The inflammasome in fibromyalgia and CRPS: a microglial hypothesis?

Cordero, Mario D.

doi:10.1038/nrrheum.2015.131

Cited by 4 publications

(3 citation statements)

References 16 publications

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“…99 Finally, an inflammasomemicroglial activation mechanism was also proposed in FM. 147 Collectively, these studies suggest that inhibition of NALP3 inflammasome activity by coenzyme Q 10 and AMPK activators may be a potentially effective therapy for the specific and nonspecific pain states associated with FM.…”

Section: Chronic Prostatitis and Chronic Pelvic Pain Syndromementioning

confidence: 99%

The inflammasome as a target for pain therapy

Zhang¹,

Li²,

Li³

et al. 2016

British Journal of Anaesthesia

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The interleukin-1 family of cytokines are potent inducers of inflammation and pain. Proteolytic activation of this family of cytokines is under the control of several innate immune receptors that coordinate to form large multiprotein signalling platforms, termed inflammasomes. Recent evidence suggests that a wide range of inflammatory diseases, cancers, and metabolic and autoimmune disorders, in which pain is a common complaint, may be coordinated by inflammasomes. Activation of inflammasomes results in cleavage of caspase-1, which subsequently induces downstream initiation of several potent pro-inflammatory cascades. Therefore, it has been proposed that targeting inflammasome activity may be a novel and effective therapeutic strategy for these pain-related diseases. The purpose of this narrative review article is to provide the reader with an overview of the activation and regulation of inflammasomes and to investigate the potential therapeutic role of inflammasome inhibition in the treatment of diseases characterized by pain, including the following: complex regional pain syndrome, gout, rheumatoid arthritis, inflammatory pain, neuropathic pain, chronic prostatitis, chronic pelvic pain syndrome, and fibromyalgia. We conclude that the role of the inflammasome in pain-associated diseases is likely to be inflammasome subtype and disease specific. The currently available evidence suggests that disease-specific targeting of the assembly and activity of the inflammasome complex may be a novel therapeutic opportunity for the treatment of refractory pain in many settings.

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Section: Chronic Prostatitis and Chronic Pelvic Pain Syndromementioning

confidence: 99%

The inflammasome as a target for pain therapy

Zhang¹,

Li²,

Li³

et al. 2016

British Journal of Anaesthesia

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“…Moreover, in mice with spinal cord injury, both microglia and astrocytes were activated with an increased release of IL-1β and caspase-1 [ 154 ]. Furthermore, the association of NLRP3 inflammasomes with neuroinflammation has been declared in fibromyalgia and CRPS [ 155 ]. Several studies reported that NLRP3 inhibitors ameliorate pain in numerous animal pain models [ 156 , 157 ].…”

Section: Role Of Curcumin On Epigenetic Modulation and Inflammasome On Neuroinflammation-driven Chronic Painmentioning

confidence: 99%

Mechanistic Insight into the Effects of Curcumin on Neuroinflammation-Driven Chronic Pain

et al. 2021

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Chronic pain is a persistent and unremitting condition that has immense effects on patients’ quality of life. Studies have shown that neuroinflammation is associated with the induction and progression of chronic pain. The activation of microglia and astrocytes is the major hallmark of spinal neuroinflammation leading to neuronal excitability in the projection neurons. Excessive activation of microglia and astrocytes is one of the major contributing factors to the exacerbation of pain. However, the current chronic pain treatments, mainly by targeting the neuronal cells, remain ineffective and unable to meet the patients’ needs. Curcumin, a natural plant product found in the Curcuma genus, improves chronic pain by diminishing the release of inflammatory mediators from the spinal glia. This review details the role of curcumin in microglia and astrocytes both in vitro and in vivo and how it improves pain. We also describe the mechanism of curcumin by highlighting the major glia-mediated cascades in pain. Moreover, the role of curcumin on inflammasome and epigenetic regulation is discussed. Furthermore, we discuss the strategies used to improve the efficacy of curcumin. This review illustrates that curcumin modulating microglia and astrocytes could assure the treatment of chronic pain by suppressing spinal neuroinflammation.

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“…FM is listed by the CDC as one of the conditions sharing symptoms with PASC 10 and recent studies showed that 30-40% of individuals with PASC meet the American College of Rheumatology (ACR) FM diagnostic criteria 11,12 . FM's underlying cause has not been proven, but it is hypothesized to involve sensory sensitization of the spinothalamic tract, possibly attributed to microglial overactivation by numerous factors, including viral infections [13][14][15] . Some researchers postulate that Sars-Cov-2 may induce central pain by interacting with ACE2 receptors in the microglia or via Spike proteins activating microglial apoptotic pathways [16][17][18] .…”

Section: Introductionmentioning

confidence: 99%

Transcutaneous Electrical Nerve Stimulation for Fibromyalgia-like Syndrome in Patients with Post-Acute Sequelae of Sars-Cov-2: A Pilot Randomized Clinical Trial

Zulbaran-Rojas,

Bara,

Lee

et al. 2024

Preprint

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This study investigated the effect of Transcutaneous Electrical Nerve Stimulation (TENS) for fibromyalgia-like symptoms including chronic widespread pain, fatigue, and gait impairment in twenty-five individuals with Post-Acute Sequelae of Sars-Cov-2 (PASC). Participants were randomized to a high dose (intervention group, IG) or low dose (placebo group, PG) TENS device. Both groups received daily 3–5 hours of TENS therapy for 4-weeks. The Brief Pain Inventory assessed functional interference from pain (BPI-I), and pain severity (BPI-S). The global fatigue index (GFI) assessed functional interference from fatigue. Wearable technology measured gait parameters during three 30-feet consecutive walking tasks. At 4-weeks, the IG exhibited a greater decrease in BPI-I compared to the PG (mean difference = 2.61, p = 0.008), and improved in gait parameters including stride time (4%-8%, test condition dependent), cadence (4%-10%, depending on condition), and double-support phase (12% in dual-task) when compared to baseline. A sub-group meeting the American College of Rheumatology Fibromyalgia diagnostic criteria undergoing high-dose TENS showed GFI improvement at 4-weeks from baseline (mean change = 6.08, p = 0.005). Daily TENS therapy showed potential in reducing functional interference from pain, fatigue, and gait alterations in PASC individuals. The study's limited power could affect the confirmation of certain observations. Extending the intervention period may improve treatment effectiveness.

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The inflammasome in fibromyalgia and CRPS: a microglial hypothesis?

Cited by 4 publications

References 16 publications

The inflammasome as a target for pain therapy

The inflammasome as a target for pain therapy

Mechanistic Insight into the Effects of Curcumin on Neuroinflammation-Driven Chronic Pain

Transcutaneous Electrical Nerve Stimulation for Fibromyalgia-like Syndrome in Patients with Post-Acute Sequelae of Sars-Cov-2: A Pilot Randomized Clinical Trial

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