Neutrophils infiltrate sensory ganglia and mediate chronic widespread pain in fibromyalgia

Fibromyalgia is a debilitating widespread chronic pain syndrome that occurs in 2 to 4% of the population. The prevailing view that fibromyalgia results from central nervous system dysfunction has recently been challenged with data showing changes in peripheral nervous system activity. Using a mouse...

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Published inProceedings of the National Academy of Sciences - PNAS Vol. 120; no. 17; p. e2211631120
Main Authors Caxaria, Sara, Bharde, Sabah, Fuller, Alice M, Evans, Romy, Thomas, Bethan, Celik, Petek, Dell'Accio, Francesco, Yona, Simon, Gilroy, Derek, Voisin, Mathieu-Benoit, Wood, John N, Sikandar, Shafaq
Format Journal Article
LanguageEnglish
Published United States National Academy of Sciences 25.04.2023
Subjects
Adoptive transfer
Biological Sciences
Central nervous system
Chronic Pain
Fibromyalgia
Ganglia
Ganglia, Sensory
Humans
Hyperalgesia
Hypersensitivity
Leukocytes (neutrophilic)
Lymphocytes
Monocytes
Neutrophils
Pain
Peripheral nerves
Peripheral nervous system
Priming
Sensory neurons
neuroimmune
pain
fibromyalgia
neutrophils
dorsal root ganglia
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Summary:Fibromyalgia is a debilitating widespread chronic pain syndrome that occurs in 2 to 4% of the population. The prevailing view that fibromyalgia results from central nervous system dysfunction has recently been challenged with data showing changes in peripheral nervous system activity. Using a mouse model of chronic widespread pain through hyperalgesic priming of muscle, we show that neutrophils invade sensory ganglia and confer mechanical hypersensitivity on recipient mice, while adoptive transfer of immunoglobulin, serum, lymphocytes, or monocytes has no effect on pain behavior. Neutrophil depletion abolishes the establishment of chronic widespread pain in mice. Neutrophils from patients with fibromyalgia also confer pain on mice. A link between neutrophil-derived mediators and peripheral nerve sensitization is already established. Our observations suggest approaches for targeting fibromyalgia pain via mechanisms that cause altered neutrophil activity and interactions with sensory neurons.
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Edited by Allan Basbaum, University of California San Francisco, San Francisco, CA; received July 7, 2022; accepted February 5, 2023
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.2211631120