Abstract
Background and Objectives: The aetiology and pathomechanism of fibromyalgia syndrome 12 (FMS) as one of chronic pain syndromes still need to be further elucidated. Mitogen-activated protein kinase (MAPK) pathway has been proposed as a novel approach in pain management. Since the major symptom of fibromyalgia syndrome (FMS) patients is pain, it became of interest whether MAPK pathways, such as the stress-activated p38 MAPK/MK2 axis, are activated in FMS patients. Therefore, this study aimed at determining p38 MAPK/MK2 in FMS patients. Materials and Methods: Phosphorylation of MAPK-activated protein kinases 2 (MK2), a direct target of p38 MAPK, was measured in monocytes of FMS and healthy controls (HCs) to monitor the activity of this pathway. Results: The mean level of phosphorylated MK2 was fivefold higher in FMS patients as compared to HCs (p < 0.001). Subgroup analysis revealed that antidepressants did not influence the activity of MK2 in FMS patients. Conclusions: This result indicates that the p38/MK2 pathway could be involved in the pathomechanism of FMS, could act as a clinical marker for FMS, and could be a possible target for pain management in FMS patients.
Highlights
The aetiology and pathomechanism of fibromyalgia syndrome (FMS) are still remaining elusive
According to the in vivo cell-based assay that was initially developed to identify specific p38 Mitogen-activated protein kinase (MAPK) inhibitors [24], we investigated the activation of the p38 MAPK pathway in monocytes of whole blood from healthy controls (HCs) and FMS patients
We investigated a possible link of activated p38 MAPK-MAPK-activated protein kinases 2 (MK2) signaling and depression in FMS patients
Summary
The aetiology and pathomechanism of fibromyalgia syndrome (FMS) are still remaining elusive. Besides the alteration of pain sensitization in the peripheral and central nervous system [1,2,3], one of the most proposed hypotheses in initiation of FMS is the aberration of the hypothalamus-pituitary-adrenal (HPA) axis [4], which leads to dysregulation of glucocorticoid levels in FMS patients [5]. This result can alter immune systems, as innate and adaptive immune systems are influenced by glucocorticoids [6]. Conclusions: This result indicates that the p38/MK2 pathway could be involved in the pathomechanism of FMS, could act as a clinical marker for FMS, and could be a possible target for pain management in FMS patients
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