School of BioSciences - Theses
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ItemA systems approach to understanding allergy, asthma and childhood wheeze( 2019)In Australia, asthma is a common respiratory disease with a significant health burden. Our current understanding of the biological mechanisms behind asthma is incomplete. It is not clear what makes a person more susceptible compared to another, nor is it clear how determinants of asthma susceptibility interact to cause disease. Childhood wheeze does not necessarily progress to asthma, and asthma itself is a heterogeneous condition that encompasses many different phenotypes, each with potentially different biology. However, we suspect that, for most affected individuals, the origins of asthma arise in early childhood, as embodied by the “hygiene hypothesis”. Events like microbial and allergen exposure in early life, as well as frequency and severity of respiratory infections, may steer the child on a course towards asthma and disease. Early prediction of disease susceptibility or severity is important because it may permit early intervention in young children, which may then limit the progression of asthma or prevent it altogether. My research thesis had three general aims: 1. To uncover hidden subgroups or “clusters” of children who share similar trajectories of immune function and susceptibility to respiratory infection; and determine how these relate to asthma and other related phenotypes. 2. To describe microbial communities in the upper respiratory tract of infants, specifically distinct patterns of change or trajectories in the microbiome that emerge as the child ages; and to determine how these relate to respiratory health, asthma, and related phenotypes. 3. To identify novel genetic determinants of asthma and related phenotypes in early childhood (including immunorespiratory clusters and microbiome trajectories), and determine how these relate to each other. Through this research, I hope to shed light on the complexity that is asthma pathogenesis. In particular, it may explain how the determinants of asthma are similar or different between individuals. With my research, it may be possible to better characterise the interlocking events that lead from disruption of normal physiology to eventual disease. Future studies can focus on the origins of asthma in specific subpopulations, as well as potential treatment targets within each subgroup. The results of this research may open up the potential for developing therapeutic and preventative measures for asthma, as well as allow earlier intervention for infants at risk of developing asthma later in life.