The expression of 11 beta hydroxysteroid dehydrogenase in severe allergic rhinitis

Author:

Ohta Nobuo1,Noguchi Naoya2,Takahashi Tomoko3,Suzuki Tatsutoshi4,Kakuta Risako5,Suzuki Yusuke6,Awataguchi Toshiichi2,Suzuki Takahiro2,Takahashi Yukiko2,Shoji Fumi2,Wada Kota7,Kawano Tasuku3,Ono Isao8,Kusano Yusuke9,Miyasaka Tomomitsu3,Osafune Hiroshi10,Matsutani Sachiko2,Yaginuma Yuji2,Ishida Yusuke11,Saito Yutaro2,Yamazaki Muneharu12,Ikeda Ryoukichi2

Affiliation:

1. ) Division of Otolaryngology, , 1-12-1, Fukumuro, Miyaginoku, Sendai 983-8512, Japan Tohoku Medical and Pharmaceutical University Hospital

2. Tohoku Medical and Pharmaceutical University Otolaryngology

3. Tohoku Medical and Pharmaceutical University Division of Pathophysiology, Department of Pharmaceutical Sciences, Faculty of Pharmaceutical Sciences,

4. Kitasato University Faculty of Medicine Otolaryngology, Head and Neck Surgery

5. Tohoku Medical and Pharmceutical University Otolaryngology

6. Yamagata University School of Medicine Otolaryngology, Head and Neck Surgery

7. Toho University Faculty of Medicine Otolaryngology

8. Tohoku Medical and Pharmaceutical University Center for Medical Education, Faculty of Medicine

9. To hoku Medical and Pharmaceutical University Otolaryngology

10. Toho University Faculty of Medicine Otolaryngology, Head and Neck Surgery

11. Tohoku Medical and Pharmaceutical University Division of Anatomy and Cell Biology

12. Tohoku Medical and Pharmaceutical University Otolarynglogy

Abstract

Objective: To clarify the roles of 11 beta-HSD in resistance to glucocorticoid therapy for allergic rhinitis, a case series study was conducted. Methods: The patient group consisted of 20 subjects with allergic rhinitis, aged from 21 to 46 years (mean age 26.5), who showed persistent GC resistance necessitating surgical removal of the inferior turbinate after 6 months’ GC treatment. The patients with poor response to GC treatment for 6 months’ were defined as GC resistance. The control group consisted of 10 subjects aged from 16 to 39 years (mean age 24.5) who underwent maxillofacial surgery, from whom nasal tissues were taken and who did not receive GC treatment. Nasal mucosal tissues from patients and cntorol subjects were examined immunohistochemically. The sections were washed with 0.01 M phosphate-buffered saline (PBS; pH 7.2) containing 0.15 M NaCl and 0.01% Triton X-100, and incubated for 2 h with rabbit polyclonal anti-11 beta HSD1 and 11 beta-HSD2 antibody (Santa Cruz Biotechnology, Inc., Santa Cruz, CA, USA), each diluted 1:200 in PBS containing 0.1% bovine serum albumin. Immunostained sections were assessed under an Olympus microscope with an eyepiece reticule at 200 X magnification. Cell counts are expressed as means per high-power field (0.202 mm2). Control group means (arithmetic mean ± SD) were compared with patient group means by Mann–Whitney U-test at P = 0.05. Results: Although 11 beta-HSD1 was expressed to a similar extent in patients and controls, 11 beta-HSD2 was expressed significantly more in patients with severe allergic rhinitis, resulting in a increased HSD-1/HSD-2 ratio. The significantly increased expression of 11 beta-HSD2 in the nasal epithelium and submucosal inflammatory cells of patients with severe nasal allergy were observed in the present study. Conclusion: Our findings suggest that 11 beta-HSD2 plays an important role in resistance to glucocorticoid therapy for allergic rhinitis, and its expression might be used as an additional parameter indicating steroid resistance in allergic rhinitis.

Publisher

Index Copernicus

Subject

Otorhinolaryngology

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