Communication between our immune system and the ECM is essential for tissue health and when dysregulated can be a factor contributing to pathology. In conditions like asthma, inflammation is often a predictor of disease severity. However, our lab has shown that allergen-induced ECM remodelling still occurs in the absence of chronic inflammation. Rather, we have discovered ECM changes are induced and sustained by chitinase-like proteins, immune-associated molecules highly upregulated in inflammatory and fibrotic diseases. More broadly, we have begun to study spatial changes of key immune cells/mediators and ECM organisation in the lung to understanding immune-ECM crosstalk during disease.