Autoantibodies to gastric mucosa in Helicobacter pylori infection

Although Helicobacter pylori is recognized as the main cause of chronic gastritis and its associated diseases, very little is known about the pathogenetic mechanisms leading to intestinal metaplasia and atrophic gastritis.

We reviewed the data regarding the possible pathogenetic role played by the anti-H. pylori immune responses in the genesis of atrophic gastritis and intestinal metaplasia.

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 autoimmune responses also in patients with H. pylori infection. In a mechanism known as antigenic mimicry, highly conserved immunogenic molecules expressed by infectious pathogens may act as a trigger for the induction of humoral and cellular immune responses that cross-react with host cellular antigens. Numerous studies support the view that H. pylori is very effective in inducing antigenic mimicry, and antibodies against H. pylori have been found to cross-react with both antral mucosal cells (the membrane of the secretory canalicular structures of the parietal cells) and gastrin-producing cells. Such autoantibodies were detected both in human infections and in experimental work in rodents.

The detection of antibodies that cross-react with H. pylori and 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.