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Terms in this set (88)

chronic airway inflammation

Higher number of activated inflammatory cells within the airway wall. Eosinophils, mast cells, macrophages and T lymphocytes (produce cytokines, leukotrienes, and bradykinins) are found in the epithelium

Airway inflammation - type 2 helper T-cell (T H2) response with predominantly eosinophilic inflammation. Severe asthma may have type 1 helper T-cell (T H1) response with predominantly neutrophilic airway inflammation and cytokine production

Airway cooling can be a significant cause of bronchospasm, in exercise induced asthma as well as winter time asthma attacks

airway hyperresponsiveness. Airways constrict in response to inhaled allergens or irritants
Inhaled allergens cause mast cell degranulation release of chemical mediators --> bronchospasm --> increased airway resistance, wheezing and mucus hypersecretion
Stimulation of irritant receptors, resp. tract infections, airway cooling

Airway remodeling; hyperplasia and hypertrophy of smooth muscle cells, edema, inflammatory infiltration, angiogenesis, increased deposition of type I and type III collagen --> thickening of subepithelium and expansion of entire airway wall.

Airway remodeling over time may lead to irreversible airflow limitation (obstructive pattern) making bronchodilators less effective
-- Airway remodeling makes distinction between asthma and COPD less clear

Bottom line: Allergic type activation of the immune system. TH2-predominant T-cell response to inhaled antigens causing IgE production and allergic airway inflammation