Hypotheses on the Pathogenesis and Natural History of Helicobacter Pylori-Induced Inflammation

Gastroenterology. 1992 Feb;102(2):720-7. doi: 10.1016/0016-5085(92)90126-j.

Abstract

Although Helicobacter pylori is now recognized as playing an etiologic role in chronic gastritis and peptic ulcer disease, information on the pathogenesis and natural history of infection is limited. A model is proposed in which luminal H. pylori secrete substances that mediate inflammation that is beneficial to the organism but ultimately deleterious for the host; in addition to tissue damage, inflammation also affects gastric secretory function. In this model, the host may attempt to suppress the inflammatory response, and the adequacy of this postulated down-regulation determines pathological and clinical outcome. The effects of the inflammatory process on gastrin-hydrochloric acid homeostasis may be of critical importance in the pathogenesis of peptic ulcer disease. Because the long-term consequences of H. pylori colonization reflect the continued presence of the organism in the host over years or decades, it may be useful to consider this as a "slow" bacterial infection.

Publication types

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

MeSH terms

  • Gastritis / immunology
  • Gastritis / microbiology*
  • Gastritis / physiopathology
  • Helicobacter Infections / immunology
  • Helicobacter Infections / physiopathology*
  • Helicobacter pylori*
  • Humans
  • Peptic Ulcer / microbiology