S100G expression and function in fibroblasts on colitis induction
S100G expression and function in fibroblasts on colitis induction
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DOI：
10.1016/j.intimp.2016.07.017
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发表时间：
2016-10-01
影响因子：
5.6
通讯作者：
Hirooka, Yoshiki
中科院分区：
文献类型：
--
作者：
Ishiguro, Kazuhiro;Watanabe, Osamu;Hirooka, Yoshiki
补充白介素10，一种重要的抗炎细胞因子，对炎症性肠病的疗效令人失望(180)。IL-10可能下调结肠炎诱导后其他抗炎介质的表达。我们使用了一种以半抗原蛋白可视化为特征的结肠炎模型，该模型指示了结肠炎诱导后半抗原蛋白形成的位置，用于组织学和基因表达分析。IL-10缺乏时，大鼠结肠炎后炎症改变减轻，S100G表达增加。S100G在成纤维细胞中表达，IL-10下调S100G的表达。S100G通过抑制核因子-kappaB的活化，抑制单核细胞趋化蛋白-1(MCP-1)的产生。因此，S100G，也被称为Calbindin-D9k，可能是结肠炎诱导后成纤维细胞中重要的抗炎介质，而S100G表达下调可能是补充IL-10效果不佳的原因之一。(C)2016爱思唯尔B.V.保留所有权利。
Supplementation with interleukin (IL)-10, an important anti-inflammatory cytokine, has shown disappointing efficacy for inflammatory bowel diseases (180). IL-10 may down-regulate the expression of other anti-inflammatory mediators following colitis induction. We used a colitis model characterized by hapten-protein visualization, which indicates the site of hapten-protein formation after colitis induction for histological and gene expression analyses. Under IL-10 deficiency, following colitis induction inflammatory changes were reduced, and S100G expression was elevated. S100G was expressed in fibroblasts, and S100G expression was down-regulated by IL-10. S100G suppressed the production of monocyte chemotactic protein-1 (MCP-1) through the inhibition of NF-kappa B activation. Therefore, S100G, also known as Calbindin-D9k, may be an important anti-inflammatory mediator in fibroblasts following colitis induction, and down-regulation of S100G expression might be one reason for the insufficient performance of IL-10 supplementation. (C) 2016 Elsevier B.V. All rights reserved.