CHEP projects

Respiratory infections are the most commonly experienced illnesses throughout life, but especially during the first two years when infants may have six to eight infections each year. Emerging evidence indicates infections early in life along with other insults to developing airways in susceptible children may contribute to later development of chronic respiratory conditions such as asthma and chronic bronchitis.

We have previously collected detailed information on respiratory infections in the first two years of life for children who have participated in the ORChID study. The purpose of this study is to follow these children in early childhood up to the age of 7 years and track their lung function as a measure of respiratory health, as well as their immune response to common environmental allergens.

Collaborations with Queensland Alliance for Environmental Health Sciences (QAESH), The University of Queensland has already been established combining expertise in quantifying exposures to harmful chemicals in the environment with paediatric epidemiology and health outcome expertise. Strong collaborative links have been established, in particular with Professor Jochen Mueller and Professor Kevin Thomas.

Collaborative studies underway or in the planning include:

• Optimising techniques for assessing exposure of infants and young children to environmental chemicals
• Measuring biomarkers of environmental exposures
• Measuring environmental exposures and their health consequences in birth cohort studies.

Evidence is accumulating that climate change is resulting in a change in the distribution of infections, especially food, water, and vector-borne diseases.

Such changes will result in Australia facing an increase in diseases our work force is not trained to handle. Collaborations within CHRC (Infection, Inflammation and the Environment theme) and with The University of Queensland Australian Infectious Disease (AID) Research Centre will see CHEP well placed to contribute to an improved outcome for Australian children.

In addition, we have seen the impact on human health of zoonoses. Existing collaborations between CHRC and the School of Veterinary Science, The University of Queensland can be extended to help address such issues in children's health.

Pollution caused three times more deaths in 2015 than AIDS, tuberculosis and malaria combined.  Exposure to air pollution and other environmental stressors have adverse effects on human health, including increasing susceptibility to acute respiratory illnesses (ARI) and chronic respiratory diseases.

While the epidemiological evidence is strong, the mechanism(s) underlying this phenomenon remains uncertain. Children exposed to second-hand tobacco smoke are at increased risk of ARI, including acute viral bronchiolitis, pneumonia and middle ear infections. Children exposed to household air pollution have increased rates of pneumonia and tuberculosis and exaggerated respiratory symptoms and ARI occur more frequently in children exposed to traffic related air pollution (TRAP). A common factor linking these combustion products is that they contain environmentally persistent free radicals (EPFRs). The premise of this research is that EPFRs cause adverse health consequences by inducing oxidative stress (OS). 

The project aims to understand the mechanisms by which EPFR exposure increases susceptibility to respiratory viral infections and to investigate mitigation strategies.

A range of environmental factors can influence the health of the population. Environmental factors such as air pollution, temperature extremes, chemical exposures and polluted water can negatively impact the health of affected communities. Conversely, green space and good urban design can improve the health of communities. This project aims to examine the environmental factors associated with child health outcomes in Queensland, Australia.

Initial studies in the project will explore birth outcomes, neurodevelopmental disorders, infectious disease and asthma. 

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 (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.

The preschool years represent a crucial period in lung development. Longitudinal studies have shown that deficits in lung function start in early life with long term consequences into adulthood. This highlights the importance of being able to reliably and accurately measure the lung function of preschool aged children to aid in the diagnosis, treatment and management of children with suspected or known respiratory disease.

Macrophages are key cells in innate immune responses and play a critical role in orchestrating both initiation and resolution of pulmonary inflammation. In response to immune insults or injury, monocytes originated from bone-marrow migrate to the tissues, differentiate into macrophages (M0) and polarize into pro-inflammatory (classically activated or M1) or inflammation-resolving (alternatively activated or M2) phenotypes. These two compartments are well characterized in mouse model. In human, the border line between M1 and M2 polarization was vague until recently. Therefore macrophage responses in cystic fibrosis (CF) were mostly studied in mouse model. We have developed an ex-vivo model of human macrophages that reliably separates un-polarized (M0), M1 and M2 macrophages. Using this model we recently reported that activation of inflammation-resolving M2 macrophages were impaired in CF. In addition, we observed early expression of pro-inflammatory M1 macrophage markers in monocyte-derived M0 macrophages in patients with CF. Similar M1 and M2 markers expression was observed when macrophages from healthy donors were treated with CFTR channel inhibitor suggesting that defection M2 polarization is CFTR-dependent. We are aiming to study the link between CFTR function and macrophage polarization and functions.

Contact: a.tarique@uq.edu.au

CHEP is collaborating on several projects investigating the impact of environmental exposures on neurodevelopment and mental health in children. CHEP and Queensland Alliance for Environmental Health Sciences (QAESH) are providing expertise in environmental monitoring to the Barwon Infant Study, co-ordinated by Dr. Peter Vuillermin and Professor Anne-Louise Ponsonby, Murdoch Children's Research Institute, Melbourne.

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.

We have a number of opportunities for parents and children to participate in our research.

Current studies are listed on the Participate in our research section of our website.