In IBD, the immune system-mediated attack is against the gastrointestinal tract. T cells that preferentially produced the Th1 cytokines (IL-2, IFN-gamma, and tumor necrosis factor alpha) were shown to transfer Crohn’s disease-like symptoms to naive mice, and the production of Th1 cytokines is associated with IBD among humans subjects. In conventional animal facilities, IL-10 KO mice develop enterocolitis within 912 wk of life. Approximately 30% of IL-10 KO mice die after the development of severe anemia and weight loss. Vitamin D deficiency accelerated the development of IBD symptoms among IL-10 KO mice.
In the clinical practice, vitamin D deficiency is common among patients with Crohn’s disease, even when the disease is in remission. It is unclear why vitamin D deficiency occurs more frequently in IBD; it is probably attributable to the combined effects of low vitamin D intake, malabsorption of many nutrients including vitamin D, and decreased outdoor activities in climates that are not optimal for vitamin D synthesis in the skin. The standard treatments for patients with IBD include short-term high-dose and long-term low-dose prednisone therapy. Prednisone and other corticosteroid therapies result in decreased bone mineral density, which increases the risks for vertebral fractures. Vitamin D deficiency has been linked to bone loss among patients with IBD, and bone loss is a problem for up to 50% of patients with IBD. A placebo-controlled study showed that calcium and vitamin D supplementation were effective for preventing bone loss among patients with Crohn’s disease. The hor- monally active form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], is known to increase bone mineralization when administered to experimental animals and human subjects. Therefore, vitamin D and/or 1,25(OH)2D3 supplementation is warranted for patients with IBD, to maintain bone mineral density and to normalize circulating vitamin D concentrations.
Vitamin D and infectious diseases
On the basis of the ability of 1,25(OH)2D3 to suppress the development of various autoimmune diseases and to prolong al- lograft survival, 1,25(OH)2D3 has been recognised as an immunosuppressive hormone. However, 1,25(OH)2D3 has been shown to have no effect on the susceptibility of mice to infections with Herpes simplex virus or Candida albicans. The doses of 1,25(OH)2D3 chosen were the same doses that had been shown previously to prolong allograft survival. Surprisingly, little is known about the effect of vitamin D status on the ability of the host to fight infections. There is an interesting but mechanistically unsubstantiated link between vitamin D deficiency and cases of tuberculosis. Experimentally, vitamin D deficiency and host resistance to infectious diseases have not been studied extensively. One experiment in VDR KO mice showed that VDR KO mice exhibited increased granulomatous inflammation (slightly more severe infection) during Schistosoma mansoni infection, compared with WT mice. Little is known about the role of vitamin D and 1,25(OH)2D3 in regulating immune responses to infectious diseases. What is known is somewhat paradoxical, on the basis of the ability of this nutrient/hormone to suppress autoimmune diseases and prolong transplant survival. Need medication you can’t afford? Buy cialis professional