Interleukin-10 inhibits tumor necrosis factor-α production in lipopolysaccharide-stimulated RAW 264.7 cells through reduced MyD88 expression
Interleukin-10 inhibits tumor necrosis factor-α production in lipopolysaccharide-stimulated RAW 264.7 cells through reduced MyD88 expression
复制标题
DOI：
10.1177/1753425908089618
复制
发表时间：
2008-04-01
期刊：
影响因子：
3.2
通讯作者：
Yokochi, Takashi
中科院分区：
文献类型：
--
作者：
Dagvadorj, Jargalsaikhan;Naiki, Yoshikazu;Yokochi, Takashi
通过脂多糖（LPS）刺激RAW 264.7巨噬细胞，研究了白细胞介素(IL)-10介导的抑制肿瘤坏死因子(TNF)- α产生的机制。IL-10在LPS刺激后早期短暂抑制tnf - α的产生。IL-10抑制lps刺激的RAW 264.7细胞中核因子(NF)- κ B、p38和应激活化蛋白激酶（SAPK）的活化。尽管MyD88蛋白水平在LPS作用下升高，但IL-10阻止了LPS诱导的MyD88增强。在LPS作用下，经IL-10预处理和不经IL-10预处理的细胞MyD88 mRNA表达无显著差异。因此，IL-10可能通过降低MyD8的表达来抑制lps诱导的tnf - α的产生。
The mechanism of interleukin (IL)-10-mediated inhibition of tumor necrosis factor (TNF)-alpha production was studied by lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. IL-10 inhibited TNF-alpha production transiently at an early stage after LPS stimulation. IL-10 inhibited the activation of nuclear factor (NF)-kappa B, p38 and stress-activated protein kinase (SAPK) in LPS-stimulated RAW 264.7 cells. Although the level of MyD88 protein increased in response to LPS, IL-10 prevented the LPS-induced MyD88 augmentation. There was no significant difference in the MyD88 mRNA expression between the cells pretreated with or without IL-10 in response to LPS. Therefore, IL-10 was suggested to inhibit LPS-induced TNF-alpha production via reduced MyD8 8 expression.