Regulation of pain by neuro-immune interactions between macrophages and nociceptor sensory neurons

Chen, Ouyang; Donnelly, Christopher R.; Ji, Ru-Rong

doi:10.1016/j.conb.2019.11.006

Cited by 171 publications

(141 citation statements)

References 52 publications

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“…M1 is characterized by a high expression of pro-inflammatory cytokines and receptors, while M2 is characterized by a good deal of anti-inflammatory cytokines [ 60 – 62 ]. There is a bilateral communication between macrophages and nociceptors, which is embodied in macrophages releasing pro-inflammatory mediators to ‘talk to’ nociceptors while macrophages showing ‘listening to’ neuropeptides and chemokines secreted by nociceptors [ 63 ]. Many experimental NP animal models exhibit the activation and accumulation of macrophages.…”

Section: Introductionmentioning

confidence: 99%

Gut microbiota regulates neuropathic pain: potential mechanisms and therapeutic strategy

et al. 2020

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Neuropathic pain (NP) is a sustained and nonreversible condition characterized by long-term devastating physical and psychological damage. Therefore, it is urgent to identify an effective treatment for NP. Unfortunately, the precise pathogenesis of NP has not been elucidated. Currently, the microbiota-gut-brain axis has drawn increasing attention, and the emerging role of gut microbiota is investigated in numerous diseases including NP. Gut microbiota is considered as a pivotal regulator in immune, neural, endocrine, and metabolic signaling pathways, which participates in forming a complex network to affect the development of NP directly or indirectly. In this review, we conclude the current understanding of preclinical and clinical findings regarding the role of gut microbiota in NP and provide a novel therapeutic method for pain relief by medication and dietary interventions.

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Section: Introductionmentioning

confidence: 99%

Gut microbiota regulates neuropathic pain: potential mechanisms and therapeutic strategy

et al. 2020

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“…It is reported that dysregulation of miR-1224, miR-46 and miR-124 participated in CFA-induced inflammatory pain. [6][7][8][9] Further, MiR-485-5p is reported to be involved in OA development and progression, 10,11 however, the effect of miR-485-5p on OA-related inflammatory pain remains unclear.…”

Section: Introductionmentioning

confidence: 99%

<p>Decreased MiR-485-5p Contributes to Inflammatory Pain Through Post-Transcriptional Upregulation of ASIC1 in Rat Dorsal Root Ganglion</p>

Xu¹,

Wu²,

Zhang³

et al. 2020

JPR

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“…Furthermore, systemic MaR1 administration caused sustained reversal of mechanical hypersensitivity and reduced inflammatory macrophage numbers in DRG [78]. Given that macrophages are critical contributors to chronic pain pathogenesis by forming bidirectional communication with nociceptors [79], it remains important to identify whether endogenous macrophagederived maresins contribute to chronic pain resolution.…”

Section: Maresinsmentioning

confidence: 99%

“…For example, the intrathecal dose required for either DHA and EPA to reduce CFA-induced heat hyperalgesia is > 1000 times higher than that of RvE1. Thus, endogenous omega-3-derived resolvins may provide a missing link between dietary omega-3 fatty acids and control of inflammation and pain 79 . In December 2019, the FDA approved an omega-3 fish oil medication, Vascepa (icosapent ethyl, EPA only), to reduce the risk of heart attack and stroke in patients at risk of cardiovascular disease, with 4 g daily taken to achieve therapeutic effects.…”

Section: Chronic Migrainementioning

confidence: 99%

Neuromodulation, Specialized Proresolving Mediators, and Resolution of Pain

et al. 2020

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The current crises in opioid abuse and chronic pain call for the development of nonopioid and nonpharmacological therapeutics for pain relief. Neuromodulation-based approaches, such as spinal cord stimulation, dorsal root ganglion simulation, and nerve stimulation including vagus nerve stimulation, have shown efficacy in achieving pain control in preclinical and clinical studies. However, the mechanisms by which neuromodulation alleviates pain are not fully understood. Accumulating evidence suggests that neuromodulation regulates inflammation and neuroinflammation-a localized inflammation in peripheral nerves, dorsal root ganglia/trigeminal ganglia, and spinal cord/brain-through neuro-immune interactions. Specialized proresolving mediators (SPMs) such as resolvins, protectins, maresins, and lipoxins are lipid molecules produced during the resolution phase of inflammation and exhibit multiple beneficial effects in resolving inflammation in various animal models. Recent studies suggest that SPMs inhibit inflammatory pain, postoperative pain, neuropathic pain, and cancer pain in rodent models via immune, glial, and neuronal modulations. It is noteworthy that sham surgery is sufficient to elevate resolvin levels and may serve as a model of resolution. Interestingly, it has been shown that the vagus nerve produces SPMs and vagus nerve stimulation (VNS) induces SPM production in vitro. In this review, we discuss how neuromodulation such as VNS controls pain via immunomodulation and neuro-immune interactions and highlight possible involvement of SPMs. In particular, we demonstrate that VNS via auricular electroacupuncture effectively attenuates chemotherapy-induced neuropathic pain. Furthermore, auricular stimulation is able to increase resolvin levels in mice. Thus, we propose that neuromodulation may control pain and inflammation/neuroinflammatioin via SPMs. Finally, we discuss key questions that remain unanswered in our understanding of how neuromodulation-based therapies provide short-term and long-term pain relief.

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Regulation of pain by neuro-immune interactions between macrophages and nociceptor sensory neurons

Cited by 171 publications

References 52 publications

Gut microbiota regulates neuropathic pain: potential mechanisms and therapeutic strategy

Gut microbiota regulates neuropathic pain: potential mechanisms and therapeutic strategy

<p>Decreased MiR-485-5p Contributes to Inflammatory Pain Through Post-Transcriptional Upregulation of ASIC1 in Rat Dorsal Root Ganglion</p>

Neuromodulation, Specialized Proresolving Mediators, and Resolution of Pain

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