NOTES Helicobacter-Associated Gastritis in SCID Mice

Immunodeficient (SCID) and immunocompetent mice were infected with Helicobacter felis to address the role of autoimmunity in Helicobacter-associated gastritis. The extents of inflammation were equivalent in the two groups. The numbers of H. felis organisms were marginally increased in the SCID mice but did not achieve statistical significance. These results indicate that autoimmunity is not necessary to induce disease and that the presence of an adaptive immune system does not significantly affect H. felis colonization. Colonization of the gastric antrum by Helicobacter pylori can result in the development of type B chronic gastritis and peptic ulcers (17) or gastric mucosa-associated lymphoid tissue lym-phomas (10, 21) and may increase the risk of developing gastric carcinoma (6). H. pylori infections rarely resolve spontane-ously, and the chronic active gastritis that accompanies colo-nization is typically maintained for the duration of infection. Previous work has established that the chronic inflammatory infiltrate associated with H. pylori and Helicobacter felis has characteristics of adaptive immunity such as lymphoid aggre