Figure 2.

Schematic demonstrating possible pathways to A. fumigatus-induced airway remodelling. The asthmatic epithelium is characterised by goblet cell hyperplasia and mucus hypersecretion, loss of ciliated cells and subepithelial fibrosis. This fibrosis is likely driven by injury signals from the epithelium activating underlying fibroblasts. Loss of cilia function coupled with increased mucus and exposure of basement membrane components may enhance A. fumigatus adhesion and allergen production. A. fumigatus-derived factors drive the upregulation of pro-inflammatory cytokines to shape the immune response. In addition, epithelial-derived growth factors such as Endothelin-1 are upregulated in response to A. fumigatus and may directly activate underlying fibroblasts. Angiogenesis and vascular permeability support the arrival of infiltrating immune cells and circulating mediators likely contribute to airway wall remodelling. Image generated in BioRender.