Corticosteroid resistance in mild asthma: markers of persistent inflammation

Citation
H. Matsuse et al., Corticosteroid resistance in mild asthma: markers of persistent inflammation, ANN ALLER A, 82(5), 1999, pp. 457-462
Citations number
30
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Clinical Immunolgy & Infectious Disease
Journal title
ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY
ISSN journal
1081-1206 → ACNP
Volume
82
Issue
5
Year of publication
1999
Pages
457 - 462
Database
ISI
SICI code
1081-1206(199905)82:5<457:CRIMAM>2.0.ZU;2-N
Abstract
Background: Bronchial hyperresponsiveness (BHR) is an important feature of asthma. Glucocorticosteroids (GCS) reduce BHR, probably by suppressing alle rgic inflammation. There are, however, two groups of asthmatics with either GCS-responsive or non-responsive BHR to methacholine. We investigated the mechanism of non-CCS-responsive BHR in mild asthma. Methods: Non-GCS-responsive BHR asthma was defined as failure of reduction of BHR to methacholine after a 2-week course of oral prednisolone (30 mg/da y). The expression of interleukin (IL)-4, IL-5, IFN-gamma mRNA in periphera l blood mononuclear cells, eosinophil count, serum cortisol, eosinophilic c ationic protein (ECP), and spirometry were measured in five non-GCS-respons ive BHR asthmatics and six patients with GCS-responsive BHR asthma before a nd after prednisolone therapy. Results: With the exception of serum ECP and expression of IL-5 mRNA, no si gnificant differences were observed between GCS-responsive BHR and non-GCS- responsive BHR asthma. The mean ECP level was significantly higher in non-G CS-responsive BHR than in GCS-responsive BHR asthma before and after predni solone therapy. Interleukin-5 mRNA was detected in all asthmatics before pr ednisolone therapy; however, after prednisolone therapy, IL-5 mRNA was only detected in non-GCS-responsive BHR asthmatics. Conclusions: Our findings suggest that activation of eosinophils appears to persist in some asthmatics with non-GCS-responsive BHR due to continuous I L-5 production by lymphocytes.