Particulate matter air pollution is the leading cause of global disease burden, with exposure causally linked to respiratory diseases driven by epithelial cell dysfunction, including lung cancers and fibrosis.
We found that acute exposure to air pollution accelerates lung tumorigenesis through the release of the inflammatory cytokine IL-1β from pulmonary macrophages (Hill*, Lim*, Weeden*, Nature 2023). However, it is unclear whether cumulative pollution exposure leads to persistent alterations in the lung, creating a prolonged susceptibility to disease beyond the initial exposure window.
This project focuses on lung-resident macrophage responses to repeated challenges with urban air pollutants and the regulators driving aberrant macrophage-epithelial cross-talk in early tumourigenesis.
Techniques employed include in vivo modeling, 3D organoid assays, live cell microscopy, immunological and molecular biology techniques.