Grimsholm Ola, Rantapää-Dahlqvist Solbritt, Dalén Tore, Forsgren Sture
Department of Integrative Medical Biology, Section for Anatomy, Umeå University, Umeå, Sweden.
Clin Rheumatol. 2008 Oct;27(10):1289-97. doi: 10.1007/s10067-008-0910-4. Epub 2008 May 17.
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 TNFalpha. 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.
脑源性神经营养因子(BDNF)在类风湿关节炎(RA)中的作用在很大程度上尚不清楚。研究了BDNF及其相关受体TrkB和p75在RA患者滑膜组织中的分布,并与骨关节炎(OA)患者进行对比。此外,还测量了滑膜组织和滑液中BDNF的水平。此外,分析了抗肿瘤坏死因子(抗TNF;英夫利昔单抗)治疗对RA患者血浆中BDNF水平的影响。滑膜中的细胞显示出BDNF免疫反应性,在神经束的神经纤维以及与感觉小体相关的部位可见BDNF、p75和TrkB受体免疫反应。滑膜组织中BDNF的水平与显微镜下观察到的炎症细胞数量或TNFα水平无关。滑液中BDNF的水平也与红细胞沉降率(ESR)或白细胞计数无关。抗TNF治疗在开始抗TNF治疗14周后,即最后一次输注8周后,导致血浆中BDNF水平下降。与健康个体相比,RA患者在基线时观察到更高水平的BDNF。然而,接受抗TNF治疗的患者血浆中BDNF的水平与ESR或疾病活动评分的变化无关。这项研究的临床意义在于,抗TNF治疗会影响血浆中BDNF的水平,尽管没有证据表明在接受英夫利昔单抗治疗或未接受英夫利昔单抗治疗的RA患者中,BDNF水平与炎症参数相关。相反,包括神经结构在内的炎症细胞以外的其他来源可能是BDNF的重要来源,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神经元的影响有关。