Saccharomyces boulardii expresses neuraminidase activity selective for alpha 2,3-linked sialic acid that decreases Helicobacter pylori adhesion to host cells

Helicobacter pylori is a major causative agent of gastritis and peptic ulcer disease and is an established risk factor for gastric malignancy. Antibiotic combination therapy can eradicate H. pylori. As these same regimens can evoke adverse effects and resistance, new alternative therapies or adjunct...

Full description

Saved in:
Bibliographic Details
Published in:APMIS : acta pathologica, microbiologica et immunologica Scandinavica microbiologica et immunologica Scandinavica, 2014-10, Vol.122 (10), p.941-950
Main Authors: Sakarya, Serhan, Gunay, Necati
Format: Article
Language:English
Subjects:
Helicobacter pylori
Lactobacillus acidophilus
Lactobacillus reuteri
Saccharomyces boulardii
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Helicobacter pylori is a major causative agent of gastritis and peptic ulcer disease and is an established risk factor for gastric malignancy. Antibiotic combination therapy can eradicate H. pylori. As these same regimens can evoke adverse effects and resistance, new alternative therapies or adjunctive treatments are needed. A probiotic approach may provide a novel strategy for H. pylori treatment. In the current study, two probiotic bacteria, Lactobacillus acidophilus and Lactobacillus reuteri, and a probiotic yeast, Saccharomyces boulardii, were evaluated for their ability to influence H. pylori viability, adherence to gastric and duodenal cells, as well as the effect of S. boulardii on cell surface expression of sialic acid. Our results indicate that S. boulardii contains neuraminidase activity selective for alpha (2-3)-linked sialic acid. This neuraminidase activity removes surface alpha (2-3)-linked sialic acid, the ligand for the sialic acid-binding H. pylori adhesin, which in turn, inhibits H. pylori adherence to duodenal epithelial cells.
ISSN:0903-4641
1600-0463
DOI:10.1111/apm.12237