LPS通过激活NF-κB，ERK和p38 MAPK信号通路在小鼠巨噬细胞中上调TLR9基因表达。,Immunology Letters

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LPS通过激活NF-κB，ERK和p38 MAPK信号通路在小鼠巨噬细胞中上调TLR9基因表达。
Immunology Letters ( IF 3.3 ) Pub Date : 2002-04-12 , DOI: 10.1016/s0165-2478(02)00010-x
Huazhang An ₁ , Hongmei Xu , Yizhi Yu , Minghui Zhang , Runzi Qi , Xiaoyi Yan , Shuxun Liu , Wenya Wang , Zhenghong Guo , Zhihai Qin , Xuetao Cao

Affiliation

Toll样受体（TLR）在细菌产品激活巨噬细胞中至关重要。已经显示TLR2和TLR4分别介导脂多糖（LPS）和脂蛋白信号转导。LPS对TLR2和TLR4表达的调节被认为是控制免疫细胞对细菌总体反应的机制之一。但是，对于TLR家族的其他成员是否受LPS监管知之甚少。最近，TLR9被证明是CpG DNA信号必不可少的。考虑到CpG DNA的有效免疫调节作用，调节TLR9表达可能在控制免疫细胞对细菌的总体反应中起重要作用。在这项研究中，研究了LPS对小鼠巨噬细胞RAW264.7细胞中TLR9基因表达的调控。进行半定量RT-PCR以确定TLR9的基因表达。LPS刺激后，TLR9基因表达在1小时内上调并在约3小时达到峰值。LPS刺激激活了NF-κB，ERK和p38 MAPK信号通路。用NF-κB，ERK和p38 MAPK信号通路抑制剂预处理巨噬细胞可抑制LPS诱导的TLR9 mRNA表达上调。我们的研究结果表明，LPS刺激可通过巨噬细胞中的NF-κB，ERK和p38 MAPK信号通路上调TLR9的基因表达，这表明LPS诱导的TLR9表达增加的巨噬细胞可能更有效地入侵细菌。LPS刺激激活了NF-κB，ERK和p38 MAPK信号通路。用NF-κB，ERK和p38 MAPK信号通路抑制剂预处理巨噬细胞可抑制LPS诱导的TLR9 mRNA表达上调。我们的研究结果表明，LPS刺激可通过巨噬细胞中的NF-κB，ERK和p38 MAPK信号通路上调TLR9的基因表达，这表明LPS诱导的TLR9表达增加的巨噬细胞可能更有效地入侵细菌。LPS刺激激活了NF-κB，ERK和p38 MAPK信号通路。用NF-κB，ERK和p38 MAPK信号通路抑制剂预处理巨噬细胞可抑制LPS诱导的TLR9 mRNA表达上调。我们的研究结果表明，LPS刺激可通过巨噬细胞中的NF-κB，ERK和p38 MAPK信号通路上调TLR9的基因表达，这表明LPS诱导的TLR9表达增加的巨噬细胞可能更有效地入侵细菌。

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Up-regulation of TLR9 gene expression by LPS in mouse macrophages via activation of NF-kappaB, ERK and p38 MAPK signal pathways.

Toll-like receptors (TLR) are critical in the activation of macrophages by bacterial products. It has been shown that TLR2 and TLR4 mediate lipopolysaccharide (LPS) and lipoproteins signal transduction, respectively. Regulation of TLR2 and TLR4 expression by LPS was considered to be one of the mechanisms to control the overall responses of immune cells to bacteria. However, little is known about whether the other members of TLR family are regulated by LPS. Recently, TLR9 was demonstrated to be essential for CpG DNA signaling. Given the effective immune modulation by CpG DNA, regulation of TLR9 expression might play important role in controlling the overall responses of immune cells to bacteria. In this study, regulation of TLR9 gene expression in mouse macrophage cell line RAW264.7 by LPS was investigated. Semiquantitative RT-PCR was performed to determine gene expression of TLR9. Following LPS stimulation, TLR9 gene expression was upregulated within 1 h and reached peak level at about 3 h. LPS stimulation activated NF-kappaB, ERK and p38 MAPK signal pathways. Pretreatment of macrophages with inhibitors of NF-kappaB, ERK and p38 MAPK signal pathways inhibited LPS-induced upregulation of TLR9 mRNA expression. Our results demonstrated that LPS stimulation could upregulate gene expression of TLR9 via NF-kappaB, ERK, and p38 MAPK signal pathways in macrophages, indicating that macrophages with increased TLR9 expression induced by LPS might respond to invading bacteria more effectively.

更新日期：2019-11-01

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