Asthma: pathology
- Lesion
Asthma is chronic airway inflammation that makes bronchi narrow in episodes. Over time the airway wall thickens and part of the narrowing becomes fixed.
What it is
Asthma is a chronic inflammatory disease of the airways with variable, largely reversible obstruction: episodes of wheeze, breathlessness, chest tightness and cough, often at night. The commonest form, atopic asthma, is a Th2- and IgE-driven type I hypersensitivity reaction to inhaled allergens. Repeated inflammation remodels the bronchial wall, which explains the fixed component some patients develop.
Structure
- Fatal attack (gross): overinflated lungs with small atelectatic areas; bronchi and bronchioles plugged by thick, tenacious mucus.
- H&E: thickened basement membrane zone (subepithelial collagen), many eosinophils in the mucosa, goblet-cell hyperplasia, enlarged submucosal glands.
- Hypertrophied and hyperplastic bronchial smooth muscle; increased vascularity; edema.
- Sputum or lavage: eosinophils, Charcot-Leyden crystals and Curschmann spirals.
Step by step
- In a genetically prone person, inhaled allergen is presented to T cells that become Th2 cells (epithelial IL-33 and TSLP push this).
- IL-4 and IL-13 switch B cells to IgE, which coats mast cells.
- On re-exposure, allergen cross-links IgE on mast cells: histamine, leukotrienes C4–E4 and prostaglandin D2 are released.
- Bronchospasm (direct and through vagal reflexes), edema and mucus narrow the airway within minutes.
- Hours later recruited eosinophils release major basic protein and cationic protein that damage the epithelium.
- Repeated cycles thicken the wall (remodeling), adding a fixed component to the obstruction.
Types of asthma by trigger
| Type | Mechanism | Clues |
|---|---|---|
| Atopic | Type I (IgE) hypersensitivity, Th2 | Childhood, family history, eczema, positive skin tests |
| Nonatopic | No allergen sensitisation; airway hyperreactivity | Viral infections, pollutants, cold, exercise as triggers |
| Drug-induced (aspirin and NSAIDs) | COX block, fall in PGE2, excess leukotrienes | Nasal polyps, rhinitis, urticaria |
| Occupational | Type I or direct release of bronchoconstrictors | Fumes, resins, wood or cotton dust, formaldehyde at work |
Markers
- Charcot-Leyden crystals
- Curschmann spirals
- Blood eosinophilia
- Raised IgE
Clinical notes
- Attacks of wheeze, cough and dyspnoea, often at night or early morning, triggered by allergens, viral infections, cold air, exercise or irritants.
- Acute severe asthma can be fatal; most patients live a normal life between episodes.
- Blood eosinophilia and high IgE support atopic asthma; type 2 biologic therapies target IL-5, the IL-4 receptor or TSLP.
- Neutrophil-rich, steroid-resistant asthma is a Th17-related minority.
Test yourself
Think of the answer, then tap the question to see it.
What are Charcot-Leyden crystals?
Crystals of galectin-10 released by eosinophils, seen in the sputum of patients with atopic asthma.
What is airway remodeling in asthma?
Structural thickening of the bronchial wall: sub-basement membrane fibrosis, larger glands and more goblet cells, smooth muscle hypertrophy and more vessels.
Why can aspirin trigger asthma in some patients?
Blocking cyclooxygenase lowers prostaglandin E2 and shunts arachidonic acid toward bronchoconstricting leukotrienes.
Which cytokine recruits and activates eosinophils in asthma?
IL-5, secreted by Th2 cells and group 2 innate lymphoid cells.
Elsewhere in DurgiPedia
- Type I hypersensitivity (immediate, IgE)
- IL-4, IL-5 and IL-13 (the Th2 cytokines)
- Mast cell and basophil
- Th1, Th2, Th17, Tfh and Treg
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Asthma (MedlinePlus, US National Library of Medicine, 2025).
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Representative model, for educational purposes only.