Cellular responses to enteropathogenic Escherichia coli infection.
Enteropathogenic Escherichia coli (EPEC), first described in the 1940's and 1950's, remain an important cause of severe infantile diarrhoea in many parts of the developing world. EPEC do not produce enterotoxins and are not invasive; instead their virulence depends upon exploitation of host cell signalling pathways and the host cell cytoskeleton both as a means of colonizing mucosal surfaces of the small intestine and causing diarrhoea. Following initial mucosal attachment, EPEC secrete 'signalling' proteins and express a surface adhesin, intimin, to produce 'attaching & effacing' lesions in the enterocyte brush border membrane characterised by localised destruction of brush border microvilli, intimate bacterial adhesion and cytoskeletal reorganisation and accretion beneath attached bacteria. The pathophysiology of EPEC diarrhoea is also complex and probably results from a combination of epithelial cell responses including both electrolyte secretion and structural damage.
Knutton
S
S
Institute of Child Health, University of Birmingham, UK.
D001422:Bacterial Adhesion; D003967:Diarrhea / Q000209:etiology* / Q000382:microbiology / Q000503:physiopathology; D004926:Escherichia coli / Q000472:pathogenicity / Q000502:physiology; D004927:Escherichia coli Infections / Q000209:etiology* / Q000382:microbiology / Q000503:physiopathology; D006801:Humans; D007223:Infant; D007413:Intestinal Mucosa / Q000382:microbiology / Q000473:pathology; D008954:Models, Biological; D015398:Signal Transduction; D014774:Virulence