变应性鼻炎大鼠IL-35的表达及对辅助性T细胞免疫调节的影响

目的 探讨变应性鼻炎(AR)大鼠IL-35的表达及对辅助性T细胞免疫调节的影响。 方法 以卵清蛋白作为致敏原,建立AR大鼠模型。大鼠随机分为对照组、模型组、地塞米松组和IL-35干预组。分析比较大鼠过敏症状评分;采用RT-PCR分析鼻黏膜中IL-35、IFN-γ、IL-4和IL-17的mRNA表达情况;酶联免疫吸附法测定IL-35、IFN-γ、IL-4和IL-17在外周血的表达水平;流式细胞术检测外周血中Th1、Th2和Th17细胞百分比。 结果 IL-35干预可明显降低AR大鼠的症状积分;AR模型组IL-35和IFN-γ的mRNA表达及在外周血的表达均显著低于对照组,而在IL-35干预组的表达高于AR模型组,AR模型组IL-4和IL-17表达显著高于对照组,而在IL-35干预组的表达低于AR模型组(P<0.05);AR模型组Th1细胞百分比显著低于对照组,而在IL-35干预组Th1细胞百分比显著高于AR模型组,Th2和Th17细胞百分比显著高于对照组,IL-35干预组Th2和Th17细胞百分比显著低于AR模型组(P<0.05)。 结论 AR大鼠IL-35的表达降低,IL-35干预可通过上调IFN-γ和下调IL-4、IL-17表达降低炎症反应,机制可能与调节Th1、Th2和Th17平衡有关。

Expression of IL-35 in allergic rhinitis and its effect on the immunoregulation of T cells

Objective To investigate the expression of IL-35 in allergic rhinitis(AR)and to explore its effect on the immunoregulation of T cells. Methods A rat model of AR was established by using ovalbumin as the allergen. Rats were randomly divided into the control group, model group, dexamethasone group, and IL-35 intervention group. Anaphylaxis score of rats was analyzed and compared. RT-PCR was used to analyze the mRNA expressions of IL-35, IFN-γ, IL-4, and IL-17 in the nasal mucosa. The expression levels of IL-35, IFN-γ, IL-4, and IL-17 in peripheral blood were measured by enzyme linked immunosorbent assay. Flow cytometry was used to detect the percentage of Th1, Th2, and Th17 cells in peripheral blood. Results IL-35 intervention can significantly reduce the symptoms of AR rats. The expression levels of IL-35 and IFN-γ in the AR model group and in peripheral blood were significantly lower than in the control group, whereas the expression levels were higher in the IL-35 intervention group than in the AR group. IL-4 and IL-17 expression levels were significantly higher in the AR model group than in the control group, whereas the expression levels were lower in the IL-35 intervention group than in the AR model group. The percentage of Th1 cells in the AR model group was significantly lower than that in the control group, whereas the percentage of Th1 cells in the IL-35 intervention group was significantly higher than that in the AR model group. The percentage of Th2 and Th17 cells was significantly higher in the AR model group than that in the control group. The percentage of Th2 and Th17 cells in the IL-35 intervention group was significantly lower than that in the AR model group(P<0.05). Conclusion IL-35 expression was downregulated in AR rats. IL-35 intervention can reduce the inflammatory response by upregulation of IFN-γ and downregulation of IL-4 and IL-17. The mechanism may be related to the regulation of Th1, Th2, and Th17 balance.