摘要
目的探讨白介素1β在煤尘诱导肺巨噬细胞释放细胞因子过程中的作用。方法通过佛波酯(PMA)刺激THP-1细胞诱导其分化为人肺泡巨噬细胞,随机分为对照组,2 000μg/ml组(高剂量组)、1 000μg/ml组(中剂量组)和500μg/ml组(低剂量组),对照+白介素1β抗体组,高剂量+白介素1β抗体组,中剂量+白介素1β抗体组和低剂量+白介素1β抗体组,煤尘染毒8h,测定白介素1β、白介素6、TNF-α。结果不同剂量的媒尘均可诱导巨噬细胞释放白介素1β、白介素6、TNF-α,其中高剂量组的细胞因子水平升高最为明显(P<0.01),分别为867.91、35.17和249.86pg/ml。不同剂量组在加入白介素1β抗体后,巨噬细胞释放的白介素6、TNF-α水平也明显降低(P<0.01),低剂量组分别下降为6.11和27.55pg/ml,中剂量组分别下降为11.53和52.73pg/ml,高剂量组分别下降为16.07和94.17pg/ml。结论IL-1β在煤工尘肺的纤维化过程中发挥了重要作用,阻断白介素1β可能减弱媒尘诱导的巨噬细胞炎性反应。
Objective To explore the role of IL-1β in the release of cytokines from pulmonary macrophages induced by Methods THP-1 ceils were stimulated by phorbol ester (PMA) to induce their differentiation into human alveolar macrophages ,and were randomly divided into 8 groups including one control group and 3 exposure groups(low- dose group,middle dose group and high dose group) and 4 IL-1β antibody groups. They received different dose of coal dust by garage for 8 hours continuously,and eytokines IL-1β,IL-6 and TNF-α were measured. Results IL-1β,IL-6 and TNF-α were induced by coal dust in the release of cytokines from macrophages,and the cytokine level were the highest in the high close group ( P 〈0.01 ), and the levels were 867.91 pg/ml, 35.17 pg/ml, and 249.86 pg/ml, respectively. After the addition of IL-1β antibody,the levels of Ig-1β,IL-6 and TNF-α released by macrophages in different dose groups significantly decreased. They dropped to 6.11 pg/ml and 7.55 pg/ml in the low dose group,11.53 pg/ml and 52.73 pg/ml in the middle dose group and 16.07 pg/ml and 94.17 pg/ml in the high dose group. Conclusion IL-1β plays an important role in the process of fibrosis of coal workers' pneumoconiosis. Blocking IL-1β may attenuate the inflammatory response of macrophages.
出处
《预防医学论坛》
2017年第10期726-728,共3页
Preventive Medicine Tribune
基金
湖南省教育厅科学研究优秀青年项目(项目编号:14B165)
湖南省卫生与计划生育委员会科研项目(项目编号:B2017044)