Helicobacter pylori infection and the pathogenesis of duodenal ulceration

Ann N Y Acad Sci. 1998 Nov 17;859:96-111. doi: 10.1111/j.1749-6632.1998.tb11114.x.

Abstract

Helicobacter pylori is a gram-negative spiral bacterium confined to the habitat of gastric-type epithelium. H. pylori causes duodenal ulceration by a cumulative effect of antral predominant gastritis with increased acid secretion, consequent gastric metaplasia in the duodenum (a site of further colonization by H. pylori), duodenitis, reduced duodenal bicarbonate secretion, and mucosal damage. Bacterial factors influence outcome. Major determinants are the production of a vacuolating toxin and the presence of CagA, an immunodominant product of a nonconserved gene cagA, a marker for the cag pathogenicity island that encodes virulence genes involved in induction of epithelial chemokine responses. In ulcer patients the mucosal immune response is polarized to a T-helper-1 (Th1) cell-mediated response, which may contribute to mucosal damage. Eradication of H. pylori restores acid output to normal. Loss of both acid and bacteria halts gastroduodenitis and allows ulcer healing. Gastric metaplasia does not regress in the short term.

Publication types

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

MeSH terms

  • Animals
  • Antigens, Bacterial*
  • Bacterial Proteins / genetics
  • Duodenal Ulcer / microbiology
  • Duodenal Ulcer / pathology
  • Duodenal Ulcer / physiopathology*
  • Duodenum / pathology
  • Gastric Acid / metabolism
  • Gastric Mucosa / pathology
  • Gastritis / etiology
  • Gastritis / microbiology
  • Gastritis / physiopathology
  • Helicobacter Infections / complications
  • Helicobacter Infections / pathology
  • Helicobacter Infections / physiopathology*
  • Helicobacter pylori* / genetics
  • Helicobacter pylori* / pathogenicity
  • Humans
  • Intestinal Mucosa / microbiology
  • Intestinal Mucosa / pathology
  • Metaplasia
  • Th1 Cells / immunology

Substances

  • Antigens, Bacterial
  • Bacterial Proteins
  • cagA protein, Helicobacter pylori