摘要
目的:研究白细胞介素27(interleukin-27,IL-27)对辅助性T细胞1(helper T cell 1,Th1)分化及急性肺损伤的影响与作用机制。方法:通过盲肠结扎穿刺(cecal ligation and puncture,CLP)构建脓毒症急性肺损伤小鼠模型,苏木精-伊红(hematoxylin-eosin staining,HE)染色评估肺组织病理损伤。采用Western Blot、RT-qPCR检测JAK/STAT通路表达与激活以及T盒转录因子21(T-box transcription factor 21,T-bet)蛋白的表达。结果:IL-27加重脓毒症小鼠肺损伤。细胞实验表明IL-27显著激活JAK2/STAT1通路磷酸化,上调T-bet蛋白(P<0.01)和mRNA水平(P<0.05)。抑制STAT1磷酸化后,T-bet表达显著下调(P<0.01)。结论:IL-27通过JAK2/STAT1通路促进Th1分化,加重脓毒症小鼠急性肺损伤。
Objective:To investigate the effect and mechanism of interleukin-27(IL-27)on the differentiation of T helper type 1(Th1)cells and acute lung injury.Methods:The method of cecal ligation and puncture was used to establish a mouse model of sepsis with acute lung injury,and hematoxylin-eosin staining was used to assess the histopathological damage of the lungs.Western blot and RT-qPCR were used to measure the expression and activation of the JAK/STAT pathway and the protein and mRNA expression levels of T-box transcription factor 21(T-bet).Results:IL-27 exacerbated lung injury in mice with sepsis.Cell experiments showed that IL-27 significantly activated the phosphorylation of the JAK2/STAT1 pathway and upregulated the protein and mRNA expression levels of T-bet(P<0.01,P<0.05).The expression of T-bet was significantly downregulated after inhibition of STAT1 phosphorylation(P<0.01).Conclusion:IL-27 promotes Th1 differentiation via the JAK2/STAT1 pathway,thereby exacerbating acute lung injury in mice with sepsis.
作者
王远扬
徐昉
祁海峰
Wang Yuanyang;Xu Fang;Qi Haifeng(Department of Critical Care Medicine,The First Affiliated Hospital of Chongqing Medical University;Department of Critical Care Medicine,Women and Children’s Hospital of Chongqing Medical University)
出处
《重庆医科大学学报》
CSCD
北大核心
2024年第12期1572-1576,共5页
Journal of Chongqing Medical University
基金
重庆市科卫联合医学科研重点资助项目(编号:2023ZDXM004)。
