A Crucial Role for the Vitamin D Receptor in Experimental Inflammatory Bowel Diseases

  • Froicu M
  • Weaver V
  • Wynn T
 et al. 
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Abstract

The active form of vitamin D (1,25D 3) suppressed the development of animal models of human auto-immune diseases including experimental inflam-matory bowel disease (IBD). The vitamin D recep-tor (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 experi-mental models of IBD. In the CD45RB transfer model of IBD, CD4 ؉ /CD45RB high T cells from VDR KO mice induced more severe colitis than wild-type CD4 ؉ /CD45RB high T cells. The second model of IBD used was the spontaneous colitis that de-velops in IL-10 KO mice. VDR/IL-10 double KO mice developed accelerated IBD and 100% mortal-ity 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 im-mune system and not a result of altered calcium homeostasis, or gastrointestinal tract function. The data establishes an essential role for VDR sig-naling in the regulation of inflammation in the gas-trointestinal tract. (Molecular Endocrinology 17: 2386–2392, 2003)

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Authors

  • Monica Froicu

  • Veronika Weaver

  • Thomas A Wynn

  • Mary Ann Mcdowell

  • Jo Ellen Welsh

  • Margherita T Cantorna

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