Helicobacter pylori LPS: molecular mimicry with the host and role in autoimmunity.

Helicobacter pylori lipopolysacchararide expresses Lewis x and/or y blood group antigens in mimicry with human gastric epithelial cells. Mimicry may have two diverging roles in pathogenesis. Infection may break tolerance and anti-Lewis antibodies may be induced that bind to gastric mucosa and cause damage. Secondly, mimicry may cause "invisibility" of the pathogen to the host, thus aiding persistence of infection. We demonstrate that Helicobacter pylori induces autoantibodies during infection. In orally infected pigs, these were specific for Lewis epitopes present on parietal cell H+K(+)-ATPase. In contrast, in infected patients the autoantibodies were directed to protein epitopes of H+K(+)-ATPase not induced through mimicry.