Why Helicobacter pylori has Lewis antigens

Institute for Biological Sciences, NRC, 100 Sussex Drive, Ottawa, Ontario, Canada K1A 0R6
Trends in Microbiology (Impact Factor: 9.81). 01/2001; 8(12):565-570. DOI: 10.1016/S0966-842X(00)01875-8

ABSTRACT 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.

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    • "However, there are contradictory observations about these hypotheses. Currently, the best evidence for the role of H. pylori Lewis glycans is that they may play a role in the adhesion or colonization of the bacterium to the host gastric mucosa (reviewed in Appelmelk et al., 2000; Gerhard et al., 2002; Moran and Prendergast, 2001). Especially, H. pylori Le x has been suggested to mediate adhesion to gastric epithelial cells and to be essential for colonization (Appelmelk and Vandenbroucke-Grauls, 2000; Edwards et al., 2000; Martin et al., 2000; Osaki et al., 1998). "
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    ABSTRACT: After the breakthroughs in genomic sequencing, one of the next challenges remains to understand the molecular biology of other classes of biomolecules, such as protein and lipids, many of which carry specific glycomodification when mediating their biological functions. This review focuses on the 6-deoxyhexose biosynthesis of cell surface glycans of three Gram-negative pathogens, Helicobacter pylori, Pseudomonas aeruginosa, and Actinobacillus actinomycetemcomitans serotype a. 6-Deoxysugars are important functional components of cell surface glycans, and their biosynthetic pathways might be suitable targets for novel interventions of antibacterial chemotherapy.
    Glycobiology 04/2004; 14(3):1R-15R. DOI:10.1093/glycob/cwh040 · 3.14 Impact Factor
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    • "To this end, we are assembling gastric histological material taken at the time of H. pylori culture from the majority of the patients. The selectin binding we have observed is distinct from the previously reported, carbohydrate-mediated interactions of H. pylori [14]. Among these are interactions with gastric epithelial cells mediated by the bacterial Fig. 2. Inhibition of E-and L-selectin binding to suspensions of H. pylori isolates by selectin ligands or EDTA. "
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    ABSTRACT: The deleterious effects of Helicobacter pylori infection of the stomach are largely the result of a vigorous chronic inflammatory response, and include chronic gastritis, peptic ulceration and gastric cancer. We are exploring the possibility that carbohydrate components on H. pylori contribute to the persistent inflammation through interactions with leukocyte-endothelial adhesion molecules of the host. Lipopolysaccharides of most H. pylori strains contain sequences related to the Lewis (Le(x) or Le(a)) antigens. Carbohydrate sequences of this family encompass ligands for the leukocyte-endothelium adhesion molecules of the host, namely, the E- and P-selectins, which are expressed on inflamed endothelia, and L-selectin, which is constitutively expressed on leukocytes. Here we investigate H. pylori isolates from patients with chronic gastritis, duodenal ulcer and gastric cancer for their interactions with the selectins. Our results provide unequivocal evidence of interactions of isolates from each of the diagnostic groups with E- and L-selectins.
    FEMS Immunology & Medical Microbiology 06/2003; 36(3):127-34. DOI:10.1016/S0928-8244(03)00021-X · 2.55 Impact Factor
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    ABSTRACT: Diss. -- Helsingin yliopisto.
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