Division of Rheumatology, Department of Internal Medicine, School of Medicine, Catholic University of Korea, Seoul St Mary's Hospital.
Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea and.
Rheumatology (Oxford). 2016 Jan;55(1):156-61. doi: 10.1093/rheumatology/kev316. Epub 2015 Aug 28.
Triggering receptor expressed on myeloid cells 1 (TREM-1), which amplifies the inflammation elicited by the Toll-like receptor pathway, was originally implicated in sepsis and bacterial infection. However, it has been suggested that TREM-1 may also play an important role in non-infectious inflammation. The present study was conducted to investigate whether TREM-1 is involved in human acute gouty inflammation.
A total of 37 gout patients were recruited between March 2011 and January 2014 from Seoul St Mary's Hospital. The expression of TREM-1 on mononuclear cells was assessed using FACS analysis, immunostaining and real-time RT-PCR. To block the TREM-1 signal, soluble TREM-1 (sTREM-1) or the synthetic blocking peptide LP17 was used. The concentration of sTREM-1 was assessed by ELISA.
FACS analysis and real-time RT-PCR demonstrated that TREM-1 expression was higher in the SF mononuclear cells of acute gouty arthritis patients than in peripheral blood mononuclear cells (PBMCs). Immunohistochemical staining of tophi tissues revealed TREM-1 expression, with confocal microscopy demonstrating TREM-1 expression on tophi tissue macrophages. We also demonstrated that MSU treatment induced TREM-1 expression on the PBMCs of acute gout patients in vitro. Although blockade of TREM-1 did not directly suppress MSU-induced IL-1β production of PBMCs in vitro, the concentration of soluble TREM-1 was higher in the SF of gout vs OA patients and was positively correlated with serum CRP.
TREM-1 is induced by MSU and is associated with the inflammation of human acute gouty arthritis.
髓系细胞触发受体 1（TREM-1）可放大 Toll 样受体途径引发的炎症反应，最初与脓毒症和细菌感染有关。然而，有人认为 TREM-1 也可能在非传染性炎症中发挥重要作用。本研究旨在探讨 TREM-1 是否参与人类急性痛风性炎症。
2011 年 3 月至 2014 年 1 月期间，共招募 37 例痛风患者，均来自首尔圣玛丽医院。采用流式细胞术分析、免疫组化和实时 RT-PCR 检测单核细胞中 TREM-1 的表达。通过使用可溶性 TREM-1（sTREM-1）或合成阻断肽 LP17 阻断 TREM-1 信号。通过 ELISA 评估 sTREM-1 的浓度。
流式细胞术分析和实时 RT-PCR 表明，急性痛风性关节炎患者关节滑液单核细胞中 TREM-1 的表达高于外周血单核细胞（PBMCs）。对痛风石组织进行免疫组织化学染色显示 TREM-1 表达，共聚焦显微镜显示痛风石组织巨噬细胞中存在 TREM-1 表达。我们还证明了 MSU 在体外诱导急性痛风患者 PBMCs 表达 TREM-1。尽管体外阻断 TREM-1 不能直接抑制 MSU 诱导的 PBMCs 产生 IL-1β，但痛风患者关节滑液中的可溶性 TREM-1 浓度高于骨关节炎患者，且与血清 CRP 呈正相关。
MSU 诱导 TREM-1 的表达，并与人类急性痛风性关节炎的炎症有关。
