Mucosal production of antigastric autoantibodies in Helicobacter pylori gastritis

Background. Apart form bacterial virulence factors of Helicobacter pylori, certain host factors influence the pathogenesis of H. pylori gastritis. In particular, antigastric autoantibodies that are detectable in the sera of a substantial proportion of H. pylori were shown to correlate with the devel opment of gastric atrophy. The aim of this study was to analyze the possibl e antigastric autoimmune response in H. pylori gastritis at the site where the action is, i.e., in the gastric mucosa. Materials and Methods. Gastric biopsy specimens from antrum and corpus muco sa of 24 H. pylori-infected and of 33 noninfected patients were cultured fo r 3 days, and tissue culture supernatants were analyzed for the amount of l ocally produced IgA and IgG. Antigastric autoantibodies were screened in th e sera and in the supernatants by means of immunohistochemistry. Results. The infected patients had significantly higher concentrations of l ocally produced IgA, whereas the IgG concentrations were virtually the same in infected and noninfected patients. IgG or IgA antigastric autoantibodie s, or both, were detectable only in the sera (38%) and supernatants (17%) o f infected patients. Interestingly, the patient with the strongest local au toimmune response showed body-predominant H. pylori gastritis, with destruc tion of gastric glands and atrophy of the body mucosa. Conclusions. These results demonstrate that antigastric autoimmune reaction s are detectable at the site of the disease and might be relevant for the p athogenesis of gastric mucosa atrophy in H. pylori gastritis.