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Infection and Immunity, October 2000, p. 5998-6004, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Saccharomyces boulardii Preserves the Barrier Function and Modulates the Signal Transduction Pathway Induced in Enteropathogenic Escherichia coli-Infected T84 Cells

Dorota Czerucka,1,* Stephanie Dahan,1 Baharia Mograbi,2 Bernard Rossi,2 and Patrick Rampal1

Laboratoire de Gastroentérologie et Nutrition1 and INSERM U364, IFR50, Faculté de Médecine,2 Université de Nice-Sophia Antipolis, 06107 Nice Cedex 2, France

Received 24 February 2000/Returned for modification 30 March 2000/Accepted 6 June 2000

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, [3H]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.

* Corresponding author. Mailing address: Laboratoire de Gastroentérologie, Université de Nice-Sophia Antipolis, 28 Avenue de Valombrose, 06107 Nice Cedex 2, France. Phone: (33) 4-93-37-76-95. Fax: (33) 4-93-81-77-10. E-mail: czerucka{at}unice.fr.

Infection and Immunity, October 2000, p. 5998-6004, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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