Up-Regulation of NOD1 and NOD2 through TLR4 and TNF-.ALPHA. in LPS-treated Murine Macrophages

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  • TAKAHASHI Yuji
    Laboratory of Animal Breeding, Graduate School of Agricultural and Life Sciences, The University of Tokyo
  • ISUZUGAWA Kazuto
    Laboratory of Animal Breeding, Graduate School of Agricultural and Life Sciences, The University of Tokyo
  • MURASE Yasunori
    Laboratory of Animal Breeding, Graduate School of Agricultural and Life Sciences, The University of Tokyo
  • IMAI Misa
    Laboratory of Animal Breeding, Graduate School of Agricultural and Life Sciences, The University of Tokyo
  • YAMAMOTO Shinya
    Laboratory of Animal Breeding, Graduate School of Agricultural and Life Sciences, The University of Tokyo
  • IIZUKA Masateru
    Laboratory of Animal Breeding, Graduate School of Agricultural and Life Sciences, The University of Tokyo
  • AKIRA Shizuo
    Department of Host Defense, Research Institute for Microbial Diseases, Osaka University
  • BAHR George M.
    Laboratory of Molecular Immunology of Infection and Inflammation, Institut Pasteur de Lille
  • MOMOTANI Ei-ichi
    National Institute of Animal Health
  • HORI Masatoshi
    Laboratory of Veterinary Pharmacology, Graduate School of Agricultural and Life Sciences, The University of Tokyo
  • OZAKI Hiroshi
    Laboratory of Veterinary Pharmacology, Graduate School of Agricultural and Life Sciences, The University of Tokyo
  • IMAKAWA Kazuhiko
    Laboratory of Animal Breeding, Graduate School of Agricultural and Life Sciences, The University of Tokyo

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Other Title
  • LPS処理されたマウスのマクロファージにおけるTLR4とTNF-αを介したNOD1とNOD2の発現亢進
  • Up-regulation of NOD1 and NOD2 through TLR4 and TNF-α in LPS-treated Murine Macrophages
  • Up regulation of NOD1 and NOD2 through TLR4 and TNF アルファ in LPS treated Murine Macrophages

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Abstract

NOD1 (Card4) and NOD2 (Card15) are thought to be responsible for cytoplasmic defense against bacterial entry. To gain further knowledge about how their expressions are regulated in murine macrophages, we investigated the expression of NOD1 and NOD2 mRNAs after stimulation with various endotoxins, lipopolysaccharide, lipoteichoic acid and peptidoglycan. In macrophage RAW264.7 cells, the first and second rises in NOD1 and NOD2 mRNAs were observed at 2 hr and at 8-12 hr after endotoxin treatment. Increases in NOD1 and NOD2 mRNAs at 2 hr in lipopolysaccharide-treated RAW264.7 cells were reduced with the use of NF-κB inhibitor, caffeic acid phenetyl ester. In RAW264.7 cells, lipopolysaccharide-induced increases in NOD1 and NOD2 mRNAs were inhibited with anti-TLR4 antibody, and partially reduced in peritoneal macrophages obtained from TLR4-deficient mice. Furthermore, NOD1 and NOD2 mRNA expressions in RAW264.7 cells were increased by the treatment with proinflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), or IL-6. In TNF-α deficient macrophages, the expression of NOD molecules was minimal at 12 hr, and the second rise in NOD mRNA seen in lipopolysaccharide-treated RAW264.7 cells was inhibited with anti-TNF-α, but not with anti-IL-1β or anti-IL-6 antibody. These observations suggest that immediate response of NODs to endotoxins could result from NF-κB activation via TLR signaling, whereas the second rise in NOD mRNAs might have resulted from TNF-α production possibly through NF-κB, TLR, and/or NOD signalings.<br>

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