Role of apoptosis in Helicobacter pylori-associated gastric mucosal injury

J Gastroenterol Hepatol. 2000 Mar:15 Suppl:D46-54. doi: 10.1046/j.1440-1746.2000.02147.x.

Abstract

Apoptosis, a programmed cell death, was ignored, just like Helicobacter pylori, only to reappear recently. However, the number of current publications dealing with apoptosis or H. pylori has increased exponentially. Although gastric epithelial apoptosis is a programmed physiological event in the superficial aspect of the mucosa and is important for healthy cell turnover, H. pylori infection reportedly promotes such a cell death sequence. Because apoptosis regulates the cycle of cell turnover in balance with proliferation, dysregulation of apoptosis or proliferation evoked by H. pylori colonization would be linked to the gastric carcinogenesis. In other words, a reduced level of apoptosis could contribute to the generation of gastric cancer. Herein, we review apoptosis as well as its associated pathological events, such as hyperproliferation, in H. pylori-colonized gastric mucosa.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis*
  • Cell Division
  • Chloramines / metabolism
  • Disease Models, Animal
  • Gastric Mucosa / microbiology*
  • Gastric Mucosa / pathology
  • Genes, bcl-2 / physiology
  • Genes, p53 / physiology
  • Gerbillinae
  • Helicobacter pylori* / metabolism
  • Humans
  • Mice
  • Oxidation-Reduction
  • Stomach Diseases / microbiology*

Substances

  • Chloramines
  • chloramine