TY - JOUR
T1 - The expression of 11 β−hydroxysteroid dehydrogenase in severe allergic rhinitis
AU - Ohta, Nobuo
AU - Suzuki, Yusuke
AU - Noguchi, Naoya
AU - Kakuta, Risako
AU - Suzuki, Takahiro
AU - Awataguchi, Toshiichi
AU - Takahashi, Yukiko
AU - Tomioka-Matsutani, Sachiko
AU - Ishida, Yusuke
AU - Ikeda, Ryokichi
AU - Yamazaki, Muneharu
AU - Kusano, Yusuke
AU - Saito, Yutarou
AU - Shoji, Fumi
AU - Yaginuma, Yuji
AU - Suzuki, Tatsutoshi
AU - Osafune, Hiroshi
AU - Kawano, Tasuku
AU - Miyasaka, Tomomitsu
AU - Takahashi, Tomoko
AU - Ohno, Isao
AU - Wada, Kota
N1 - Funding Information:
This work was supported by JSPS KAKENHI Grant Number JP17K11363 and the Ministry of Health, Labor, and Welfare of Japan. We express our sincere thanks to Mrs. Yuko Ohta, Uyo Gakuen college, for her editorial assistance.
Publisher Copyright:
Copyright © 2019 Polish Society of Otorhinolaryngologists Head and Neck Surgeons. Published by Index Copernicus Sp. z o.o. All rights reserved.
PY - 2019
Y1 - 2019
N2 - objective: To clarify the roles of 11 β-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 of GC treatment. The patients with poor response to GC treatment for 6 months were defined as GC-resistant. 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 control subjects were examined immuno-histochemically. 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 β−HSD1 and 11 β−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× 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 β−HSD1 was expressed to a similar extent in patients and controls, 11 β−HSD2 was expressed more significantly in patients with severe allergic rhinitis, resulting in an increased HSD-1/HSD-2 ratio. The significantly increased expression of 11 β−HSD2 in the nasal epithelium and submucosal inflammatory cells of patients with severe nasal allergy was observed in the present study. conclusion: Our findings suggest that 11 β-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.
AB - objective: To clarify the roles of 11 β-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 of GC treatment. The patients with poor response to GC treatment for 6 months were defined as GC-resistant. 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 control subjects were examined immuno-histochemically. 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 β−HSD1 and 11 β−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× 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 β−HSD1 was expressed to a similar extent in patients and controls, 11 β−HSD2 was expressed more significantly in patients with severe allergic rhinitis, resulting in an increased HSD-1/HSD-2 ratio. The significantly increased expression of 11 β−HSD2 in the nasal epithelium and submucosal inflammatory cells of patients with severe nasal allergy was observed in the present study. conclusion: Our findings suggest that 11 β-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.
KW - 11 β-hydroxysetroid dehydrogenase
KW - Allergic rhinitis
KW - Glucocorticoid resistance
KW - Glucocorticoid response
KW - Glucocorticoid therapy
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U2 - 10.5604/01.3001.0012.6143
DO - 10.5604/01.3001.0012.6143
M3 - Article
C2 - 30919824
AN - SCOPUS:85063957994
SN - 0030-6657
VL - 73
SP - 18
EP - 21
JO - Otolaryngologia Polska
JF - Otolaryngologia Polska
IS - 2
ER -