Effect of fluticasone propionate on soluble CD30 release in patients with severe allergic asthma

Citation
F. Purello-d'Ambrosio et al., Effect of fluticasone propionate on soluble CD30 release in patients with severe allergic asthma, J INVES ALL, 10(5), 2000, pp. 283-285
Citations number
16
Categorie Soggetti
Clinical Immunolgy & Infectious Disease
Journal title
JOURNAL OF INVESTIGATIONAL ALLERGOLOGY & CLINICAL IMMUNOLOGY
ISSN journal
10189068 → ACNP
Volume
10
Issue
5
Year of publication
2000
Pages
283 - 285
Database
ISI
SICI code
1018-9068(200009/10)10:5<283:EOFPOS>2.0.ZU;2-B
Abstract
Previous studies have demonstrated improvements in health-related quality o f life in asthmatic patients after treatment with fluticasone propionate. C D30 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) rel eased by CD30+ cells. Since serum sCD30 levels are high in allergic patient s, in our study we examined the possible role of fluticasone propionate in modulating sCD30 release in patients with severe allergic asthma. In additi on, we evaluated a possible correlation between sCD30 and FEV, in these pat ients. To this end two groups of subjects were enrolled: 20 healthy nonatop ic control subjects (group A) and 20 atopic patients with severe bronchial asthma receiving fluticasone propionate at the total dosage of I mg/day for 8 weeks (group B). Serum samples were examined before and after the treatm ent 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 +/- 4.88vs. <1 IU/ml, respective ly). In addition, we found that sCD30 serum levels were undetectable in pat ients of group B after fluticasone propionate therapy. In group B a positiv e correlation between serum sCD30 levels and FEV, values before fluticasone propionate treatment was noted (Rho = -0.644, p <0.005). The fluticasone p ropionate inhibition of sCD30 release may partly explain how fluticasone pr opionate exerts its antiinflammatory activity, through the modulation of Th 2 cells.