Abstract
1. We have recently demonstrated that airway eosinophilic inflammation can be transferred to unprimed mice by infusing interleukin (IL)-5-producing T cell clones. Using that murine model, we performed this study to delineate the mechanism of cyclosporin A and dexamethasone to inhibit allergic airway eosinophilic inflammation. 2. The ovalbumin-reactive murine T cell clones, FJ17, produced IL-2, IL-4 and IL-5 upon stimulation with relevant antigen. In FJ17-transferred mice, messenger RNA (mRNA) of IL-2 and IL-5 expressed in the lungs, the number of eosinophils in bronchoalveolar lavage fluid (BALF) was increased and the bronchial responsiveness to acetylcholine was enhanced after antigen provocation. 3. Cyclosporin A (10, 100 ng ml(-1)) and dexamethasone (10, 100 ng ml(-1) suppressed the production of IL-5 as well as IL-2 and IL-4 by FJ17 in vitro. 4. Subcutaneously administered cyclosporin A (30 mg kg(-1)) and dexamethasone (10 mg kg(-1)) inhibited antigen-induced mRNA expression of IL-2 and IL-5, increase of BALF eosinophils and bronchial hyperresponsiveness of FJ17-transferred mice in vivo. The number of BALF eosinophils was correlated with the bronchial responsiveness to acetylcholine (r=0.672). 5. The results clearly indicated that the suppression of IL-5 synthesis by T cells is involved in the effects of cyclosporin A and dexamethasone to inhibit allergic airway eosinophilic inflammation.
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