Evidence of both systemic inflammation and neuroinflammation in fibromyalgia patients, as assessed by a multiplex protein panel applied to the cerebrospinal fluid and to plasma.
Evidence of both systemic inflammation and neuroinflammation in fibromyalgia patients, as assessed by a multiplex protein panel applied to the cerebrospinal fluid and to plasma.
复制标题
DOI：
10.2147/jpr.s128508
复制
发表时间：
2017
影响因子：
2.7
通讯作者：
Gordh T
中科院分区：
文献类型：
--
作者：
Bäckryd E;Tanum L;Lind AL;Larsson A;Gordh T
除了中枢过度兴奋和自上而下调节受损之外，慢性炎症可能在纤维肌痛（FM）的病理生理学中发挥作用。事实上，根据涉及不同体液中细胞因子和其他炎症相关蛋白分析的动物实验和人体研究，神经炎症机制被认为是许多慢性疼痛病症病理生理学的核心。然而，关于 FM，之前的人血浆/血清和/或脑脊液 (CSF) 细胞因子研究仅关注了一些预先确定的候选细胞因子。我们不是一次只分析几种物质，而是使用了一种新的多重蛋白质面板，可以同时分析 92 种炎症相关蛋白质。因此，我们研究了 40 名 FM 患者的脑脊液和血浆炎症特征，并与健康对照 (n=10) 的脑脊液和献血者对照 (n=46) 的血浆进行比较。通过投影进行多变量数据分析，我们发现了神经炎症（在脑脊液中评估）和慢性全身炎症（在血浆中评估）的证据。两组蛋白质（一组用于脑脊液，一组用于血浆）在患者和对照之间具有高度区分性。值得注意的是，我们发现高水平的脑脊液趋化因子 CX3CL1（也称为 fractalkine）。此外，之前有关 FM 中 IL-8 的研究结果在 CSF 和血浆中得到了重复。这是首次描述 FM 患者的如此广泛的炎症特征。因此，FM 的特征似乎是客观的生化改变，而将其机制本质上视为特发性甚至心因性的挥之不去的特征应该被视为绝对过时的。
In addition to central hyperexcitability and impaired top–down modulation, chronic inflammation probably plays a role in the pathophysiology of fibromyalgia (FM). Indeed, on the basis of both animal experiments and human studies involving the analysis of cytokines and other inflammation-related proteins in different body fluids, neuroinflammatory mechanisms are considered to be central to the pathophysiology of many chronic pain conditions. However, concerning FM, previous human plasma/serum and/or cerebrospinal fluid (CSF) cytokine studies have looked only at a few predetermined cytokine candidates. Instead of analyzing only a few substances at a time, we used a new multiplex protein panel enabling simultaneous analysis of 92 inflammation-related proteins. Hence, we investigated the CSF and plasma inflammatory profiles of 40 FM patients compared with CSF from healthy controls (n=10) and plasma from blood donor controls (n=46). Using multivariate data analysis by projection, we found evidence of both neuroinflammation (as assessed in CSF) and chronic systemic inflammation (as assessed in plasma). Two groups of proteins (one for CSF and one for plasma) highly discriminating between patients and controls are presented. Notably, we found high levels of CSF chemokine CX3CL1 (also known as fractalkine). In addition, previous findings concerning IL-8 in FM were replicated, in both CSF and plasma. This is the first time that such an extensive inflammatory profile has been described for FM patients. Hence, FM seems to be characterized by objective biochemical alterations, and the lingering characterization of its mechanisms as essentially idiopathic or even psychogenic should be seen as definitively outdated.