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The skin produces vitamin D3 after exposure to sunlight. Activated vitamin D3 interacts with genes to regulate microbial recognition and defense. Specifically, vitamin D3 upregulates genes to induce Toll-like receptor-2 (TLR-2) on keratinocytes and to increase the expression of antimicrobial peptides such as cathelicidin. Cathelicidin activates innate immune mechanisms that protect and defend the skin against infecting and invading organisms.
Schauber and colleagues recently found that such activation also requires histone acetylation. They found that inhibitors of histone deacetylase increased epidermal cathelicidin and enhanced antimicrobial actions against Staphylococcus aureus. Blocking the vitamin D receptor or steroid receptor coactiva…