INFECTION OF T84 CELLS WITH ENTEROPATHOGENIC ESCHERICHIA-COLI ALTERS BARRIER AND TRANSPORT FUNCTIONS

The effect of enteropathogenic Escherichia coli (EPEC) infection on el ectrophysiology of T84 cell monolayers was examined. After 18 h of inf ection with EPEC (E2348), transepithelial electrical resistance was de creased (30 +/- 5%, of uninfected values) compared with monolayers inf ected with a nonpathogenic E. coli strain (104 +/- 13%). Resistance of monolayers infected with EPEC mutant strain CVD206, deficient in atta ching and effacing lesion formation, was partially reduced (66 +/- 10% ). In addition, permeability of EPEC-infected T84 monolayers increased compared with uninfected cells. Associated with these changes was an altered distribution of the tight junction protein, ZO-1. Taken togeth er, these findings suggest that the barrier defect induced by EPEC was at the level of the tight junction. Adenosine 3',5'-cyclic monophosph ate-stimulated chloride secretion was also diminished in EPEC-infected cells, whereas Ca2+-dependent chloride secretion was not different fr om uninfected cells. These findings indicate that EPEC infection alter s intestinal epithelial barrier and transport functions. Furthermore, these results provide a possible mechanism for EPEC-induced diarrheal disease.