Figure 2

Intervention of ADAM/ADAMTS proteinases in asthma and COPD. Succinctly, in asthma, inhaled allergens provoke the degranulation of sensitized mast cells and the activation of epithelial cells (EC) while in COPD, inhaled cigarette smoke activates epithelial cells and macrophages. After a first challenge in both diseases, an inflammatory reaction occurs resulting in the recruitment of eosinophils and CD4⁺ T cells for asthma, neutrophils and CD8⁺ T cells for COPD. Following a chronic inflammation, tissue alterations such as mucus hypersecretion, bronchoconstriction appear in asthma while small airway fibrosis, alveolar destruction (emphysema) and mucus hypersecretion occur in COPD. An airway hyperresponsiveness is linked to both diseases. However, it is reversible in asthma but not in COPD. ADAM-8 plays a role in asthma-related inflammation while ADAM-33 is associated to remodeling processes and hyperresponsiveness associated to asthma. In COPD, ADAM-17 acts on mucus hypersecretion process while ADAM-33 is associated with COPD-related hyperresponsiveness.