Bifidobacterium catabolism of human milk oligosaccharides overrides endogenous competitive exclusion driving colonization and protection
Understanding how exogenous microbes stably colonize the animal gut is essential to reveal mechanisms of action and tailor effective probiotic treatments. Bifidobacterium species are naturally enriched in the gastrointestinal tract of breast-fed infants. Human milk oligosaccharides (HMOs) are associ...
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Taylor & Francis Group
2021
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oai:doaj.org-article:d99be7dd45d74118a4b98cf46d46f0022021-11-04T15:00:42ZBifidobacterium catabolism of human milk oligosaccharides overrides endogenous competitive exclusion driving colonization and protection1949-09761949-098410.1080/19490976.2021.1986666https://doaj.org/article/d99be7dd45d74118a4b98cf46d46f0022021-01-01T00:00:00Zhttp://dx.doi.org/10.1080/19490976.2021.1986666https://doaj.org/toc/1949-0976https://doaj.org/toc/1949-0984Understanding how exogenous microbes stably colonize the animal gut is essential to reveal mechanisms of action and tailor effective probiotic treatments. Bifidobacterium species are naturally enriched in the gastrointestinal tract of breast-fed infants. Human milk oligosaccharides (HMOs) are associated with this enrichment. However, direct mechanistic proof of the importance of HMOs in this colonization is lacking given milk contains additional factors that impact the gut microbiota. This study examined mice supplemented with the HMO 2ʹfucosyllactose (2ʹFL) together with a 2ʹFL-consuming strain, Bifidobacterium pseudocatenulatum MP80. 2ʹFL supplementation creates a niche for high levels of B.p. MP80 persistence, similar to Bifidobacterium levels seen in breast-fed infants. This synergism impacted gut microbiota composition, activated anti-inflammatory pathways and protected against chemically-induced colitis. These results demonstrate that bacterial-milk glycan interactions alone drive enrichment of beneficial Bifidobacterium and provide a model for tunable colonization thus facilitating insight into mechanisms of health promotion by bifidobacteriain neonates.Britta E. HeissAmy M. EhrlichMaria X. Maldonado-GomezDiana H. TaftJules A. LarkeMichael L. GoodsonCarolyn M. SlupskyDaniel J. TancrediHelen E. RaybouldDavid A. MillsTaylor & Francis Grouparticlegut microbiotahuman milk oligosaccharidesbifidobacteriumcolonizationprobioticsDiseases of the digestive system. GastroenterologyRC799-869ENGut Microbes, Vol 13, Iss 1 (2021) |
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gut microbiota human milk oligosaccharides bifidobacterium colonization probiotics Diseases of the digestive system. Gastroenterology RC799-869 |
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gut microbiota human milk oligosaccharides bifidobacterium colonization probiotics Diseases of the digestive system. Gastroenterology RC799-869 Britta E. Heiss Amy M. Ehrlich Maria X. Maldonado-Gomez Diana H. Taft Jules A. Larke Michael L. Goodson Carolyn M. Slupsky Daniel J. Tancredi Helen E. Raybould David A. Mills Bifidobacterium catabolism of human milk oligosaccharides overrides endogenous competitive exclusion driving colonization and protection |
description |
Understanding how exogenous microbes stably colonize the animal gut is essential to reveal mechanisms of action and tailor effective probiotic treatments. Bifidobacterium species are naturally enriched in the gastrointestinal tract of breast-fed infants. Human milk oligosaccharides (HMOs) are associated with this enrichment. However, direct mechanistic proof of the importance of HMOs in this colonization is lacking given milk contains additional factors that impact the gut microbiota. This study examined mice supplemented with the HMO 2ʹfucosyllactose (2ʹFL) together with a 2ʹFL-consuming strain, Bifidobacterium pseudocatenulatum MP80. 2ʹFL supplementation creates a niche for high levels of B.p. MP80 persistence, similar to Bifidobacterium levels seen in breast-fed infants. This synergism impacted gut microbiota composition, activated anti-inflammatory pathways and protected against chemically-induced colitis. These results demonstrate that bacterial-milk glycan interactions alone drive enrichment of beneficial Bifidobacterium and provide a model for tunable colonization thus facilitating insight into mechanisms of health promotion by bifidobacteriain neonates. |
format |
article |
author |
Britta E. Heiss Amy M. Ehrlich Maria X. Maldonado-Gomez Diana H. Taft Jules A. Larke Michael L. Goodson Carolyn M. Slupsky Daniel J. Tancredi Helen E. Raybould David A. Mills |
author_facet |
Britta E. Heiss Amy M. Ehrlich Maria X. Maldonado-Gomez Diana H. Taft Jules A. Larke Michael L. Goodson Carolyn M. Slupsky Daniel J. Tancredi Helen E. Raybould David A. Mills |
author_sort |
Britta E. Heiss |
title |
Bifidobacterium catabolism of human milk oligosaccharides overrides endogenous competitive exclusion driving colonization and protection |
title_short |
Bifidobacterium catabolism of human milk oligosaccharides overrides endogenous competitive exclusion driving colonization and protection |
title_full |
Bifidobacterium catabolism of human milk oligosaccharides overrides endogenous competitive exclusion driving colonization and protection |
title_fullStr |
Bifidobacterium catabolism of human milk oligosaccharides overrides endogenous competitive exclusion driving colonization and protection |
title_full_unstemmed |
Bifidobacterium catabolism of human milk oligosaccharides overrides endogenous competitive exclusion driving colonization and protection |
title_sort |
bifidobacterium catabolism of human milk oligosaccharides overrides endogenous competitive exclusion driving colonization and protection |
publisher |
Taylor & Francis Group |
publishDate |
2021 |
url |
https://doaj.org/article/d99be7dd45d74118a4b98cf46d46f002 |
work_keys_str_mv |
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