کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3417124 1225181 2008 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Caspases-3, -8, and -9 are required for induction of epithelial cell apoptosis by enteropathogenic E. coli but are dispensable for increased paracellular permeability
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی میکروب شناسی
پیش نمایش صفحه اول مقاله
Caspases-3, -8, and -9 are required for induction of epithelial cell apoptosis by enteropathogenic E. coli but are dispensable for increased paracellular permeability
چکیده انگلیسی

Enteropathogenic Escherichia coli (EPEC) is an important cause of diarrhea, particularly among infants in developing countries. An increase in intestinal permeability due to EPEC infection has been suggested as a factor in the development of diarrhea. Abnormally high levels of programmed cell death (apoptosis) of intestinal epithelial cells can lead to increased intestinal permeability. The effects of EPEC on cell apoptosis remain incompletely understood. This study characterized the mechanisms of EPEC-induced epithelial apoptosis and examined whether this effect contributes to heightened permeability in an in vitro model of infection. We report that EPEC-induced apoptosis in T84 intestinal epithelial cells via a mechanism involving caspases-3, -6, -8, and -9, the cleavage of PARP, and oligonucleosome formation. In addition, EPEC time-dependently increased paracellular permeability as assessed by transepithelial resistance and the apical-to-basolateral movement of 3000 MW dextran. Furthermore, EPEC infection led to the cleavage and mislocalization of tight junctional ZO-1 and occludin. However, pharmacological inhibition of caspases did not prevent the EPEC-induced disruptions in epithelial barrier structure and function. Taken together, these results suggest that a caspase-dependent upregulation in epithelial cell apoptosis during EPEC infection occurs independent of impaired intestinal barrier function.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Microbial Pathogenesis - Volume 44, Issue 4, April 2008, Pages 311–319
نویسندگان
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