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A number of studies have examined the effects of 1,25‐dihydroxyvitamin D₃(1,25(OH)₂D₃) on intestinal inflammation driven by immune cells, while little information is currently available about its impact on inflammation caused by intestinal epithelial cell (IEC) defects. Mice lacking IEC‐specificRab11aa recycling endosome small GTPase resulted in increased epithelial cell production of inflammatory cytokines, notably IL‐6 and early onset of enteritis. To determine whether vitamin D supplementation may benefit hosts with epithelial cell‐originated mucosal inflammation, we evaluated in vivo effects of injected 1,25(OH)₂D₃or dietary supplement of a high dose of vitamin D on the gut phenotypes of IEC‐specificRab11aknockout mice (Rab11a^ΔIEC). 1,25(OH)₂D₃administered at 25 ng, two doses per mouse, by intraperitoneal injection, reduced inflammatory cytokine production in knockout mice compared to vehicle‐injected mice. Remarkably, feeding mice with dietary vitamin D supplementation at 20,000 IU/kg spanning fetal and postnatal developmental stages led to improved bodyweights, reduced immune cell infiltration, and decreased inflammatory cytokines. We found that these vitamin D effects were accompanied by decreased NF‐κB (p65) in the knockout intestinal epithelia, reduced tissue‐resident macrophages, and partial restoration of epithelial morphology. Our study suggests that dietary vitamin D supplementation may prevent and limit intestinal inflammation in hosts with high susceptibility to chronic inflammation.