The role of vitamin D in asthma.
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.


METHODS
PubMed database was searched from 1950 to 2009. Keywords used included asthma, vitamin D, inflammation, airway smooth muscle and cytokines.


METHODS
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.
Sandhu
Manbir S
MS
Creighton University, Department of Medicine, Division of Allergy and Immunology, Omaha, Nebraska 68131, USA.
Casale
Thomas B
TB
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000276:immunology* / Q000627:therapeutic use; D001249:Asthma / Q000188:drug therapy / Q000453:epidemiology / Q000276:immunology*; D002117:Calcitriol / Q000378:metabolism / Q000494:pharmacology; D003713:Dendritic Cells / Q000187:drug effects / Q000276:immunology; D019587:Dietary Supplements; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors; D016753:Interleukin-10 / Q000378:metabolism; D020545:Respiratory Mucosa / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D012307:Risk Factors; D013254:Steroid 17-alpha-Hydroxylase / Q000276:immunology / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000276:immunology; D014807:Vitamin D / Q000276:immunology* / Q000627:therapeutic use; D014808:Vitamin D Deficiency / Q000188:drug therapy / Q000453:epidemiology / Q000276:immunology*
D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; D016753:Interleukin-10; D014807:Vitamin D; D013254:Steroid 17-alpha-Hydroxylase; D002117:Calcitriol