Papers of the Week

Fibromyalgia (FM) is a disease characterized by chronic widespread pain, fatigue, aches, joint stiffness, depression, cognitive dysfunction and non-restorative sleep. In FM, neurotransmission and glial activation can occur with an increase in inflammatory cytokines and involvement of mast cells (MCs) in the skin. FM skin biopsies show an increased number of MCs, as well as the production of corticotropin releasing hormone (CRH) and substance P (SP) by the neurons, which in turn activate MCs to release neurosensitizing pro-inflammatory substances, such as cytokines, secreted preformed mediators and lipids, which can exacerbate low-grade inflammation. In fact, certain pro-inflammatory cytokines are higher in FM and mediate muscle pain, the mechanism of which is not yet clear. MC-derived tumor necrosis factor (TNF) induces nerve growth factor (NGF) and participates in nerve fiber elongation in skin hypersensitivity. IL-37 is an inhibitor of pro-inflammatory IL-1 family members which are generated and released by MCs. The goal of this article is to demonstrate that inflammatory cytokines and MC products play a role in fibromyalgia and that inflammation may be inhibited by IL-37. Here, we propose IL-37 as a cytokine that contributes to improve the pathogenesis of FM by blocking IL-1 family members. This article is protected by copyright. All rights reserved.