Peripheral mechanisms of pain in fibromyalgia

Fibromyalgia (FM) is a common chronic disorder characterized by widespread musculoskeletal pain, hypersensitivity, and fatigue. The causes of pathology in FM remain unknown and this gap in knowledge underlies the lack of therapeutic options. The common view is that FM is a CNS disease. However, new research points to an involvement of the peripheral nervous system.

We recently discovered that transfer of antibodies (IgG) from FM patients to mice induces several aspects of the disease, including widespread pain.

We found that FM IgG binds to satellite glial cells (SGC) in both human and mouse dorsal root ganglia (DRG) and that binding intensity to SGCs correlates with FM disease severity.Our preliminary data show striking cellular changes in skin biopsies from FM patients and that transfer of FM IgG to mice induces cellular changes in skin and mitochondrial dysfunction in DRG cells.

Based on our this we aim to: 1. Characterize the cell landscape in human fibromyalgia skin using single cell RNA sequencing and advanced imaging. 2.

Examine if IgG from FM patients induce cellular changes in mouse skin and how this correlates to induction of pain-related behaviors. 3.

Investigate what aspects of mitochondrial function is affected by FM IgG mitochondrial in DRG and skin and it relates to pain.Our project will provide new insights peripheral mechanisms underpinning FM symptoms and potentially to pave the way for new treatment strategies for sub-populations of individuals with FM.