Interleukin-1α: a key player for epithelial-to-mesenchymal signalling in COPD?

The lungs are continuously exposed to inhaled particles and irritants. Tobacco smoking is the leading cause of several airway diseases, including lung cancer, idiopathic pulmonary fibrosis and chronic obstructive pulmonary disease (COPD). In COPD, repeated exposure to cigarette smoke induces chronic inflammation and structural remodelling of the airways, with peribronchial fibrosis and epithelial-to-mesenchymal transition [1], resulting in (mostly irreversible) airway obstruction. Thus, abnormal airway responses to noxious gases probably results from aberrant signalling and crosstalk between epithelial, mesenchymal and immune cells.