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Glycobiology Advance Access originally published online on January 15, 2009
Glycobiology 2009 19(5):453-461; doi:10.1093/glycob/cwp004
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© The Author 2009. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Review

Roles of gastric mucin-type O-glycans in the pathogenesis of Helicobacter pylori infection

Motohiro Kobayashi2, Heeseob Lee3, Jun Nakayama2 and Minoru Fukuda1,4

2 Department of Molecular Pathology, Shinshu University Graduate School of Medicine, Matsumoto 390-8621, Japan
3 Department of Food Science and Nutrition, Pusan National University, Busan 609-735, Korea
4 Tumor Microenvironment Program, Cancer Research Center, Burnham Institute for Medical Research, La Jolla, CA 92037, USA

1 To whom correspondence should be addressed: Tel: +1-858-646-3144; Fax: +1-858-646-3193; e-mail: minoru{at}burnham.org

Received on September 3, 2008; revised on January 9, 2009; accepted on January 9, 2009

Helicobacter pylori is a Gram-negative bacterium that infects over 50% of the world's population. This organism causes various gastric diseases such as chronic gastritis, peptic ulcer, and gastric cancer. H. pylori possesses lipopolysaccharides that share structural similarity to Lewis blood group antigens in gastric mucosa. Such antigenic mimicry could result in immune tolerance against antigens of this pathogen. On the other hand, H. pylori colonizes gastric mucosa by utilizing adhesins that bind Lewis blood group antigen-related carbohydrates expressed on gastric epithelial cells. After colonization, H. pylori induces acute inflammatory responses mainly by neutrophils. This acute phase is gradually replaced by a chronic inflammatory response. In chronic gastritis, lymphocytes infiltrate the lamina propria, and such infiltration is facilitated by the interaction between L-selectin on lymphocytes and peripheral lymph node addressin (PNAd), which contains 6-sulfo sialyl Lewis X-capped O-glycans, on high endothelial venule (HEV)-like vessels. H. pylori barely colonizes gland mucous cell-derived mucin where {alpha}1,4-GlcNAc-capped O-glycans exist. In vitro experiments show that {alpha}1,4-GlcNAc-capped O-glycans function as a natural antibiotic to inhibit H. pylori growth. These findings show that distinct sets of carbohydrates expressed in the stomach are closely associated with pathogenesis and prevention of H. pylori-related diseases, providing therapeutic potentialities based on specific carbohydrate modulation.

Key words: 6-sulfo sialyl Lewis X-capped O-glycan / {alpha}1, 4-GlcNAc-capped O-glycan / cholesterol {alpha}-glucoside / cholesterol {alpha}-glucosyltransferase / Helicobacter pylori


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