Chemokine induction by the adipocyte-derived cytokine adiponectin
Chemokine induction by the adipocyte-derived cytokine adiponectin
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DOI：
10.1016/j.clim.2006.01.010
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发表时间：
2006-07-01
影响因子：
8.6
通讯作者：
Song, HJ
中科院分区：
文献类型：
--
作者：
Rovin, BH;Song, HJ
脂联素是一种脂肪细胞来源的细胞因子，在肥胖和糖尿病等代谢疾病中发挥作用。最近的研究表明，脂联素也可能影响免疫反应，主要作为抗炎因子发挥作用。鉴于我们观察到SLE炎症性肾炎患者血浆和尿脂联素水平升高，我们评价了脂联素对与SLE肾炎发病相关的促炎化学因子的影响。据推测，脂联素可以减弱细胞因子诱导的趋化因子表达。用脂联素处理培养的人微血管内皮细胞和单核细胞，用ELISA法测定细胞培养上清液中IL-8和MCP-1的水平。出乎意料的是，全长脂联素显著增加了IL-8和MCIP-1的产生，但并没有消除细胞因子诱导的趋化因子的表达。此外，脂联素激活了前炎症转录因子NF-kappa B，脂联素诱导的趋化因子不是通过参与代谢信号转导的脂联素受体介导的，提示一个新的受体可能参与了炎症效应。我们得出结论，脂联素可能具有促炎和抗炎作用，其在特定炎症性疾病中的确切作用仍有待研究。(C)2006 Elsevier Inc.保留所有权利。
Adiponectin is an adi pocyte- derived cytokine that p ays a ro e in metabo ic disorders such as obesity and diabetes mellitus. Recent work suggests that adiponectin may also affect the immune response, primarily acting as an anti-inflammatory factor. Given our observation that plasma and urine adiponectin levels are increased in SLE patients with inflammatory glomerutonephritis, we evaluated the effect of adiponectin on proinflammatory chemokines relevant to the pathogenesis of SLE nephritis. It was postulated that adiponectin would attenuate cytokine-induced chemokine expression. Cultured human microvascular endothelial cells and monocytes were treated with adiponectin, and IL-8 and MCP-1 levels were measured in the cell-culture supernatants by ELISA. Unexpectedly, full-length adiponectin significantly increased IL-8 and MCIP-1 production, and did not abrogate cytokine-induced chemokine expression. Furthermore, adiponectin activated the proinflammatory transcription factor NF-kappa B. Chemokine induction by adiponectin was not mediated by the well-characterized adiponectin receptors involved in metabolic signaling, suggesting a novel receptor may be responsible for the inflammatory effect. We conclude that adiponectin may have pro- and anti-inflammatory effects, and its exact role in specific inflammatory diseases remains to be worked out. (c) 2006 Elsevier Inc. All rights reserved.