Lung injury is consistently associated with the rapid accumulation of hyaluronan (HA), an extracellular matrix component that plays critical roles in tissue structure, repair and inflammation. Elevated HA levels are observed in a variety of pulmonary insults, including viral infections such as SARS-CoV-2 and influenza, allergic inflammation, and exposure to environmental pollutants. Our recent work has identified the type-2 cytokine IL-13 as an important regulator of hyaluronan matrix formation across multiple models of lung injury. However, the mechanisms by which IL-13 influences hyaluronan metabolism and matrix organisation remain unclear. Our on-going studies aim to determine how IL-13 shapes hyaluronan matrices through changes in cellular phenotype and function. By understanding how immune signals (like IL-13) regulate hyaluronan deposition and matrix structure, we aim to determine whether specific hyaluronan matrices promote effective tissue repair and recovery of lung function or contribute to chronic inflammation and pathological tissue remodelling.