Cord blood vitamin D concentrations are un- related to atopy and wheeze in 2 diverse birth cohort studies

epithelia abolished the cell’s ability to respond to stressors adequately (Fig 2, G). To test whether the assumption that ORMDL overexpression impairs epithelial repair thus promoting the development toward an asthmatic phenotype, we performed a simple wound repair assay using cultured human lung epithelial cells (BEAS-2B). This scratch assay was performed with control BEAS-2B cells (transfected with an empty vector) and those transfected with an ORMDL3 overexpression vector (Fig 2, H). The wound repair assay demonstrated that ORMDL3-overexpressing BEAS-2B cellsshow adelay inwound closure, implying that their repair capacity is reduced. In conclusion, we found that increased epithelial ORMDL expression, which mimics the situation found in carriers of the risk allele, changes cellular response characteristics in a way that promote asthma development. ORMDL overexpression changes 1) terminal airway structures, 2) increases the susceptibility to stressors such as CS and hypoxia, 3) abolishes the airway epithelial’s ability to react adequately to stressors, and 4) reduces the repair capacities of the epithelium substantially. We hypothesize that these ORMDL overexpression-induced changes are of central importance for the observed phenotypes that collectively lead to an increased susceptibility to acquire asthma.