奥洛他定联合卡介菌多糖核酸对慢性荨麻疹患者的免疫应答机制探讨

Mechanism of Olopatatadine combined with BCG polysaccharide nucleic acid onimmune response in patients with chronicurticaria through TLR2 pathway

摘要:

目的 研究奥洛他定联合卡介菌多糖核酸治疗前后慢性荨麻疹患者Toll 样受体2（TLR2）表达 量的变化及其与免疫球蛋白E（IgE）、补体C3、补体C4、细胞因子含量的相关性。方法 选取2016 年1 月- 2016 年11 月在佛山市中医院接受奥洛他定联合卡介菌多糖核酸治疗的慢性荨麻疹患者作为研究对象。治 疗前和治疗后2、4 及6 周时，采集外周血并测定TLR2、TLR4、TLR7、TLR9 的表达量，采集血清并测 定IgE、C3、C4、Th1、Th2 细胞因子的含量。结果 治疗后2、4 及6 周时，外周血单个核细胞中TLR2 的 mRNA 含量均低于治疗前，TLR4、TLR7 及TLR9 的mRNA 含量与治疗前比较，差异无统计学意义（P >0.05）； 血清中IgE、白细胞介素4（IL-4）、白细胞介素10（IL-10）的含量均低于治疗前，C3、C4、IFN-γ、白细 胞介素2（IL-2）的含量高于治疗前；外周血中TLR2 的表达量与血清中IgE、IL-4、IL-10 的含量呈正相关， 与C3、C4、IFN-γ、IL-2 的含量呈负相关。结论 奥洛他定联合卡介菌多糖核酸治疗可能通过TLR2 通路 调节慢性荨麻疹患者体内的免疫应答。

Abstract:

Objective To study TLR2 expression in patients with chronic urticaria pre- and post-treatment of olopatatadine combined with BCG polysaccharide nucleic acid and its correlation with IgE, C3, C4 and cytokine levels. Methods Patients with chronic urticaria who received olopatatadine combined with BCG polysaccharide nucleic acid treatment in our hospital from January 2016 to November 2016 were selected as the research subjects; pre- and 2 weeks, 4 weeks and 6 weeks post- treatment, peripheral blood was collected to determine expression levels of TLR2, TLR4, TLR7 and TLR9, and serum was collected to determine levels of IgE, C3, C4 and Th1 and Th2 cytokines. Results About 2 weeks, 4 weeks and 6 weeks post-treatment, TLR2 mRNA levels in peripheral blood mononuclear cells were lower than those pre-treatment while TLR4, TLR7 and TLR9 mRNA levels were not significantly different from those pre-treatment, and serum IgE, IL-4 and IL-10 levels were lower than those pretreatment while C3, C4, IFN-γ and IL-2 levels were higher than those pre-treatment; TLR2 expression in peripheral blood was positively correlated with serum IgE, IL-4 and IL-10 levels, and negatively correlated with C3, C4, IFN-γ and IL-2 levels. Conclusion Treatment of Olopatatadine combined with BCG polysaccharide nucleic acid can regulate the immune response in patients with chronic urticaria through TLR2 pathway.