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By – Dr. SAMIA FATIMA
1. Eosinophils 2. Mast cells 3. T-lymphocytes 4. Neutrophils 5. Basophils
Acute inflammation
Chronic inflammation
Remodeling of airways
Symptoms of bronchoconstriction
Exacerbationnonspecific hyperreactivity
Ongoing obstruction of airways
Pathogenesis of asthma
1.Early phase Inhaled Antigen
Sensitised mast cells on the mucosal surface bronchoconstriction
Histamine bronchoconstriction, increased vascular permeability.
prostaglandin D 2 bronchoconstriction, vasodilatation.
Leucotriene C4,D4, E4 Increased vascular permeability, mucus secretion and bronchoconstriction.
Direct subepithelial parasympathetic stimulation bronchoconstriction.
2.Late phase starts 4 to 8 hours later Mast cell release additional cytokine Influx of leukocytes(neutrophil,eosinophil) Eosinophils are particularly important-
exert a variety of effect
MAST CELLS release histamine,cysteinyl-leukotrienes,cytokines,chemokines, growth factors and neutrophins
causes bronchoconstriction
MACROPHAGES AND DENDRITIC CELLs release cytokines,IL-10. dendritic cells are the antigen presenting cells
EOSINOPHILS release of basic proteins and oxygen derived free
radicals causes airway hyperresponsiveness
NEUTROPHILS increased numbers of activated neutrophils are found in sputum and airways of patients with severe asthma.
T Lymphocytes Th2 cells release IL-5 eosinophilic inflammation IL-4,13 increased IgE formation
PRIMARY MEDIATORS
1.Th2 cells > IL 4,5 > IgE production & Mast cell recruitment
2.Histamine - bronchconstriction by direct and cholinergic reflex actions
3.ECF and NCF
Secondary mediators LT C4, D4, and E4. prolonged bronchospasm increased vascular permeability increased mucus secretion. Prostaglandins (D2) Bronchospasm Vasodilation PAF platelet aggregation granule secretion.
i. Inflammatory cell infiltration of the airwaysii. Increased thickness of the bronchial
smooth muscleiii. Partial or full loss of the respiratory
epitheliumiv. Subepithelial fibrosisv. Hypertrophy and hyperplasia of the
submucosal glands and goblet cellsvi. Partial or full occlusion of the airway lumen
by mucous plugsvii. Enlarged mucous glands and blood vessels
Acute bronchoconstriction
Swelling of bronchial wall
Chronic production of mucous
Remodeling of airways walls