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Carbohydrate-Dependent and Antimicrobial Peptide Defence Mechanisms Against Helicobacter pylori Infections

Chapter in book
Authors Médea Padra
John Benktander
K. Robinson
Sara K. Lindén
Published in Molecular Mechanisms of Inflammation: Induction, Resolution and Escape by Helicobacter pylori
Pages 179-207
ISBN 978-3-030-15138-6
Publisher Springer
Publication year 2019
Published at Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 179-207
Language en
Links dx.doi.org/10.1007/978-3-030-15138-...
Keywords gastric epithelial-cells, outer-membrane proteins, neutrophil-activating, protein, lewis antigen-expression, blood-group antigens, binding-specificity, innate immunity, beta-defensins, alpha-defensin, iv, secretion, bolos c, 1995, gastroenterology, v109, p723
Subject categories Gastroenterology and Hepatology, Internal medicine

Abstract

The human stomach is a harsh and fluctuating environment for bacteria with hazards such as gastric acid and flow through of gastric contents into the intestine. H. pylori gains admission to a stable niche with nutrient access from exudates when attached to the epithelial cells under the mucus layer, whereof adherence to glycolipids and other factors provides stable and intimate attachment. To reach this niche, H. pylori must overcome mucosal defence mechanisms including the continuously secreted mucus layer, which provides several layers of defence: (1) mucins in the mucus layer can bind H. pylori and transport it away from the gastric niche with the gastric emptying, (2) mucins can inhibit H. pylori growth, both via glycans that can have antibiotic like function and via an aggregation-dependent mechanism, (3) antimicrobial peptides (AMPs) have antimicrobial activity and are retained in a strategic position in the mucus layer and (4) underneath the mucus layer, the membrane-bound mucins provide a second barrier, and can function as releasable decoys. Many of these functions are dependent on H. pylori interactions with host glycan structures, and both the host glycosylation and concentration of antimicrobial peptides change with infection and inflammation, making these interactions dynamic. Here, we review our current understanding of mucin glycan and antimicrobial peptide-dependent host defence mechanisms against H. pylori infection.

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Denna text är utskriven från följande webbsida:
http://gu.se/english/research/publication/?publicationId=284835
Utskriftsdatum: 2019-12-06