COPD and asthma are both obstructive airway diseases but differ fundamentally in pathophysiology, cellular mechanisms, and reversibility. Asthma is characterized by chronic airway inflammation driven by type 2 (Th2) immune responses: allergen exposure triggers mast cell degranulation and Th2 cell activation, releasing IL-4 (IgE class switching), IL-5 (eosinophil recruitment), and IL-13 (mucus hypersecretion, airway hyperresponsiveness). This causes bronchial smooth muscle hyperreactivity, mucosal edema, mucus plugging, and reversible airway obstruction. Airway remodeling (subepithelial fibrosis, smooth muscle hypertrophy) occurs with chronic poorly controlled asthma. COPD involves two overlapping pathologies: chronic bronchitis (mucus gland hyperplasia, chronic productive cough ≥ 3 months/year for ≥ 2 consecutive years, neutrophilic inflammation) and emphysema (destruction of alveolar walls by neutrophil-derived elastase and proteinases, with loss of elastic recoil and gas exchange surface area). COPD inflammation is primarily neutrophilic and CD8+ T cell-driven (unlike Th2/eosinophilic in asthma), and airflow obstruction is progressive and largely irreversible. The protease-antiprotease imbalance theory explains emphysema: cigarette smoke recruits neutrophils and macrophages that release elastase; simultaneously, oxidative stress inactivates alpha-1 antitrypsin (the main elastase inhibitor). Alpha-1 antitrypsin deficiency is a genetic cause of...