what are the pathogenesis of asthma?

 Pathogenesis of Asthma a detailed guide

Asthma is a chronic inflammatory disease of the airways characterized by

  • Recurrent episodes of wheezing, dyspnea, chest tightness, and cough

  • Reversible airflow obstruction

  • Airway hyperresponsiveness to various stimuli

The pathogenesis of asthma involves complex interactions between genetic and environmental factors, leading to airway inflammation, bronchial hyperresponsiveness, and episodic bronchoconstriction.

Pathogenesis of Asthma

1. Genetic Predisposition

  • Individuals with atopy (a tendency to develop allergic diseases) are more likely to develop allergic (extrinsic) asthma.

  • Associated genes: IL-4, IL-5, IL-13, ADAM33, and HLA genes.

2. Environmental Triggers

  • Allergens: dust mites, pollen, pet dander, mold

  • Infections: especially viral respiratory infections

  • Pollutants: smoke, fumes, cold air

  • Exercise: especially in cold or dry environments

  • Drugs: aspirin (in aspirin-sensitive asthma)

3.  Immune Response (Type I Hypersensitivity in Atopic Asthma)

🔸 Sensitization Phase

  • Initial exposure to allergen → activation of Th2 cells.

  • Th2 cells release cytokines:

    • IL-4: promotes B-cell class switching to IgE

    • IL-5: recruits eosinophils

    • IL-13: enhances mucus production and airway hyperreactivity

  • IgE binds to mast cells, sensitizing them.

🔸 Re-exposure Phase

  • Allergen cross-links IgE on mast cells → mast cell degranulation → release of:

    • Histamine: causes bronchoconstriction, mucus secretion

    • Leukotrienes (LTC₄, LTD₄): potent bronchoconstrictors

    • Prostaglandins: contribute to inflammation

4.  Inflammatory Cell Recruitment

  • Eosinophils: Major role in tissue damage; release toxic granules and cytokines

  • Mast cells and basophils: drive immediate and late-phase reactions

  • T-lymphocytes (Th2 subtype): sustain and amplify inflammation

  • Neutrophils: more prominent in severe or non-atopic asthma

5.  Late-Phase Reaction (4–8 hours after exposure)

  • Further infiltration of eosinophils and T cells

  • Sustained bronchoconstriction, edema, mucus secretion, and airway remodeling

 Structural Changes (Airway Remodeling)

Chronic inflammation leads to irreversible changes in airway architecture:

  • Goblet cell hyperplasia → ↑ mucus production

  • Subepithelial fibrosis (thickening of basement membrane)

  • Smooth muscle hypertrophy and hyperplasia

  • Angiogenesis (increased blood vessel formation)

  • Mucus plugging of bronchioles

These changes contribute to persistent airflow limitation, especially in long-standing asthma.

 Summary of Key Pathogenic Steps

Step Description
Genetic predisposition Th2-skewed immune response
Trigger exposure Allergen or irritant activates immune system
IgE production Sensitization of mast cells
Mast cell degranulation Immediate bronchoconstriction and inflammation
Eosinophilic inflammation Late-phase response and tissue damage
Airway remodeling Chronic structural changes impairing airflow

 Types of Asthma (based on pathogenesis)

Type Characteristics
Atopic (allergic) IgE-mediated, most common in children, family history
Non-atopic Triggered by infections, pollution; no allergy history
Drug-induced Aspirin-sensitive asthma
Occupational Due to workplace exposure (chemicals, dust)


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