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Review: Molecular mimicry of host structures by lipopolysaccharides of Campylobacter and Helicobacter spp.: implications in pathogenesis

Department of Microbiology, University College, Galway, Ireland, anthony.moran{at}ucg.ie

B.J. Appelmelk

Department of Medical Microbiology, School of Medicine, Vrije Universiteit, Amsterdam, The Netherlands

G.O. Aspinall

Department of Chemistry, York University, Toronto, Ontario, Canada

Molecular mimicry of host structures by the saccharide portion of lipopolysaccharide (LPS) contributes to the virulence of certain strains of mucosal pathogens. Mimicry by the low molecular weight (low-M_r) LPSs of Neisseria and Haemophilus spp. have been the most extensively studied. However, studies within the last decade have revealed other types of mimicry within the saccharide moieties of LPSs of the enteric pathogen Campylobacter jejuni and the gastroduodenal pathogen Helicobacter pylori. The core oligosaccharides of low-M_r LPSs of C. jejuni serotypes which are associated with the development of Guillain-Barré syndrome (GBS), a neurological disorder, exhibit mimicry of gangliosides. Cross-reactive antibodies between LPSs and gangliosides which are induced during antecedent C. jejuni infection are considered to play an important 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 infection, the mimicry may play a role in immune response regulation and the induction of autoantibodies against the gastric proton pump, a glycoprotein that also expresses Lewis antigens.

Journal of Endotoxin Research, Vol. 3, No. 6, 521-531 (1996)
DOI: 10.1177/096805199600300611


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