Asthma

Asthma is a chronic inflammatory airway disease characterized by reversible airflow obstruction, bronchial hyperresponsiveness, and airway remodeling. At the cellular level, the pathogenesis involves a complex interplay between innate and adaptive immune responses. In allergic (Type 2-high) asthma, inhaled allergens are processed by dendritic cells, which present antigens to naive T helper cells, driving Th2 polarization. Th2 cells secrete signature cytokines: IL-4 (promotes IgE class switching in B cells), IL-5 (recruits and activates eosinophils via the IL-5 receptor), and IL-13 (induces goblet cell metaplasia, mucus hypersecretion, and smooth muscle hypercontractility). IgE binds high-affinity FcεRI receptors on mast cells; upon re-exposure, allergen cross-linking of IgE triggers mast cell degranulation releasing preformed mediators (histamine, tryptase, prostaglandin D2) and newly synthesized lipid mediators (leukotrienes C4/D4/E4 — potent bronchoconstrictors 1000x more potent than histamine). The late-phase response (4–8 hours post-exposure) involves eosinophil infiltration with release of major basic protein (MBP) and eosinophil cationic protein (ECP), causing epithelial damage and sustained inflammation. Airway remodeling — subepithelial fibrosis from myofibroblast collagen deposition, smooth muscle hypertrophy/hyperplasia, angiogenesis, and goblet cell hyperplasia — leads to progressive fixed airflow...