There has been a striking increase in the incidence of asthma in Australia over recent decades. The general consensus in the field is that major underlying causes of this increase are changes in lifestyle, diet and hygiene. A commonality between all of these factors is shifts in the constituents of the microbial communities resident in our mucosal tissues, most notably the gut. Accordingly, there has been a surge of interest in trying to characterize and manipulate this ‘microbiota’ as a means of improving prognostic tools and health. The majority of research in the field has focused solely upon the bacterial communities within the microbiota, disregarding its other members, such as fungi. Although the fungal component of the microbiota comprises of approximately 0.03-2% of total intestinal microbes, fungal cells are >100 fold larger than bacterial cells and thus represent a substantial biomass within the gut ecosystem. Bacteria and fungi co-inhabit and interact within the gut, thus it is important to consider that influencing bacterial communities could affect fungal communities, and vice versa. The hypothesis behind this project is that interplay between fungal and bacterial communities within the microbiota underpin susceptibility to asthma. There are fundamental questions that need to be addressed. How do fungal and bacterial communities influence each other? Which bacteria and fungi are the most immunomodulatory members of the community? What is the mechanism of action through which bacterial and fungal communities influence susceptibility to asthma? In order to address these questions, this research project has the following two aims: 1. Determine the microbial, metabolic and immunological mechanisms through which commensal bacteria and fungi influence susceptibility to asthma. 2. Identify the links between fungal-bacterial interactions and the development of atopy and wheeze in early childhood. This project involves a range of techniques and approaches including cellular immunology, bioinformatics and both mouse models of disease and analysis of a human birth cohort study.
asthma, microbiota, bacteria, fungi, microbes, inflammation, lung, gut, immunology, bioinformatics, human cohort
Central Clinical School
Top-up scholarship funding available