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糖皮质激素对卵清蛋白致敏和 RSV 感染致哮喘小鼠的作用。

Effect of glucocorticoid in mice of asthma induced by ovalbumin sensitisation and RSV infection.

机构信息

Department of Healthcare, Provincial Hospital Affiliated to Shandong University, 324#, Jingwu Road, Jinan, 250021, PR China.

出版信息

Asian Pac J Allergy Immunol. 2011 Jun;29(2):176-80.

PMID:21980833
Abstract

OBJECTIVE

To investigate the inflammatory changes and the airway hyper-responsiveness in the asthma mouse model infected by respiratory syncytial virus and elucidate the relationship between the infection and the effect of glucocorticoid.

METHODS

60 BALB/c mice were randomly divided into 6 groups. One of these is the control group; the others are the OVA/sham group, the OVA/sham +Dex group, the PBS/RSV group, the OVA/RSV group and the OVA/RSV+Dex group. The airway resistance was measured using a sealed body plethysmograph. Pathological slides were stained with hematoxylin-eosin, and the peribronchial inflammation was observed microscopically. The concentrations of IL-4, IFN-gamma, TGF-beta1 in lung tissues were detected by ELISA.

RESULTS

Compared with the control group, the degree of the airway inflammation and hyperresponsiveness and the concentrations of IL-4/IFN-gamma, TGF-beta1 in all four OVA groups increased significantly. And there was a statistically significant difference between the OVA/sham group and the OVA/sham+Dex group, and between the OVA/RSV group and the OVA/RSV+Dex group respectively. Compared with the OVA/RSV group, there was an obvious aggravation of airway inflammation and hyper-responsiveness in the OVA/RSV+Dex group.

CONCLUSIONS

Glucocorticoid significantly reduces airway inflammation and hyper-responsiveness induced by repetitive OVA challenge in the mouse model of asthma. However, the significant decrease in Th1 and increase in Th2 inflammation and aggravation of airway hyper-responsiveness in the mice in OVA/RSV group show that they are not sensitive to glucocorticoid. The effects of infection with RSV on the mouse model of asthma could be the cause of the glucocorticoid resistance during the therapy.

摘要

目的

研究呼吸道合胞病毒感染哮喘小鼠模型的炎症变化和气道高反应性,并阐明感染与糖皮质激素作用之间的关系。

方法

将 60 只 BALB/c 小鼠随机分为 6 组,其中一组为对照组;其余为 OVA/假手术组、OVA/假手术+地塞米松组、PBS/RSV 组、OVA/RSV 组和 OVA/RSV+地塞米松组。使用密封体描记法测量气道阻力。苏木精-伊红染色病理切片,显微镜下观察支气管周围炎症。酶联免疫吸附试验检测肺组织中 IL-4、IFN-γ、TGF-β1 的浓度。

结果

与对照组相比,所有 4 个 OVA 组的气道炎症和高反应性程度以及 IL-4/IFN-γ、TGF-β1 浓度均显著增加,且 OVA/假手术组与 OVA/假手术+地塞米松组、OVA/RSV 组与 OVA/RSV+地塞米松组之间存在统计学差异。与 OVA/RSV 组相比,OVA/RSV+地塞米松组气道炎症和高反应性明显加重。

结论

糖皮质激素可显著减轻哮喘小鼠模型反复 OVA 攻击引起的气道炎症和高反应性。然而,OVA/RSV 组小鼠 Th1 减少和 Th2 炎症增加以及气道高反应性加重,表明它们对地塞米松不敏感。RSV 感染对哮喘小鼠模型的影响可能是治疗过程中糖皮质激素抵抗的原因。

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