摘要
目的通过观察人支气管上皮细胞(BEAS-2B)株释放IL-8I、L-1β、SICAM-1等的变化,探讨PM2.5有机提取物(EOM)对气道上皮细胞的炎性损伤作用;并研究BEAS-2B损伤后释放的炎症因子诱导T淋巴细胞表达CD25,从而可能参与类似于过敏性哮喘的变态反应过程。方法BEAS-2B暴露于3.75、7.5、15μg/mlPM2.5有机提取物,双抗夹心ELISA法检测培养上清液中IL-8I、L-1β、SICAM-1的变化;将BEAS-2B细胞损伤后释放的炎症因子作用于人外周血淋巴细胞,流式细胞仪检测淋巴细胞CD25阳性表达率。结果阴性对照组有少量IL-8I、L-1β、SICAM-1表达,且随着时间延长略有增加;与阴性对照组相比,随着PM2.5有机提取物染毒剂量的增加和作用时间的延长,IL-8I、L-1β、SICAM-1的表达也增高,差异具有统计学意义(P<0.01)。结论BEAS-2B细胞暴露于PM2.5有机提取物后,释放与气道炎症反应及气道高变应性相关的IL-8I、L-1β、SICAM-1等炎性因子;BEAS-2B细胞损伤后释放的IL-1β等炎性因子能够促进T淋巴细胞表达CD25分子,从而可能参与类似于过敏性哮喘的变态反应过程。
Objective To ascertain the effect of extractable organic matters(EOM) of PM2.5 on inducing inflammation through observing the altertion of IL-8, IL-1β, sICAM-1 that BEAS-2B release, and study the expression of surface molecule CD25 on lymphocyte to find the role of PM2.5 in the process of immunity. Methods To expose BEAS-2B to EOM of PM2.5 and examine the cytokine in culture medium by ELISA, exposing cytokines that BEAS-2B release on human blood lymphocyte and measure the expression of CD25 with flow cytometry. Results The control group has a small quantity IL-8,IL-1β,sICAM-1 expressing and increase a little with the prolongation of time. Exposure groups have more notable expression of IL-8, IL-1β, sICAM-1 than control group, and the difference has sataistical significance ( P 〈 0.01 ) . Conclusions BEAS-2B cells exposed to EOM of PM2.5 could release IL-8,IL-1β,sICAM-1, which maybe played a role in airway inflammation and airway high responses, and the cytokines released by BEAS-2B cells could advance T lymphocyte proliferate and express molecule CD25, consequently inspired the inflammatory process of airway high responses.
出处
《卫生研究》
CAS
CSCD
北大核心
2006年第6期687-689,共3页
Journal of Hygiene Research
基金
广东省科技计划项目(No.2002C31612)