Previous studies have demonstrated improvements in health-related quality of life in asthmatic patients after treatment with fluticasone propionate. CD30 is a marker of Th2 lymphocytes, which are key cells in the pathogenesis of allergic inflammation. There is also a soluble form of CD30 (sCD30) released by CD30+ cells. Since serum sCD30 levels are high in allergic patients, in our study we examined the possible role of fluticasone propionate in modulating sCD30 release in patients with severe allergic asthma. In addition, we evaluated a possible correlation between sCD30 and FEV1 in these patients. To this end two groups of subjects were enrolled: 20 healthy nonatopic control subjects (group A) and 20 atopic patients with severe bronchial asthma receiving fluticasone propionate at the total dosage of 1 mg/day for 8 weeks (group B). Serum samples were examined before and after the treatment period. sCD30 serum levels were determined by the commercial ELISA-kit (Dako). The limit of detection of the assay was 1 U/ml. Our data show that sCD30 basal serum levels were significantly (p <0.05) higher in patients of group B respect to group A subjects (8.35+/-4.88 vs. <1 IU/ml, respectively). In addition, we found that sCD30 serum levels were undetectable in patients of group B after fluticasone propionate therapy. In group B a positive correlation between serum sCD30 levels and FEV1 values before fluticasone propionate treatment was noted (Rho = -0.644, p <0.005). The fluticasone propionate inhibition of sCD30 release may partly explain how fluticasone propionate exerts its antiinflammatory activity, through the modulation of Th2 cells.