Pathophysiology

Asthma is an inflammatory disease driven by T-helper type 2 cells (Th2-cell) that manifests in individuals with a genetic predisposition. It consists of the following three pathophysiologic processes:

1. Bronchial hyperresponsiveness

2. Bronchial inflammation

   • Symptoms are primarily caused by inflammation of the terminal bronchioles, which are lined with smooth muscle but lack the cartilage found in larger airways.

   • Overexpression of Th2-cells → inhalation of antigen results in production of cytokines (IL-3, IL-4, IL-5, IL-13) → activation of eosinophils and induction of cellular response (B-cell IgE production) → bronchial submucosal edema and smooth muscle contraction → bronchioles collapse [4][5]

3. Endobronchial obstruction caused by:

   • Increased parasympathetic tone

     • Reversible bronchospasm

     • Increased mucus production

     • Mucosal edema and leukocyte infiltration into the mucosa with hyperplasia of goblet cells

   • Hypertrophy of smooth muscle cells

• Allergic asthma

  • IgE-mediated type 1 hypersensitivity to a specific allergen

  • Characterized by mast cell degranulation and release of histamine after a prior phase of sensitization

• Nonallergic asthma

  • Irritant asthma: irritant enters lung → ↑ release of neutrophils → submucosal edema → airway obstruction

  • Aspirin-induced asthma (NSAID-exacerbated respiratory disease) is characterized by the Samter triad:

    • Inhibition of COX-1 → ↓ PGE2 → ↑ leukotrienes and inflammation → submucosal edema → airway obstruction

    • Chronic rhinosinusitis with nasal polyposis

    • Asthma symptoms