抄録
Corticosteroids and theophylline have been used widely for the treatment of asthma. These two classes of drugs appear to reduce the tissue infiltration of eosinophils, predominant inflammatory cells in the airways of asthmatic patients. Corticosteroids inhibit the generation of both endothelial-activating Th2 cytokines (e.g. interleukin (IL)-4/IL-13) and eosinophil growth factors (e.g. IL-5/granulocyte-macrophage colony stimulating factor) and also attenuate the effects of eosinophil growth factors on the differentiation and prolonged survival of eosinophils. However, corticosteroids modulate directly neither eosinophil adhesiveness nor the expression of adhesion proteins on endothelial cells in vitro. Therefore, it is likely that the inhibitory effect of corticosteroids on the tissue infiltration of eosinophils is the consequence of indirect mechanisms, mainly via the inhibition of cytokines. Interestingly, theophylline, which is generally accepted as a bronchodilator, attenuates eosinophil adhesion to endothelial cells in vitro at a clinically therapeutic concentration. Furthermore, theophylline inhibits the expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 on endothelial cells that had been stimulated with IL-4 plus tumor necrosis factor-α. Thus, theophylline possibly exerts an inhibitory effect on both the adhesive property of eosinophils and the expression of adhesion molecules on endothelial cells. These findings possibly indicate that theophylline would be adequate to supplement the actions of corticosteroids in asthmatic airway inflammation, partly via its inhibitory effect on the interaction between blood eosinophils and endothelial cells.
