Helicobacter infections in laboratory animals: a model for gastric neoplasias?

Ann Med. 1995 Oct;27(5):575-82. doi: 10.3109/07853899509002472.

Abstract

Evidence is rapidly accumulating that Helicobacter pylori is a major risk factor for human gastric adenocarcinomas and all low-grade B-cell gastric lymphomas. Given this, there is a need to develop animal models with a view to discovering not only how carcinogenesis is initiated, but also how the process can be prevented. The lack of H. pylori animal models suitable for long-term studies means that alternatives are needed. The most productive models are likely to be the Helicobacter mustelae-infected ferret or the mouse infected with either Helicobacter felis or 'Helicobacter heilmannii'. The first evidence that helicobacter infection induces a chronic inflammation that progresses to gastric atrophy, the precursor lesion to gastric adenocarcinoma in humans, has come from the mouse model. The severity of inflammation is dependent on the type of mouse strain used, highlighting the importance of host factors in the development of gastritis. Carcinogenesis studies should only be done with mouse strains known to cause atrophy. The H. mustaelae-infected ferret appears very susceptible to the development of adenocarcinoma following ingestion of chemical carcinogens. Long-term infection of mice with H. felis results in the development of low-grade B-cell gastric lymphomas indistinguishable to those found in H. pylori-infected humans. Helicobacter-infected animals, rodents in particular are going to provide exciting opportunities to investigate not only important aspects of gastric cancer and lymphoma but also fundamental issues of carcinogenesis in general.

MeSH terms

  • Animals
  • Disease Models, Animal*
  • Ferrets
  • Gastritis, Atrophic / complications
  • Gastritis, Atrophic / microbiology*
  • Gastritis, Atrophic / pathology
  • Helicobacter Infections / complications
  • Helicobacter Infections / pathology
  • Mice
  • Stomach / microbiology
  • Stomach Neoplasms* / etiology