Adiponectin differentially regulates cytokines in porcine macrophages
Adiponectin differentially regulates cytokines in porcine macrophages
复制标题
DOI：
10.1016/j.bbrc.2004.02.130
复制
发表时间：
2004-04-09
影响因子：
3.1
通讯作者：
Spurlock, ME
中科院分区：
文献类型：
--
作者：
Wulster-Radcliffe, MC;Ajuwon, KM;Spurlock, ME
脂联素是一种脂肪细胞衍生的激素，可减弱活化的人巨噬细胞产生TNF α。在本研究中，我们使用猪血液来源的巨噬细胞来测试的假设，即脂联素的抗炎作用包括抑制IL 6和诱导IL 10。脂联素抑制脂多糖激活的巨噬细胞产生TNF α和IL 6（P < 0.01）。脂联素可增加IL 10的表达（P < 0.05），并增强脂多糖（LPS）对IL 10的诱导作用（P < 0.05）。从机制上讲，脂联素对促炎细胞因子产生的减弱与NF κ B向细胞核转运的减弱有关。脂联素或U 0126抑制ERK 1/2均能抑制LPS诱导的IL 6产生（P < 0.05），但脂联素与ERK 1/2抑制剂联用不能进一步抑制IL 6的产生。而脂联素和p38 MAPK抑制剂SB 203580的抑制作用是相加的（P < 0.05）。这些数据表明，脂联素的抗炎作用包括抑制IL 6和诱导IL 10。此外，我们提供的证据表明，脂联素的一些抗炎作用部分是通过抑制NF κ B信号和ERK 1/2活性介导的。(C)2004年爱思唯尔公司All rights reserved.
Adiponectin, an adipocyte-derived hormone, attenuates the production of TNFalpha by activated human macrophages. In the present study, we used porcine blood-derived macrophages to test the hypothesis that the anti-inflammatory action of adiponectin includes suppression of IL6 and an induction of IL10. Adiponectin suppressed both TNTalpha and IL6 production in macrophages activated with lipopolysaccharide (P < 0.01). In contrast, adiponectin increased IL10 expression (P < 0.05) and augmented (P < 0.05) the induction of this cytokine by lipopolysaccharide (LPS). Mechanistically, the attenuation of proinflammatory cytokine production by adiponectin was associated with an attenuation of the translocation of NFkappaB to the nucleus. Either adiponectin or inhibition of ERK1/2 with U0126 diminished the induction of IL6 by LPS (P < 0.05), but the combination of adiponectin and the inhibitor did not further reduce IL6 production. In contrast, the inhibitory actions of adiponectin and a p38 MAPK inhibitor (SB203580) were additive (P < 0.05). These data indicate that the anti-inflammatory actions of adiponectin include suppression of IL6 and induction of ILIO. In addition, we provide evidence that some of the anti-inflammatory actions of adiponectin are mediated in part by suppression of NFkappaB signaling and ERK1/2 activity. (C) 2004 Elsevier Inc. All rights reserved.