Helicobacter pylori, neutrophils, interleukins, and gastric epithelial proliferation

J Clin Gastroenterol. 1997;25 Suppl 1:S198-202. doi: 10.1097/00004836-199700001-00031.

Abstract

Infection of Helicobacter pylori causes chronic gastritis and plays an important role in the pathogenesis of gastroduodenal ulceration. H. pylori has also been suggested to be involved in the genesis of adenocarcincoma and MALT lymphoma of the stomach. H. pylori infection is associated with increased gastric epithelial proliferation, which can be reversed by a successful eradication of the organism. Although the mechanisms of increased gastric epithelial proliferation is not known, the enhanced epithelial proliferation is important in developing gastric carcinoma. Whether or not H. pylori de nove stimulates gastric epithelial proliferation is controversial, but gastric infection with H. pylori activates a mucosal inflammatory response by consisting of large numbers of polymorphonuclear and mononuclear cells, that also includes expression of various cytokines including interleukin-8. We review the mechanisms of H. pylori in enhanced gastric epithelial cell proliferation and cytokines in patients with H. pylori infection.

Publication types

  • Review

MeSH terms

  • Animals
  • Cytokines / metabolism*
  • Gastric Mucosa / microbiology
  • Gastric Mucosa / pathology
  • Gastritis / microbiology*
  • Gastritis / pathology
  • Helicobacter Infections / pathology*
  • Helicobacter pylori*
  • Humans
  • Interleukin-8 / metabolism*
  • Neutrophils*
  • Peptic Ulcer / microbiology*
  • Peptic Ulcer / pathology
  • Stomach Neoplasms / microbiology*
  • Stomach Neoplasms / pathology

Substances

  • Cytokines
  • Interleukin-8