B-cell and plasma cell activation in a mouse model of chronic muscle pain

Melissa E. Lenert, Audrey R. Green, Ericka N. Merriwether, Michael D. Burton

Research output: Contribution to journalArticlepeer-review

Abstract

Fibromyalgia (FM) is a complex chronic musculoskeletal pain disorder with an elusive pathogenesis, with a strong implication of immune interactions. We recently found that IL-5 and the adaptive immune system mediates pain outcomes in fibromyalgia (FM) patients and preclinical models of FM-like chronic widespread pain (CWP). However, there is an active debate if FM/CWP has an autoimmune etiology. Preclinical models of CWP utilize a repeated insult paradigm, which resembles a primary, then secondary response similarly observed in the antibody response, in which the subsequent event causes a potentiated pain response. Recent translational studies have implicated immunoglobulins (Ig) and B-cells in FM/CWP pathophysiology. To understand if these are involved in preclinical models of CWP, we performed comprehensive B-cell phenotyping in the bone marrow, circulation, and popliteal (draining) lymph nodes in the two-hit acidic saline model of CWP. We found increased MHC class II-expressing B-cells in peripheral blood, increased activated plasma cells in peripheral blood, and increased memory B-cells in the bone marrow. Interestingly, acidic pH (4.0) injected mice have reduced levels of IgG1, independent of treatment with IL-5. We have demonstrated that the acidic saline model of CWP induces T-cell mediated activation of B-cells, increased active plasma cells, and increased memory B-cells in female mice.

Original languageEnglish (US)
Article number100169
JournalNeurobiology of Pain
Volume16
DOIs
StatePublished - Jul 1 2024

Keywords

  • Autoimmune
  • B-cell
  • Female
  • Fibromyalgia
  • Musculoskeletal pain

ASJC Scopus subject areas

  • Neuroscience (miscellaneous)
  • Clinical Neurology
  • Anesthesiology and Pain Medicine

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