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Microbial Superantigens Induce Glucocorticoid Receptor β and Steroid Resistance in a Nasal Explant Model
Author(s) -
Fakhri Samer,
Tulic Meri,
Christodoulopoulos Pota,
Fukakusa Motonori,
Frenkiel Saul,
Leung Donald Y. M.,
Hamid Qutayba A.
Publication year - 2004
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1097/00005537-200405000-00019
Subject(s) - superantigen , glucocorticoid receptor , in situ hybridization , explant culture , receptor , biology , microbiology and biotechnology , medicine , endocrinology , glucocorticoid , immunology , messenger rna , immune system , t cell , in vitro , biochemistry , gene
Objective: To study the role of superantigen (SAg) in inducing glucocorticoid (GC) receptor β and steroid resistance in an explant model of nasal tissue. Methods: Nasal tissue was obtained from inferior turbinates of controls and ragweed (RW)‐sensitive patients. Tissue samples were incubated with SAg of staphylococcal enterotoxin B. In addition, tissue samples from RW‐sensitive patients were incubated with RW allergen in the presence and absence of both SAg and dexamethasone (DEX). The expression of GC receptor β was assessed by immunocytochemistry. The expression of interleukin (IL)‐2 and IL‐4 mRNA was assessed by in situ hybridization. Results: SAg induced an increase in the expression of GC receptor β in atopic tissue and to a lesser extent in nonatopic tissue. The most significant induction of GC receptor β was observed in response to SAg and RW in atopic tissue. Stimulation of atopic tissue with RW alone and SAg alone induced IL‐4 and IL‐2 mRNA, respectively. Incubation of atopic tissue with both SAg and RW induced both IL‐2 and IL‐4 mRNA. The increase in IL‐4 mRNA expression was blunted by the addition of DEX to atopic tissue stimulated with RW alone but not to tissue stimulated by both RW and SAg. Conclusion: Our results demonstrate that SAgs induce steroid resistance in atopic nasal explant tissue by up‐regulating the expression of GC receptor β. Furthermore, we have shown that the up‐regulation of GC receptor β is a local event that is associated with the coexpression of IL‐2 and IL‐4 mRNA.