Infection of T84 cells with enteropathogenic Escherichia coli alters barrier and transport functions

Am J Physiol. 1996 Apr;270(4 Pt 1):G634-45. doi: 10.1152/ajpgi.1996.270.4.G634.


The effect of enteropathogenic Escherichia coli (EPEC) infection on electrophysiology of T84 cell monolayers was examined. After 18 h of infection with EPEC (E2348), transepithelial electrical resistance was decreased (30 +/- 5% of uninfected values) compared with monolayers infected with a nonpathogenic 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 with 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. Adenosine 3'5'-cyclic monophosphate-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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Bacterial Adhesion
  • Biological Transport
  • Calcium / metabolism
  • Cell Line
  • Cell Survival
  • Chlorides / metabolism
  • Electrophysiology
  • Escherichia coli Infections / metabolism*
  • Escherichia coli Infections / pathology
  • Escherichia coli Infections / physiopathology
  • Humans
  • Intestinal Diseases / metabolism*
  • Intestinal Diseases / pathology
  • Intestinal Diseases / physiopathology
  • Intestines / microbiology
  • Intestines / pathology
  • Intestines / physiopathology
  • Intracellular Membranes / metabolism
  • Membrane Proteins / metabolism
  • Permeability
  • Phosphoproteins / metabolism
  • Zonula Occludens-1 Protein


  • Actins
  • Chlorides
  • Membrane Proteins
  • Phosphoproteins
  • TJP1 protein, human
  • Zonula Occludens-1 Protein
  • Calcium