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首页> 外文期刊>Life sciences >Dextran sulfate sodium enhances interleukin-1 beta release via activation of p38 MAPK and ERK1/2 pathways in murine peritoneal macrophages
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Dextran sulfate sodium enhances interleukin-1 beta release via activation of p38 MAPK and ERK1/2 pathways in murine peritoneal macrophages

机译：硫酸右旋糖酐钠通过激活小鼠腹膜巨噬细胞中的p38 MAPK和ERK1 / 2途径增强白介素1β的释放

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摘要

Interleukin (IL)-1 beta is a pro-inflammatory cytokine that has been shown to play a pivotal role in the onset of inflammatory bowel disease (IBD), however, the molecular mechanisms underlying the production of IL-1 beta in IBD are not fully understood. We investigated dextran sulfate sodium (DSS)-induced IL-1 beta production and caspase-1 activities in murine peritoneal macrophages (pMempty set). Further, the activation status of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase 1/2 (ERK1/2), and c-Jun NH2-terminal kinase (JNK1/2), as well as their upstream target kinases, were examined by Western blotting. In addition, mRNA expression was assessed by RT-PCR and CXC chemokine ligand 16 (CXCL16) protein was detected by immunocytochemistry. DSS-treated pMempty set released IL-1 beta protein in a time-dependent manner without affecting mRNA levels during 3-24 h, and caspase-1 activity peaked at 5 min (29-fold). IL-1 beta release and caspase-1 activity induced by DSS were significantly inhibited by a MAPK kinase 1/2 inhibitor, a p38 MAPK inhibitor, and NAC, however, not by JNK1/2 or a protein kinase C inhibitor. In addition, DSS strikingly induced the phosphorylation of p38 MAPK and ERK1/2 within 2 and 10 min, respectively. DSS also induced intracellular generation of reactive oxygen species (ROS). Pre-treatment with anti-CXCL16 for 24 h, but not anti-scavenger receptor-A, anti-CD36, or anti-CD68 antibodies, significantly suppressed DSS-induced IL-1 beta production. Our results suggest that DSS triggers the release of IL-1 beta protein from murine pMempty set at a post-translational level through binding with CXCL16, ROS generation, and resultant activation of both p38 MAPK and ERK1/2 pathways, and finally caspase-1 activation. (c) 2007 Elsevier Inc. All rights reserved.
机译：白介素（IL）-1β是一种促炎性细胞因子，已被证明在炎症性肠病（IBD）发作中起关键作用，但是，IBD中IL-1β产生的分子机制尚不明确。完全了解。我们调查了小鼠腹膜巨噬细胞（pMempty集）中的葡聚糖硫酸钠（DSS）诱导的IL-1β产生和caspase-1活性。此外，p38丝裂原活化蛋白激酶（MAPK），细胞外信号调节激酶1/2（ERK1 / 2）和c-Jun NH2-末端激酶（JNK1 / 2）的激活状态及其上游靶标通过蛋白质印迹检查激酶。另外，通过RT-PCR评估mRNA表达，并通过免疫细胞化学检测CXC趋化因子配体16（CXCL16）蛋白。经DSS处理的pMempty集以时间依赖性方式释放IL-1β蛋白，而在3-24小时内不影响mRNA水平，并且caspase-1活性在5分钟达到峰值（29倍）。 MAPK激酶1/2抑制剂，p38 MAPK抑制剂和NAC显着抑制了DSS诱导的IL-1β释放和caspase-1活性，但是JNK1 / 2或蛋白激酶C抑制剂则没有。此外，DSS分别在2分钟和10分钟内惊人地诱导了p38 MAPK和ERK1 / 2的磷酸化。 DSS还诱导细胞内产生活性氧（ROS）。用抗CXCL16预处理24小时，但不使用抗清道夫受体A，抗CD36或抗CD68抗体进行预处理，可以显着抑制DSS诱导的IL-1β产生。我们的研究结果表明，DSS通过与CXCL16结合，ROS产生以及p38 MAPK和ERK1 / 2途径以及最终caspase-1的激活，触发了小鼠pMempty在翻译后水平上释放IL-1β蛋白。激活。 （c）2007 Elsevier Inc.保留所有权利。

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