副干酪乳酸杆菌通过诱导负调控因子抑制单核巨噬细胞对脂多糖刺激的炎性细胞因子应答
作者:
作者单位:

作者简介:

通讯作者:

中图分类号:

基金项目:


L.paracasei inhibits LPS-induced mononuclear phagocytes inflammatory cytokine response through negative regulators
Author:
Affiliation:

Fund Project:

  • 摘要
  • |
  • 图/表
  • |
  • 访问统计
  • |
  • 参考文献
  • |
  • 相似文献
  • |
  • 引证文献
  • |
  • 资源附件
  • |
  • 文章评论
    摘要:

    目的:探讨副干酪乳酸杆菌(Lactobacillus paracacei,L.para)预刺激抑制脂多糖(Lipopolysacchride,LPS)诱导的炎性细胞因子释放的调节机制-方法:用佛波酯诱导THP-1细胞分化为巨噬细胞样细胞;以L.para预刺激为实验组,小剂量LPS(10 ng/ml)预刺激和TLR2激动剂Pam3CSK4预刺激为对照组,预刺激24 h后,再用LPS大剂量(1 -滋g/ml)刺激经分化的THP-1细胞;检测预刺激对TLR信号通路负调控因子A20-SOCS1-SOCS3-IRAK3的表达水平,对TLR4和CD14的膜表达水平和mRNA水平,以及对大剂量LPS诱导的炎性细胞因子IL-1β-TNF-α水平的影响-各目的蛋白mRNA水平检测采用实时荧光定量聚合酶链式反应(real-time quantitative polymerase chain reaction,RT-qPCR)法,TLR4和CD14的膜表达检测采用流式细胞术-结果:L.para等预刺激能够降低LPS诱导的IL-1β-TNF-α表达水平;并能够上调细胞TLR信号途径负调控因子A20-SOCS1-SOCS3-IRAK3的mRNA水平,但不影响细胞膜的TLR4和CD14阳性百分率;IRAK1/4抑制剂能够减弱预刺激诱导的负调控因子表达水平,并减弱预刺激对LPS诱导炎症因子释放的抑制作用-结论:副干酪乳酸杆菌预刺激能够通过上调TLR信号通路负调控因子A20-SOCS1-SOCS3-IRAK3等的表达抑制单核巨噬细胞对LPS刺激的炎性细胞因子的释放-

    Abstract:

    Objective:To investigate the regulation mechanism of prestimulation of Lactobacillus paracacei (L.para) inhibited on LPS-induced inflammatory cytokine release. Methods:THP-1 cells were differentiated to macrophage-like cells by PMA stimulation. Cells were then pretreated by L.para (the experimental group),a lower dose LPS (10 ng/ml) and TLR2 agonist Pam3CSK4 respectively (the control group). After 24 hours pretreatment,THP-1 cells were further stimulated with a higher dose LPS (1 -滋g/ml). The influence of this prestimulation on the expression of TLR signaling pathway negative regulators,membrane expression and mRNA levels in TLR4 and CD14 and IL-1β and TNF-α levels in a higher dose LPS-induced inflammatory cytokines were respectively detected. mRNA levels were measured by real-time quantitative polymerase chain reaction (RT-qPCR). Membrane expressions of TLR4 and CD14 after pretreatment were confirmed by flow cytometry. Results:LPS-induced IL-1β and TNF-α levels were significantly reduced by L.para pretreatment;In addition,the mRNA level of TLR signaling pathway negative regulators A20,SOCS1,SOCS3 and IRAK3 were upregulated while membrane expression of TLR4 and CD14 unaltered. Prestimulation-reduced negative regulators expression levels along with the release of LPS-reduced inflammatory cytokines were weaken by a IRAK1/4 inhibitor. Conclusion:L.para prestimulation could enhance negative regulators of TLR signaling A20,SOC1,SOCS3 and IRAK3 expression thus inhibits inflammatory response of macrophage after LPS stimulation.

    参考文献
    相似文献
    引证文献
引用本文

谢 超,孙可一,季晓辉.副干酪乳酸杆菌通过诱导负调控因子抑制单核巨噬细胞对脂多糖刺激的炎性细胞因子应答[J].南京医科大学学报(自然科学版),2014,(9):1184-1191

复制
分享
文章指标
  • 点击次数:
  • 下载次数:
  • HTML阅读次数:
  • 引用次数:
历史
  • 收稿日期:2014-04-08
  • 最后修改日期:
  • 录用日期:
  • 在线发布日期: 2014-09-11
  • 出版日期:
通知关闭
郑重声明