The biofilm lifestyle involves bacteria adhering to a surface and building a protective slime shield to encase them. Biofilms enhance antimicrobial resistance by providing physical protection as well as through the coordinated release of molecules to disable antibiotics. These dynamic communities can grow and spread causing large scale and chronic infections. The US National Institutes of Health estimates that more than 80 per cent of problematic infections are caused by biofilms. And 65 per cent of hospital-acquired infections can be traced back to biofilms accessing the body via catheters.
We are primarily using real time microscopy to study the various roles of different biofilm components in establishment, maintenance, and growth and survival – including adapting to environmental changes - with one aim being to develop new ways to combat pathogenesis and reduce biofilm formation.
To date, our discoveries include: how pieces of broken and dispersed membrane can form reusable ‘shopping bags’ aka transport vesicles; how large populations of bacteria self-organise individual behaviours to enable active expansion of biofilm communities; how eDNA functions as a biofilm ‘glue’ that assists coordinated behaviour and motility, as well as its role in cell traffic control; and how bacteria escape the actions of antibiotics that target the bacterial cell wall by transitioning into an alternate cell wall deficient lifestyle.
More recently, we have discovered that vestiges of viruses which infect bacteria (bacteriophages) can trigger a cell ‘explosion’ (explosive cell lysis, ECL) that releases extracellular DNA (eDNA), moonlighting proteins (a single protein with multiple functions) and other cellular components that function as shared resources, or ‘public goods’ back into the biofilm where they are used by other members of the community.
While we have established that ECL is required for biofilm development in vitro, its role in infection and inflammation is unknown. To that end, we have assembled a team of experts to test our hypothesis that ECL leads to the release of factors that contribute to immunopathogenic processes. Our model is based around the ability of Pseudomonas aeruginosa to cause acute and chronic respiratory infections. Specifically, we will study immune stimulation and inflammation, programmed cell death pathways, intracellular survival, and inflammasome activation, by using ECL mutant bacteria, and in vitro macrophage and mouse lung infection models.
Research focus: Biofilm architecture and dynamics and the lifestyles of bacteria
Tags: Pathogen evolution, Biofilms, Cell-to-cell communication, Quorum sensing, Pseudomonas, Antibiotic resistance, Inflammation
Phone: +61 2 9514 4144