Please use this identifier to cite or link to this item: https://scholarhub.balamand.edu.lb/handle/uob/2695
Title: Up-Regulation of NOD1 and NOD2 through TLR4 and TNF- alpha in LPS-treated Murine Macrophages
Authors: Takahasi, Yuji
Isuzugawa, Kazuto
Murase, Yasunori
Imai, Misa
Yamamoto, Shinya
Iizuka, Masateru
Akira, Shizuo
Bahr, George M. 
Momotani, Ei-ichi
Hori, Masatoshi
Ozaki, Hiroshi
Imakawa, Kazuhiko
Affiliations: Faculty of Medicine 
Keywords: Murine
NOD1
NOD2
TNF-α
Subjects: Macrophages
Issue Date: 2006
Part of: Journal of veterinary medical science
Volume: 68
Issue: 5
Start page: 471
End page: 478
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.
URI: https://scholarhub.balamand.edu.lb/handle/uob/2695
Open URL: Link to full text
Type: Journal Article
Appears in Collections:Faculty of Medicine

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