Expression of Glucocorticoid Receptor in Nasal Polyps and Nasal Mucosa.
- Author:
Jun Myung KANG
1
;
Jin Hee CHO
;
Yu Sung WON
;
Sung Shik KIM
;
Han Sung CHANG
;
He Ro YOON
Author Information
1. Department of Otolaryngology-Head and Neck Surgery, College of Medicine, The Catholic University of Korea, Seoul, Korea. entkjm@cmc.cuk.ac.kr
- Publication Type:Original Article
- Keywords:
Glucocorticoid receptors;
Nasal polyps;
Allergir rhinitis
- MeSH:
Cytoplasm;
Endothelial Cells;
Eosinophils;
Epithelial Cells;
Glucocorticoids;
Humans;
Hypersensitivity;
Inflammation;
Mucous Membrane;
Nasal Mucosa*;
Nasal Polyps*;
Receptors, Glucocorticoid*;
Rhinitis;
Sinusitis;
Steroids;
Turbinates
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2000;43(7):731-736
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: Glucocorticoids are currently the most potent medication available for the treatment of nasal polyposis and allergic rhinitis, but exact mechanisms and cellular targets in the nasal mucosa are uncertain. Multifactorial effects of glucocorticoid are initiated by their binding to a specific cytoplasmic glucocorticoid receptor (GR). We performed this study to investigate the localization and distribution ot' human 4R and GR j3 isoform in nasal mucosa and to examine the influence of allergy and eosinophilic infiltration on GR and GR betaisoform expression in nasal polyps. MATERIALS AND METHODS: Nasal polyps (NP), middle turbinate mucosa (MT) and inferior turbinate (IT) mucosa were taken from 40 patients with chronic sinusitis and nasal polyps. We examined to have concomitant allergic rhinitis. Specimens were stained to quantify eosinophils and immunohistochemically stained to quantify GR and GR beta isaform in the unit area of tissues. RESULTS: Immunostaining of GR and GR betaisoform was predominantly localized in epithelial cell and infiltrating inflammatory cell in subepithelial layer, with lesser amounts in the endothelial cells and in the cells surrounding glands. Immunostaining of GR was mostly co-expressed with GR beta isoform. No correlation was found between Gk and GR beta isoform expression in subepithelial layer and the intensity of eosinophilic inflammation and allergy in NP. There was no significant differences in GR and GR beta isoform expression between NP, MT, and IT. CONCLUSION: Epithelial cells may be an important site of action for intranasal steroids, and the increased number of eosinophils infiltrating the mucosa and allergy did not amplify the number of immunostaining of GK and GR beta isoform.
