AUTOANTIBODIES TO GASTRIC-MUCOSA IN HELICOBACTER-PYLORI INFECTION

Background. Although Helicobacter pylori is recognized as the main cau se of chronic gastritis and its associated diseases, very little is kn own about the pathogenetic mechanisms leading to intestinal metaplasia and atrophic gastritis.Methods. We reviewed the data regarding the po ssible pathogenetic role played by the anti-H. pylori immune responses in the genesis of atrophic gastritis and intestinal metaplasia. Resul ts. Although only type A (corpus-restricted atrophic gastritis), often associated to pernicious anemia, is considered autoimmune in nature, abundant evidence supports the presence of cellular and humoral autoim mune responses also in patients with H. pylori infection. In a mechani sm known as antigenic mimicry, highly conserved immunogenic molecules expressed by infectious pathogens may act as a trigger for the inducti on of humoral and cellular immune responses that cross-react with host cellular antigens. Numerous studies support the view that H. pylori i s very effective in inducing antigenic mimicry, and antibodies against H. pylori have been found to cross-react with both antral mucosal cel ls (the membrane of the secretory canalicular structures of the pariet al cells) and gastrin-producing cells. Such autoantibodies were detect ed both in hu man infections and in experimental work in rodents. Conc lusions. The detection of antibodies that cross react with H. pylori a nd various components of the gastric mucosa provides strong support to the view that immune responses against H. pylori not only participate in the pathogenetic mechanisms leading to atrophy in the progressive atrophic gastritis associated with Helicobacter infection but also in the corpus-restricted autoimmune gastritis.