Soluble fractalkine in the plasma of fibromyalgia patients

Garcı́a, Juan José; Ortega, Eduardo

doi:10.1590/0001-3765201420130081

Cited by 4 publications

(5 citation statements)

References 8 publications

(9 reference statements)

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“…They increase sensitivity to pain by direct action of their receptors expressed in nociceptive neurons, 3 and also serve to regulate the inflammatory response, acting simultaneously on elements of the nervous system, 4,5 suggesting an important role in the pathophysiology of autoimmune diseases such as rheumatoid arthritis, multiple sclerosis, systemic lupus erythematosus and fibromyalgia (FM). [5][6][7] According to the American College of Rheumatology (ACR), FM is defined as the presence of widespread pain and tenderness at 11 or more of 18 specific tender point sites. 8 Thus, core symptoms of the FM include pain, fatigue, and mood and sleep disturbances.…”

Section: Introductionmentioning

confidence: 99%

Altered release of chemokines by phagocytes from fibromyalgia patients: a pilot study

2015

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Fibromyalgia (FM) is a syndrome characterized by widespread chronic pain and is associated with elevated systemic inflammatory biomarkers, and an elevated innate cellular response. The aim of this study was to determine if fibromyalgia patients have altered ability to release pro-inflammatory chemokines by isolated neutrophils and monocytes. The study participants were women diagnosed with FM (n ¼ 6) and a control group of healthy women (HW) (n ¼ 6). Supernatant concentrations of eotaxin (CCL11), human macrophage-derived chemokine (MDC) (CCL22) and growth regulatedoncogene (GRO-a) (CXCL1) released by both monocytes and neutrophils either resting or stimulated by LPS were determined by ELISA and compared between the FM and HW groups. Both resting and activated monocytes from FM patients released more eotaxin, MDC and GRO-a than those from HW. However, there were no significant differences in the release of chemokines from neutrophils of FM patients and the ones from healthy women. In conclusion, monocytes from women with FM are deregulated, releasing higher amounts of eotaxin, MDC and GRO-a than healthy individuals. This fact does not occur in neutrophils from women with FM.

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Section: Introductionmentioning

confidence: 99%

Altered release of chemokines by phagocytes from fibromyalgia patients: a pilot study

2015

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“…Differentially methylated PRKCA contributes to the risk of developing fibromyalgia in women (26). Patients with fibromyalgia typically suffer from rheumatic symptoms, which are likely to be associated with inflammatory cytokines (27). LIF, which encodes a member of the IL-6 cytokine family, downregulates autoimmune responses by enhancing the number of regulatory T cells (28).…”

Section: Discussionmentioning

confidence: 99%

Differentially methylated regions in patients with rheumatic heart disease and secondary pulmonary arterial hypertension

Zheng

Chen

et al. 2017

Experimental and Therapeutic Medicine

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The aim of the present study was to identify differentially methylated regions (DMRs) in patients with rheumatic heart disease and secondary pulmonary arterial hypertension (RHD-PAH). A genome-wide DNA methylation assay was performed between 6 patients with RHD-PAH and 6 healthy controls using an Illumina Infinium HumanMethylation450 BeadChip kit. The Limma software package was subsequently used to identify significant DMRs. A total of 40 hypome-thylated and 64 hypermethylated CpG sites were identified between the RHD-PAH group and the control group. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes term and signaling pathway enrichment analyses revealed that the DMRs, mapped to the genes including protein kinase C α, protein kinase AMP-activated non-catalytic subunit γ2, sprouty related EVH1 domain containing 2 and LIF interleukin 6 family cytokine, were significantly enriched in the negative regulation of protein kinase/transferase activity and the positive regulation of protein amino acid phosphorylation/phosphate metabolic process. The identified DMRs may provide novel insights into the pathogenesis of RHD-PAH.

