TH2 cells secrete cytokines like IL-4, IL-5, and IL-13 that stimulate B cells to produce IgE antibodies and recruit eosinophils. Upon exposure to allergens, IgE binds to mast cells, which then release mediators like histamine and leukotrienes upon re-exposure. This causes bronchospasm, edema, and mucus production. In the late phase, recruited leukocytes release more mediators that damage the epithelium. In asthma, there is thickening of the basement membrane, accumulation of mucus, and chronic inflammation from increased eosinophils and goblet cells.

1. PBL Session 3
Rosshini Jagatheswaran

2. Describe the
PATHOGENESIS of
bronchial asthma
MUST KNOW
Learning Outcome

3. How T helper cells work?

4. TH2cells
secrete cytokines IL-4, IL-5, IL-13
stimulate B cells to produce IgE and other
antibodies.
 IL-4 stimulates the production of IgE
 IL-5 activates locally recruited eosinophils
 IL-13 stimulates mucus secretion from
bronchial submucosal glands and also
promotes IgE production by B cells

6. Sensitization to Allergen
• Inhaled allergens
• TH2– dominated response
• IgE productions
• Eosinophil recruitment
• Release of granules and mediators

8. Allergen-Triggered Asthma
• Re-exposure
• Ag-induced cross linking of IgE bound to IgE
receptors on mast cell
• Mediators released – histamine, leukotrienes
• Tight junctions between epithelial cells open
• Antigen enter mucosa
• Mucosal mast cells activated
• Eosinophil release other mediators

9. • Leukotrienes
- constriction of bronchi  bronchospasm
- increased mucus production  mucosal
accumulation
• Histamine
- increased vascular permeability  swelling &
redness  edema
- increased mucus production  mucosal
accumulation
• Eosinophilic chemotactic factor
- Chemotaxis of eosinophils accumulation of
eosinophils

10. Late Phase
• Recruited leukocytes
initiate late phase
• Mediators release
from endothelium,
epithelial cells,
leukocytes
• Eosinophils  MBP,
ECP – damage
epithelium

12. Comparison of a normal bronchiole
with that in a patient with asthma
• Increase in the number of mucus-secreting
goblet cells in the mucosa and hypertrophy of
submucosal mucus glands  Accumulation of
mucus in the bronchial lumen
• Recruitment of eosinophils & macrophages
intense chronic inflammation
• Thickened basement membrane
• Hypertrophy & hyperplasia of smooth muscle
cells

13. POP-QUIZ
Which T Helper Cell plays an important
role in bronchial asthma?
What happens after IgE binds to the
mast cell in the first phase-sensitization
phase?
Leukotrienes causes …?
Upon re-exposure of Ag, what happens
after binding of IgE?

14. Some factors released by eosinophils in
the late phase causes damage to the
epithelium. Give 2 examples of the
factors.
Give 2 differences of a normal
bronchiole and bronchiole of an
asthmatic patient.

15. THANK YOU