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Impact of mast cells in fibromyalgia and low‐grade chronic inflammation: Can IL‐37 play a role?
Author(s) -
Conti Pio,
Gallenga Carla Enrica,
Caraffa Alessandro,
Ronconi Gianpaolo,
Kritas Spyros K.
Publication year - 2019
Publication title -
dermatologic therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.595
H-Index - 68
eISSN - 1529-8019
pISSN - 1396-0296
DOI - 10.1111/dth.13191
Subject(s) - proinflammatory cytokine , medicine , inflammation , fibromyalgia , immunology , tumor necrosis factor alpha , pathogenesis , cytokine , nerve growth factor , receptor
Fibromyalgia (FM) is a disease characterized by chronic widespread pain, fatigue, aches, joint stiffness, depression, cognitive dysfunction, and nonrestorative 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 increase in the number of MCs, as well as the production of corticotropin releasing hormone and substance P (SP) by the neurons, which in turn activate MCs to release neurosensitizing proinflammatory substances, such as cytokines, secreted preformed mediators, and lipids, which can exacerbate low‐grade inflammation. In fact, certain proinflammatory 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 proinflammatory 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 FM 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.