Evidence of both systemic inflammation and neuroinflammation in fibromyalgia patients, as assessed by a multiplex protein panel applied to the cerebrospinal fluid and to plasma

Bäckryd, Emmanuel; Tanum, Lars; Lind, Anne-Li; Larsson, Anders; Gordh, Torsten

doi:10.2147/jpr.s128508

Cited by 168 publications

(156 citation statements)

References 64 publications

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“…CX3CL1 could, in turn, stimulate microglia thus establishing positive feedback. Therefore it is possible that chemokines and cytokines secreted by activated microglia can be involved in establishing a state of neuronal hyperactivity and central sensitization [13,[43][44][45][46]. Overall, microglia, through these mechanisms, can contribute to brain inflammation and to the pathogenesis of different brain disorders [41,[47][48][49][50][51][52].…”

Section: Inflammatory Mediators and Innate Immunity In The Generationmentioning

confidence: 99%

T Cell Subpopulations in the Physiopathology of Fibromyalgia: Evidence and Perspectives

Banfi

Diani

Pigatto

et al. 2020

IJMS

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Fibromyalgia is one of the most important "rheumatic" disorders, after osteoarthritis. The etiology of the disease is still not clear. At the moment, the most defined pathological mechanism is the alteration of central pain pathways, and emotional conditions can trigger or worsen symptoms. Increasing evidence supports the role of mast cells in maintaining pain conditions such as musculoskeletal pain and central sensitization. Importantly, mast cells can mediate microglia activation through the production of proinflammatory cytokines such as IL-1β, IL-6, and TNFα. In addition, levels of chemokines and proinflammatory cytokines are enhanced in serum and could contribute to inflammation at systemic level. Despite the well-characterized relationship between the nervous system and inflammation, the mechanism that links the different pathological features of fibromyalgia, including stress-related manifestations, central sensitization, and dysregulation of the innate and adaptive immune responses is largely unknown. This review aims to provide an overview of the current understanding of the role of adaptive immune cells, in particular T cells, in the physiopathology of fibromyalgia. It also aims at linking the latest advances emerging from basic science to envisage new perspectives to explain the role of T cells in interconnecting the psychological, neurological, and inflammatory symptoms of fibromyalgia.

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Section: Inflammatory Mediators and Innate Immunity In The Generationmentioning

confidence: 99%

T Cell Subpopulations in the Physiopathology of Fibromyalgia: Evidence and Perspectives

Banfi

Diani

Pigatto

et al. 2020

IJMS

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“…These studies typically examine plasma levels of various cytokines following administration of painful stimuli. In addition, other studies have examined immune biomarkers in chronic pain samples 6–8…”

Section: Introductionmentioning

confidence: 99%

Age differences in salivary markers of inflammation in response to experimental pain: does venipuncture matter?

Cruz-Almeida

Aguirre

Sorenson³

et al. 2017

JPR

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An important consideration in mechanistic research using biomarkers should include the use of saliva as an alternative to blood. The use of saliva would allow the study of susceptible populations such as older adults where venipuncture may not be feasible. Although saliva has been most commonly used to measure cortisol and tumor necrosis factor-α (TNFα), there is limited evidence that other cytokines found in saliva significantly change in response to laboratory-induced pain. Therefore, the aim of the current preliminary study was to characterize the time course, duration and magnitude of changes of commonly measured pro- (interleukin [IL]-6, IL-8) and anti-inflammatory (IL-10, IL-4) cytokines in saliva samples and to test for age-related differences in separate experimental painful and non-painful control sessions. In addition, we also tested whether venipuncture results in significant cytokine alterations similar to a painful stimulus in a non-painful, non-venipuncture control session. All cytokines were significantly induced by the cold pressor task compared to a warm control session (p < 0.001). Specifically, healthy older adults experienced greater salivary changes in all cytokines during the cold pressor session compared to younger adults in the non-painful sessions (p < 0.001). There were no significant differences between the venipuncture and non-venipuncture sessions across all cytokines (p > 0.05). Our findings support the use of saliva as a substitute for blood in both young and older healthy individuals to measure changes after experimental pain stimulation. In addition, venipuncture alone is not sufficient to induce IL-6, IL-8, IL-10 and IL-4. Future studies in the community are urgently needed to validate and further move translational mechanistic pain research to those populations most underrepresented in clinical research.

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“…In addition, inflammation can promote gliogenesis 8 , which may also contribute to the observed association between higher genetic risk and larger striatal 6 volume. Interestingly, increased striatal volume was also found in fibromyalgia patients 3 , another disease characterized by systemic inflammation 9 .…”

Section: Discussionmentioning

confidence: 93%

Genetic Risk for Rheumatoid Arthritis is Associated with Increased Striatal Volume in Healthy Young Adults

Avinun

Nevo

Hariri

2019

Preprint

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Rheumatoid arthritis (RA), an autoimmune disease, has recently been associated with increased striatal volume and decreased intracranial volume (ICV) in longstanding patients. As inflammation has been shown to precede the clinical diagnosis of RA and it is a known moderator of neuro-and gliogenesis, we were interested in testing whether these brain morphological changes appear before the clinical onset of disease in healthy young adult volunteers, as a function of relative genetic risk for RA. Genetic and structural MRI data were available for 516 healthy non-Hispanic Caucasian university students (275 women, mean age 19.78±1.24 years). Polygenic risk scores were computed for each individual based on a genomewide association study of RA, so that higher scores indicated higher risk. Striatal volume (sum of caudate, putamen, and nucleus accumbens volumes) and ICV were derived for each individual from high-resolution T1-weighted images. After controlling for sex, age, genetic components of ethnicity, socioeconomic status, and depressive symptoms, we found that higher RA polygenic risk scores were associated with increased striatal volume, but not decreased ICV. Our findings suggest that increased striatal volume may be linked to processes that precede disease onset, such as inflammation, while decreased ICV may relate to disease progression.

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Evidence of both systemic inflammation and neuroinflammation in fibromyalgia patients, as assessed by a multiplex protein panel applied to the cerebrospinal fluid and to plasma

Cited by 168 publications

References 64 publications

T Cell Subpopulations in the Physiopathology of Fibromyalgia: Evidence and Perspectives

T Cell Subpopulations in the Physiopathology of Fibromyalgia: Evidence and Perspectives

Age differences in salivary markers of inflammation in response to experimental pain: does venipuncture matter?

Genetic Risk for Rheumatoid Arthritis is Associated with Increased Striatal Volume in Healthy Young Adults

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