Vitamin D and The Microbiota Cooperate to Regulate Gastrointestinal Homeostasis and Inflammatory Bowel Disease
M. T. Cantorna, PhD
Department of Veterinary and Biomedical Sciences
Center for Molecular Immunology and Infectious Diseases
Pennsylvania State University
Abstract
Evidence from animal models of inflammatory bowel disease (IBD) clearly show that vitamin D deficiency results in more severe disease and that treatment with 1,25(OH)2D can suppress the symptoms. Vitamin D is an environmental factor that affects susceptibility and severity of experimental IBD in mice and likely Crohn’s disease in humans.
The mechanisms by which vitamin D would regulate IBD include regulation of innate and adaptive immunity and control of gastrointestinal permeability. Newer evidence shows that vitamin D, likely via regulation of immune cells, regulates the microbiota. The effectiveness of vitamin D to regulate IBD was inhibited by disruptions of the microbiota using broad spectrum antibiotics. More specifically the Helicobacteraceae family members within the Proteobacteria pyhlum were higher in vitamin D deficient mice and this was associated with more severe colitis. 1,25(OH)2D or antibiotics treatment reduced Helicobacteraceae numbers and was associated with less severe disease. The ability of the host to metabolize vitamin D depends on the microbiota. Colonization of germfree mice resulted in increased 25(OH)D and 24,25(OH)2D in the blood. The potential mechanisms by which the microbiota regulate systemic vitamin D metabolism will be discussed. The major finding of the present study is that there is a symbiotic relationship between vitamin D and the microbiota that influences the development of immune mediated diseases like IBD.
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