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PM2.5氧化应激对变应性哮喘气道上皮固有免疫调控因子表达的刺激作用
鲍志坚, 胡旭, 沈晓强
杭州市红十字会医院结核科
摘要:
目的探讨PM2.5氧化应激对变应性哮喘气道上皮固有免疫调控因子表达的刺激作用。方法将24只BALB/c雌性小鼠采用随机数字表法分为哮喘模型组、PM2.5轻度污染组、PM2.5重度污染组和正常对照组4组,每组6只。其中哮喘模型组、PM2.5轻度污染组和PM2.5重度污染组均利用含卵清蛋白的磷酸盐缓冲液制造哮喘模型,成功后分别用卵清蛋白溶液、90滋g/m3的PM2.5和雾化的1%卵清蛋白溶液、200滋g/m3的PM2.5和雾化的1%卵清蛋白溶液进行激发。正常对照组注射不含卵清蛋白的磷酸盐缓冲液,激发方法同哮喘模型组。采用ELISA法检测各组小鼠血清IL-4、IL-5、IL-13和IFN-γ水平并观察小鼠气道及肺组织的病理变化。结果PM2.5轻度污染组、PM2.5重度污染组小鼠IL-4、IL-5、IL-13和IFN-γ水平均高于哮喘模型组,差异均有统计学意义(均P<0.05)。PM2.5重度污染组小鼠血清IL-4、IL-5、IL-13和IFN-γ水平均高于PM2.5轻度污染组,差异均有统计学意义(均P<0.05)。随着PM2.5浓度的升高,小鼠气道上皮增厚程度逐渐加重,气道及血管周围炎性细胞浸润水平也逐渐加重,气道分泌物及官腔狭窄或闭塞发生率逐渐升高。结论PM2.5可增加变应性哮喘发病的风险,其机制可能是通过调节气道自身的固有免疫调控因子实现的,且PM2.5浓度越高,该效应也越明显。
关键词:  PM2.5 氧化应激 变应性哮喘 免疫
DOI:10.12056/j.issn.1006-2785.2018.40.2.2017-1966
分类号:
基金项目:浙江省医药卫生科技计划项目(2015KYB312)
Stimulatory effect of PM2.5 oxidative stress on expression of innate immune regulatory factors in airway epithelia of allergic asthma mice
Hangzhou Red Cross Hospital
Abstract:
Objective To investigate the stimulatory effect of PM2.5 oxidative stress on the expression of innate immune regulatory factors in airway epithelia of allergic asthma mice. Methods Twenty four BALB/c female mice were randomly divided into 4 groups with 6 in each group: normal control group, asthma model group, PM2.5 mild pollution group and PM2.5 severe pollution group. The asthma model was induced by intraperitoneal injection of ovalbumin (OVA). Mice in asthma model group, PM2.5 mild pollution group and PM2.5 severe pollution group were stimulated by inhalation of 1% OVA solution, PM2.5 90滋g/m3+1%OVA and PM2.5 200滋g/m3+1%OVA, respectively. Serum levels of IL-4, IL-5, IL-13 and IFN-γ were detected, and the pathological changes of airway and lung tissues were observed in all groups. Results Serum levels of IL-4, IL-5, IL-13 and IFN-γ in PM2.5 pollution groups were significantly higher than those in asthma model group (all P<0.05); and the levels in PM2.5 severe pollution group were higher than those in PM2.5 mild pollution group (all P<0.05). The pathological examination showed that the changes in lung structure were increased, airway epithelial thickening aggravated, vascular infiltration of inflammatory cells and lumen stenosis or occlusion were more severe with the increased PM2.5 pollution. Conclusion PM2.5 may increase the risk of allergic asthma, which may be associated with the increased secretion of immune regulatory factors in the airways; and the higher the PM2.5, the more pronounced the effect.
Key words:  PM2 .5 Oxidative stress Allergic asthma Immunity