Puri Basant K, Preyer Rosemarie, Lee Gary S, Schwarzbach Armin
Faculty of Health and Wellbeing, University of Winchester, Winchester, UK.
Department of Immune Analytics, GenID, Strassberg, Germany.
CNS Neurol Disord Drug Targets. 2024;23(11):1392-1399. doi: 10.2174/0118715273274091231207101522.
The aetiology of fibromyalgia is unknown; its symptoms may be related to a T-lymphocyte-mediated response to infectious organisms.
First, to test the hypothesis that fibromyalgia is associated with increased interferon (IFN)-γ-secreting T-lymphocytes after stimulation with Anaplasmataceae-related major surface proteins (MSPs) and the macromolecular translocation type IV secretion system effector ankyrin repeat domain-containing protein A (AnkA). Second, to ascertain the relationship in fibromyalgia between (i) the IFN-γ-secreting T-lymphocyte response to stimulation with Anaplasmataceae-related MSPs and AnkA, and (ii) co-infection by and spp., and antinuclear antibodies.
Using a case-control design, patients fulfilling the American College of Rheumatology revised criteria for fibromyalgia, and controls, underwent the following blinded assessments: (i) enzyme- linked immune absorbent spot (ELISpot) IFN-γ release assay of T-lymphocyte reactivity to Anaplasmataceae-related MSPs and AnkA; (ii) ELISpot IFN-γ release assays of T-lymphocyte reactivity to three antigens, namely full antigen (B31); peptide mix (from sensu stricto, ); and lymphocyte function-associated antigen-1; (iii) immunoglobulin (Ig) A assay by enzyme-linked immunosorbent assay (ELISA) of antibodies to spp.; (iv) IgG (ELISA) antibodies to spp.; (v) serum antinuclear antibodies (immunofluorescence).
The groups were age- and sex-matched. The mean (standard error) value of IFN-γ release for the fibromyalgia group was 1.52 (0.26), compared with 1.00 (0.22) for the controls. Generalised linear modelling (p<0.001) of IFN-γ release in the fibromyalgia patients showed significant main effects of all three indices of infection and of antinuclear antibodies.
Anaplasmataceae may play an aetiological role in fibromyalgia.
纤维肌痛的病因尚不清楚；其症状可能与T淋巴细胞介导的对感染性生物体的反应有关。
第一，检验纤维肌痛与无形体科相关主要表面蛋白（MSP）和大分子易位IV型分泌系统效应蛋白含锚蛋白重复结构域蛋白A（AnkA）刺激后干扰素（IFN）-γ分泌性T淋巴细胞增加相关的假说。第二，确定纤维肌痛中（i）无形体科相关MSP和AnkA刺激下IFN-γ分泌性T淋巴细胞反应与（ii）伯氏疏螺旋体和伽氏疏螺旋体共同感染及抗核抗体之间的关系。
采用病例对照设计，符合美国风湿病学会修订的纤维肌痛标准的患者及对照进行以下盲法评估：（i）T淋巴细胞对无形体科相关MSP和AnkA反应性的酶联免疫斑点（ELISpot）IFN-γ释放试验；（ii）T淋巴细胞对三种伯氏疏螺旋体抗原反应性的ELISpot IFN-γ释放试验，即全抗原（B31）；肽混合物（来自狭义伯氏疏螺旋体）；以及伯氏疏螺旋体淋巴细胞功能相关抗原-1；（iii）通过酶联免疫吸附测定（ELISA）检测抗伯氏疏螺旋体属抗体的免疫球蛋白（Ig）A；（iv）抗伽氏疏螺旋体属IgG（ELISA）抗体；（v）血清抗核抗体（免疫荧光法）。
两组在年龄和性别上匹配。纤维肌痛组IFN-γ释放的平均（标准误）值为1.52（0.26），而对照组为1.00（0.22）。纤维肌痛患者IFN-γ释放的广义线性模型（p<0.001）显示，所有三种伯氏疏螺旋体感染指标和抗核抗体均有显著的主要效应。
无形体科可能在纤维肌痛的病因中起作用。
