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
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
收藏
页码:109 / 115
页数:7
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