Philippe D, Favre L, Foata F, Adolfsson O, Perruisseau-Carrier G, Vidal K, Reuteler G, Dayer-Schneider J, Mueller C, Blum S. Bifidobacterium lactis attenuates onset of inflammation in a murine model of colitis. World J Gastroenterol 2011; 17(4): 459-469 [PMID: 21274375 DOI: 10.3748/wjg.v17.i4.459]
Corresponding Author of This Article
David Philippe, PhD, Department of Nutrition and Health, Nestlé Research Centre, Vers-chez-les-Blanc, PO Box 44, CH-1000 Lausanne 26, Switzerland. david.philippe@rdls.nestle.com
Article-Type of This Article
Original Article
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World J Gastroenterol. Jan 28, 2011; 17(4): 459-469 Published online Jan 28, 2011. doi: 10.3748/wjg.v17.i4.459
Bifidobacterium lactis attenuates onset of inflammation in a murine model of colitis
David Philippe, Laurent Favre, Francis Foata, Oskar Adolfsson, Genevieve Perruisseau-Carrier, Karine Vidal, Gloria Reuteler, Johanna Dayer-Schneider, Christoph Mueller, Stéphanie Blum
David Philippe, Laurent Favre, Francis Foata, Oskar Adolfsson, Genevieve Perruisseau-Carrier, Karine Vidal, Gloria Reuteler, Stéphanie Blum, Department of Nutrition and Health, Nestlé Research Centre, CH-1000 Lausanne 26, Switzerland
Johanna Dayer-Schneider, Christoph Mueller, Department of Pathology, University of Bern, CH-3010 Bern, Switzerland
Author contributions: Philippe D and Favre L wrote the manuscript and contributed equally to this work; Philippe D, Favre L, Adolfsson O, Vidal K, Mueller C, Foata F and Blum S designed the study and participated in data analysis; Foata F, Perruisseau-Carrier G, Dayer-Schneider J and Reuteler G performed research; all authors approved the final manuscript.
Correspondence to: David Philippe, PhD, Department of Nutrition and Health, Nestlé Research Centre, Vers-chez-les-Blanc, PO Box 44, CH-1000 Lausanne 26, Switzerland. david.philippe@rdls.nestle.com
Telephone: +41-21-7858967 Fax: +41-21-7858544
Received: July 8, 2010 Revised: July 30, 2010 Accepted: August 7, 2010 Published online: January 28, 2011
Abstract
AIM: To assess the anti-inflammatory effect of the probiotic Bifidobacterium lactis (B. lactis) in an adoptive transfer model of colitis.
METHODS: Donor and recipient mice received either B. lactis or bacterial culture medium as control (deMan Rogosa Sharpe) in drinking water for one week prior to transfer of a mix of naive and regulatory T cells until sacrifice.
RESULTS: All recipient mice developed signs of colonic inflammation, but a significant reduction of weight loss was observed in B. lactis-fed recipient mice compared to control mice. Moreover, a trend toward a diminution of mucosal thickness and attenuated epithelial damage was revealed. Colonic expression of pro-inflammatory and T cell markers was significantly reduced in B. lactis-fed recipient mice compared to controls. Concomitantly, forkhead box protein 3, a marker of regulatory T cells, was significantly up-regulated by B. lactis.
CONCLUSION: Daily oral administration of B. lactis was able to reduce inflammatory and T cells mediators and to promote regulatory T cells specific markers in a mouse model of colitis.
