Cigarette smoke induces overexpression of cathepsin S in active smokers with and without COPD

Background: Cigarette smoking induces molecular changes within the lung, including oxidative stress, inflammatory cell recruitment and a protease/anti-protease imbalance, which contributes in part to emphysema, airway remodeling and airway obstruction. Nevertheless, little is known on cathepsin S (CatS), a cysteine protease that plays a key role in tissue remodeling (elastin degradation) during chronic inflammatory lung diseases. Aims and objectives: We evaluated whether cigarette smoke activity modulates CatS expression and activity in human lung tissues and in cellulo. Methods: Lung tissue extracts were obtained from forty-two COPD patients (current and former smokers), non-COPD smokers (n=20) and never-smokers (n=10). Primary human bronchial epithelial cells (pHBECs) were challenged by non-toxic doses of cigarette smoke extracts (CSE). CatS activity was determined using fluorogenic substrates and its protein expression was analyzed by western-blot, ELISA and immunohistochemistry studies. Results: CatS expression and activity increased significantly in current smokers with or without COPD compared to never and former smokers (p Conclusion: CatS participates in ECM remodeling during lung inflammation associated to tobacco.