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

Jargalsaikhan Dagvadorj; Yoshikazu Naiki; Gantsetseg Tumurkhuu; Ferdaus Hassan; Shamima Islam; Naoki Koide; Isamu Mori; Tomoaki Yoshida; Takashi Yokochi

doi:10.1177/1753425908089618

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

Jargalsaikhan Dagvadorj, Yoshikazu Naiki, Gantsetseg Tumurkhuu, Ferdaus Hassan, Shamima Islam, Naoki Koide, Isamu Mori, Tomoaki Yoshida, Takashi Yokochi

Medical Biology

Research output: Contribution to journal › Article › peer-review

33 Citations (Scopus)

Abstract

The mechanism of interleukin (IL)-10-mediated inhibition of tumor necrosis factor (TNF)-α production was studied by lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. IL-10 inhibited TNF-α production transiently at an early stage after LPS stimulation. IL-10 inhibited the activation of nuclear factor (NF)-κB, 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-α production via reduced MyD88 expression.

Original language	English
Pages (from-to)	109-115
Number of pages	7
Journal	Innate Immunity
Volume	14
Issue number	2
DOIs	https://doi.org/10.1177/1753425908089618
Publication status	Published - 04-2008

All Science Journal Classification (ASJC) codes

Microbiology
Immunology
Molecular Biology
Cell Biology
Infectious Diseases

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1177/1753425908089618

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

abstract = "The mechanism of interleukin (IL)-10-mediated inhibition of tumor necrosis factor (TNF)-α production was studied by lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. IL-10 inhibited TNF-α production transiently at an early stage after LPS stimulation. IL-10 inhibited the activation of nuclear factor (NF)-κB, 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-α production via reduced MyD88 expression.",

author = "Jargalsaikhan Dagvadorj and Yoshikazu Naiki and Gantsetseg Tumurkhuu and Ferdaus Hassan and Shamima Islam and Naoki Koide and Isamu Mori and Tomoaki Yoshida and Takashi Yokochi",

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AU - Dagvadorj, Jargalsaikhan

AU - Naiki, Yoshikazu

AU - Tumurkhuu, Gantsetseg

AU - Hassan, Ferdaus

AU - Islam, Shamima

AU - Koide, Naoki

AU - Mori, Isamu

AU - Yoshida, Tomoaki

AU - Yokochi, Takashi

PY - 2008/4

Y1 - 2008/4

N2 - The mechanism of interleukin (IL)-10-mediated inhibition of tumor necrosis factor (TNF)-α production was studied by lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. IL-10 inhibited TNF-α production transiently at an early stage after LPS stimulation. IL-10 inhibited the activation of nuclear factor (NF)-κB, 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-α production via reduced MyD88 expression.

AB - The mechanism of interleukin (IL)-10-mediated inhibition of tumor necrosis factor (TNF)-α production was studied by lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. IL-10 inhibited TNF-α production transiently at an early stage after LPS stimulation. IL-10 inhibited the activation of nuclear factor (NF)-κB, 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-α production via reduced MyD88 expression.

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

Abstract

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