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Intrauterine growth restriction (IUGR) is associated with asthma. Murine models of IUGR have altered airway responsiveness in the absence of any inflammatory exposure. Given that a primary feature of asthma is airway inflammation, IUGR-affected individuals may develop more substantial respiratory impairment if subsequently exposed to an allergen. This study used a maternal hypoxia-induced mouse model of IUGR to determine the combined effects of IUGR and allergy on airway responsiveness.

The dramatic rise in allergic disease has occurred in tandem with recent environmental changes and increasing indoor lifestyle culture. While multifactorial, one consistent allergy risk factor has been reduced sunlight exposure. However, vitamin D supplementation studies have been disappointing in preventing allergy, raising possible independent effects of ultraviolet (UV) light exposure.

Findings provide further proof of concept that pharmacological targeting of airway smooth muscle thickness will be beneficial and may be facilitated by azithromycin

We propose that propensity for viral exacerbations of asthma and COPD relate to delayed expression of epithelial cell innate anti-viral immune genes

Our findings provide new insight into the molecular mechanisms operative at baseline in the airway mucosa in atopic asthmatic with natural aeroallergen exposure

We identified new asthma loci, found new associations at loci implicated in the comorbidity of asthma plus hay fever and confirmed nine known loci.

Identify entrenched areas of asthma management and treatment in which progress has stalled and to challenge current principles

To determine the contribution of RSV to the subsequent development of severe asthma in different subgroups of children at risk of severe RSV disease.

We sought to assess whether the trajectory to asthma begins already at birth and whether epigenetic mechanisms, contribute to asthma inception.

High fractional exhaled nitric oxide and sputum eosinophils are associated with an increased risk of future virus-induced exacerbations.