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Project Manager, Respiratory Health
The airway epithelium is the primary structural and functional airway barrier and orchestrates innate immunity. Some children may have underlying epithelial vulnerabilities that contribute to the pathogenesis of acute wheeze and asthma.
Type 1 interferons (T1IFNs) are typically expressed in low concentrations under homeostatic conditions, but upon pathogenic insult or perturbation of the pathway, these critical immune signaling molecules can become either protectors from or drivers of pathology. While essential for initiating antiviral defense and modulating inflammation, dysregulation of T1IFN signaling can contribute to immunopathology, making it and its associated pathways prime targets for immune evasion and disruption by pathogens.
National policies are essential for countries to adapt to the negative health impacts of climate change. Children are disproportionately affected by these impacts and must be at the heart of adaptation policies to address their vulnerabilities. Adaptation commitments worldwide are integrated into national adaptation plans, nationally determined contributions, national communications, and other multisectoral policies. We aimed to evaluate how effectively national climate change policies worldwide plan to protect child health, considering a range of determinants for successful child-health adaptation.
Newborn screening (NBS) for cystic fibrosis (CF) provides an opportunity to commence management and therapeutic interventions significantly earlier
Guideline to provide evidence-based recommendations on diagnostic testing for primary ciliary dyskinesia
Preterm children have worse lung function than healthy controls
PLA2R1 is increased in the airway epithelium in asthma, and serves as a regulator of airway hyperresponsiveness, airway permeability, antigen sensitization, and airway inflammation
Human rhinovirus infection delays repair and inhibits apoptotic processes in epithelial cells from non-asthmatic and asthmatic children
HRV-1B infection directly alters human airway epithelial TJ expression leading to increased epithelial permeability potentially via antiviral response of IL-15