MOLECULAR MIMICRY OF HOST STRUCTURES BY LIPOPOLYSACCHARIDES OF CAMPYLOBACTER AND HELICOBACTER SPP - IMPLICATIONS IN PATHOGENESIS

Molecular mimicry of host structures by the saccharide portion of lipo polysaccharide (LPS) contributes to the virulence of certain strains o f mucosal pathogens. Mimicry by the low molecular weight (low-M(r)) LP Ss of Neisseria and Haemophilus spp. have been the most extensively st udied. However, studies within the last decade have revealed other typ es of mimicry within the saccharide moieties of LPSs of the enteric pa thogen Campyiobacter jejuni and the gastroduodenal pathogen Helicobact er pylori The core oligosaccharides of low-M(r) LPSs of C. jejuni sero types which are associated with the development of Guillain-Barre synd rome (GBS), a neurological disorder, exhibit mimicry of gangliosides. Cross-reactive antibodies between LPSs and gangliosides which are indu ced during antecedent C. jejuni infection are considered to play an im portant role in GBS pathogenesis. The O-polysaccharide chains of high- M(r) LPSs of a number of H. pylori strains mimic Lewis(x) and/or Lewis (Y) blood group antigens. This mimicry may camouflage the bacterium in the gastric mucosa upon initial infection. With the progression of in fection, the mimicry may play a role in immune response regulation and the induction of autoantibodies against the gastric proton pump, a gl ycoprotein that also expresses Lewis antigens.