Infection with Helicobacter pylori leads to persistent gastric inflammation and gastric and duodenal ulceration, and is associated with development of mucosa-associated lymphoid tissue (MALT) lymphoma and with loss of gastric glands in the antrum and corpus. This disappearance of mucus- and acid-secreting cells from the mucosa is referred to as atrophy (43). Atrophy is a precursor of gastric adenocarcinoma. As yet, the mechanisms responsible for the induction of atrophy are not defined and the induction of atrophy is enigmatic. Although H. pylori is not invasive and usually resides in the antrum, glands deep in the mucosa of antrum and corpus disappear. Experimental infection in mice shows that colonization takes place mainly in the antrum, but atrophy occurs in the corpus (62). Recent data in humans suggest that an H. pylori-driven autoimmune process causes gastric corpus atrophy.
In this chapter, the antigastric antibody responses to H. pylori infection in humans are described. Particular types of antibodies, those directed against parietal cell canaliculi, are likely to be clinically relevant in H. pylori-associated antigastric autoimmunity. Second, the pathogenesis of classical autoimmune gastritis and pernicious anemia (AIG/PA) and the pathogenesis of H. pylori-associated atrophic gastritis are reviewed. Because of the striking similarities between AIG/PA and H. pylori gastritis accompanied by corpus atrophy and autoantibodies, it seems plausible to consider an initiating role of H. pylori in AIG/PA.
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