IL-6通过激活JAK2/STAT3信号通路增强小鼠肺泡巨噬细胞的吞噬功能
IL-6 enhances the phagocytic function of mouse alveolar macrophages by activating the JAK2/STAT3 signaling pathway
华梦晴 1高培宇 2方芳 1苏浩宇 2宋传旺1
作者信息
- 1. 蚌埠医学院检验医学院免疫学教研室,安徽蚌埠 233030;蚌埠医学院慢性疾病免疫学基础与临床安徽省重点实验室,安徽蚌埠 233030
- 2. 蚌埠医学院慢性疾病免疫学基础与临床安徽省重点实验室,安徽蚌埠 233030
- 折叠
摘要
目的 探讨白细胞介素6(IL-6)对MH-S小鼠肺泡巨噬细胞吞噬功能的影响及其相关机制.方法 脂多糖(LPS)经气道滴入激发构建小鼠急性肺损伤(ALI)模型,ELISA检测支气管肺泡灌洗液(BALF)中IL-6的含量.体外培养MH-S细胞,在信号转导子与转录激活子3(STAT3)抑制剂Stattic(5 μmol/L)存在与否的情况下,再加入IL-6(10 ng/mL～500 ng/mL)刺激6 h,加入荧光微球孵育2 h后,采用流式细胞术检测MH-S细胞吞噬荧光微球情况;Western blot法检测磷酸化的Janus激酶2(p-JAK2)、磷酸化的STAT3(p-STAT3)、肌动蛋白相关蛋白2(Arp2)、纤维型肌动蛋白(F-actin)的表达水平.结果 鼻腔滴入LPS后,小鼠BALF中IL-6含量显著升高.随着IL-6刺激剂量的增加,MH-S细胞吞噬荧光微球的作用增强,Arp2、F-actin蛋白的表达水平升高.100 ng/mL IL-6刺激MH-S细胞后,p-JAK2和p-STAT3蛋白的表达水平升高.阻断MH-S细胞STAT3信号后,IL-6促进细胞吞噬的效应完全消失,IL-6诱导的Arp2、F-actin蛋白表达增加被抑制.结论 IL-6通过激活JAK2/STAT3信号通路促进MH-S细胞Arp2、F-actin蛋白的表达增强吞噬功能.
Abstract
Objective To investigate the effect of interleukin-6(IL-6)on the phagocytosis of MH-S alveolar macrophages and its related mechanisms.Methods A mouse acute lung injury(ALI)model was constructed by instilling lipopolysaccharide(LPS)into the airway.ELISA was used to detect the content of IL-6 in bronchoalveolar lavage fluid(BALF).In vitro cultured MH-S cells,in the presence or absence of signal transducer and activator 3 of transcription(STAT3)inhibitor Stattic(5 μmoVL),IL-6(10 ng/mL～500 ng/mL)was added to stimulate for 6 hours,and then incubated with fluorescent microspheres for 2 hours.The phagocytosis of MH-S cells was detected by flow cytometry.Western blot analysis was used to detect the expression levels of phosphorylated Janus kinase 2(p-JAK2),phosphorylated STAT3(p-STAT3),actin-related protein 2(Arp2)and filamentous actin(F-actin).Results The content of IL-6 in BALF was significantly increased after the mice were injected with LPS through the airway.With the increase of IL-6 stimulation concentration,the phagocytic function of MH-S cells was enhanced,and the expression levels of Arp2 and F-actin proteins in MH-S cells were increased.The expression levels of p-JAK2 and p-STAT3 proteins increased in MH-S cells stimulated with IL-6(100 ng/mL).After blocking STAT3 signaling,the effect of IL-6 in promoting phagocytosis of MH-S cells disappeared completely,and the increased expression of Arp2 and F-actin proteins in MH-S cells induced by IL-6 was also inhibited.Conclusion IL-6 promotes the expression of Arp2 and F-actin proteins by activating the JAK2/STAT3 signaling pathway,thereby enhancing the phagocytic function of MH-S cells.
关键词
白细胞介素6(IL-6)/MH-S细胞/吞噬功能/Janus激酶2(JAK2)/信号转导子与转录激活子3(STAT3)/肺泡巨噬细胞Key words
interleukin-6/MH-S cells/phagocytosis/JAK2/STAT3/alveolar macrophages引用本文复制引用
基金项目
安徽高校自然科学研究项目重大项目(KJ2020ZD49)
安徽高校自然科学研究项目重点项目(KJ2020A0583)
蚌埠医学院自然科学重点项目(2020byzd024)
蚌埠医学院省级重点科研平台开放课题基金(KLICD-2022-D2)
2021年安徽省大学生创新创业训练计划项目(S202110367103)
出版年
2024
NETL
NSTL
万方数据