Bronchial Asthma

Introduction & disease concept

• Definition — a chronic inflammatory disorder of the airways with hyper-responsiveness of tracheobronchial smooth muscle, producing recurrent, variable and reversible airflow obstruction with wheeze, dyspnoea, chest tightness and (often nocturnal) cough.
• Three defining features — chronic airway inflammation, bronchial hyper-reactivity, and variable/reversible airflow limitation — a heterogeneous, primarily inflammatory disease in which inflammation underlies the hyper-reactivity and drives airway remodeling.
• Dual pathology — both an obstructive disease (reversible bronchoconstriction) and an inflammatory disease (oedema, mucus, eosinophil/TH2 infiltration) — so treatment must address both: bronchodilators (relievers) + anti-inflammatory agents (controllers).
• Early & late response — allergen cross-links IgE on mast-cell FcεRI → early response (histamine, tryptase, PGD₂, cysteinyl-LTs → immediate FEV₁ fall); 3–6 h later a late response driven by TH2 cytokines IL-4/IL-5/IL-13 recruiting eosinophils → sustained obstruction + rising bronchial reactivity.
• T2-high vs T2-low — the key molecular split — T2-high (eosinophilia, high IgE/FeNO, periostin) responds well to inhaled corticosteroids and type-2 biologics; T2-low (non-T2) responds poorly to ICS. FeNO and blood eosinophils are the working biomarkers.