| Literature DB >> 29684996 |
F Mastrangelo1, I Frydas2, G Ronconi3, S K Kritas4, L Tettamanti5, Al Caraffa6, C D Ovidio7, A Younes8, C E Gallenga9, P Conti10.
Abstract
It has been observed that acute stress causes the activation of TH1 cells, while TH2 cells regulate and act on chronic inflammation. Fibromyalgia (FM) is a chronic, idiopathic disorder which affects about twelve million people in the United States. FM is characterized by chronic widespread pain, fatigue, aching, joint stiffness, depression, cognitive dysfunction and non-restorative sleep. The mechanism of induction of muscle pain and inflammation is not yet clear. In FM there is an increase in reactivity of central neurons with increased sensitivity localized mainly in the CNS. Mast cells are involved in FM by releasing proinflammatory cytokines, chemokines, chemical mediators, and PGD2. TNF is a cytokine generated by MCs and its level is higher in FM. The inhibition of pro-inflammatory IL-1 family members and TNF by IL-37 in FM could have a therapeutic effect. Here, we report for the first time the relationship between MCs, inflammatory cytokines and the new anti-inflammatory cytokine IL-37 in FM.Entities:
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Year: 2018 PMID： 29684996
Source DB: PubMed Journal: J Biol Regul Homeost Agents ISSN： 0393-974X Impact factor: 1.711