TY - JOUR
T1 - Adiponectin inhibits Toll-like receptor family-induced signaling
AU - Yamaguchi, Noboru
AU - Argueta, Jose Guillermo Martinez
AU - Masuhiro, Yoshikazu
AU - Kagishita, Maki
AU - Nonaka, Kazuaki
AU - Saito, Toshiyuki
AU - Hanazawa, Shigemasa
AU - Yamashita, Yoshihisa
N1 - Funding Information:
We thank Drs. I. Shimomura and N. Maeda for generously providing the mouse globular adiponectin cDNA. Support for this research was provided by Grant-in-Aid for Scientific Research (C) 17592184 from the Ministry of Education, Science, Sports, and Culture of Japan.
PY - 2005/12/19
Y1 - 2005/12/19
N2 - Recent studies have shown that adiponectin, an adipocyte-derived cytokine, acts as a potent inhibitor of inflammatory responses. It has been also demonstrated that bacterial and viral signalings in host cells are triggered via Toll-like receptor (TLR) molecules. Therefore, in the present study, we investigated whether globular adiponectin (gAd) would be able to inhibit TLR-mediated nuclear factor-κB (NF-κB) signaling in mouse macrophages (RAW264). gAd predominantly bound to the AdipoR1 receptor and suppressed TLR-mediated NF-κB signaling. gAd-mediated inhibition of TLR-mediated IκB phosphorylation and NF-κB activation was eliminated by the pretreatment of cycloheximide. Also their inhibitions of gAd were blocked by preincubation of the cells with an antibody against AdipoR1, but not with an antibody against AdipoR2. Taken together, these findings indicate that adiponectin negatively regulates macrophage-like cell response to TLR ligands via an unknown endogenous product(s).
AB - Recent studies have shown that adiponectin, an adipocyte-derived cytokine, acts as a potent inhibitor of inflammatory responses. It has been also demonstrated that bacterial and viral signalings in host cells are triggered via Toll-like receptor (TLR) molecules. Therefore, in the present study, we investigated whether globular adiponectin (gAd) would be able to inhibit TLR-mediated nuclear factor-κB (NF-κB) signaling in mouse macrophages (RAW264). gAd predominantly bound to the AdipoR1 receptor and suppressed TLR-mediated NF-κB signaling. gAd-mediated inhibition of TLR-mediated IκB phosphorylation and NF-κB activation was eliminated by the pretreatment of cycloheximide. Also their inhibitions of gAd were blocked by preincubation of the cells with an antibody against AdipoR1, but not with an antibody against AdipoR2. Taken together, these findings indicate that adiponectin negatively regulates macrophage-like cell response to TLR ligands via an unknown endogenous product(s).
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U2 - 10.1016/j.febslet.2005.11.019
DO - 10.1016/j.febslet.2005.11.019
M3 - Article
C2 - 16325814
AN - SCOPUS:28844494503
SN - 0014-5793
VL - 579
SP - 6821
EP - 6826
JO - FEBS Letters
JF - FEBS Letters
IS - 30
ER -