The CHEP Laboratory Science team

Innate immune response in respiratory epithelium

Lower respiratory illnesses in the first year or two of life, especially those associated with wheeze and/or fever, are major risk factors for poor respiratory health. Recent data suggests that bacteria and viruses commonly found in the nose in early life may increase the risk of subsequent disease.

This project will take advantage of a unique, community-based birth cohort (Early Life Lung Function and Respiratory Health Study - ELLF), in whom the presence of respiratory viruses and bacteria in the upper airway and respiratory symptoms during the first 2 years of life have been determined from weekly nasal swabs and a daily symptom diary. This project will determine how nasal cells obtained from either adults (asthmatic or healthy) and the children birth cohort respond in laboratory-based culture when infected with bacteria, in addition to assessing the cell response when co-infected with respiratory viruses.

Innate immunity and response to oxidative stress in the airway epithelium

The airway epithelium provides the first line of innate immune protection to defend against environmental stressors and infections. A decline in airway epithelial innate immune system functionality is associated with many medical conditions and can result in chronic inflammation and compromised immunity of the lung. Oxidative stress can be generated by environmental exposure. Increase in oxidative stress cause airway and lung damage, which may initiate or worsen respiratory disease. Redox regulation maintains the equilibrium of pro-oxidant/anti-oxidant reactions but can be disturbed by environmental exposures. How this impacts on respiratory disease and whether anti-oxidants can provide protection is unknown.

This project aims to investigate the innate immune responses in environmental exposure; how the airway epithelium response to oxidative stress; and examine the utility of antioxidants to restore redox homeostasis.

Identifying biomarkers of susceptibility to air pollution-induced oxidative stress and respiratory disease 

Air pollution is a major driver of respiratory disease, affecting millions of people worldwide and placing a significant burden on health systems and communities. Oxidative stress and epithelial injury are key biological mechanisms linking air pollution exposure to adverse respiratory health outcomes. However, not everyone responds to air pollution in the same way. Understanding why some individuals are more susceptible than others is critical for developing targeted prevention strategies and improving public health. Our research group investigates the biological pathways underlying individual susceptibility to oxidant-induced respiratory injury. Using primary human nasal epithelial cells cultured as fully differentiated respiratory epithelium at the air-liquid interface, we have developed innovative models to assess susceptibility to oxidative stress. We have also established a simplified screening approach using mitochondrial respiration measurements in monolayer cell cultures. This HDR project aims to take the next step by identifying transcriptomic and DNA methylation signatures of oxidative stress susceptibility that can be detected from simple nasal swab samples. The development of a reliable molecular signature would create powerful new opportunities to: investigate susceptibility to air pollution in large population studies and birth cohorts; expand research into regional and remote communities where advanced laboratory facilities are unavailable; improve understanding of how environmental exposures influence respiratory health across the lifespan; and support future precision health approaches for prevention and intervention. 

Bushfire smoke, environmental contamination, and respiratory health in a changing climate  

Climate change is increasing the frequency, intensity, and duration of bushfires worldwide. In Australia, major bushfire events have devastating environmental, economic, and health consequences, impacting ecosystems, biodiversity, agriculture, water quality, and communities. While the immediate dangers of bushfires are well recognised, the long-term health impacts of bushfire smoke remain poorly understood. Bushfire smoke can travel vast distances and contains a complex mixture of hazardous pollutants, including fine particulate matter and highly reactive oxidant species known as environmentally persistent free radicals (EPFRs). These pollutants can settle on soil, agricultural land, home gardens, and water systems, potentially creating long-lasting environmental contamination. Emerging evidence suggests that EPFRs may persist in burned environments for years after a fire event, yet little is known about their long-term effects on human health. This project will investigate how persistent pollutants from bushfires affect respiratory health and environmental safety. Using environmental samples collected from bushfire-affected regions and advanced cellular models of the human airway, the project aims to determine how long these harmful compounds persist and how they interact with respiratory epithelial cells, the first line of defence against inhaled pollutants.