Seminar Abstract: Chronic lung diseases like asthma are characterised by airway remodelling and inflammation, including changes to the extracellular matrix (ECM) environment. Whilst the complex and dynamic processes of ECM remodelling has traditionally been attributed to persistent and aberrant immune cell activation, many questions remain over which specific immune cells and mediators influence discrete lung remodelling events. Using mouse models of allergic airway pathology, our lab has shown that type 2 and IL-17a signalling are not required for the development of airway remodelling. Instead, our findings highlight a central role for targeting chitinase-like proteins, as potential targets to prevent or reverse ECM changes in the lung. In addition, the localisation of macrophages and fibroblasts around active ECM remodelled sites suggests that communication between these cell types may may an important role in driving ECM remodelling processes.

Biosketch: "I studied at the University of Melbourne, embarking on a PhD in Pharmacology studying oestrogen metabolites and models of breast tumour growth. With an interest in vivo model system, I moved to the University of Edinburgh, UK to explore immune responses and how the lung responds to infections, allergens and injury. I obtained an Asthma UK and Medical Research Fellowship and moved to the University of Manchester to develop and utilise models of allergic airway pathology to better understand immune responses and extracellular matrix remodelling. In 2022 I relocated to the University of Aberdeen with a growing interest in using spatial methods to uncover key immuno-matrix networks that drive lung disease."