A genetic basis for atrophy: Dominant non-responsiveness and helicobacter induced gastritis in F1 hybrid mice

P. Sutton, J. Wilson, R. Genta, D. Torrey, A. Savinainen, J. Pappo, A. Lee

Research output: Contribution to journalArticlepeer-review

34 Scopus citations


Background - The importance of host factors in helicobacter induced gastritis has been shown in animal models. Infection of most mouse strains with Helicobacter felis results in a functional atrophic gastritis, while other strains remain gastritis free. Aims - To investigate these host factors further by using genetic crosses of responder and non-responder mice. Methods - F1 hybrids of the non-responder CBA/Ca strain and three strains of mice known to develop H felis induced gastritis were infected for three months with H felis. Gastritis was assessed by histopathology and serum antibody responses by ELISA. Results - Infection of CBA/Ca mice and F1 hybrids induced little or no gastritis. Analyses of the antibody responses in these mice revealed virtually undetectable anti-helicobacter antibody levels despite colonisation with high numbers of H felis. In contrast, infection of H felis responsive strains induced gastritis and a significant humoral immune response. Conclusions - The non-responsiveness of CBA/Ca mice to H felis infection is dominantly inherited. The lack of gastritis in GBA mice and their offspring is probably due to active suppression of the immune response normally mounted against H felis. Investigation of these mechanisms will provide important insights relevant to induction of gastric atrophy and cancer in humans.

Original languageEnglish (US)
Pages (from-to)335-340
Number of pages6
Issue number3
StatePublished - 1999


  • CBA
  • F hybrid
  • Gastritis
  • Helicobacter
  • Non-responsiveness

ASJC Scopus subject areas

  • Gastroenterology


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