[1]刘 姗,宋政文,郑晨晨,等.CD11b调控LPS刺激下巨噬细胞表达IL-12的分子机制[J].南京师范大学学报(自然科学版),2018,41(02):71.[doi:10.3969/j.issn.1001-4616.2018.02.013]
　Liu Shan,Song Zhengwen,Zheng Chenchen,et al.Molecular Mechanism of CD11b Regulated IL-12Expression in LPS-Stimulated Macrophages[J].Journal of Nanjing Normal University(Natural Science Edition),2018,41(02):71.[doi:10.3969/j.issn.1001-4616.2018.02.013]
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CD11b调控LPS刺激下巨噬细胞表达IL-12的分子机制()
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《南京师范大学学报》（自然科学版）[ISSN:1001-4616/CN:32-1239/N]

卷:
第41卷
期数:
2018年02期
页码:
71
栏目:
·生命科学·
出版日期:
2018-06-30

文章信息/Info

Title:
Molecular Mechanism of CD11b Regulated IL-12Expression in LPS-Stimulated Macrophages
文章编号:
1001-4616(2018)02-0071-07
作者:
刘 姗; 宋政文; 郑晨晨; 张国秀; 赵智辉
南京师范大学生命科学学院,生物化学与生物制品研究所,江苏省分子与医学生物技术重点实验室,江苏 南京 210023
Author(s):
Liu Shan; Song Zhengwen; Zheng Chenchen; Zhang Guoxiu; Zhao Zhihui
School of Life Sciences,Nanjing Normal University,Institute of Biochemistry and Biological Products,Jiangsu Key Laboratory for Molecular and Medical Biotechnology,Nanjing 210023,China
关键词:
CD11b; 白细胞介素12; 脂多糖; 巨噬细胞; JNK; NF-κB
Keywords:
CD11b; interleukin 12; lipopolysaccharides; macrophage; JNK; NF-κB
分类号:
R363.2
DOI:
10.3969/j.issn.1001-4616.2018.02.013
文献标志码:
A
摘要:
CD11b是白细胞整合素家族成员之一,在炎症的发生和发展中发挥重要作用. 在内毒素血症小鼠模型,发现脂多糖(LPS)导致外周血白细胞介素12(IL-12)水平降低,而CD11b抑制剂能防止此现象发生. 为阐明CD11b调控LPS刺激下IL-12产生的分子机制,本文利用RAW264.7细胞开展了进一步研究. 酶联免疫吸附、实时定量PCR和Western Blot等检测结果表明,CD11b可抑制LPS刺激下RAW264.7细胞IL-12的表达; 利用shRNA敲低CD11b的表达则能提高LPS刺激下RAW264.7细胞IL-12p35、IL-12p40的转录水平和蛋白水平的表达; JNK和 NF-κB 信号通路与CD11b调控IL-12的产生关系密切,而p38、ERK信号通路影响较小. 因此,研究结果提示,CD11b通过JNK和NF-κB信号通路抑制LPS刺激下巨噬细胞IL-12的产生,抑制CD11b的功能可能有助于削弱LPS引起的炎症反应.
Abstract:
CD11b is a member of the leukocyte integrin family,which plays a significant role in the pathogenesis of inflammation. In an endotoxemia mouse model,we found that lipopolysaccharide(LPS)caused a significant decrease of interleukin-12(IL-12)in peripheral blood,and pretreatment with CD11b inhibitor effectively prevented the occurrence of such event. To elucidate the underlying molecular mechanism that CD11b regulates the production of IL-12 under LPS stimulation,we performed further studies using RAW264.7 cells. Results from Enzyme-linked immunosorbent assay,real-time quantitative PCR,and Western Blot demonstrated that,CD11b inhibited the expression of IL-12 in LPS-stimulated RAW264.7 cells. Knocking down the expression of CD11b increased the expression of IL-12p35 and IL-12p40 at both transcription and protein levels in RAW264.7 cells stimulated with LPS. The regulation of CD11b on IL-12 expression was closely associated with the activation of JNK and NF-κB signaling pathways,while p38 and ERK signaling pathways were less involved. Thus,this study suggested that CD11b inhibited IL-12 production in LPS-stimulated macrophages mainly via JNK and NF-κB signaling pathways,and inhibiting the function of CD11b may be of help for attenuating excessive inflammatory responses induced by LPS.

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备注/Memo

备注/Memo:
收稿日期:2018-01-26.
基金项目:国家自然科学基金面上项目(81273232).
通讯联系人:赵智辉,博士,教授,研究方向:炎症相关信号通路. E-mail:zhaozhihui_1964@aliyun.com
更新日期/Last Update: 2018-11-06