Background: Vitamin D, a common food additive, has been shown to prevent the induction of experimental autoimmune diseases in mice. A possible immune deviation from T(H)1 to T(H)2 responses has been postulated. Although there is no doubt about the beneficial effects of vitamin D, its role in allergy has not been investigated.
Objective: To define the role of vitamin D in modulating the development of a T(H)2-mediated disease, we used a murine model of pulmonary eosinophilic inflammation.
Methods: Five-week-old mice were primed on day 0 with ovalbumin intraperitoneally. Then they were nasally challenged with ovalbumin on days 7, 8, 9, and 10, and on day 11, samples were studied. Some mice received subcutaneous injections of vitamin D every second day as follows: days -3, -1, 1, 3, 5, 7, and 9. The control groups received PBS on the same days.
Results: Early treatment with vitamin D augmented allergen-induced T-cell proliferation along with T(H)2 cytokine (IL-4 and IL-13) and IgE production. Surprisingly, the local inflammatory response in bronchoalveolar lavage fluid and lung tissue was significantly ameliorated with impaired recruitment of eosinophils and inferior levels of IL-5. These findings were attributed to late treatment with vitamin D after establishment of an early immune response.
Conclusion: We suggest that excess supplementation of vitamin D could influence the development of a sustained T(H)2 response, leading to an increasing prevalence of allergy, whereas vitamin D might hold promising beneficial effects in airway eosinophilia.