Why Helicobacter pylori has Lewis antigens
Department of Microbiology, National University of Ireland, Galway, Gaillimh, Connaught, Ireland Trends in Microbiology
(Impact Factor: 9.19).
01/2001; 8(12):565-570. DOI: 10.1016/S0966-842X(00)01875-8
In mimicry with human gastric epithelial cells, the lipopolysaccharide of Helicobacter pylori expresses Lewis blood group antigens. Recent data suggest that molecular mimicry does not promote immune evasion, nor does it lead to induction of autoantibodies, but that H. pylori Lewis X mediates adhesion to gastric epithelial cells and is essential for colonization.
Available from: PubMed Central
- "It is interesting that Lewis blood group antigens are also expressed on the O-specific chain of the lipopolysaccharide (LPS) of H. pylori. This can be understood as a kind of molecular mimicry between bacteria and host and could be involved in colonization process [9, 10]. "
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ABSTRACT: To assess the influence of monoclonal anti-Lewis b, anti-H type 1, and anti-sialyl Lewis x addition on interactions of sugar structures of MUC1 mucin with Helicobacter pylori. The investigations were carried out on gastric juices of 11 patients and 12 H. pylori strains. The levels of Lewis b and sialyl Lewis x antigens on MUC1 were assessed by sandwich ELISA tests. Anti-Lewis b, anti-H type 1 or anti-sialyl Lewis x monoclonal antibodies were added to MUC1 to determine whether the adhesion activities of H. pylori isolates to examined mucin would be affected. Binding of bacteria to MUC1 was assessed by ELISA test. Clear inhibitory effect of examined antibodies was revealed in 6 of 12 examined H. pylori isolates independently on babA2 status. In the rest of strains this effect was negligible. We confirmed participation of Lewis b, H type 1 and also sialyl Lewis x of MUC1 mucin in interactions with H. pylori independently on babA genopositivity. Not full inhibition and a lack of this effect in some strains suggest an existence of other mechanisms of H. pylori adherence to mucin.
Available from: europepmc.org
- "Heneghan et al.  proposed that anti-Lewis antibodies were present in most patients with H. pylori infection and that this response is independent from the host Lewis phenotype but is related to the bacterial Lewis phenotype. However, Appelmelk et al.  suggested that the molecular similarity of the H. pylori LPS to the Lewis antigens did not promote immune evasion, nor does it lead to induction of autoantibodies. We also reported that, although high titers of antibodies to H. pylori LPS were found in the sera of infected patients, these antibodies were not autoreactive and were not directed against the Lewis antigens . "
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ABSTRACT: We compared the serological reactivity of lipopolysaccharides (LPS) isolated from Japanese and Western strains of Helicobacter pylori against anti-Lewis antigen monoclonal antibodies and H. pylori-positive Japanese sera. The two LPS from Western strains (26695 and O:2) did not react with any sera from Japanese patients, while all LPS from Japanese strains and the Sydney strain reacted with these sera. We propose that LPS of all Japanese smooth strains share either one of two epitopes, which are termed highly antigenic and weakly antigenic epitopes, present in the O-polysaccharide portion, and these epitopes are independent the Lewis antigens. The present findings indicated that the two Western strains lacked the two epitopes, which are shared by all Japanese strains.
Available from: David J Mcgee
- "These surface LPS antigens are necessary for the establishment of infection, because mutant strains defective for LPS O-antigen synthesis or for Lewis X/Y expression fail to colonize mice [11-13]. There is evidence that Lewis antigens expressed on the bacterial surface contribute to adherence of H. pylori to gastric epithelial cells [10,14], and play a role in tissue tropism [15-17]. Gastric epithelial cells also express Lewis antigens [18,19], suggesting that the display of Lewis antigens on the bacterial surface may serve as a mimicry strategy. "
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ABSTRACT: Helicobacter pylori specifically takes up cholesterol and incorporates it into the bacterial membrane, yet little is currently known about cholesterol's physiological roles. We compared phenotypes and in vivo colonization ability of H. pylori grown in a defined, serum-free growth medium, F12 with 1 mg/ml albumin containing 0 to 50 mug/ml cholesterol.
While doubling times were largely unaffected by cholesterol, other overt phenotypic changes were observed. H. pylori strain SS1 grown in defined medium with cholesterol successfully colonized the stomach of gerbils, whereas SS1 grown without cholesterol failed to colonize. H. pylori lipopolysaccharide often displays Lewis X and/or Y antigens. Expression of these antigens measured by whole-cell ELISA was markedly enhanced in response to growth of strain SS1, 26695, or G27 in cholesterol. In addition, electrophoretic analysis of lipopolysaccharide in wild type G27 and in mutants lacking the O-chain revealed structural changes within the oligosaccharide core/lipid A moieties. These responses in Lewis antigen levels and in lipopolysaccharide profiles to cholesterol availability were highly specific, because no changes took place when cholesterol was substituted by beta-sitosterol or bile salts. Disruption of the genes encoding cholesterol alpha-glucosyltransferase or lipid A phosphoethanolamine transferase had no effect on Lewis expression, nor on lipopolysaccharide profiles, nor on the cholesterol responsiveness of these properties. Disruption of the lipid A 1-phosphatase gene eliminated the effect of cholesterol on lipopolysaccharide profiles but not its effect on Lewis expression.
Together these results suggest that cholesterol depletion leads to aberrant forms of LPS that are dependent upon dephosphorylation of lipid A at the 1-position. A tentative model for the observed effects of cholesterol is discussed in which sequential steps of lipopolysaccharide biogenesis and, independently, presentation of Lewis antigen at the cell surface, depend upon membrane composition. These new findings demonstrate that cholesterol availability permits H. pylori to modify its cell envelope in ways that can impact colonization of host tissue in vivo.
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