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Innate Immunity, Vol. 14, No. 2,
109-115 (2008)
DOI: 10.1177/1753425908089618
© 2008 SAGE Publications
Interleukin-10 inhibits tumor necrosis factor- production in lipopolysaccharide-stimulated RAW 264.7 cells through reduced MyD88 expression
Jargalsaikhan Dagvadorj
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Yoshikazu Naiki
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Gantsetseg Tumurkhuu
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Ferdaus Hassan
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Shamima Islam
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Naoki Koide
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Isamu Mori
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Tomoaki Yoshida
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Takashi Yokochi
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan, yokochi{at}aichi-med-u.ac.jp
The mechanism of interleukin (IL)-10-mediated inhibition of tumor necrosis factor (TNF)- production was studied by lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. IL-10 inhibited TNF- production transiently at an early stage after LPS stimulation. IL-10 inhibited the activation of nuclear factor (NF)- 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- production via reduced MyD88 expression.
Key Words: IL-10 LPS MyD88 TNF- TLR4

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