Asthma is a chronic inflammatory airway disease characterized by variable airflow obstruction, bronchial hyperresponsiveness, and airway remodeling. The inflammatory cascade is predominantly Th2-mediated: inhaled allergens are processed by dendritic cells, which present antigens to naive CD4+ T cells, driving Th2 differentiation. Th2 cells release IL-4 (promotes B-cell IgE class switching), IL-5 (eosinophil recruitment and survival), and IL-13 (goblet cell metaplasia and mucus hypersecretion, smooth muscle hypercontractility, subepithelial fibrosis). IgE binds high-affinity FcepsilonRI receptors on mast cells; upon re-exposure, allergen cross-links surface IgE triggering mast cell degranulation, releasing histamine, prostaglandin D2, leukotrienes (LTC4/D4/E4 - 1000x more potent bronchoconstrictors than histamine), and tryptase. The early-phase response (minutes) involves bronchospasm and edema; the late-phase response (4-8 hours) involves eosinophilic infiltration, mucus plugging, and epithelial damage. Chronic inflammation leads to airway remodeling: subepithelial fibrosis (collagen I, III, V deposition beneath basement membrane), smooth muscle hypertrophy/hyperplasia, goblet cell hyperplasia (mucus hypersecretion), angiogenesis, and neural plasticity (increased cholinergic tone). These structural changes cause fixed airflow obstruction that becomes less responsive to bronchodilators over time. Non-Th2 (non-eosinophilic) asthma involves neutrophilic inflammation driven by IL-17, IL-8, and often...