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EN
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.
EN
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.
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