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首页> 外文期刊>Molecular pharmacology. >Nicotinic acid-induced flushing is mediated by activation of epidermal langerhans cells.
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Nicotinic acid-induced flushing is mediated by activation of epidermal langerhans cells.

机译：烟酸诱导的潮红是由表皮朗格汉斯细胞的活化介导的。

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摘要

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 [Ca(2+)](i) to nicotinic acid and express prostanoid synthases required for the formation of the vasodilatory prostanoids prostaglandin E(2) and prostaglandin D(2). Depletion of epidermal Langerhans cells but not of macrophages or dendritic cells abrogates nicotinic acid-induced flushing. These data unexpectedly identify epidermal Langerhans cells as essential mediators of nicotinic acid-induced flushing and may help to generate new strategies to suppress the unwanted effects of nicotinic acid. In addition, our results suggest that Langerhans cells besides their immunological roles are also involved in the local regulation of dermal blood flow.
机译：抗血脂异常药物烟酸（烟酸）已经使用了数十年。烟酸治疗用途的主要问题之一是称为冲洗的强烈皮肤血管舒张，几乎所有服用烟酸的患者都会出现这种情况。烟酸引起的潮红已被证明是由烟酸受体GPR109A介导的，并涉及血管舒张性前列腺素的形成。然而，这种短期作用的细胞机制尚不清楚。在这里，我们显示表皮朗格汉斯细胞对于烟酸诱导的皮肤潮红反应至关重要。朗格汉斯细胞以[Ca（2 +）]（i）对烟酸的增加作出反应，并表达形成血管扩张性前列腺素前列腺素E（2）和前列腺素D（2）所需的前列腺素合酶。表皮朗格汉斯细胞的耗竭，而不是巨噬细胞或树突状细胞的耗竭，消除了烟酸引起的潮红。这些数据出乎意料地确定了表皮朗格汉斯细胞为烟酸诱导潮红的重要介质，并可能有助于产生新的策略来抑制烟酸的有害作用。此外，我们的结果表明，朗格汉斯细胞除了具有免疫功能外，还参与了真皮血流的局部调节。

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