In asthmatic patients, antioxidant defence is decreased. Although inhaled corticosteroids decrease asthmatic inflammation and modulate reactive oxygen species (ROS) generation, little is known of their effect on cellular antioxidant levels. The aim of this study was to evaluate the effect of inhaled beclomethasone dipropionate (BDP; 1,000 mg . day -1 ) on erythrocyte antioxidant levels in stable asthmatic patients.Forty patients with stable, mild asthma were treated in a double-blind, placebocontrolled, parallel-group study with BDP 250 mg, two puffs b.i.d. for 6 weeks. At entry and every 2 weeks during treatment, erythrocyte antioxidant levels, haematological parameters, pulmonary function tests and asthma symptoms were determined.The results show that during treatment with BDP, erythrocyte catalase levels increased (at entry (meanSEM) 414, after 6 weeks 544 mmol H 2 O 2 . min -1 . g haemoglobin (Hb) -1 , p=0.05 in comparison with placebo). Erythrocyte total glutathione levels significantly decreased after 6 weeks treatment with BDP (from 7.00.4 to 6.60.3 mmol . g Hb -1 (p=0.04)). In the BDP-treated patients, blood eosinophil counts were higher in patients who responded with an increase in erythrocyte catalase levels during BDP treatment, as compared to those not responding ((meanSEM) 34039 and 15352610 6 cells . L -1, respectively, p=0.05). The present study shows that treatment with inhaled bedomethasone dipropionate results in changes in antioxidant levels in erythrocytes of patients with stable, mild asthma. Eur Respir J 1999; 13: 1260±1266.

To study the effect of IL-13 on CD69 expression and cell viability in human eosinophils, purified human peripheral blood eosinophils from healthy donors were incubated with increasing concentrations of IL-13. The expression of CD69 was analyzed by flow cytometry (FACS). Surface expression of CD69, which was absent on untreated eosinophils, was induced by IL-13 at concentrations ranging from 1 ng/ml to 1 microgram/ml in a concentration-dependent manner. In contrast, neutrophils expressed CD69 neither spontaneously nor following incubation with IL-13. Semiquantitative reverse transcription-PCR for CD69 mRNA showed constitutive CD69 mRNA expression in purified human eosinophils. Incubation of eosinophils with IL-13 further increased CD69-specific mRNA. Analysis of intracellularly stored CD69 in eosinophils permeabilized with saponin revealed intracellular binding of anti-CD69 Abs in all isolated eosinophils. After stimulation with 100 ng/ml IL-13 for 24 h, the concentration of intracellular CD69 decreased by 41 +/- 9%. Furthermore, IL-13 at a concentration of 100 ng/ml enhanced eosinophil viability, as assessed by propidium iodide staining after 4 days in culture from 8.6 +/- 5.5% in control medium to 50.7 +/- 6.8% following stimulation with IL-13 treatment. The effect of Il-13 on eosinophil viability as well as that on CD69 expression were both neutralized by anti-IL-13 Abs. In conclusion, our results demonstrate that IL-13 specifically activates human eosinophils, as determined by the expression of CD69 cell surface protein and mRNA expression. Furthermore, IL-13 significantly prolongs eosinophil survival in vitro. The data suggest that IL-13 may play a role in the activation of eosinophils.