Mast Cells, Neuroinflammation and Pain in Fibromyalgia Syndrome

Frontiers in Cellular Neuroscience

Mona Bawazeer¹  Theoharis C. Theoharides³  Irene Tsilioni⁴ 

[1] Department of Basic Medical Sciences, College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia;Department of Internal Medicine, Tufts Medical Center, Tufts University School of Medicine, Boston, MA, United States;Department of Psychiatry, Tufts Medical Center, Tufts University School of Medicine, Boston, MA, United States;Laboratory of Molecular Immunopharmacology and Drug Discovery, Department of Immunology, Tufts University School of Medicine, Boston, MA, United States;Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, MA, United States;

关键词: mast cells;    pain;    neuroinflammation;    fibromyalgia syndrome;    proinflammatory cytokines (TNF-alpha;    IL-1 beta;   

DOI  :  10.3389/fncel.2019.00353

来源: DOAJ

【 摘 要 】

Fibromyalgia Syndrome (FMS) is a disorder of chronic, generalized muscular pain, accompanied by sleep disturbances, fatigue and cognitive dysfunction. There is no definitive pathogenesis except for altered central pain pathways. We previously reported increased serum levels of the neuropeptides substance P (SP) and its structural analogue hemokinin-1 (HK-1) together with the pro-inflammatory cytokines IL-6 and TNF in FMS patients as compared to sedentary controls. We hypothesize that thalamic mast cells contribute to inflammation and pain, by releasing neuro-sensitizing molecules that include histamine, IL-1β, IL-6 and TNF, as well as calcitonin-gene related peptide (CGRP), HK-1 and SP. These molecules could either stimulate thalamic nociceptive neurons directly, or via stimulation of microglia in the diencephalon. As a result, inhibiting mast cell stimulation could be used as a novel approach for reducing pain and the symptoms of FMS.

【 授权许可】

Unknown