Enteropathogenic and enterohemorrhagic
E. coli are important causes of gastrointestinal disease worldwide. As part of their pathogenesis, EPEC and EHEC cause a distinctive lesion on the intestinal mucosa known as an attaching and effacing (A/E) lesion. A/E lesion formation requires a type III secretion system that injects multiple effector proteins into the cell. Despite their shared mechanism of intestinal colonization, EPEC and EHEC exhibit substantial differences in epidemiology and clinical disease. In particular, EHEC produces a potent Shiga toxin that is associated with development of the haemolytic uremic syndrome (HUS), an acute form of renal failure. This Research Topic will examine interactions between attaching and effacing bacteria and the host cell, and discuss EPEC/EPEC ecology, genomics and animal models of disease. Articles will centre on pathogen evolution, novel adhesins, type III effector biology and bacterium-host responses during infection.
Click here to access the Editorial Article summarizing the contributions to this Research Topic Abstract Submission Deadline:
November 15, 2011 Full Article Submission Deadline:
January 1, 2011Enteropathogenic and enterohemorrhagic
E. coli are important causes of gastrointestinal disease worldwide. As part of their pathogenesis, EPEC and EHEC cause a distinctive lesion on the intestinal mucosa known as an attaching and effacing (A/E) lesion. A/E lesion formation requires a type III secretion system that injects multiple effector proteins into the cell. Despite their shared mechanism of intestinal colonization, EPEC and EHEC exhibit substantial differences in epidemiology and clinical disease. In particular, EHEC produces a potent Shiga toxin that is associated with development of the haemolytic uremic syndrome (HUS), an acute form of renal failure. This Research Topic will examine interactions between attaching and effacing bacteria and the host cell, and discuss EPEC/EPEC ecology, genomics and animal models of disease. Articles will centre on pathogen evolution, novel adhesins, type III effector biology and bacterium-host responses during infection.
Click here to access the Editorial Article summarizing the contributions to this Research Topic Abstract Submission Deadline:
November 15, 2011 Full Article Submission Deadline:
January 1, 2011