Increased contact hypersensitivity response in mice by topical application of 1?,25-dihydroxyvitamin D3 to elicitation site

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Abstract
Recent evidence indicates that the biologically active metabolite of vitamin D3, 1α,25-dihydroxy-vitamin D3 [1α,25(OH)2D3], has an effect on the regulation of the immune response. We investigated whether topical treatment of mice with 1α,25(OH)2D3 influences the contact hypersensitivity (CHS) response to trinitrochlorobenzene (TNCB). 1α,25(OH)2D3 was applied to the dorsal trunk of A/J mice on days 0–3, and on day 4 topical application of 5% TNCB on the 1α,25(OH)2D3-treated site was performed. The mice were tested for CHS on day 10 by applying 1% TNCB to the ears. No effect on induction of CHS response to TNCB was observed in 1α,25(OH)2D3-treated mice compared with 24,25-dihydroxyvitamin D3[24,25-(OH)2D3]-treated mice as control. In a second experiment, the dorsal trunk of A/J mice was treated with 5% TNCB on day 0. The topical application of 1α,25(OH)2D3 on the ears was performed from days 2 to 5. On day 6, the mice were tested for CHS by applying 1% TNCB to the 1α,25(OH)2D3-treated ears. When 1α,25(OH)2D3 increased their response to TNCB by 40% compared with 24,25(OH)2D3-treated mice as 1α,25(OH)2D3 increased their response to TNCB by 40% compared with 24,25(OH)2D3-treated mice as control (P2D3 induced an irritant dermatitis that was superimposed on a subsequent CHS reaction. The 1α,25(OH)2D3 modulation of CHS response to TNCB in mice suggests that the hormone may play a role in the regulation of the immune response in vivo.

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