In vitro effect of glucocorticoids on nasal polyps (original) (raw)
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Quantitative Analysis of Activated Glucocorticoid Receptors in Nasal Polyps
Nihon Bika Gakkai Kaishi (Japanese Journal of Rhinology), 2006
Objective: The purpose of our study was to measure the activated glucocorticoid receptor (GR) protein level in the nuclei of nasal polyp cells and compare the results in nasal polyposis patients with chronic rhinosinusitis alone and with chronic rhinosinusitis associated with asthma, before and after glucocorticoid (GC) therapy. Methods: We used enzyme-linked immunosorbentassay (ELISA) techniques to quantitatively measure the activated-GR protein level in the nuclei of the nasal polyp cells. Nasal polyp tissues were obtained from patients with chronic rhinosinusitis alone and with both chronic rhinosinusitis and bronchial asthma. In the latter, polyp tissues were separately obtained before and after GC therapy. Results: Our data showed no significant differences between the activated-GR protein level of the nasal polyposis patients with chronic rhinosinusitis alone and with both chronic rhinosinusitis and bronchial asthma before GC therapy. However, the activated-GR protein level was significantly upregulated after GC therapy in the patients with both chronic rhinosinusitis and bronchial asthma. Conclusion: The result of our research clearly showed that GCs upregulated the activated-GR protein level in the nuclei of nasal polyp cells and that the upregulation is essential for the anti-inflammatory action of GCs.
In vivo (Athens, Greece)
Glucocorticoids (GCs) bind to the cellular glucocorticoid receptors (GRs) to exert anti-inflammatory and immunosuppressive actions. We investigated the changes in the expressions of the two GR isoforms, GR-alpha and GR-beta, in nasal polyps treated with GC. Immunofluorescent staining revealed prominent expression of GR-alpha in the inflammatory cell infiltrate in the polyps obtained from patients with chronic sinusitis and bronchial asthma. Furthermore, while the expression of GR-alpha was significantly reduced following GC treatment, that of GR-beta remained unchanged. The results of real-time PCR also revealed that the prominent expression of GR-alpha mRNA in the polyps decreased following GC treatment, while the expression of GR-beta mRNA remained unchanged. The observations indicate that GR-alpha may play the major role in the inflammation associated with nasal polyps and the ratio of the expression level of GR-beta to that of GR-alpha may serve as a useful index of the clinical...
Respiratory Medicine, 2003
The lower sensitivity of the inflamed nasal mucosa to glucocorticoids might be related to an increased expression of the glucocorticoid receptor (GR) beta isoform.We investigated GRa and GRb mRNA expression in epithelial cells from nasal mucosa and nasal polyps.GRa mRNA was at least1000 times more expressed than GRb mRNA in both tissues.GRb expression (mean7SEM of 10 3 cDNA copies/mg of total RNA) was higher in nasal polyps (1.1570.19; n=27; Po0.01) than in nasal mucosa (0.6270.10; n=32). Nasal polyps with43% of inflammatory cells had higher GRb levels (1.4070.29; n=16) than both nasal mucosa (Po0.01) and polyps with r3% of inflammatory cells (0.8070.18; n=11; Po0.05).No difference in GRbexpression was found between nasalmucosa and polyps with r 3% of inflammatory cells. GRb expression correlated with the inflammatory cell number, especially with mast cells (r=0.50, Po0.0001). There was no difference in GRa mRNA expression between nasal mucosa and nasal polyps. In summary,GRa is far more expressed than GRbin bothtissues.The increased expression of GRb may be related to the presence of inflammatory cells.
