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Background  The active form of vitamin D (1,25(OH) 2 D 3 ) has been shown to inhibit development of inflammatory bowel disease (IBD) in IL-10 KO mice. Here, the role of the vitamin D receptor (VDR) and 1,25(OH) 2 D 3  in acute experimental IBD was probed.    Results  VDR KO mice were extremely sensitive to dextran sodium sulfate (DSS) and there was increased mortality of the VDR KO mice at doses of DSS that only caused a mild form of colitis in wildtype (WT) mice. DSS colitis in the VDR KO mice was accompanied by high colonic expression of TNF-α, IL-1 α, IL-1β, IL-12, IFN-γ, IL-10, MIP-1α and KC. DSS concentrations as low as 0.5% were enough to induce bleeding, ulceration and weight loss in VDR KO mice. VDR KO mice failed to recover following the removal of DSS, while WT mice showed signs of recovery within 5 days of DSS removal. The early mortality of DSS treated VDR KO mice was likely due to perforation of the bowel and resulting endotoxemia. VDR KO mice were hyper-responsive to exogenously injected LPS and cultures of the peritoneal exudates of moribund DSS treated VDR KO mice were positive for bacterial growth. 1,25(OH) 2 D 3  in the diet or rectally decreased the severity and extent of DSS-induced inflammation in WT mice.    Conclusion  The data point to a critical role for the VDR and 1,25(OH) 2 D 3  in control of innate immunity and the response of the colon to chemical injury.

Vitamin D and the vitamin D receptor are critical for control of the innate immune response to colonic injury