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Department of Nutrition (M.F., V.W., M.T.C.), University Park, Pennsylvania 16802; Immunopathogenesis Section (T.A.W.), National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892; and Department of Biology (M.A.M., J.E.W.), Notre Dame University, South Bend, Indiana 46556
Address all correspondence and requests for reprints to: Dr. Margherita T. Cantorna, Department of Nutrition, 126 South Henderson Building, University Park, Pennsylvania 16802. E-mail: mxc69{at}psu.edu.
The active form of vitamin D (1,25D3) suppressed the development of animal models of human autoimmune diseases including experimental inflammatory bowel disease (IBD). The vitamin D receptor (VDR) is required for all known biologic effects of vitamin D. Here we show that VDR deficiency (knockout, KO) resulted in severe inflammation of the gastrointestinal tract in two different experimental models of IBD. In the CD45RB transfer model of IBD, CD4+/CD45RBhigh T cells from VDR KO mice induced more severe colitis than wild-type CD4+/CD45RBhigh T cells. The second model of IBD used was the spontaneous colitis that develops in IL-10 KO mice. VDR/IL-10 double KO mice developed accelerated IBD and 100% mortality by 8 wk of age. At 8 wk of age, all of the VDR and IL-10 single KO mice were healthy. Rectal bleeding was observed in every VDR/IL-10 KO mouse. Splenocytes from the VDR/IL-10 double KO mice cells transferred IBD symptoms. The severe IBD in VDR/IL-10 double KO mice is a result of the immune system and not a result of altered calcium homeostasis, or gastrointestinal tract function. The data establishes an essential role for VDR signaling in the regulation of inflammation in the gastrointestinal tract.
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