Neutrophils infiltrate sensory ganglia and mediate chronic widespread pain in fibromyalgia

Sara Caxaria, Sabah Bharde, Alice M. Fuller, Romy Evans, Bethan Thomas, Petek Celik, Francesco Dell’Accio, Simon Yona, Derek Gilroy, Mathieu Benoit Voisin, John N. Wood*, Shafaq Sikandar*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

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.

Original languageAmerican English
Article numbere2211631120
JournalProceedings of the National Academy of Sciences of the United States of America
Volume120
Issue number17
DOIs
StatePublished - 25 Apr 2023

Bibliographical note

Publisher Copyright:
Copyright © 2023 the Author(s). Published by PNAS.

Keywords

  • dorsal root ganglia
  • fibromyalgia
  • neuroimmune
  • neutrophils
  • pain

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