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 3:0049C, 1996.
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 13 November 1995; accepted in final form 17 January
1996.
APS Manuscript Number C688-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 February 96