Augmentation of water-immersion stress- induced gastric mucosal lesions in BALB/c mice infected with Helicobacter felis

Digestion. 1999 Jan-Feb;60(1):34-40. doi: 10.1159/000007586.

Abstract

Background and aims: Inoculation of Helicobacter felis into the murine stomach has been reported to induce chronic gastric inflammation and may be a model of Helicobacter pylori-induced chronic gastritis. In this study, to characterize H. felis-induced gastritis, the gastric production of interleukin-1beta (IL-1beta) and hepatocyte growth factor (HGF) was measured in mice.

Methods: Gastric mucosal lesions were induced in H. felis-infected BALB/c mice by water-immersion stress. The severity score of gastric erosions per stomach was measured as the sum of the length of erosions. Gene expression of IL-1beta and HGF were analyzed by Northern blot analysis and production of HGF was examined using the enzyme immunoassay method.

Results: Water-immersion stress induced gastric mucosal lesions accompanied by increased expression of IL-1beta mRNA. H. felis infection evoked enhanced expression of IL-1beta and HGF genes. When H. felis-infected mice were stressed by water immersion, the mucosal lesions were more severe than those in non-infected mice. Moreover, IL-1beta gene expression as well as HGF production was further increased.

Conclusions: Although H. felis inoculation did not cause gastric mucosal erosions by itself, it augmented the stress-induced erosions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Northern
  • Female
  • Gastric Mucosa / pathology
  • Gastritis / microbiology*
  • Gastritis / physiopathology
  • Helicobacter / pathogenicity*
  • Helicobacter Infections / pathology*
  • Helicobacter Infections / physiopathology
  • Hepatocyte Growth Factor / biosynthesis
  • Immersion / physiopathology
  • Interleukin-1 / biosynthesis
  • Mice
  • Mice, Inbred BALB C
  • RNA, Messenger / genetics
  • Stomach Ulcer / microbiology
  • Stomach Ulcer / pathology*
  • Stomach Ulcer / physiopathology
  • Stress, Physiological / physiopathology*
  • Time Factors

Substances

  • Interleukin-1
  • RNA, Messenger
  • Hepatocyte Growth Factor