Human gastric mucins differently regulate Helicobacter pylori proliferation, gene expression and interactions with host cells.

PloS One
Emma C SkoogSara K Lindén

Abstract

Helicobacter pylori colonizes the mucus niche of the gastric mucosa and is a risk factor for gastritis, ulcers and cancer. The main components of the mucus layer are heavily glycosylated mucins, to which H. pylori can adhere. Mucin glycosylation differs between individuals and changes during disease. Here we have examined the H. pylori response to purified mucins from a range of tumor and normal human gastric tissue samples. Our results demonstrate that mucins from different individuals differ in how they modulate both proliferation and gene expression of H. pylori. The mucin effect on proliferation varied significantly between samples, and ranged from stimulatory to inhibitory, depending on the type of mucins and the ability of the mucins to bind to H. pylori. Tumor-derived mucins and mucins from the surface mucosa had potential to stimulate proliferation, while gland-derived mucins tended to inhibit proliferation and mucins from healthy uninfected individuals showed little effect. Artificial glycoconjugates containing H. pylori ligands also modulated H. pylori proliferation, albeit to a lesser degree than human mucins. Expression of genes important for the pathogenicity of H. pylori (babA, sabA, cagA, flaA and ureA) appeared ...Continue Reading

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Citations

Mar 26, 2014·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Jutta MessingAndreas Hensel
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Datasets Mentioned

BETA
AE001439

Methods Mentioned

BETA
glycosylation
PCR
flow cytometry
density gradient centrifugation
enzyme-linked immunosorbent assays
ELISA
reverse transcription PCR

Software Mentioned

SPSS Statistics
Primer3

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