Search
One in eight children have asthma, a chronic disease of the airways in the lungs. It results in shortness of breath, chest tightness, wheezing and coughing.
Respiratory infection and wheezing illness are leading causes of hospitalisation in childhood, placing a significant burden on families and healthcare systems. However, reliably distinguishing children at risk of developing persistent disease from those likely to outgrow their symptoms remains a clinical challenge. Earlier identification would allow clinicians to focus care and resources on those most likely to benefit from long-term management, while reducing anxiety and uncertainty about the future for families.
The Respiratory Environmental Health team conducts research in early life determinants of lung growth and development, respiratory environmental health, and mechanisms of airway dysfunction in asthma and other respiratory disease.
The Foundations of Lung Disease Team is focused on improving the diagnosis, treatment, and lifelong care of childhood lung disease.
We’ve heard from families that trustworthy information about preterm-associated lung disease is difficult to find. In response, we’ve created resources to empower families with the knowledge they need to manage these challenges.
This project investigates how different populations of cells within the respiratory tract immune system are altered during a viral infection.
Obesity is a contributing factor to asthma severity; while it has long been understood that obesity is related to greater asthma burden, the mechanisms though which this occurs have not been fully elucidated. One common explanation is that obesity mechanically reduces lung volume through accumulation of adipose tissue external to the thoracic cavity.
The twenty-first century has seen a fundamental shift in disease epidemiology with anthropogenic environmental change emerging as the likely dominant factor affecting the distribution and severity of current and future human disease. This is especially true of allergic diseases and asthma with their intimate relationship with the natural environment.
The earliest respiratory function assessments, within or close to the neonatal period, consistently show correlations with lung function and with the development of asthma into adulthood. Measurements of lung function in infancy reflect the in utero period of lung development, and if early enough, show little influence of postnatal environmental exposures.
Patients with comorbid asthma-obesity experience greater disease severity and are less responsive to therapy. We have previously reported adipose tissue within the airway wall that positively correlated with body mass index. Accumulation of biologically active adipose tissue may result in the local release of adipokines and disrupt large and small airway function depending on its anatomical distribution. This study therefore characterized airway-associated adipose tissue distribution, lipid composition, and adipokine activity in a porcine model.