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The antidyslipidemic drug nicotinic acid (niacin) has been used for decades. One of the major problems of the therapeutical use of nicotinic acid is a strong cutaneous vasodilation called flushing, which develops in almost every patient taking nicotinic acid. Nicotinic acid-induced flushing has been shown to be mediated by the nicotinic acid receptor GPR109A and to involve the formation of vasodilatory prostanoids. However, the cellular mechanisms underlying this short-term effect are unknown. Here, we show that epidermal Langerhans cells are essential for the cutaneous flushing response induced by nicotinic acid. Langerhans cells respond with an increase in [Ca²⁺]_i to nicotinic acid and express prostanoid synthases required for the formation of the vasodilatory prostanoids prostaglandin E₂ and prostaglandin D₂. Depletion of epidermal Langerhans cells but not of macrophages or dendritic cells abrogates …