Open AccessSaccharomyces boulardiiPreserves the Barrier Function and Modulates the Signal Transduction Pathway Induced in EnteropathogenicEscherichia coli-Infected T84 Cells
Author(s) -
Dorota Czerucka,
Stéphanie Dahan,
Baharia Mograbi,
Bernard Rossi,
Patrick Rampal
Publication year - 2000
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.68.10.5998-6004.2000
Subject(s) - saccharomyces boulardii , enteropathogenic escherichia coli , microbiology and biotechnology , biology , signal transduction , yeast , internalization , intracellular , escherichia coli , bacteria , biochemistry , cell , gene , genetics , probiotic
Use of the nonpathogenic yeastSaccharomyces boulardii in the treatment of infectious diarrhea has attracted growing interest. The present study designed to investigate the effect of this yeast on enteropathogenicEscherichia coli (EPEC)-associated disease demonstrates thatS. 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 ofS. 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 ofS. 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 ofS. boulardii . Altogether, this study demonstrated thatS. boulardii exerts a protective effect on epithelial cells after EPEC adhesion by modulating the signaling pathway induced by bacterial infection.