Jiang Tingting, Wang Weihua, Zhu Zhenghua, Zhu Liwei, Ma Zhaoxin
Lin Chuang Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2015 Jun;29(12):1121-5.
To investigate the effect of dxamethasone (DEX) on the expression of Tregs in allergic rhinitis (AR) mice, and explore the mechanism of glucocorticoid in the treatment of AR.
AR murine model was established by sensitization and challenge with OVA, besides intervention treatment with DEX was carried out in AR model. The behavior observation was used to evaluate the improvement effect of DEX on AR symptoms. The morphological characteristics of nasal tissues were observed by HE staining after fixation and decalcification. The mononuclear cells were obtained by grinding spleens, and the total RNA was extracted for reverse transcriptase polymerase chain reaction to investigate the level of mRNA expression of Foxp3. The changes of CD4+ Foxp3+ Tcells in spleen of mice were analyzed by flow cytometry.
BALB/c mice received OVA sensitization followed by OVA intranasal challenge, the frequencies of sneezing and nose-scratching increased significantly in AR group (44. 50 ± 5. 61 and 72. 94 ± 8. 76) compared with control group (12. 68 ± 1. 87 and 26. 76 ± .2. 89), P<0. 01; The frequencies decreased significantly in DEX group (26. 04 ± 3. 93 and 56. 79 ± 5. 64), P< 0. 05 compared with AR group. The continuity of nasal mucosa ciliated columnar epithelium in AR group was destroyed and appeared to be repaired in DEX group. Inflammatory cells infiltration was also markedly decreased by DEX treatment. The proportion of CD4+ Foxp3+ T cells in AR group (3. 89 ± 0. 39)% decreased, P<0. 01 vs control group (4. 63 ± 0. 15) %. DEX treatment induced production of Tregs (6. 89 ± 0. 49)%, P<0. 05 vs control group. DEX significantly increased the expression of Foxp3 mRNA (P<0. 05) compared with AR and control group.
DEX reduce upper airway allergic inflammation effectively, which may be mediated by promoting the expression of Foxp3 and inducing the amplification of Tregs in vivo.
探讨地塞米松（DEX）对变应性鼻炎（AR）小鼠调节性T细胞（Tregs）表达的影响，以阐明糖皮质激素治疗AR的机制。
采用卵清蛋白（OVA）致敏和激发建立AR小鼠模型，并对模型小鼠进行DEX干预治疗。通过行为学观察评价DEX对AR症状的改善作用。固定、脱钙后行苏木精-伊红（HE）染色观察鼻黏膜组织形态学特征。研磨脾脏获取单个核细胞，提取总RNA，采用逆转录聚合酶链反应检测叉头框蛋白3（Foxp3）mRNA表达水平。采用流式细胞术分析小鼠脾脏中CD4+Foxp3+T细胞的变化。
OVA致敏并滴鼻激发后，AR组小鼠喷嚏和挠鼻次数频率（44.50±5.61、72.94±8.76）较对照组（12.68±1.87、26.76±2.89）显著增加，P<0.01；DEX组上述指标（26.04±3.93、56.79±5.64）较AR组显著降低，P<0.05。AR组鼻黏膜纤毛柱状上皮连续性破坏，DEX组可见修复迹象。DEX治疗后炎症细胞浸润亦显著减少。AR组CD4+Foxp3+T细胞比例（3.89±0.39）%较对照组（4.63±0.15）%降低，P<0.01。DEX治疗后可诱导Tregs产生（6.89±0.49）%，与对照组比较，P<0.05。与AR组和对照组比较，DEX可显著上调Foxp3mRNA表达（P<0.05）。
DEX可有效减轻上呼吸道变应性炎症，其机制可能与促进Foxp3表达、诱导体内Tregs扩增有关。
