@article{discovery10169224,
           month = {April},
          number = {17},
         journal = {Proceedings of the National Academy of Sciences of the United States of America},
            year = {2023},
           title = {Neutrophils infiltrate sensory ganglia and mediate chronic widespread pain in fibromyalgia},
       publisher = {Proceedings of the National Academy of Sciences},
            note = {Copyright {\copyright} 2023 the Author(s). Published by PNAS. This open access article is distributed under Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND).},
          volume = {120},
        keywords = {dorsal root ganglia, fibromyalgia, neuroimmune, neutrophils, pain, Humans, Chronic Pain, Fibromyalgia, Neutrophils, Hyperalgesia, Ganglia, Sensory},
          author = {Caxaria, S and Bharde, S and Fuller, AM and Evans, R and Thomas, B and Celik, P and Dell'Accio, F and Yona, S and Gilroy, D and Voisin, MB and Wood, JN and Sikandar, S},
            issn = {0027-8424},
        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.},
             url = {https://doi.org/10.1073/pnas.2211631120}
}