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Higher Bifidobacteria counts in male offspring exposed to supplemental levels of vitamin D in utero and during suckling in IBD‐prone mice
Author(s) -
Glenn Andrea J.,
Li Sophia,
Fielding Kristina A,
Chen Jianmin C,
Comelli Elena M,
Ward Wendy E
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb430
Subject(s) - bacteroides , dysbiosis , feces , inflammation , biology , offspring , microbiome , vitamin d and neurology , gut flora , immunology , clostridium , vitamin , in utero , physiology , medicine , microbiology and biotechnology , endocrinology , bacteria , pregnancy , fetus , genetics , bioinformatics
Vitamin D deficiency has been linked to an increased risk of inflammatory bowel disease (IBD), and microbial dysbiosis has been implicated in IBD. Our objective was to determine if exposure to supplemental levels of vitamin D can favourably modulate microbiota composition pre‐inflammation in the male interleukin‐10 knockout (IL‐10 KO) mouse that spontaneously develops intestinal inflammation at 6–8 weeks of age. The mice were randomized to a diet containing 25 IU (low group) or 5000 IU (high group) of vitamin D/kg of diet in utero and during suckling, and fecal samples were collected at 5 weeks of age. Fecal microbiota composition was determined by qPCR. Mice in the supplemental group had higher (p = 0.01) counts of Bifidobacteria than mice in the low group. Total bacteria, Bacteroides, Clostridium leptum , Clostridium coccoides and Escherichia coli counts were unaffected. Bifidobacteria have been found to sustain intestinal homeostasis and inhibit Th1‐driven inflammation and may favourably alter gut microbial composition to a more health‐promoting phenotype. Further investigation is needed to determine if this results in protection against developing intestinal inflammation.