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

Abstract

BACKGROUND The importance of host factors in helicobacter induced gastritis has been shown in animal models. Infection of most mouse strains withHelicobacter 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 CBA 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.

  • helicobacter
  • non-responsiveness
  • gastritis
  • F1 hybrid
  • CBA
  • Abbreviations used in this paper

    LPS
    lipopolysaccharide
    MHC
    major histocompatibility complex
    BHI
    brain heart infusion
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  • Abbreviations used in this paper

    LPS
    lipopolysaccharide
    MHC
    major histocompatibility complex
    BHI
    brain heart infusion
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