Abstract: @@ Bronchial asthma is characterized by chronic recruitment of eosinophils in the airways. It has been reported that bronchial eosinophil recruitment and activation may even occur in mild-moderate stable asthma and that bronchial epithelium damage and airway responsiveness may be partially associated with the eosinophilic inflammatory reaction.1 There is increasing evidence that the eosinophil-rich bronchial inflammation characteristic of asthma is orchestrated, at least partly, by cytokine products of activated T lymphocytes. Of particular interest is T-helper type 2 (Th2) cell-derived interleukin-5 (IL-5). 2 This cytokine mediates the terminal differentiation of committed eosinophil precursors, activates mature eosinophils, and prolongs their survivals in culture and, presumably, at sites of allergic inflammation.3-6 IL-5 also selectively enhances eosinophil degranulation, antibody-dependent cytotoxicity, 3 and adhesion to vascular endothelium.4