Fibromyalgia patients with elevated levels of anti–satellite glia cell immunoglobulin G antibodies present with more severe symptoms

Author:

Krock Emerson1ORCID,Morado-Urbina Carlos E.1,Menezes Joana1,Hunt Matthew A.1,Sandström Angelica2,Kadetoff Diana2,Tour Jeanette2,Verma Vivek3,Kultima Kim4,Haglund Lisbet5,Meloto Carolina B.3,Diatchenko Luda3,Kosek Eva26,Svensson Camilla I.1ORCID

Affiliation:

1. Department of Physiology and Pharmacology, Centre for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden

2. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Sandström is now with the Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School and Department of Radiology, Massachusetts General Hospital, Boston, MA, United States. Tour is now with the Oncology Surgery Department, Blekinge Hospital, Karlskrona, Sweden

3. Faculty of Dental Medicine and Oral Health Sciences, Department of Anesthesia, Faculty of Medicine and Health Sciences, Alan Edwards Centre for Research on Pain, McGill University, Montreal, QC, Canada

4. Department of Medical Sciences, Uppsala University, Uppsala, Sweden

5. Division of Orthopaedic Surgery, Department of Surgery, McGill University, Montreal, QC, Canada

6. Department of Surgical Sciences, Uppsala University, Uppsala, Sweden

Abstract

Abstract Transferring fibromyalgia patient immunoglobulin G (IgG) to mice induces pain-like behaviour, and fibromyalgia IgG binds mouse and human satellite glia cells (SGCs). These findings suggest that autoantibodies could be part of fibromyalgia pathology. However, it is unknown how frequently fibromyalgia patients have anti-SGC antibodies and how anti-SGC antibodies associate with disease severity. Here, we quantified serum or plasma anti-SGC IgG levels in 2 fibromyalgia cohorts from Sweden and Canada using an indirect immunofluorescence murine cell culture assay. Fibromyalgia serum IgG binding to human SGCs in human dorsal root ganglia tissue sections was also assessed by immunofluorescence. In the cell culture assay, anti-SGC IgG levels were increased in both fibromyalgia cohorts compared with control group. Elevated anti-SGC IgG was associated with higher levels of self-reported pain in both cohorts, and higher fibromyalgia impact questionnaire scores and increased pressure sensitivity in the Swedish cohort. Anti-SGC IgG levels were not associated with fibromyalgia duration. Swedish fibromyalgia (FM) patients were clustered into FM-severe and FM-mild groups, and the FM-severe group had elevated anti-SGC IgG compared with the FM-mild group and control group. Anti-SGC IgG levels detected in culture positively correlated with increased binding to human SGCs. Moreover, the FM-severe group had elevated IgG binding to human SGCs compared with the FM-mild and control groups. These results demonstrate that a subset of fibromyalgia patients have elevated levels of anti-SGC antibodies, and the antibodies are associated with more severe fibromyalgia symptoms. Screening fibromyalgia patients for anti-SGC antibodies could provide a path to personalized treatment options that target autoantibodies and autoantibody production.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Anesthesiology and Pain Medicine,Neurology (clinical),Neurology

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