Apoptosis in gastric epithelial cells is induced by Helicobacter pylori and accompanied by increased expression of BAK

Biochem Biophys Res Commun. 1997 Oct 20;239(2):626-32. doi: 10.1006/bbrc.1997.7485.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Apoptosis*
  • Cell Line
  • Coculture Techniques
  • Epithelial Cells / metabolism*
  • Epithelial Cells / microbiology*
  • Epithelial Cells / ultrastructure
  • Gastric Mucosa / metabolism*
  • Helicobacter pylori / growth & development
  • Helicobacter pylori / physiology*
  • Helicobacter pylori / ultrastructure
  • Humans
  • Membrane Proteins / biosynthesis*
  • Nucleic Acid Hybridization
  • Pyloric Antrum / chemistry
  • Pyloric Antrum / microbiology
  • Pyloric Antrum / ultrastructure
  • Staining and Labeling
  • Stomach / microbiology*
  • Stomach / ultrastructure
  • bcl-2 Homologous Antagonist-Killer Protein


  • BAK1 protein, human
  • Membrane Proteins
  • bcl-2 Homologous Antagonist-Killer Protein