ICAM-1 and alpha 3 beta l expression by bronchial epithelial cells and their in vitro modulation by inflammatory and anti-inflammatory mediators

Background: Adhesion molecules are involved in inflammatory and repair proc esses of the bronchial epithelium. ICAM-1 is mainly involved in inflammator y reactions, whereas integrins, such as alpha 3 beta 1, are mainly involved in repair processes. Methods: Using bronchial biopsies from 10 asthmatics and eight controls, we first evaluated by immunohistochemistry expression of alpha 3 beta 1 and I CAM-1 in intact and damaged epithelium. Then, using the human pulmonary epi thelial cell line WI-26 VA, we studied, by flow-cytometry, the modulation o f ICAM-1 and alpha 2 beta 1 expression, and, by ELISA, the release of fibro nectin by proinflammatory cytokines, such as IL-5, and anti-inflammatory cy tokines, such as IL-4, TGF-beta, and EGF. Results: alpha 3 beta 1 expression was slightly higher in asthma than in co ntrols, as well as in damaged epithelium than in undamaged epithelium. ICAM -1 expression was higher in asthma than in controls, and similarly distribu ted in intact or damaged epithelium. In vitro, alpha 3 beta 1 was significa ntly increased by TGF-beta, EGF, and IL-4, and significantly decreased by I L-5. Fibronectin release was significantly increased by TGF-beta and IL-4, unchanged by EGF, and slightly but significantly decreased by IL-5. ICAM-1 expression was significantly decreased by TGF-beta and IL-4, unchanged by E GF, and significantly increased by IL-5. Conclusions: These differences in adhesion molecule expression and fibronec tin release may be important in epithelial cell inflammation and repair.