Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Department of Psychosomatic Medicine, Kyushu University Hospital, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Sci Rep. 2017 Sep 19;7(1):11882. doi: 10.1038/s41598-017-11506-4.
Fibromyalgia is a refractory disease characterized by chronic intractable pain and psychological suffering, the cause of which has not yet been elucidated due to its complex pathology. Activation of immune cells in the brain called microglia has attracted attention as a potential underlying pathological mechanism in chronic pain. Until recently, however, technological and ethical considerations have limited the ability to conduct research using human microglia. To overcome this limitation, we have recently developed a technique to create human-induced microglia-like (iMG) cells from human peripheral blood monocytes. In this study, we created the iMG cells from 14 patients with fibromyalgia and 10 healthy individuals, and compared the activation of iMG cells between two groups at the cellular level. The expression of tumor necrosis factor (TNF)-α at mRNA and protein levels significantly increased in ATP-stimulated iMG cells from patients with fibromyalgia compared to cells from healthy individuals. Interestingly, there was a moderate correlation between ATP-induced upregulation of TNF-α expression and clinical parameters of subjective pain and other mental manifestations of fibromyalgia. These findings suggest that microglia in patients with fibromyalgia are hypersensitive to ATP. TNF-α from microglia may be a key factor underlying the complex pathology of fibromyalgia.
纤维肌痛是一种难治性疾病,其特征为慢性难治性疼痛和心理痛苦,由于其复杂的病理学,其病因尚未阐明。大脑中被称为小胶质细胞的免疫细胞的激活已引起人们的关注,作为慢性疼痛的潜在潜在病理机制。然而,直到最近,技术和道德方面的考虑限制了使用人类小胶质细胞进行研究的能力。为了克服这一限制,我们最近开发了一种从人外周血单核细胞中产生人类诱导的小胶质细胞样(iMG)细胞的技术。在这项研究中,我们从 14 名纤维肌痛患者和 10 名健康个体中创建了 iMG 细胞,并在细胞水平上比较了两组 iMG 细胞的激活情况。与健康个体的细胞相比,纤维肌痛患者的 ATP 刺激的 iMG 细胞中肿瘤坏死因子(TNF)-α的 mRNA 和蛋白水平的表达显着增加。有趣的是,ATP 诱导的 TNF-α表达上调与纤维肌痛的主观疼痛和其他精神表现的临床参数之间存在中度相关性。这些发现表明,纤维肌痛患者的小胶质细胞对 ATP 敏感。来自小胶质细胞的 TNF-α可能是纤维肌痛复杂病理学的关键因素。