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The role of vitamin D in asthma.

机译:维生素D在哮喘中的作用。

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OBJECTIVE: To review the current literature on vitamin D and asthma, discussing the possible roles of vitamin D on asthma pathogenesis and the potential consequences of vitamin D deficiency. DATA SOURCES: PubMed database was searched from 1950 to 2009. Keywords used included asthma, vitamin D, inflammation, airway smooth muscle and cytokines. STUDY SELECTION: Articles were selected based on relevance to the subject. RESULTS: Vitamin D deficiency has been associated with epidemiologic patterns observed in the asthma epidemic. Vitamin D deficiency is more common with obesity, African American ethnicity, and westernization of countries with higher-risk populations for asthma. Evidence suggests that vitamin D deficiency is associated with increased airway hyperresponsiveness, lower pulmonary functions, worse asthma control, and possibly steroid resistance. Lung epithelial cells express high baseline levels of 1alpha-hydroxylase. This allows the conversion of inactive calcidiol to active calcitriol locally within the lung. Calcitriol has been shown to inhibit the synthesis and release of certain cytokines, such as RANTES, platelet-derived growth factor, and matrix metalloproteinases, from bronchial smooth muscle cells, thereby leading to decreased lung inflammation and smooth muscle cell proliferation. Vitamin D also increases synthesis of interleukin 10 by CD4+CD25+Foxp3+ T-regulatory cells and dendritic cells, while concurrently inhibiting dendritic cell activation by downregulating expression of costimulatory molecules CD40 and CD80/86. Vitamin D is also capable of inducing the expression of several anti-infective molecules, such as cathelicidin. Thus, vitamin D has a number of biologic effects that are likely important in regulating key mechanisms in asthma. CONCLUSIONS: We hypothesize that vitamin D supplementation may lead to improved asthma control by inhibiting the influx of inflammatory cytokines in the lung and increasing the secretion of interleukin 10 by T-regulatory cells and dendritic cells.
机译:目的:回顾有关维生素D和哮喘的最新文献,讨论维生素D在哮喘发病机理中的可能作用以及维生素D缺乏症的潜在后果。数据来源:PubMed数据库的检索时间为1950年至2009年。使用的关键词包括哮喘,维生素D,炎症,气道平滑肌和细胞因子。研究选择:基于与主题的相关性选择文章。结果:维生素D缺乏与哮喘流行中的流行病学模式有关。维生素D缺乏症在肥胖症,非裔美国人以及哮喘风险较高的国家的西化中更为常见。有证据表明,维生素D缺乏与气道高反应性增加,肺功能降低,哮喘控制不佳以及类固醇抵抗有关。肺上皮细胞表达较高的1α-羟化酶基线水平。这允许在肺内局部将非活性骨化二醇转化为活性骨化三醇。骨化三醇已显示抑制支气管平滑肌细胞合成和释放某些细胞因子,例如RANTES,血小板衍生的生长因子和基质金属蛋白酶,从而导致肺部炎症减少和平滑肌细胞增殖。维生素D还可以通过CD4 + CD25 + Foxp3 + T调节性细胞和树突状细胞增加白介素10的合成,同时通过下调共刺激分子CD40和CD80 / 86的表达来抑制树突状细胞的活化。维生素D还能够诱导几种抗感染分子(例如cathelicidin)的表达。因此,维生素D具有许多生物学作用,可能对调节哮喘的关键机制很重要。结论:我们假设补充维生素D可以通过抑制肺中炎性细胞因子的流入并通过T调节细胞和树突状细胞增加白介素10的分泌来改善哮喘控制。

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