Characterisation of Escherichia coli strains involved in transcytosis across gut epithelial cells exposed to metabolic and inflammatory stress.

Translocation of normally non-pathogenic bacteria across the gut may drive inflammatory responses associated with sepsis and inflammatory bowel disease. Recent evidence suggests translocation may not be purely passive, but occurs via novel transcellular pathways activated in enterocytes by inflammatory and metabolic stress. The specificity of this pathway with respect to different E. coli strains and other bacterial species, and possible molecular determinants of the "translocating" phenotype have been investigated. Translocation of E. coli strains and other bacteria was studied across Caco-2 monolayers exposed to different forms of cellular stress. All bacteria, apart from the pathogen Shigella sonnei, exhibited low levels of translocation in untreated monolayers. However, following enterocyte stress, translocation of E. coli strains C25 and HBTEC-1 was markedly stimulated, accompanied by increased internalisation into enterocytes. C25 and HBTEC-1 were typed to ECOR group A and group D respectively. Pathoarray analysis showed both strains had profiles quite different to those predicted for typical ExPEC isolates, lacking many of the genes associated with pathogenicity, although they contained several ORFs in common with ExPEC isolates. These data suggest translocating E. coli strains associated with infections are not opportunistic ExPEC strains but may comprise a separate group of E. coli strains.