BDNF in RA:: Downregulated in plasma following anti-TNF treatment but no correlation with inflammatory parameters
BDNF in RA:: Downregulated in plasma following anti-TNF treatment but no correlation with inflammatory parameters
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DOI：
10.1007/s10067-008-0910-4
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发表时间：
2008-10-01
影响因子：
3.4
通讯作者：
Forsgren, Sture
中科院分区：
文献类型：
--
作者：
Grimsholm, Ola;Rantapaa-Dahlqvist, Solbritt;Forsgren, Sture
脑源性神经营养因子（BDNF）在类风湿关节炎（RA）中的作用尚不清楚。检测了类风湿关节炎（RA）患者滑膜组织中BDNF及其相关受体TrkB和p75的分布，并与骨关节炎（OA）患者进行对比。此外，测量了滑膜组织和滑液中BDNF的水平。此外，抗肿瘤坏死因子（抗TNF;英夫利西单抗）治疗对RA患者血浆中BDNF水平的影响进行了分析。滑膜细胞呈BDNF免疫反应性，BDNF、p75和TrkB受体免疫反应见于神经束的神经纤维和感觉小体。滑膜组织中的BDNF水平与显微镜下观察到的炎性细胞数量或TNF α水平无关。滑液中的BDNF水平也与红细胞沉降率（ESR）或白色血细胞计数无关。抗TNF治疗导致抗TNF治疗开始后14周BDNF血浆水平降低，即，末次输注后8周。与健康个体相比，RA患者基线时观察到更高水平的BDNF。然而，抗TNF治疗患者血浆中BDNF水平与ESR或疾病活动评分的变化无关。本研究的临床意义在于抗TNF治疗影响血浆BDNF水平，尽管没有证据表明BDNF水平与接受英夫利昔单抗治疗或未接受英夫利昔单抗治疗的RA患者的炎症参数相关。相反，可能的是，除了炎性细胞以外的来源，包括神经结构，是BDNF的重要来源，并且抗TNF治疗对BDNF水平的影响可能与对循环和各种局部细胞和/或含BDNF的神经元的影响有关。
The involvement of brain-derived neurotrophic factor (BDNF) in rheumatoid arthritis (RA) is largely unknown. The distribution of BDNF and its associated receptors, TrkB and p75, in the synovial tissue of patients with RA was examined and contrasted with that in patients with osteoarthritis (OA). Additionally, levels of BDNF in both synovial tissue and synovial fluid were measured. Furthermore, the effects of anti-tumour necrosis factor (anti-TNF; infliximab) treatment on BDNF levels in the plasma of RA patients were analysed. Cells in the synovium showed immunoreactivity for BDNF and BDNF-, p75- and TrkB-receptor immunoreactions were seen in nerve fibres of nerve fascicles and in association with sensory corpuscles. The levels of BDNF in synovial tissue were not correlated with the number of inflammatory cells observed microscopically or with levels of TNF alpha. Nor did the BDNF levels in synovial fluid correlate with erythrocyte sedimentation rate (ESR) or white blood cell counts. Anti-TNF treatment lead to a decrease in plasma levels of BDNF 14 weeks after the initiation of anti-TNF therapy, i.e., 8 weeks after the last infusion. Higher levels of BDNF were observed in RA patients at baseline compared with those for healthy individuals. However, the levels of BDNF in plasma of patients treated with anti-TNF did not correlate with the changes in ESR or a disease activity score. The clinical significance of this study is that anti-TNF treatment influences plasma levels of BDNF although there was no evidence that BDNF levels correlate with inflammatory parameters in either infliximab-treated or non-infliximab-treated patients with RA. Instead it is likely that sources other than inflammatory cells, including nerve structures, are important sources of BDNF and that the effects of anti-TNF treatment on BDNF levels may be related to effects on circulating and various local cells and/or BDNF-containing neurons.