Apoptosis in Gastric Epithelial Cells Is Induced byHelicobacter pyloriand Accompanied by Increased Expression of BAK

G. Chen, Emilia Mia Sordillo, William G. Ramey, Jason Reidy, Peter R. Holt, Stanisław Krajewski, John C. Reed, Martin J. Blaser, Steven F. Moss

Biochemical and Biophysical Research Communications · 1997 · 110 citations · 21 references

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Abstract

Carriage of the bacterium H. pylori in the human stomach is associated with evidence of increased epithelial cell apoptosis. This may be of significance in the etiology of gastritis, peptic ulcers, and neoplasia. The ability of H. pylori to directly induce epithelial apoptosis was examined in vitro by fluorescence and electron microscopy, flow cytometry, and DNA fragmentation ELISA. The induction of apoptosis by H. pylori was time and concentration-dependent and inhibited by preventing direct bacterial-epithelial cell contact. Apoptosis was accompanied by increased expression of Bak, with little change in expression of other Bcl-2 family proteins. The expression of Bak was also increased in gastric biopsies from patients colonized by H. pylori. Thus, H. pylori induces gastric epithelial cell apoptosis, by a Bak-dependent pathway.

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