Administration of oral vitamin D induces cathelicidin production in atopic individuals

To the Editor: Atopic dermatitis (AD) is a chronic skin condition that affects 10% to 20% of children and 1% to 3% of adults.1 Individuals with atopic dermatitis are at an increased risk for cutaneous infections with Staphylococcus aureus, herpes simplex, and the small pox or vaccinia virus.2 Recently, it has been shown that defects in the innate immune system, such as the capacity to increase the production of broad spectrum antimicrobial peptides like cathelicidin, may account for this increase in infections.3,4 Important insight into the mechanism responsible for the production of antimicrobial peptides came with the discovery of the vitamin D response element in the cathelicidin promoter and the finding that the conversion of 25-hydroxyvitamin D to the active 1,25 dihydroxyvitamin D by CYP27B1 can occur in keratinocytes and monocytes and is under the control of Toll-like receptor 2.4-6 Thus, with infection or wounding, activation of Toll-like receptor 2 results in expression of CYP27B1, causing conversion of 25-hydroxyvitamin D to the active 1,25 dihydroxyvitamin D, and subsequent induction of cathelicidin.5,6 Our study sought to examine whether supplementation with oral cholecalciferol could provide the CYP27B1 enzyme enough substrate to overcome this relative deficiency in induction of cathelicidin in atopic patients. Because this increase is primarily seen in lesional skin, it is hypothesized that only with the supplementation with oral vitamin D can AD lesional skin be allowed to increase cathelicidin to its normal level seen postinjury.