Saccharomyces boulardii preserves the barrier function and modulates the signal transduction pathway induced in enteropathogenic Escherichia coli-infected T84 cells

Use of the nonpathogenic yeast Saccharomyces boulardii in the treatment of infectious diarrhea has attracted growing interest. The present study desig ned to investigate the effect of this yeast on enteropathogenic Escherichia coli (EPEC)-associated disease demonstrates that S. boulardii abrogated th e alterations induced by an EPEC strain on transepithelial resistance, [H-3 ]inulin flux, and ZO-1 distribution in T84 cells. Moreover, EPEC-mediated a poptosis of epithelial cells was delayed in the presence of S. boulardii. T he yeast did not modify the number of adherent bacteria but lowered by 50% the number of intracellular bacteria. Infection by EPEC induced tyrosine ph osphorylation of several proteins in T84 cells, including p46 and p52 SI-IC isoforms, that was attenuated in the presence of S. boulardii. Similarly, EPEC-induced activation of the ERK1/2 mitogen-activated protein (MAP) kinas e pathway was diminished in the presence of the yeast. Interestingly, inhib ition 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 obse rved in the presence of S. boulardii. Altogether, this study demonstrated t hat S. boulardii exerts a protective effect on epithelial cells after EPEC adhesion by modulating the signaling pathway induced by bacterial infection .