Passive transfer of fibromyalgia pain from patients to mice

Fibromyalgia syndrome (FMS) is a chronic pain condition characterized by widespread pain and tenderness. The etiology and pathophysiology of fibromyalgia are unknown and there are no effective treatments. Here we show that sensory hypersensitivity in FMS is caused by autoantibodies that act by sensi...

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Published inbioRxiv
Main Authors Goebel, Andreas, Gentry, Clive, Cuhadar, Ulku, Krock, Emerson, Vastani, Nisha, Sensi, Serena, Sandor, Katalin, Jurczak, Alexandra, Baharpoor, Azar, Brieskorn, Louisa, Carlos Morado Urbina, Sandstrom, Angelika, Tour, Janette, Kadetoff, Diana, Kosek, Eva, Bevan, Stuart, Svensson, Camilla, Andersson, David A
Format Paper
LanguageEnglish
Published Cold Spring Harbor Cold Spring Harbor Laboratory Press 24.07.2019
Subjects
Autoantibodies
Chronic pain
Dorsal root ganglia
Endothelial cells
Etiology
Fibromyalgia
Glial cells
Hypersensitivity
Immunoglobulin G
Macrophages
Mechanical stimuli
Pain
Pain perception
Sensory neurons
Skin
Spinal cord
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Summary:Fibromyalgia syndrome (FMS) is a chronic pain condition characterized by widespread pain and tenderness. The etiology and pathophysiology of fibromyalgia are unknown and there are no effective treatments. Here we show that sensory hypersensitivity in FMS is caused by autoantibodies that act by sensitizing nociceptive sensory neurons. Administration of IgG from FMS patients increased mouse pain sensitivities to stimulation with mechanical pressure and cold. In contrast, transfer of IgG depleted samples from FMS patients or IgG from healthy control subjects had no effect on pain sensitivity. Sensory nerve fibres in ex vivo skin-nerve preparations from mice treated with FMS IgG were hypersensitive to mechanical stimulation. Immunohistochemical analysis revealed that IgG from FMS patients specifically labeled satellite glial cells and myelinated fibre tracts, as well as a small number of macrophages and endothelial cells in mouse dorsal root ganglia but not skin, muscle, spinal cord and brain. Our results demonstrate that fibromyalgia pain is caused by IgG autoantibodies that sensitize peripheral nociceptive afferents neurons and suggest that therapies that reduce patient IgG titres may be effective treatments of fibromyalgia pain.
DOI:10.1101/713495