Bronchial asthma pathology with pictures
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Bronchial Asthma - Pathology
Bronchial asthma is a chronic inflammatory disorder of the airways characterized by episodic, reversible airway obstruction, bronchial hyperresponsiveness, and structural airway remodeling. The pathology involves both acute and chronic changes.
1. Pathogenesis Overview
Asthma is fundamentally an exaggerated Th2-mediated immune response to environmental antigens in genetically susceptible individuals. The central cytokines driving pathology are:
| Cytokine | Effect |
|---|---|
| IL-4 | IgE production by B cells, vessel wall priming (VCAM-1/ICAM-1) |
| IL-5 | Eosinophil development and activation |
| IL-13 | Goblet cell metaplasia, mucus hypersecretion, bronchial hyperreactivity |
| TSLP/IL-33 | Activation of ILC2s and mast cells |
The diagram below (from Robbins Pathology) shows the full pathogenic sequence:
Fig. 15.10 - Robbins Pathology: (A) Normal airway vs. (B) asthmatic airway showing goblet cell proliferation, basement membrane thickening, inflammation, and smooth muscle hypertrophy; (C) Th2 sensitization; (D) immediate-phase reaction; (E) late-phase reaction.
2. Two-Phase Inflammatory Response
Immediate Phase (within minutes)
- Allergen re-exposure cross-links IgE on mast cells → mast cell degranulation
- Release of: histamine, serotonin, prostaglandin D2, leukotrienes (LTC4, LTD4, LTE4), tryptase, chymase
- Results in: bronchospasm, vascular permeability, mucus secretion
- Vagal efferent reflexes amplify bronchoconstriction
Late Phase (2-6 hours later, lasting 24-48 hours)
- Influx of eosinophils, neutrophils, basophils, Th2 cells, DCs
- Eosinophil products (major basic protein, eosinophil cationic protein) damage the epithelium and perpetuate hyperreactivity
3. Central Role of Mast Cells and Basophils
Fig. 60.6 (Murray & Nadel's): Allergen triggers IgE cross-linking on mast cells → release of chymase, tryptase, PGD2, histamine, serotonin → early bronchoconstriction and vessel wall priming for leukocyte extravasation.
4. T2 Immunity and Airway Remodeling
Fig. 60.5 (Murray & Nadel's): IL-5 drives tissue eosinophilia. IL-13 drives goblet cell metaplasia, iNOS, airway remodeling, and bronchial hyperreactivity. IL-4 drives IgE production.
ILC2s (Group 2 innate lymphoid cells) are activated by epithelial cytokines (TSLP, IL-33) independently of allergen recognition - they share GATA3 expression and cytokine production with Th2 cells, making them especially important in severe/late-onset asthma.
5. Mucus Plugging Mechanism
Fig. 60.7 (Murray & Nadel's): IL-13 drives goblet cell metaplasia and MUC5AC-rich mucin overproduction. IL-5 activates eosinophils, which release eosinophil peroxidase (EPO). EPO + thiocyanate + H₂O₂ cross-links mucin polymers → stiff, inspissated gel → plugged airway. Charcot-Leyden crystals form from galectin-10 released during EETosis.
6. Gross and Histological Morphology (MORPHOLOGY)
Gross Findings (Fatal Cases - Status Asthmaticus)
- Overinflated lungs with air trapping
- Small areas of atelectasis
- Thick, tenacious mucus plugs occluding bronchi and bronchioles
- Plugs contain shed epithelium forming Curschmann spirals
Histological / Microscopic Findings
Acute findings:
- Numerous eosinophils in mucus and wall
- Charcot-Leyden crystals (bipyramidal crystals of galectin-10 from eosinophil granules)
- Curschmann spirals (whorls of shed epithelium in mucus plugs)
Airway Remodeling (chronic):
- Thickening of the airway wall overall
- Sub-basement membrane fibrosis - deposition of type I and III collagens beneath the epithelial basement membrane (a hallmark finding)
- Goblet cell metaplasia - increased number of goblet cells replacing ciliated cells
- Hypertrophy of submucosal glands
- Smooth muscle hypertrophy and hyperplasia of bronchial wall
- Increased vascularity (angiogenesis)
Acute airflow obstruction = bronchoconstriction + edema + mucus plugging. Airway remodeling contributes to chronic irreversible obstruction.
Histological Biopsy (Robbins & Kumar Basic Pathology, Fig. 11.11)
Bronchial biopsy specimen: sub-basement membrane fibrosis (pale acellular zone beneath epithelium), dense eosinophilic inflammation in the lamina propria, and smooth muscle hyperplasia in the lower layers.
7. Subtypes and Their Pathological Basis
| Subtype | Key Pathologic Feature |
|---|---|
| Atopic (extrinsic) | Th2/IgE-mediated; eosinophilic; responds to steroids |
| Non-atopic (intrinsic) | Triggered by respiratory infections; less IgE involvement |
| Aspirin-sensitive | Leukotriene overproduction (COX-1 inhibition shifts arachidonic acid to 5-LOX); adult-onset with nasal polyps |
| Occupational | Sensitization to workplace antigens (fumes, organic dusts, isocyanates) |
| T2-low / neutrophilic | Less eosinophilic; steroid-resistant; associated with severe/late-onset disease |
8. Key Pathologic Features - Summary Table
| Feature | Description |
|---|---|
| Cells | Eosinophils, mast cells, Th2 lymphocytes, ILC2s, basophils |
| Key cytokines | IL-4, IL-5, IL-13, TSLP, IL-33 |
| Sputum findings | Curschmann spirals, Charcot-Leyden crystals, eosinophils |
| Basement membrane | Sub-BM fibrosis (type I and III collagen) |
| Smooth muscle | Hypertrophy + hyperplasia |
| Mucus glands | Goblet cell metaplasia, submucosal gland hypertrophy |
| Vasculature | Increased (angiogenesis) |
| Fatal cases | Overinflation, mucus plugging, atelectasis |
Sources: Robbins, Cotran & Kumar Pathologic Basis of Disease (10th ed.), pp. 638-640; Robbins & Kumar Basic Pathology, pp. 442-456; Murray & Nadel's Textbook of Respiratory Medicine, Chapters 60-61 (Figs. 60.5-60.7).
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