up of EspA. This protruding organelle may be necessary to bypass microvilli or mucus layers. EspA makes filamentous appendages surrounding the bacterium and forms a needle structure through which various proteins including Esp (E. coli secreted protein) proteins and Tir are secreted. These secreted proteins drive the intimate association of the bacterium with the host epithelial cell, resulting in histological changes of epithelial cells, which is called attaching-and-effacing (A/E) lesion including F-actin aggregation. EspA not only has initial role in adherence of O157 with host cell, but also build a bridge of effect protein translocation between them. Consequently, study on biological action of EspA is very important in controlling, preventing and curing the infection of O157.In view of these, this study investigated biological function of EHEC O157 EspA from the following aspects:... |
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