Molecular mimicry in Campylobacter jejuni and Helicobacter pylori lipopolysaccharides: contribution of gastrointestinal infections to autoimmunity.

Molecular mimicry of host structures by the saccharide portion of lipopolysaccharides (LPS) of the gastrointestinal pathogens Campylobacter jejuni and Helicobacter pylori is thought to be associated with the development of autoimmune sequelae. C. jejuni, a leading cause of gastroenteritis, is the most common antecedent infection in Guillain-Barré syndrome (GBS), an inflammatory neuropathy. Chemical analyses of the core oligosaccharides of neuropathy-associated C. jejuni strains have revealed structural homology with human gangliosides. Serum antibodies against gangliosides are found in one third of GBS patients but are generally absent in enteritis cases. Collective data suggest that the antibodies are induced by antecedent infection with C. jejuni, and subsequently react with nerve tissue causing damage. The O-chains of most H. pylori strains express Lewis blood group antigens which are thought to have a role in camouflage of the bacterium as these antigens are also present on human gastric epithelial cells. In chronic H. pylori infections, bacterial expression of Lewis antigens is suggested to be involved in the induction of autoantibodies against the Lewis antigen-expressing gastric proton pump. Many aspects of the autoimmune mechanisms in C. jejuni -associated GBS and H. pylori -induced atrophic gastritis remain unclear, such as the involvement of T cells and the role of host factors.