Role of Various Mediators in Inflammation of Asthmatic Airways

Abstract

The degree of airway inflammation is directly related to asthma severity and associated hyper-responsiveness. Airway inflammation is categorized into three types: (a) acute asthmatic inflammation featured by early recruitment of cells into the airways, (b) subacute asthmatic inflammation involving activation of recruited cells in continual inflammation, and (c) chronic inflammation characterized by cellular damage. T-helper lymphocytes, the key factor in the pathogenesis of bronchial asthma, induce B cells to synthesize and secrete IgE through production of IL-4 and induce eosinophil-mediated inflammation. Mediators such as histamine, PG, leukotrienes, and kinins contract airway smooth muscle, increase microvascular leakage, increase airway mucus secretion, and attract other inflammatory cells into airway epithelia that initiate mucociliary clearance signaling pathways through special Toll-like receptor 4 expressed on epithelial cells activated by allergic and infectious triggers. These cells form barrier against mechanical stress, oxidant stress, allergens, pollutants, infectious agents, and leakage of endogenous solutes. Various adhesion molecules and costimulatory factors also promote infiltration of inflammatory cells at the site of inflammation.