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

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.