Abstract
Bronchial asthma is characterized by eosinophilic inflammation, desquamation of airway epithelium and bronchial hyperresponsiveness. Eosinophil causes desquamations of epithelium and damages to epithelial cells, following the reduction of the mediators which relaxes bronchial muscle.
Human epithelial cells can produce PGE2, 15-HETE, 8, 15-diHETE, 8, 15-LT. PGE2 causes the relaxation of airway smooth muscle. 15-HETE inhibits LT B4 release from rabbit neutrophil and LT C4 release from human eosinophil, respectively. Furthermore, epithelial cells may release epithelium-derived relaxing factor (s) (EpDRF) which cause airway muscle relaxation. Neutral endopeptidase (NEP, enkephalinase) in the epithelium destroys substance P and neurokinin A which induce bronchoconstriction.
Desquamations and damages of airway epithelium reduce these relaxing factors and cause bronchial hyperresponsiveness to bronchoconstractive effects.