The Laryngoscope, 2012
Objectives/Hypothesis: To investigate the histologic consequences of simultaneous nasal glucocorticosteroid and xylometazoline HCl administration in the rabbit nasal mucosa. Study Design: Prospective randomized study. Methods: Twenty New Zealand male rabbits were randomly placed into three groups: group I, control (n ¼ 6); group II, xylometazoline HCl (n ¼ 8); or group III, xylometazoline HCl-fluticasone furoate (n ¼ 6). Group I received no treatment. Groups II and III received two intranasal puffs of xylometazoline HCl 0.5 mg/mL twice daily or two puffs of xylometazoline HCl 0.5 mg/mL twice daily plus one puff of 27.5 lg fluticasone furoate twice daily to each nostril (110 lg), respectively. At the end of 3 weeks, the rabbits were sacrificed. The mucosa of the nasal cavities was excised. Specimen sections (5 lm) were stained with hematoxylin and eosin, mucicarmine, and Gomori one-step trichrome and were examined under a light microscope. The presence of edema, congestion, inflammatory cell infiltration, nasociliary loss, epithelial and nerve-ending degeneration, and goblet cell increase were evaluated semiquantitatively (grades 0-3). Results: Statistically significant differences were detected between groups II and III in terms of edema, congestion, inflammatory cell infiltration, nasociliary loss, and epithelial degeneration (P ¼ .006, P ¼ .049, P ¼ .015, P ¼ .014, and P ¼ .049, respectively). Nerve-ending degeneration, goblet cell increase, and quantitative goblet and neutrophil cell counts did not yield statistically significant differences between groups II and III (P ¼ .137, P ¼ .580, P ¼ .770, and P ¼ .616, respectively). Conclusions: The combined simultaneous intranasal administration of xylometazoline HCl and fluticasone furoate appears to be beneficial in minimizing the long-term usage-associated congestion, edema, inflammatory cell infiltration, epithelial degeneration, and nasociliary loss in the rabbit model nasal mucosa.
Glucocorticoid therapy increases COX-2 gene expression in nasal polyps in vivo
European Respiratory Journal, 2009
The aim of the present study was to evaluate the in vivo regulation of cyclooxygenase-2 in nasal polyps. In total, 65 patients with nasal polyps were randomly (3:1) treated with (n551; 33 with asthma) or without (n514) oral prednisone and intranasal budesonide for 2 weeks plus intranasal budesonide for 10 additional weeks. Biopsies were obtained at baseline and after 2 and 12 weeks of treatment. All samples were analysed for cyclooxygenase-1 and cyclooxygenase-2 mRNA. Attempts were made to detect cyclooxygenase-2 protein. At baseline, cyclooxygenase-1 and cyclooxygenase-2 expression did not differ between polyps from nonasthmatic and asthmatic patients. Cyclooxygenase-1 mRNA was unchanged by glucocorticoid treatment, while cyclooxygenase-2 mRNA increased in glucocorticoid-treated patients at week 2 compared with baseline and then decreased at week 12. Within subgroups, increased cyclooxygenase-2 mRNA was found at week 2 in polyps from nonasthmatic and asthmatic patients compared with baseline. At week 12, cyclooxygenase-2 expression remained high in nonasthmatics while it decreased in asthmatics. Cyclooxygenase-2 protein was not detected under any circumstances. Glucocorticoid therapy enhances cyclooxygenase-2 expression in vivo in nasal polyps, a finding that does not follow the generally accepted assumption that cyclooxygenase-2 expression is suppressed by glucocorticoids.
Journal of inflammation (London, England), 2016
The pathogenesis of non-allergic rhinitis (NAR) is still largely unknown. Furthermore, it is unclear whether there is a correlation between the effect of nasal glucocorticoids on nasal inflammation and on nasal symptoms and quality of life. In this pilot study we recruited 12 healthy subjects and 24 patients with recently diagnosed persistent NAR [12 untreated and 12 under regular treatment with nasal fluticasone furoate (two sprays of 27.5 μg each in each nostril once daily, total daily dose = 110 μg) for at least 20 days]. Each subject filled a mini rhinoconjunctivitis quality of life questionnaire (mini RQLQ). Nasal scrapings were obtained from each subject and used to prepare slides for Diff-Quik and immunocytochemical staining for inflammatory and epithelial cells count, MUC5AC expression and the general pro-inflammatory transcription factor nuclear factor kB (NF-kB) activation. The nasal score of the mini RQLQ, the number of nasal inflammatory cells (neutrophils, eosinophils) ...