Infection of t84 intestinal epithelial cells with enteropathogenic
escherichia coli alters barrier and transport functions.
Philpott, Dana J., Derek M. McKay*, Philip M. Sherman, and Mary H.
Perdue.
Division of Gastroenterology, Research Institute, The Hospital for
Sick Children and Departments of Pediatrics and Microbiology,
University of Toronto, Toronto, Ontario, Canada; Intestinal Disease
Research Program, McMaster University, Hamilton, Ontario, Canada
APStracts 2:0207G, 1995.
The effects of enteropathogenic Escherichia coli (EPEC) infection on
electrophysiology of T84 cell monolayers was examined. After 18 hours
of infection with EPEC (E2348), transepithelial electrical resistance
was decreased (30 + 5 % of uninfected values) compared to monolayers
infected with a non-pathogenic E. coli strain (104 + 13 %).
Resistance of monolayers infected with EPEC mutant strain CVD206,
deficient in attaching and effacing lesion formation, was partially
reduced (66 + 10 %). In addition, permeability of EPEC-infected T84
monolayers increased compared to uninfected cells. Associated with
these changes was an altered distribution of the tight junction
protein, ZO-1. Taken together, these findings suggest that the
barrier defect induced by EPEC was at the level of the tight
junction. Cyclic AMP-stimulated chloride secretion was also
diminished in EPEC-infected cells whereas Ca2+-dependent chloride
secretion was not different from uninfected cells. These findings
indicate that EPEC infection alters intestinal epithelial barrier and
transport functions. Furthermore, these results provide a possible
mechanism for EPEC-induced diarrheal disease.
Received 14 December 1994; accepted in final form 30 September
1995.
APS Manuscript Number G490-4.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95