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Section: Chemokines In Fmmentioning

confidence: 99%

“…So, monocytes, isolated by magnetic separation from the rest of peripheral blood mononuclear cells (PBMC), produce greater amounts of 91,135], 91,135], 91,135], 91] and 91,135]; also, these cells from women with FM produce a greater amount of inflammatory chemokines, such as MCP-1 (CCL2) [54], eotaxin (CCL11), MDC (CCL22), . This increase of the chemokines, at the local level, produced by monocytes from FM patients would be stimulating the sensation of pain in these patients because chemokines increase pain sensitivity by directly acting on their receptors (wich are present along the entire pathway of pain in peripheral nerves, the sites of nerve damage, the dorsal root ganglia and the spinal cord) [123], as most of these chemokines are molecules that mediate both inflammatory and neuropathic pain [124,155,156]. Only one study has reported that monocytes from patients with FM produce less RANTES than monocytes of healthy individuals [54], while Garcia and Ortega [125] found no difference in the production of fractalkine (CX3CL1) by monocytes on FM patients and healthy people.…”

Section: Altered Functionality Of Monocytes In Fibromyalgiamentioning

confidence: 99%

“…In addition, chemokines appear to be molecules with a role in the coordination of nociceptive events associated with the injury. Increase sensitivity to pain by direct action on chemokine receptors expressed in nociceptive neurons [123], and also serve to regulate the inflammatory response simultaneously acting on components of the nervous system [124].The fact that the main symptom of fibromyalgia is chronic widespread pain, suggests that chemokines, such as inflammatory mediators and nociceptor's modulators [123], may be involved in the pathophysiology of this disease. In fact, in pain mechanisms, chemokines increase sensitivity directly acting on its receptors (which are present along the entire path of pain -in peripheral nerves,the site of damage to nerves, dorsal root ganglia and spinal cord) [123].…”

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Altered Inflammatory Mediators in Fibromyalgia

Garcı́a¹,

Carvajal-Gil²,

Herrero-Olea³

et al. 2017

Rheumatology

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Fibromyalgia (FM) is a syndrome characterized by widespread chronic pain, tenderness, stiffness, fatigue, and sleep and mood disturbances. Current evidences suggest that inflammatory mediators may have an important role in the pathogenesis of fibromyalgia. Every day new evidences emerging of the role of the immune system and the inflammatory process in the pathophysiology of this disease. Thus, the aim of this work has been review that altered inductors, inflammatory mediators and effectors have been reported in fibromyalgia, and its relationship to disease's symptoms. If in fibromyalgia underlies widespread disruption of most characteristic components on the inflammatorý s process (endogenous inductors, mediators and effectors) is logical to think that fibromyalgia is producing a sustained inflammatory response in time, unregulated, responsible for the disease´s symptoms. Keywords:Fibromyalgia; Inflammation; HMGB1; Age; Inflammasome; Cytokines; Chemokines; Pentraxins; Lipid mediators; Monocytes; Neutrophils FibromyalgiaFibromyalgia (FM) is a chronic disease characterized by a widespread pain, tenderness, stiffness, fatigue, and sleep and mood disturbances. The prevalence of FM in the world ranges between 0.7% and 3.2%. It is more prevalent on women than men with a ratio women/men 20:1 (4.2% prevalence on women compared with 0.2% on men) [1] and it can develop at any age [2].The exact cause of fibromyalgia is unknown, but it has been proposed that the FM is a stress-related disorder that may involve a dysfunction of the hypothalamic-pituitary-adrenal axis (HPA) [3,4]. Thus, adverse life events, such as emotional, physical and sexual abuse on children and adults have been suggested to contribute to the development of FM [5][6][7].Risk factors FM have been the subject of much debate in recent research. There is no doubt that the experience of an abusive relationship, maintained over time, is a stressful situation that could be related to the presence of FM [8,9].Like all physiological systems, the immune system is under the control of the neuro-endocrine system and interacts and works in concert with other regulatory body systems, thus immune cells respond to neuroendocrine signals through specific receptors for hormones, neurotransmitters and neuropeptides. Therefore, dysregulation of the hypothalamic-pituitary-adrenal axis by chronic stress situations necessarily lead to a dysregulation of the immune function. Thus, inflammation is a characteristic process of the immune system, considered a defense response that is induced by infection or trauma. However, inflammation may also be induced by stress and tissue dysfunction in the absence of infection, there is a close relationship between body homeostasis, stress response and inflammation, since inflammation has both a component response to stress as a component defense response. Inflammation and FibromyalgiaIn 2001, Wallace et al. [10] were the first to suggest that inflammatory mediators, such as cytokines, could play a role in fibromyalgia. Prior results...

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Soluble fractalkine in the plasma of fibromyalgia patients

Cited by 4 publications

References 8 publications

Altered release of chemokines by phagocytes from fibromyalgia patients: a pilot study

Altered release of chemokines by phagocytes from fibromyalgia patients: a pilot study

Differentially methylated regions in patients with rheumatic heart disease and secondary pulmonary arterial hypertension

Altered Inflammatory Mediators in Fibromyalgia

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