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This Article Full Text Full Text (PDF) All Versions of this Article: 294/1/G295    most recent 00173.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wu, X. Articles by Jacobson, K. Search for Related Content PubMed PubMed Citation Articles by Wu, X. Articles by Jacobson, K.

INFLAMMATION/IMMUNITY/MEDIATORS

Saccharomyces boulardii ameliorates Citrobacter rodentium-induced colitis through actions on bacterial virulence factors

¹Children and Family Research Institute and ²Division of Gastroenterology, BC Children's Hospital, Vancouver, British Columbia; ³Department of Medicine, University of Alberta, Edmonton, Alberta; and ⁴Department of Pathology and Laboratory Medicine and ⁵Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, British Columbia, Canada

Submitted 18 April 2007 ; accepted in final form 10 November 2007

Saccharomyces boulardii has received increasing attention as a probiotic effective in the prevention and treatment of infectious and inflammatory bowel diseases. The aim of this study was to examine the ameliorating effects of S. boulardii on Citrobacter rodentium colitis in vivo and identify potential mechanisms of action. C57BL/6 mice received 2.5 x 10⁸ C. rodentium by gavage on day 0, followed by S. boulardii (25 mg; 5 x 10⁸ live cells) gavaged twice daily from day 2 to day 9. Animal weights were monitored until death on day 10. Colons were removed and assessed for epithelial barrier function, histology, and myeloperoxidase activity. Bacterial epithelial attachment and type III secreted proteins translocated intimin receptor Tir (the receptor for bacterial intimin) and EspB (a translocation apparatus protein) required for bacterial virulence were assayed. In infected mice, S. boulardii treatment significantly attenuated weight loss, ameliorated crypt hyperplasia (234.7 ± 7.2 vs. 297.8 ± 17.6 µm) and histological damage score (0.67 ± 0.67 vs. 4.75 ± 0.75), reduced myeloperoxidase activity (2.1 ± 0.4 vs. 4.7 ± 0.9 U/mg), and attenuated increased mannitol flux (17.2 ± 5.0 vs. 31.2 ± 8.2 nm·cm^–2·h^–1). The ameliorating effects of S. boulardii were associated with significantly reduced numbers of mucosal adherent C. rodentium, a marked reduction in Tir protein secretion and translocation into mouse colonocytes, and a striking reduction in EspB expression and secretion. We conclude that S. boulardii maintained colonic epithelial barrier integrity and ameliorated inflammatory sequelae associated with C. rodentium infection by attenuating C. rodentium adherence to host epithelial cells through putative actions on the type III secretion system.

infectious colitis; probiotics; bacterial adherence; Tir; EspB