Affiliation:
1. Laboratoire de Gastroentérologie et Nutrition1 and
2. INSERM U364, IFR50, Faculté de Médecine,2Université de Nice-Sophia Antipolis, 06107 Nice Cedex 2, France
Abstract
ABSTRACT
Use of the nonpathogenic yeast
Saccharomyces boulardii
in the treatment of infectious diarrhea has attracted growing interest. The present study designed to investigate the effect of this yeast on enteropathogenic
Escherichia coli
(EPEC)-associated disease demonstrates that
S. boulardii
abrogated the alterations induced by an EPEC strain on transepithelial resistance, [
3
H]inulin flux, and ZO-1 distribution in T84 cells. Moreover, EPEC-mediated apoptosis of epithelial cells was delayed in the presence of
S. boulardii
. The yeast did not modify the number of adherent bacteria but lowered by 50% the number of intracellular bacteria. Infection by EPEC induced tyrosine phosphorylation of several proteins in T84 cells, including p46 and p52 SHC isoforms, that was attenuated in the presence of
S. boulardii
. Similarly, EPEC-induced activation of the ERK1/2 mitogen-activated protein (MAP) kinase pathway was diminished in the presence of the yeast. Interestingly, inhibition of the ERK1/2 pathway with the specific inhibitor PD 98059 decreased EPEC internalization, suggesting that modulation of the ERK1/2 MAP pathway might account for the lowering of the number of intracellular bacteria observed in the presence of
S. boulardii
. Altogether, this study demonstrated that
S. boulardii
exerts a protective effect on epithelial cells after EPEC adhesion by modulating the signaling pathway induced by bacterial infection.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
156 articles.
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