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[1]陈向军,王在强,王博荣,等.PM2.5通过激活颗粒酶B/IL-18信号通路促进炎症因子表达[J].中华肺部疾病杂志,2024,(02):207-211.[doi:10.3877/cma.j.issn.1674-6902.2024.02.007]
 Chen Xiangjun,Wang Zaiqiang,Wang Borong,et al.PM2.5 promoted the expression of inflammatory cytokines by activating granzyme B/IL-18 signaling pathway[J].,2024,(02):207-211.[doi:10.3877/cma.j.issn.1674-6902.2024.02.007]
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PM2.5通过激活颗粒酶B/IL-18信号通路促进炎症因子表达(PDF)

《中华肺部疾病杂志》[ISSN:1006-6977/CN:61-1281/TN]

卷:
期数:
2024年02期
页码:
207-211
栏目:
论著
出版日期:
2024-04-20

文章信息/Info

Title:
PM2.5 promoted the expression of inflammatory cytokines by activating granzyme B/IL-18 signaling pathway
作者:
陈向军1王在强2王博荣1王 莉1方 芳1金发光2王光辉1
710100 西安,西安市胸科医院重症医学二科1
710038 西安,空军军医大学第二附属医院呼吸与危重症医学科2
Author(s):
Chen Xiangjun1 Wang Zaiqiang2 Wang Borong1 Wang Li1 Fang Fang1 Jin Faguang2 Wang Guanghui1.
1The second Department of Intensive Care Medicine, Xi'an Chest Hospital, Xi'an 710100, China; 2Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Air Force Medical University, Xi'an 710038, China
关键词:
PM2.5 颗粒酶B 自然杀伤细胞 炎症因子
Keywords:
Particulate Matter 2.5 Granzyme B Natural killer cell Inflammatory cytokine
分类号:
R563
DOI:
10.3877/cma.j.issn.1674-6902.2024.02.007
摘要:
目的 分析颗粒酶B在PM2.5促进自然杀伤(natural killer, NK)细胞炎症因子表达中的作用。方法(1)通过设置PM2.5染毒剂量梯度,分组为空白对照组(0 μg/ml)、PM2.5(50 μg/ml)组、PM2.5(150 μg/ml)组和PM2.5(450 μg/ml)组,观察PM2.5暴露与NK细胞颗粒酶B和炎症因子TNF-α、IL-1β表达间有无相关性;(2)为明确PM2.5上调NK细胞炎症因子表达中颗粒酶B是否发挥促进作用,根据是否行PM2.5染毒和颗粒酶B抑制剂Serpina3n预处理,实验分为空白对照组、Serpina3n组、PM2.5组和Serpina3n+PM2.5组。在PM2.5染毒前1h,Serpina3n组和Serpina3n+PM2.5组加入Serpina3n(100 ng/ml);(3)为明确在PM2.5上调NK细胞炎症因子表达中颗粒酶B是否通过IL-18发挥作用,根据是否行PM2.5染毒和IL-18抑制剂IL-18BP预处理,实验分为空白对照组、IL-18BP、PM2.5组、IL-18BP+PM2.5组。在PM2.5染毒前1 h,IL-18BP组和IL-18BP+PM2.5组加入IL-18BP(100 ng/ml)。分别检测每组NK细胞蛋白表达情况和细胞培养液TNF-α、IL-1β水平。结果 PM2.5促进了NK细胞颗粒酶B和炎症因子TNF-α、IL-1β表达; 阻断颗粒酶B抑制NK细胞IL-18表达和NF-κB磷酸化,降低TNF-α和IL-1β表达; 阻断IL-18抑制了NF-κB磷酸化,降低TNF-α和IL-1β表达。结论 PM2.5可能通过激活颗粒酶B/IL-18信号通路促进NK细胞TNF-α和IL-1β表达,机制可能与激活NF-κB信号通路有关。
Abstract:
Objective To explore the role of granzyme B in PM2.5 promoting the expression of inflammatory cytokines in natural killer(NK)cells. Methods First, the PM2.5 dose gradient was set. The experiment was divided into blank control group(0 μg/ml), PM2.5 group(50 μg/ml), PM2.5 group(150 μg/ml), and PM2.5 group(450 μg/ml). By setting the PM2.5 dose gradient, we observed the correlation between the expression of NK cell granzyme B and inflammatory cytokines TNF-α and IL-1β. Second, in order to determine whether granzyme B plays a promoting role in the expression of inflammatory cytokines in NK cells promoted by PM2.5, the experiment was divided into blank control group, Serpina3n group, PM2.5 group and Serpina3n+PM2.5 group according to whether PM2.5 exposure and Serpina3n inhibitor were pretreated. Serpina3n group and Serpina3n+PM2.5 group were added Serpina3n(100 ng/ml)1 hour before PM2.5 poisoning. Third, in order to determine whether granzyme B plays a role through IL-18 in PM2.5 promoting the expression of inflammatory cytokines in NK cells, the experiment was divided into blank control group, IL-18BP, PM2.5 group, and IL-18BP+PM2.5 group according to whether PM2.5 exposure and IL-18BP inhibitor were pretreated. One hour before PM2.5 exposure, IL-18BP group and IL-18BP+PM2.5 group were added with IL-18BP(100 ng/ml). The expression of NK cell protein and the levels of TNF-α and IL-1β in cell culture medium were detected in each group separately. Results PM2.5 promoted the expression of granzyme B and inflammatory factors TNF-α and IL-1β in NK cells. Blocking granzyme B inhibited IL-18 expression and NF-κB phosphorylation, and decreased TNF-α and IL-1β expression in NK cells. Blocking IL-18 inhibited the phosphorylation of NF-κB and decreased the expression of TNF-α and IL-1β. Conclusion PM2.5 may promote the expression of TNF-α and IL-1β in NK cells by activating granzyme B/IL-18 signaling pathway, and the mechanism may be related to the activation of NF-κB signaling pathway.

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备注/Memo

备注/Memo:
基金项目: 陕西省重点研发计划(2018ZDCXL-SF-02-03-02) 通信作者: 王光辉, Email: hxkwgh@163.com
更新日期/Last Update: 2024-04-20