Jansen Tim L, Berendsen Dianne, Crisan Tania O, Cleophas Maartje C P, Janssen Mirian C H, Joosten Leo A B
Department of Rheumatology, Radboud University Medical Centre, Geert Grooteplein Noord 8, 6525 GA, Nijmegen, The Netherlands,
Clin Rheumatol. 2014 Sep;33(9):1341-6. doi: 10.1007/s10067-014-2620-4. Epub 2014 Apr 24.
Monosodium urate (MSU) monohydrate crystals synergize with various toll-like receptor (TLR) ligands to induce interleukin-(IL)-1β production. Data are shown from a young male with mitochondriopathy in Kearns-Sayre syndrome (KSS) who developed gout and underwent urate-lowering therapy (ULT) versus a group of common gout patients. Peripheral blood mononuclear cells (PBMCs) are exposed in vitro to MSU crystals in the presence/absence of TLR2 ligands palmitic acid (C16:0) or palmitoyl-3-cysteine (Pam3Cys); proinflammatory cytokine production (IL-1β, IL-6, IL-8) is assessed by specific ELISA's. MSU crystals alone failed to induce IL-1beta, IL-6, or IL-8 in both the KSS patient and gout controls. A strong synergy between MSU crystals and C16:0 or Pam3Cys for induction of IL-1 beta/IL-6 is found in gout patients, but in gout with KSS, we found even more response than in control gout patients. Pam3Cys exposure reveals an enhanced response in cells originating from the KSS patient, indicating a high producer phenotype in response to TLR2 stimulation. During ULT, serum urate levels dropped in the KSS case. The hyperresponse of TLR2 may be secondary to the high serum urate concentration of 0.92 mmol/l that was initially found in circulation in vivo. Within a 6-month period, the serum urate concentration dropped, and the in vitro stimulation tests improved but did not fully normalize yet. The ex vivo cytokine production in gout patients is promising a novel gout test; PBMCs' responses in the mitochondriopathic gout patient is enhanced when compared with common gout patients, indicating a supersensitive gout patient profile. The non-inflammatory presentation in the KSS case with bulky gout is due to less inflammatory MSU crystals, i.e., specific crystal stereochemical/conformational properties. For developing gout attacks, the serum urate level and specific crystal properties both are of importance. Key Messages 1. Ex vivo cell tests are promising to serve as a novel gout lab test for screening purposes. 2. Ex vivo cellular responses are reduced following intraarticular glucocorticoid injection and/or urate-lowering therapy. 3. Crystal conformation properties play a role in the inflammatory in vivo and ex vivo response in gout. 4. A young male with Kearns-Sayre syndrome is described with less pronounced inflammatory PMBC responses to his own MSU crystals which explains the advanced stage of urate accumulation in this individual.
尿酸单钠(MSU)一水合物晶体与各种Toll样受体(TLR)配体协同作用,诱导白细胞介素-(IL)-1β的产生。数据展示了一名患有卡恩斯-塞尔综合征(KSS)线粒体病的年轻男性,他患了痛风并接受了降尿酸治疗(ULT),与一组普通痛风患者进行对比。外周血单个核细胞(PBMCs)在体外暴露于MSU晶体,同时存在/不存在TLR2配体棕榈酸(C16:0)或棕榈酰-3-半胱氨酸(Pam3Cys);通过特异性酶联免疫吸附测定(ELISA)评估促炎细胞因子的产生(IL-1β、IL-6、IL-8)。单独的MSU晶体在KSS患者和痛风对照组中均未能诱导IL-1β、IL-6或IL-8的产生。在痛风患者中发现MSU晶体与C16:0或Pam3Cys之间在诱导IL-1β/IL-6方面有很强的协同作用,但在患有KSS的痛风患者中,我们发现其反应比对照痛风患者更强。暴露于Pam3Cys显示来自KSS患者的细胞反应增强,表明对TLR2刺激有高产生者表型。在ULT期间,KSS病例的血清尿酸水平下降。TLR2的高反应性可能继发于最初在体内循环中发现的0.92 mmol/l的高血清尿酸浓度。在6个月内,血清尿酸浓度下降,体外刺激试验有所改善但尚未完全恢复正常。痛风患者的体外细胞因子产生有望成为一种新型痛风检测方法;与普通痛风患者相比,线粒体病性痛风患者的PBMCs反应增强,表明其为超敏痛风患者特征。KSS病例中伴有大量痛风的非炎症表现是由于炎症性较低的MSU晶体,即特定的晶体立体化学/构象特性。对于痛风发作的发生,血清尿酸水平和特定的晶体特性都很重要。关键信息:1. 体外细胞试验有望作为一种新型痛风实验室检测方法用于筛查。2. 关节内注射糖皮质激素和/或降尿酸治疗后,体外细胞反应降低。3. 晶体构象特性在痛风的体内和体外炎症反应中起作用。4. 描述了一名患有卡恩斯-塞尔综合征的年轻男性,其对自身MSU晶体的炎症性PBMC反应不明显,这解释了该个体尿酸积累的晚期阶段。