Background-Previous research supports a possible link between low vitamin D levels and atopic disease. However, the association between low vitamin D levels and total and allergenspecific IgE levels has not been studied.

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To cite this article: Benson AA, Toh JA, Vernon N, Jariwala SP. The role of vitamin D in the immunopathogenesis of allergic skin diseases. Allergy 2012; 67: 296–301. Abstract Vitamin D plays key roles in innate and adaptive immunity through the stimulation of Toll‐like receptors, increasing pro‐inflammatory cytokine production, and possibly enhancing T helper type 2 responses. These mechanisms may explain the growing body of evidence connecting vitamin D to allergic diseases, including asthma, food allergies, and allergic rhinitis. The data relating vitamin D to allergic skin diseases are equivocal with studies linking both high and low vitamin D levels to an increased risk of developing atopic dermatitis. In this paper, we describe the role of vitamin D in the immunopathogenesis of atopic dermatitis and other allergic skin diseases.

A "call to action" has been issued for scholars in landscape and urban planning, natural science, and public health to conduct interdisciplinary research on the human health effects of spending time in or near greenspaces. This is timely in light of contemporary interest in municipal tree planting and urban greening, defined as organized or semi-organized efforts to introduce, conserve, or maintain outdoor vegetation in urban areas. In response to injunctions from scholars and urban greening trends, this article provides an interdisciplinary review on urban trees, air quality, and asthma. We assess the scientific literature by reviewing refereed review papers and empirical studies on the biophysical processes through which urban trees affect air quality, as well as associated models that extend estimates to asthma outcomes. We then review empirical evidence of observed links between urban trees and asthma, followed by a discussion on implications for urban landscape planning and design. This review finds no scientific consensus that urban trees reduce asthma by improving air quality. In some circumstances, urban trees can degrade air quality and increase asthma. Causal pathways between urban trees, air quality, and asthma are very complex, and there are substantial differences in how natural science and epidemiology approach this issue. This may lead to ambiguity in scholarship, municipal decision-making, and landscape planning. Future research on this topic, as well as on urban ecosystem services and urban greening, should embrace epistemological and etiological pluralism and be conducted through interdisciplinary teamwork.

Atopic dermatitis (AD), a skin disease characterized by pruritus and chronic inflammation, results from a complex interplay between environmental and genetic factors. Thymic stromal lymphopoietin (TSLP), an IL-7-like cytokine, is believed to propagate AD lesions through T helper 2 (Th2) polarization. This paper describes the immunologic mechanisms involving TSLP in the generation of allergic disease. Specifically in AD, TSLP has been shown to be an inducer of myeloid dendritic cells, Th2 responses, mast cells, and natural killer T cells, thereby leading to cytokine secretion and the development of AD. We hope that further understanding of the TSLP pathway and its role in the pathogenesis of AD will lead to improved clinical management of AD in the future.

Psoriasis vulgaris is a chronic inXammatory skin disease that is marked by a complex interplay of dendritic cells (DCs), T-cells, cytokines, and downstream transcription factors as part of a self-sustaining type 1 cytokine network. As integral players of the immune system, DCs represent antigen-presenting cells that are crucial for eYcient activation of T-cells and B-cells. DCs have also been linked to distinct chronic inXammatory conditions, including psoriasis. In the setting of psoriasis therapy, DC/T cell interactions serve as a potential target for biologic response modiWers. Here we describe the major DC subsets as well as the immunologic involvement of DCs within the context of psoriatic lesions.

Summary Objective Asthma-related morbidity is higher among children with vitamin D deficiency and obesity, morbidities that frequently co-exist among minority children. However, the effect of co-existent obesity and vitamin D deficiency on pulmonary function is poorly understood. Methods We compared percent-predicted values of pulmonary function across vitamin D categories among 72 obese and 71 normal-weight Hispanic and African-American children with asthma recruited at an urban children’s hospital. Serum cytokines associated with Th1 and Th2 inflammation and 25-hydroxyvitamin D (25-OHD) were quantified in fasting serum. 25-OHD levels ≥30 ng/ml were categorized as sufficient, <30 and ≥20 ng/ml as insufficient, and <20 ng/ml as deficient. The role of inflammation was investigated by regression analysis. Results Vitamin D deficiency was present in 50% of children and did not differ by obese status. Forced Expiratory Volume in the first second (84.5 ± 9.4 vs. 94.8 ± 8.4, P<0.001), and Functional Residual Capacity (67.5 ± 20.1 vs. 79.3 ± 19, P=0.01) were lower among vitamin D deficient obese asthmatics than their sufficient counterparts, and Total Lung Capacity was lower than their insufficient counterparts (86.9 ± 14.3 vs. 96.6 ± 10, P=0.01); similar associations were not observed in normal-weight asthmatics and were not influenced by systemic inflammation. No association between Th1 and Th2 inflammatory measures, vitamin D deficiency, and pulmonary function tests was found. Conclusions Vitamin D deficiency was associated with pulmonary function deficits among obese children, but not among normal-weight children with asthma, an association that was independent of Th1 and Th2 serum inflammatory measures. Vitamin D deficiency may be one potential mechanism underlying the obese-asthma phenotype.

The spring asthma peak is closely associated with increased tree pollen counts, and the asthma increase at this time is likely due to allergic reactions to pollen. No significant associations could be established with the fall peak. The winter peak correlates with elevated SO(2) and NO(x) levels.