Interleukin-10 inhibits tumor necrosis factor-α production in lipopolysaccharide-stimulated RAW 264.7 cells through reduced MyD88 expression

被引：32

作者：

Dagvadorj, Jargalsaikhan ^{[1
]}

Naiki, Yoshikazu ^{[1
]}

Tumurkhuu, Gantsetseg ^{[1
]}

Hassan, Ferdaus ^{[1
]}

Islam, Shamima ^{[1
]}

Koide, Naoki ^{[1
]}

Mori, Isamu ^{[1
]}

Yoshida, Tomoaki ^{[1
]}

Yokochi, Takashi ^{[1
]}

机构：

[1] Aichi Med Univ, Sch Med, Dept Microbiol & Immunol, Aichi 4801192, Japan

来源：

INNATE IMMUNITY | 2008年 / 14卷 / 02期

关键词：

IL-10; LPS; MyD88; TNF-alpha; TLR4;

D O I：

10.1177/1753425908089618

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：109 / 115

页数：7

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