论文部分内容阅读
目的:观察阿奇霉素对支气管哮喘患儿外周血单个核细胞(PBMC)来源树突状细胞(DCs)功能的影响,探讨阿奇霉素免疫调节作用的机制。方法:选择16例支气管哮喘发作期患儿为研究对象,18例健康儿童为对照组。无菌条件下采用密度梯度离心法获取PBMC,体外经rhGM-CSF、rhIL-4诱生DCs。哮喘组置于不同浓度阿奇霉素(0 mg/L、0.1 mg/L、10.0 mg/L)条件下,对照组无阿奇霉素干预。采用流式细胞仪检测DCs表面CD83、CD80和CD86的表达率;ELISA法检测培养上清液中IL-10和IL-12水平。结果:(1)哮喘组CD83表达率与对照组比较差异无统计学意义(t=1.17,P>0.05),CD86的表达率明显高于对照组(t’=2.27,P<0.05),CD80表达率与对照组比较差异无统计学意义(t=1.34,P>0.05)。(2)哮喘组IL-10、IL-12水平均明显低于对照组(t’=3.31、3.39,P<0.01)。(3)浓度为0.1 mg/L组和10.0 mg/L组CD83、CD80和CD86的表达与0 mg/L组比较差异无统计学意义(q=0.031～1.022,P均>0.05)。(4)浓度为0.1 mg/L组和10.0 mg/L组IL-10水平均明显低于0 mg/L组(q=3.042或4.502,P<0.01),前两者间比较差异无统计学意义(q=1.460,P>0.05);浓度为0.1 mg/L组IL-12水平明显低于0 mg/L组和10.0 mg/L组(q=3.148或3.940,P<0.01),后两者比较差异无统计学意义(q=0.792,P>0.05)。(5)哮喘组DCs分泌IL-10与IL-12成正相关(r=0.740,P<0.01),而对照组IL-10与IL-12无相关性(r=0.232,P>0.05)。结论:(1)支气管哮喘患儿DCs存在功能缺陷,主要表现在CD86表达升高、IL-10、IL-12分泌减少;(2)阿奇霉素对哮喘患儿DCs表面CD80、CD86、CD83的表达无明显影响,但可抑制DCs分泌IL-10、IL-12且具有一定浓度依赖性,对DCs有负向免疫调节作用。
Objective: To observe the effect of azithromycin on the function of peripheral blood mononuclear cells (PBMC) derived dendritic cells (DCs) in children with bronchial asthma and to explore the mechanism of azithromycin immunoregulation. Methods: Twenty-six children with bronchial asthma attack were selected as study subjects and 18 healthy children as control group. PBMCs were obtained by density gradient centrifugation under aseptic conditions, DCs were induced by rhGM-CSF and rhIL-4 in vitro. The asthma group was treated with different concentrations of azithromycin (0 mg / L, 0.1 mg / L, 10.0 mg / L) and the control group without azithromycin intervention. The expression of CD83, CD80 and CD86 on DCs was detected by flow cytometry. The levels of IL-10 and IL-12 in culture supernatants were detected by ELISA. Results: (1) The expression of CD83 in asthma group was not significantly different from that in control group (t = 1.17, P> 0.05). The expression of CD86 in asthma group was significantly higher than that in control group (t ’= 2.27, There was no significant difference in expression rate between the two groups (t = 1.34, P> 0.05). (2) The levels of IL-10 and IL-12 in asthma group were significantly lower than those in control group (t ’= 3.31,3.39, P <0.01). (3) The expression of CD83, CD80 and CD86 in 0.1 mg / L and 10.0 mg / L groups had no significant difference compared with 0 mg / L group (q = 0.031-1.022, P> 0.05). (4) The levels of IL-10 in 0.1 mg / L and 10.0 mg / L groups were significantly lower than those in 0 mg / L group (q = 3.042 or 4.502, P <0.01). There was no significant difference between the two groups (Q = 1.460, P> 0.05). The level of IL-12 in 0.1 mg / L group was significantly lower than that in 0 mg / L group and 10.0 mg / L group (q = 3.148 or 3.940, P <0.01) The difference was not statistically significant (q = 0.792, P> 0.05). (5) There was a positive correlation between IL-10 and IL-12 secreted by DCs in asthma group (r = 0.740, P <0.01), but no correlation between IL-10 and IL-12 in control group (r = 0.232, P> 0.05). Conclusions: (1) DCs in children with bronchial asthma have defects in function, mainly in the increase of CD86 expression and decrease of IL-10 and IL-12 secretion; (2) The expression of CD80, CD86 and CD83 on DCs of asthmatic children without azithromycin But could inhibit the secretion of IL-10 and IL-12 in DCs in a concentration-dependent manner and negatively regulate DCs.