Tsilioni Irene, Russell Irwin J, Stewart Julia M, Gleason Rae M, Theoharides Theoharis C
Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine (I.T., J.M.S., T.C.T.); Department of Internal Medicine, Department of Psychiatry, and Sackler School of Graduate Biomedical Sciences, Tufts University, and Tufts Medical Center, Boston, Massachusetts (T.C.T.); Fibromyalgia Research and Consulting, Arthritis and Osteoporosis Center of South Texas, San Antonio, Texas (I.J.R.); National Fibromyalgia and Chronic Pain Association, Logan, Utah (R.M.G.).
Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine (I.T., J.M.S., T.C.T.); Department of Internal Medicine, Department of Psychiatry, and Sackler School of Graduate Biomedical Sciences, Tufts University, and Tufts Medical Center, Boston, Massachusetts (T.C.T.); Fibromyalgia Research and Consulting, Arthritis and Osteoporosis Center of South Texas, San Antonio, Texas (I.J.R.); National Fibromyalgia and Chronic Pain Association, Logan, Utah (R.M.G.)
J Pharmacol Exp Ther. 2016 Mar;356(3):664-72. doi: 10.1124/jpet.115.230060. Epub 2016 Jan 13.
Fibromyalgia syndrome (FMS) is a chronic, idiopathic condition of widespread musculoskeletal pain affecting more women than men. Even though clinical studies have provided evidence of altered central pain pathways, the lack of definitive pathogenesis or reliable objective markers has hampered development of effective treatments. Here we report that the neuropeptides corticotropin-releasing hormone (CRH), substance P (SP), and SP-structurally-related hemokinin-1 (HK-1) were significantly (P = 0.026, P < 0.0001, and P = 0.002, respectively) elevated (0.82 ± 0.57 ng/ml, 0.39 ± 0.18 ng/ml, and 7.98 ± 3.12 ng/ml, respectively) in the serum of patients with FMS compared with healthy controls (0.49 ± 0.26 ng/ml, 0.12 ± 0.1 ng/ml, and 5.71 ± 1.08 ng/ml, respectively). Moreover, SP and HK-1 levels were positively correlated (Pearson r = 0.45, P = 0.002) in FMS. The serum concentrations of the inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF) were also significantly (P = 0.029 and P = 0.006, respectively) higher (2.97 ± 2.35 pg/ml and 0.92 ± 0.31 pg/ml, respectively) in the FMS group compared with healthy subjects (1.79 ± 0.62 pg/ml and 0.69 ± 0.16 pg/ml, respectively). In contrast, serum IL-31 and IL-33 levels were significantly lower (P = 0.0001 and P = 0.044, respectively) in the FMS patients (849.5 ± 1005 pg/ml and 923.2 ± 1284 pg/ml, respectively) in comparison with healthy controls (1281 ± 806.4 pg/ml and 3149 ± 4073 pg/ml, respectively). FMS serum levels of neurotensin were not different from controls. We had previously shown that CRH and SP stimulate IL-6 and TNF release from mast cells (MCs). Our current results indicate that neuropeptides could stimulate MCs to secrete inflammatory cytokines that contribute importantly to the symptoms of FMS. Treatment directed at preventing the secretion or antagonizing these elevated neuroimmune markers, both centrally and peripherally, may prove to be useful in the management of FMS.
纤维肌痛综合征(FMS)是一种慢性、特发性的广泛性肌肉骨骼疼痛疾病,女性患者多于男性。尽管临床研究已提供中枢性疼痛通路改变的证据,但缺乏明确的发病机制或可靠的客观标志物阻碍了有效治疗方法的开发。在此我们报告,与健康对照组(分别为0.49±0.26 ng/ml、0.12±0.1 ng/ml和5.71±1.08 ng/ml)相比,FMS患者血清中的神经肽促肾上腺皮质激素释放激素(CRH)、P物质(SP)以及与SP结构相关的Hemokinin-1(HK-1)显著升高(分别为P = 0.026、P < 0.0001和P = 0.002,血清浓度分别为0.82±0.57 ng/ml、0.39±0.18 ng/ml和7.98±3.12 ng/ml)。此外,在FMS患者中,SP和HK-1水平呈正相关(Pearson相关系数r = 0.45,P = 0.002)。FMS组炎症细胞因子白细胞介素(IL)-6和肿瘤坏死因子(TNF)的血清浓度也显著高于健康受试者(分别为P = 0.029和P = 0.006,血清浓度分别为2.97±2.35 pg/ml和0.92±0.31 pg/ml)(健康受试者分别为1.79±0.62 pg/ml和0.69±0.16 pg/ml)。相反,与健康对照组(分别为1281±806.4 pg/ml和3149±4073 pg/ml)相比,FMS患者血清IL-31和IL-33水平显著降低(分别为P = 0.0001和P = 0.044,血清浓度分别为849.5±1005 pg/ml和923.2±1284 pg/ml)。FMS患者血清中神经降压素水平与对照组无差异。我们之前已表明CRH和SP可刺激肥大细胞(MCs)释放IL-6和TNF。我们目前的结果表明,神经肽可刺激MCs分泌炎症细胞因子,这些细胞因子对FMS的症状起重要作用。针对在中枢和外周预防这些升高的神经免疫标志物的分泌或拮抗其作用的治疗方法,可能被证明对FMS的管理有用。