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

被引:126
作者
Philpott, DJ
McKay, DM
Sherman, PM
Perdue, MH
机构
[1] HOSP SICK CHILDREN, RES INST, DIV GASTROENTEROL, TORONTO, ON M5G 1X8, CANADA
[2] UNIV TORONTO, DEPT PEDIAT, TORONTO, ON M5G 1X8, CANADA
[3] UNIV TORONTO, DEPT MICROBIOL, TORONTO, ON M5G 1X8, CANADA
[4] MCMASTER UNIV, INTESTINAL DIS RES PROGRAM, HAMILTON, ON L8N 3Z5, CANADA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY | 1996年 / 270卷 / 04期
关键词
enteropathogenic Escherichia coli; diarrhea; electrophysiology; permeability;
D O I
10.1152/ajpgi.1996.270.4.G634
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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.
引用
收藏
页码:G634 / G645
页数:12
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