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Epithelial cell turnover and apoptosis.

M Anti1, A Armuzzi, G Gasbarrini

  • 1Chair of Internal Medicine, Catholic University, Rome, Italy. iclcm@rm.unicatt.it

Italian Journal of Gastroenterology and Hepatology
|March 17, 1999
PubMed
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Gastric epithelial cell turnover, involving proliferation and apoptosis, is disrupted in stomach diseases. Helicobacter pylori infection alters cell proliferation, but its impact on apoptosis remains unclear.

Area of Science:

  • Gastroenterology
  • Cell Biology
  • Oncology

Background:

  • Gastric epithelial homeostasis relies on balanced cell proliferation and apoptosis.
  • Alterations in these processes are linked to chronic stomach pathologies like gastritis, atrophy, metaplasia, dysplasia, and cancer.
  • Helicobacter pylori infection is implicated in altered gastric epithelial cell turnover.

Purpose of the Study:

  • To investigate the role of cell proliferation and apoptosis in gastric diseases.
  • To examine the impact of Helicobacter pylori infection on gastric epithelial cell turnover.
  • To clarify the controversial effects of H. pylori on gastric epithelial apoptosis.

Main Methods:

  • Review of existing literature on gastric epithelial cell proliferation and apoptosis in various pathological conditions.

Related Experiment Videos

  • Analysis of studies investigating the association between Helicobacter pylori infection and changes in gastric epithelial cell turnover.
  • Examination of research exploring the influence of H. pylori cagA status on epithelial apoptosis.

    • Main Results:

    • Increased epithelial cell proliferation and altered distribution are common in chronic gastritis, atrophy, metaplasia, dysplasia, and gastric cancer.
    • Apoptosis is impaired in intestinal metaplasia, gastric dysplasia, and cancer.
    • H. pylori infection increases cell proliferation, which is reversible upon eradication, but this reversibility may be lost in later stages of carcinogenesis.
    • The effect of H. pylori on apoptosis is controversial and may depend on the cagA status of the bacteria.

    Conclusions:

    • Disrupted cell proliferation and apoptosis are key features of gastric carcinogenesis.
    • H. pylori significantly influences gastric epithelial cell proliferation, with potential implications for early carcinogenesis.
    • Further research is required to fully understand H. pylori's impact on gastric epithelial apoptosis in humans, particularly concerning cagA variations.