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Effects of Helicobacter pylori Infection and Eradication on Gastric Mucin Expression Hiroyoshi Ota 1 , Taiji Akamatsu 2 1Department of Biomedical Laboratory Sciences, School of Health Sciences, Shinshu University School of Medicine, Matsumoto, Japan 2Endoscopy Center, Suzaka Hospital, Nagano Prefectural Hospital Organization, Suzaka, Japan Keyword: adhesin , H. pylori , 胃ムチン , 血液型物質 , 接着分子 pp.1671-1677
Published Date 2012/10/25
DOI https://doi.org/10.11477/mf.1403113623
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 H. pylori(Helicobacter pylori)characteristically attaches to mucous cells on the gastric surface and preferentially colonizes and forms microcolonies within the mucous gel layer of gastric surface mucous cell type mucins. Mucins are the main components in the mucus that covers the epithelium, and they function to protect the epithelium against noxious agents, including digestive fluids, microorganisms, and toxins. Biochemically, mucins are high molecular-weight glycoproteins with complex oligosaccharide side-chains, including blood-group antigens, attached to the mucus core-protein backbone. Lewis(Le)-associated antigens are carbohydrates and may have a role in H. pylori adherence. Type 1H and Le(b)and type 2 antigens(Le[X], Le[Y], and type 2H)are present in surface mucous cells, and both types are under the control of the secretor gene. In addition, type 2 antigens are present in the fundic and pyloric gland cells, but they are not controlled by the secretor gene.

 The patterns of glycosylation of gastric mucins vary in different gastric compartments and are reversibly altered by H. pylori infection. Gastric mucosa infected by H. pylori expressed higher levels of Le(b), sialyl-Le(a), and sialyl-Le(x). The BabA adhesion of H. pylori recognizes both types 1H and Le(b)blood-group antigens expressed on normal gastric mucosa of secretor individuals, contributing to the initial steps of infection. With persistent H. pylori infection, an inflammatory response with concomitant expression of sialylated antigens is induced in the gastric mucosa. The SabA adhesin mediates the binding of H. pylori to inflamed gastric mucosa by recognizing sialyl-Le(a)and sialyl-Le(X)antigens.

 Mucins secreted from the gastric gland mucous cells have O-glycans with terminalα-1,4-linked N-acetylglucosamine that exhibit an antimicrobial effect against H. pylori by inhibiting the biosynthesis of the cell wall of H. pylori. The mucin secretion from gastric gland mucus cells in patients infected by H. pylori are increased. This upregulation of the mucin secretion may be involved in a defense mechanism against H. pylori infection. Further insight into the complex interactions between the H. pylori adhesins and the host receptors will contribute to the design of alternative strategies for the eradication of H. pylori.


Copyright © 2012, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 1882-1219 印刷版ISSN 0536-2180 医学書院

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