首页|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

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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。
IL-6 enhances the phagocytic function of mouse alveolar macrophages by activating the JAK2/STAT3 signaling pathway
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.

interleukin-6MH-S cellsphagocytosisJAK2STAT3alveolar macrophages

华梦晴、高培宇、方芳、苏浩宇、宋传旺

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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

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

安徽高校自然科学研究项目重大项目安徽高校自然科学研究项目重点项目蚌埠医学院自然科学重点项目蚌埠医学院省级重点科研平台开放课题基金2021年安徽省大学生创新创业训练计划项目

KJ2020ZD49KJ2020A05832020byzd024KLICD-2022-D2S202110367103

2024

10.13423/j.cnki.cjcmi.009693

细胞与分子免疫学杂志
中国免疫学会,第四军医大学

细胞与分子免疫学杂志

CSTPCD北大核心
影响因子：0.817
ISSN：1007-8738
年,卷(期)：2024.40(1)
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