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.