Bifidobacterium animalis subsp. lactis fermented milk product reduces inflammation by altering a niche for colitogenic microbes

Intestinal health requires the coexistence of eukaryotic self with the gut microbiota and dysregulated host-microbial interactions can result in intestinal inflammation. Here, we show that colitis improved in T-bet -/- Rag2 -/- mice that consumed a fermented milk product containing Bifidobacterium a...

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Published inProceedings of the National Academy of Sciences - PNAS Vol. 107; no. 42; pp. 18132 - 18137
Main Authors Veiga, Patrick, Gallini, Carey Ann, Beal, Chloé, Michaud, Monia, Delaney, Mary L., DuBois, Andrea, Khlebnikov, Artem, van Hylckama Vlieg, Johan E.T., Punit, Shivesh, Glickman, Jonathan N., Onderdonk, Andrew, Glimcher, Laurie H., Garrett, Wendy S., Vogt, Peter K.
Format Journal Article
LanguageEnglish
Published United States National Academy of Sciences 19.10.2010
National Acad Sciences
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Summary:Intestinal health requires the coexistence of eukaryotic self with the gut microbiota and dysregulated host-microbial interactions can result in intestinal inflammation. Here, we show that colitis improved in T-bet -/- Rag2 -/- mice that consumed a fermented milk product containing Bifidobacterium animalis subsp. lactis DN-173 010 strain. A decrease in cecal pH and alterations in short chain fatty acid profiles occurred with consumption, and there were concomitant increases in the abundance of select lactate-consuming and butyrate-producing bacteria. These metabolic shifts created a nonpermissive environment for the Enterobacteriaceae recently identified as colitogenic in a T-bet -/- Rag2 -/- ulcerative colitis mouse model. In addition, 16S rRNA-based analysis of the T-bet -/- Rag2 -/- fecal microbiota suggest that the structure of the endogenous gut microbiota played a key role in shaping the host response to the bacterial strains studied herein. We have identified features of the gut microbiota, at the membership and functional level, associated with response to this B. lactis-containing fermented milk product, and therefore this model provides a framework for evaluating and optimizing probiotic-based functional foods.
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1Present address: Department of Cell and Developmental Biology, University of Southern California, Health Sciences Campus, Los Angeles, CA 90089.
2Present address: GI Pathology, Boston Caris Diagnostics, Newton, MA 02464.
Edited by Peter K. Vogt, The Scripps Research Institute, La Jolla, CA, and approved September 8, 2010 (received for review August 5, 2010)
Author contributions: P.V., A.K., J.E.T.v.H.V., A.O., L.H.G., and W.S.G. designed research; P.V., C.A.G., C.B., M.M., M.L.D., A.D., S.P., and W.S.G. performed research; P.V., C.A.G., C.B., M.M., M.L.D., A.D., J.E.T.v.H.V., J.N.G., A.O., and W.S.G. analyzed data; and P.V. and W.S.G. wrote the paper.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.1011737107