Novel effects of the prototype translocating Escherichia coli , strain C25 on intestinal epithelial structure and barrier function

Summary Intestinal bacteria play an etiologic role in triggering and perpetuating chronic inflammatory bowel disorders. However, the precise mechanisms whereby the gut microflora influences intestinal cell function remain undefined. Therefore, the effects of the non‐pathogenic prototype translocating Escherichia coli , strain  C25  on  the  barrier  properties  of  human  T84  and Madine‐Darby canine kidney type 1 epithelial cells  were  examined.  T‐84  cells  were  also  infected  with commensal E. coil , strains F18 and HB101, and enterohaemorrhagic E. coli , serotype O157:H7. Strains F18 and HB101 had no effect on transepithelial electrical resistance (TER) of T84 monolayers. By contrast, epithelial cells infected with strain C25 displayed a time‐dependent decrease in TER, preceded by an altered distribution of the cytoskeletal protein alpha‐actinin, comparable to infection with E. coli O157:H7. E. coli C25 infection also led to activation of nuclear factor κB (NF‐κB), interleukin‐8 secretion and alterations in localization of claudin‐1, but not zona occludens‐1 or claudin‐4, in T84 cells. There were adherent C25 bacteria on the intact apical surface of infected T84 cells, while mitochondria appeared swollen and vacuolated. These novel findings demonstrate the ability of a translocating commensal bacterium to adhere to and modulate intestinal epithelial barrier function and to induce morphological changes in a manner distinct from the known enteric pathogen,  E. coli O157:H7.