High intestinal and systemic levels of decoy receptor 3 (DcR3) and its ligand TL1A in active ulcerative colitis
High intestinal and systemic levels of decoy receptor 3 (DcR3) and its ligand TL1A in active ulcerative colitis
复制标题
DOI：
10.1016/j.clim.2010.07.001
复制
发表时间：
2010-11-01
影响因子：
8.6
通讯作者：
Ladas, Spiros D.
中科院分区：
文献类型：
--
作者：
Bamias, Giorgos;Kaltsa, Garyfallia;Ladas, Spiros D.
诱饵受体-3 （DcR3）是TNF受体超家族蛋白的一员，通过与TL1A、LIGHT和Fas-L结合，参与抗凋亡和抗炎途径。TL1A/DcR3配体/受体对在溃疡性结肠炎（UC）中的作用尚未研究。我们研究了64名UC患者和56名健康对照者的全身（外周血）和局部（大肠）DcR3和TL1A的表达。活动性UC患者的DcR3血清浓度高（与健康对照组相比P < 0.0001）。这种升高显然与肠道炎症的存在有关，因为在缓解期患者中观察到的肠道炎症较少（P=0.003与活动性UC相比），而有效治疗导致血清DcR3消失或显着降低（P=0.006与治疗前相比）。此外，DcR3 mRNA转录物在结肠炎症区域显著升高（P=0.002与未受影响的同一患者相比）。除了DcR3升高外，我们还发现与健康对照相比，活动性或非活动性UC患者的TL1A循环水平升高（两者均P < 0.001）。我们得出结论，血清DcR3升高可能是UC患者活动性结肠炎症的一个指标。TL1A/ dcr3介导的通路可能参与UC的发病机制。(C) 2010爱思唯尔公司版权所有。
Decoy receptor-3 (DcR3) is a member of the TNF receptor superfamily of proteins, which has been implicated in anti-apoptotic and anti-inflammatory pathways, via binding to TL1A, LIGHT and Fas-L. The role of the TL1A/DcR3 ligand/receptor pair in ulcerative colitis (UC) has not been studied. We investigated the systemic (peripheral blood) and local (large intestine) expression of DcR3 and TL1A in 64 patients with UC and 56 healthy controls. DcR3 serum concentrations were highly elevated in patients with active UC (P < 0.0001 vs. healthy controls). This elevation was clearly related to the presence of intestinal inflammation as it was less frequently observed in patients in remission (P=0.003 vs. active UC) whereas effective treatment resulted in disappearance or significant decrease of serum DcR3 (P=0.006 vs. pre-treatment). Furthermore, DcR3 mRNA transcripts were significantly elevated in inflamed areas of the colon (P=0.002 vs. non-affected of the same patient). In addition to DcR3 elevation, we found increased circulating levels of TL1A in patients with either active or inactive UC in comparison to healthy controls (P < 0.001 for both). We conclude that elevated serum DcR3 may serve as an indicator of active colonic inflammation in patients with UC. TL1A/DcR3-mediated pathways may participate in the pathogenesis of UC. (C) 2010 Elsevier Inc. All rights reserved.