Adiponectin inhibits Toll-like receptor family-induced signaling
Adiponectin inhibits Toll-like receptor family-induced signaling
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DOI：
10.1016/j.febslet.2005.11.019
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发表时间：
2005-12-19
期刊：
影响因子：
3.5
通讯作者：
Yamashita, Y
中科院分区：
文献类型：
--
作者：
Yamaguchi, N;Guillermo, J;Yamashita, Y
最近的研究表明，脂联素，脂肪细胞衍生的细胞因子，作为一种有效的炎症反应抑制剂。还已经证明，宿主细胞中的细菌和病毒信号传导通过Toll样受体（TLR）分子触发。因此，在本研究中，我们研究了球状脂联素（gAd）是否能够抑制小鼠巨噬细胞（RAW 264）中TLR介导的核因子-κ B（NF-κ B）信号传导。gAd主要与Adi-poR 1受体结合，并抑制TLR介导的NF-κ B信号传导。放线菌酮预处理可消除gAd介导的TLR介导的I κ B磷酸化和NF-κ B活化抑制。此外，通过将细胞与针对Adipo-R1的抗体预孵育而不是与针对AdipoR 2的抗体预孵育来阻断它们对gAd的抑制。总之，这些发现表明脂联素通过未知的内源性产物负调节巨噬细胞样细胞对TLR配体的反应。(c)2005年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
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-kappa B (NF-kappa B) signaling in mouse macrophages (RAW264). gAd predominantly bound to the Adi-poR1 receptor and suppressed TLR-mediated NF-kappa B signaling. gAd-mediated inhibition of TLR-mediated I kappa B phosphorylation and NF-kappa B activation was eliminated by the pretreatment of cycloheximide. Also their inhibitions of gAd were blocked by preincubation of the cells with an antibody against Adipo-R1, 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). (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.