BML-111对PM2.5诱导外周血Th1/Th2及ILC2失调的影响  

Effect of BML-111 on PM2.5-induced dysregulation of Th1/Th2 and ILC2 in the peripheral blood of mice

作　　者：陆小霞 付慧聪 韩锋 方玉蓉 徐佳莉[1] 张李琼 杜青 LU Xiao xia;FU Hui-cong;HAN Feng;FANG Yu-rong;XU Jia-li;ZHANG Li-qiong;DU Qing(Department of Respiration,Wuhan Children＇s hospital,Tongji Medical College,Huazhong University of Science ＆ Technology,Wuhan 430016,China)

机构地区：[1]华中科技大学同济医学院附属武汉儿童医院呼吸科,武汉430016

出　　处：《现代免疫学》2018年第5期400-405,共6页Current Immunology

基　　金：国家自然科学基金重大研究计划(91643207);湖北省自然科学基金面上项目(2016CFB663);武汉市科技局应用基础研究计划[武科计(2015)203号应用基础2015061701011632]

摘　　要：本文主要探究PM2.5对小鼠外周血Th1/Th2及ILC2水平的影响以及BML-111的作用。通过分离培养小鼠PBMC,采用不同剂量PM2.5处理细胞,检测细胞增殖活性,筛选PM2.5适宜剂量。同时将细胞随机分为NC组、PM2.5组、BML-111组和拮抗剂Boc-2组,分别使用0 μg/mL PM2.5、50 μg/mL PM2.5、10 μmol/L BML-111和10 μmol/L Boc-2处理细胞,检测炎性因子的含量、Th1和Th2以及ILC2百分比、T-bet和GATA3的mRNA表达。结果发现,不同剂量PM2.5均能抑制PBMC的增殖率;PM2.5能够促使PBMC释放炎性因子,增加T-bet和GATA3的mRNA表达,诱导Th2分化,导致Th1/Th2失衡,同时提高ILC2水平。BML-111可降低炎性因子水平,抑制T-bet和GATA3的mRNA表达,降低免疫细胞水平,恢复Th1/Th2平衡,但拮抗剂Boc-2能部分逆转BML-111的作用。因此,脂氧素受体激动剂BML-111能够对PM2.5诱导的免疫炎性反应发挥有效抑制作用,这一作用可能是通过降低炎性因子的表达和ILC2百分比并维持免疫细胞Th1/Th2平衡来实现的。We aimed to investigate the effects of PM2.5 on Th1/Th2 status and ILC2 cells in the peripheral blood of mice and the effects of BML-111 on it.The peripheral blood mononuclear cells（PBMC）were isolated and cultured.The cells were treated with different doses of PM2.5 and the appropriate dose of PM2.5 was determined.The cells were randomly divided into NC,PM2.5,BML-111 and antagonist Boc-2 groups and treated with 0 μg/mL PM2.5,50 μg/mL PM2.5,10 μmol/L BML-111 and 10 μmol/L Boc-2,respectively.The levels of inflammatory factors,the percentages of Th1,Th2 and ILC2 cells,the mRNA expression levels of T-bet and GATA3 were measured.The results showed that different dosages of PM2.5 could suppress the proliferation rate of PBMCs.PM2.5 could promote the release of inflammatory factors by PBMCs,increase the mRNA expression of T-bet and GATA3,induce Th2 cell differentiation,lead to Th1/Th2 imbalance,and simultaneously raise the percentage of ILC2 cells.BML-111 reduced the levels of inflammatory factors and inhibited the mRNA expression of T-bet and GATA3,reduced the percentages of immune cells and recovered Th1/Th2 balance.But the antagonist Boc-2 partially reversed the effects of BML-111.Thus,lipoxin receptor agonist BML-111 could effectively inhibit immune inflammatory response induced by PM2.5 through reducing the levels of inflammatory factors and ILC2 cells and maintaining reestablishing Th1/Th2 balance.

关 键 词：炎症反应 PM2.5 脂氧素受体激动剂BML-111 TH1/TH2 

分 类 号：R392.11[医药卫生—免疫学]