Molecular mimicry between Helicobacter pylori and the host

Abstract

The presence of autoantibodies directed against gastric mucosa in sera of patients infected with H. pylori was first demonstrated by Negrini et al.1 To detect these antibodies, immunohistochemistry was performed with patient sera tested on sections of gastric corpus mucosal tissue from a non-infected person. Two autoimmune targets were identified: the luminal membrane of foveolar epithelium and the canaliculi (Figure 1) of the parietal cells2-4. It is known that a major fraction of the parietal cell canaliculi consists of H+,K+-ATPase, the enzyme that pumps protons into the lumen of the stomach5. Peptide epitopes present on gastric H+,K+-ATPase are known to be targets for autoantibodies present in autoimmune gastritis (AIG) and pernicious anaemia (PA)6. It is also known that H. pylori lipopolysaccharide (LPS) expresses Lewis blood group antigens (see below), similar to those occurring in the gastric mucosa7. Hence, at least theoretically, autoantibodies may be induced by molecular mimicry, i.e. during infection antibodies are induced to H. pylori LPS (= anti-Lewis x/y) that also recognize gastric Lewis antigens. The occurrence of anti-canalicular antibodies in sera of H. pylori-infected patients correlated with the presence of corpus glandular atrophy and with other histopathological and physi-ological changes (Table 1)2-4,8. The nature of the process that leads to corpus atrophy is not well understood, but an autoimmune mechanism seems plausible.