Expression of glucocorticoid receptor beta in peripheral blood mononuclear cells of asthmatics experiencing exacerbation after upper respiratory infection.
- Author:
Tae Hoon LEE
1
;
Keun Ae MOON
;
Su Jin KOH
;
Wook Jang SEO
;
YounYee KIM
;
Jaechun LEE
;
Chang Keun LEE
;
Bin YOO
;
Hee Bom MOON
;
You Sook CHO
Author Information
1. Division of Allergy and Rheumatology, Department of Medicine, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea. yscho@amc.seoul.kr
- Publication Type:Original Article
- Keywords:
Glucocorticoid receptor;
asthma;
upper respiratory infection;
steroid resistance
- MeSH:
Asthma;
Glucocorticoids;
Inflammation;
Receptors, Glucocorticoid*;
Respiratory Tract Infections;
RNA, Messenger
- From:Journal of Asthma, Allergy and Clinical Immunology
2003;23(3):525-533
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: Glucocorticoids have demonstrated excellent efficacy in decreasing airway inflammation and controlling bronchial asthma symptoms. However, exacerbations of asthma are frequently observed even during treatment with inhaled glucocorticoids, and most of these episodes occur following viral upper respiratory infections (URI). Recently, it has been suggested that transient resistance to glucocorticoid developed after URI and this resistance to glucocorticoid in asthmatics was related to the increased expression of glucocorticoid receptor beta (GCRbeta). The aim of this study is to evaluate the expression of GCRbeta in asthmatics experiencing exacerbation after an episode of URI. METHODS: Peripheral blood mononuclear cells (PBMCs) were obtained from asthmatics experiencing exacerbation after URI (n=15), stable asthmatics (n=23), and normal controls (n= 12). Exacerbated asthmatics were started on systemic glucocorticoids upto two weeks and PBMCs were obtained again after the treatment. The degree of expression of GCRbeta mRNA and ratio of GCRbeta/GCRalpha mRNA were calculated using the semi-quantitative RT-PCR. RESULTS: Compared with stable asthmatics and normal control, exacerbated asthmatics showed significantly higher expression of GCRbeta mRNA and ratio of GCRbeta/GCRalpha mRNA. However, comparing exacerbated asthmatics before and after treatment, we found no significant difference but trends of reduction in expression of GCRbeta mRNA and ratio of GCRbeta/GCRalpha mRNA after treatment. CONCLUSION: These findings suggest that transient resistance to corticosteroid in asthmatics experiencing exacerbation after an episode of URI may be related to increased expression of GCRbeta.
