Cruz-Almeida Yenisel, King Christopher D, Wallet Shannon M, Riley Joseph L
Pain Research and Intervention Center of Excellence, University of Florida, P.O. Box 103628, Gainesville, FL 32610-3628, USA ; Department of Community Dentistry and Behavioral Science, College of Dentistry, University of Florida, P.O. Box 103628, Gainesville, FL 32610-3628, USA.
Pain Res Treat. 2012;2012:538739. doi: 10.1155/2012/538739. Epub 2012 Nov 20.
Few studies in healthy subjects have examined the neuroimmune responses associated with specific experimental pain stimuli, while none has measured multiple biomarkers simultaneously. The aim of the present study was to compare the neuro-immune responses following two common experimental pain stimuli: cold pressor test (CPT) and focal heat pain (FHP). Eight adults participated in two counterbalanced experimental sessions of FHP or CPT with continuous pain ratings and blood sampling before and 30 minutes after the sessions. Despite similar pain intensity ratings (FHP = 42.2 ± 15.3; CPT = 44.5 ± 34.1; P = 0.871), CPT and FHP induced different neuro-immune biomarker responses. CPT was accompanied by significant increases in cortisol (P = 0.046) and anti-inflammatory cytokine IL-10 (P = 0.043) with significant decreases in several pro-inflammatory mediators (IL-1β (P = 0.028), IL-12 (P = 0.012), TNF-α (P = 0.039), and MCP-1 (P = 0.038)). There were nonsignificant biomarker changes during the FHP session. There were close to significant differences between the sessions for IL-1β (P = 0.081), IFN-γ (P = 0.072), and IL-12 (P = 0.053) with biomarkers decreasing after CPT and increasing after FHP. There were stronger associations between catastrophizing and most biomarkers after CPT compared to FHP. Our results suggest that CPT is a stressful and painful stimulus, while FHP is mostly a painful stimulus. Thus, each experimental pain stimulus can activate different neuro-immune cascades, which are likely relevant for the interpretation of studies in chronic pain conditions.
在健康受试者中,很少有研究考察与特定实验性疼痛刺激相关的神经免疫反应,同时也没有研究同时测量多种生物标志物。本研究的目的是比较两种常见实验性疼痛刺激后的神经免疫反应:冷加压试验(CPT)和局部热痛(FHP)。八名成年人参加了FHP或CPT的两个平衡实验环节,在实验前和实验后30分钟进行持续疼痛评分和血液采样。尽管疼痛强度评分相似(FHP = 42.2±15.3;CPT = 44.5±34.1;P = 0.871),但CPT和FHP诱导了不同的神经免疫生物标志物反应。CPT伴随着皮质醇(P = 0.046)和抗炎细胞因子IL-10(P = 0.043)的显著增加,同时几种促炎介质显著减少(IL-1β(P = 0.028)、IL-12(P = 0.012)、TNF-α(P = 0.039)和MCP-1(P = 0.038))。在FHP环节中,生物标志物变化不显著。IL-1β(P = 0.081)、IFN-γ(P = 0.072)和IL-12(P = 0.053)在两个环节之间接近显著差异,生物标志物在CPT后下降,在FHP后上升。与FHP相比,CPT后灾难化与大多数生物标志物之间的关联更强。我们的结果表明,CPT是一种有压力的疼痛刺激,而FHP主要是一种疼痛刺激。因此,每种实验性疼痛刺激都可以激活不同的神经免疫级联反应,这可能与慢性疼痛状况研究的解释相关。