Exploring the transcriptome of resident spinal microglia after collagen antibody–induced arthritis

Fernández-Zafra, Teresa; Gao, Tianle; Jurczak, Alexandra; Sándor, Katalin; Hore, Zoe; Agalave, Nilesh M.; Su, Jie; Estelius, Johanna; Lampa, Jon; Hökfelt, Tomas; Wiesenfeld‐Hallin, Zsuzsanna; Xu, Xiao‐Jun; Denk, Franziska; Svensson, Camilla I.

doi:10.1097/j.pain.0000000000001394

Cited by 54 publications

(53 citation statements)

References 58 publications

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“…However, BCP has the advantage of also directly attenuating established mechanical allodynia via CB2 receptors, whereas previous preclinical studies show that minocycline cannot attenuate established hyperalgesia and allodynia [78][79][80], which is possibly one of the reasons we postulated [50] for its failure in clinical trials for neuropathic pain [81]. Moreover, BCP alleviates allodynia in both female (current study and in another study [43]) and male mice [42], whereas a recent study showed that minocycline and pentoxifylline could reverse mechanical thresholds in males, but not in female mice [82]. Treatment with drugs that prevent astrocyte and microglia activation has been found to prevent or reduce neuropathic pain in various models [56,[83][84][85].…”

Section: Discussioncontrasting

confidence: 57%

β-Caryophyllene, a CB2-Receptor-Selective Phytocannabinoid, Suppresses Mechanical Allodynia in a Mouse Model of Antiretroviral-Induced Neuropathic Pain

2019

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Neuropathic pain associated with nucleoside reverse transcriptase inhibitors (NRTIs), therapeutic agents for human immunodeficiency virus (HIV), responds poorly to available drugs. Smoked cannabis was reported to relieve HIV-associated neuropathic pain in clinical trials. Some constituents of cannabis (Cannabis sativa) activate cannabinoid type 1 (CB1) and cannabinoid type 2 (CB2) receptors. However, activation of the CB1 receptor is associated with side effects such as psychosis and physical dependence. Therefore, we investigated the effect of β-caryophyllene (BCP), a CB2-selective phytocannabinoid, in a model of NRTI-induced neuropathic pain. Female BALB/c mice treated with 2′-3′-dideoxycytidine (ddC, zalcitabine), a NRTI, for 5 days developed mechanical allodynia, which was prevented by cotreatment with BCP, minocycline or pentoxifylline. A CB2 receptor antagonist (AM 630), but not a CB1 receptor antagonist (AM 251), antagonized BCP attenuation of established ddC-induced mechanical allodynia. β-Caryophyllene prevented the ddC-induced increase in cytokine (interleukin 1 beta, tumor necrosis factor alpha and interferon gamma) transcripts in the paw skin and brain, as well as the phosphorylation level of Erk1/2 in the brain. In conclusion, BCP prevents NRTI-induced mechanical allodynia, possibly via reducing the inflammatory response, and attenuates mechanical allodynia through CB2 receptor activation. Therefore, BCP could be useful for prevention and treatment of antiretroviral-induced neuropathic pain.

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Section: Discussioncontrasting

confidence: 57%

β-Caryophyllene, a CB2-Receptor-Selective Phytocannabinoid, Suppresses Mechanical Allodynia in a Mouse Model of Antiretroviral-Induced Neuropathic Pain

2019

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“…These authors have also shown that TNF neutralization by intrathecal administration of infliximab, or spinal prevention of microglial activation by minocycline or fluorocitrate injection, ameliorates AIA-induced hypernociception. Similarly, reversion of persistent pain hypersensitivity in a model of collagen antigen-induced arthritis was induced by spinal inhibition of microglia and astrocyte activation after intrathecal minocycline and pentoxifylline administration, respectively (55). In contrast, we did not observe spinal overexpression of TNF, TNFR1, and TNFR2, nor did we observe overexpression of Iba1 + and GFAP + cells, which are glial cell activation markers, during the persistent joint nociception.…”

Section: Discussionmentioning

confidence: 42%

Sensory Ganglia-Specific TNF Expression Is Associated With Persistent Nociception After Resolution of Inflammation

et al. 2020

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systemic injection of etanercept, an agent clinically utilized for TNF neutralization, at day 7 post arthritis induction, alleviated the persistent joint hyperalgesia by specific action in DRG. Our data suggest that neuroinflammation in DRG after the resolution of acute joint inflammation drives continuous neural sensitization resulting in persistent joint nociception in a TNF-dependent mechanism.

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“…The K/BxN model exhibits persistent pain with mechanical hypersensitivity, which does not return to baseline levels during disease progression and outlasts inflammation [155]. Table 2 briefly summarizes the pathology and pain behaviors reported in RA models [134,137,[153][154][155][156][157][158][159][160][161][162][163][164][165][166][167]. CIA, collagen-induced arthritis; CAIA, collagen antibody-induced arthritis; AIA, antigen-induced arthritis; TNF-Tg, tumor necrosis factor transgene; IL-1RA-/-, interleukin-1 receptor antagonist knockout; CII, collagen type II; Ab, antibody; mBSA, methylated bovine serum albumin; GPI, glucose-6-phosphateisomerase; hTNF, human tumor necrosis factor; RA, rheumatoid arthritis; d, day; wk, week(s); Cat S, cathepsin S; FKN, fractalkine; TLR-4, toll-like receptor 4; IL-1RI, interleukin-1 receptor type I; pCREB, phospho-CREB.…”

Section: Behavioral Tests To Assess Pain In Ra Animal Modelsmentioning

confidence: 99%

Understanding the Molecular Mechanisms Underlying the Pathogenesis of Arthritis Pain Using Animal Models

Hong

Park

Kim

2020

IJMS

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Arthritis, including osteoarthritis (OA) and rheumatoid arthritis (RA), is the leading cause of years lived with disability (YLD) worldwide. Although pain is the cardinal symptom of arthritis, which is directly related to function and quality of life, the elucidation of the mechanism underlying the pathogenesis of pain in arthritis has lagged behind other areas, such as inflammation control and regulation of autoimmunity. The lack of therapeutics for optimal pain management is partially responsible for the current epidemic of opioid and narcotic abuse. Recent advances in animal experimentation and molecular biology have led to significant progress in our understanding of arthritis pain. Despite the inherent problems in the extrapolation of data gained from animal pain studies to arthritis in human patients, the critical assessment of molecular mediators and translational studies would help to define the relevance of novel therapeutic targets for the treatment of arthritis pain. This review discusses biological and molecular mechanisms underlying the pathogenesis of arthritis pain determined in animal models of OA and RA, along with the methodologies used.

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Exploring the transcriptome of resident spinal microglia after collagen antibody–induced arthritis

Abstract: Supplemental Digital Content is Available in the Text.Glial inhibitors only reverse mechanical hypersensitivity in male mice subjected to arthritis. No obvious arthritis-related transcriptional difference was identified between male and female spinal microglia.

Cited by 54 publications

References 58 publications

β-Caryophyllene, a CB2-Receptor-Selective Phytocannabinoid, Suppresses Mechanical Allodynia in a Mouse Model of Antiretroviral-Induced Neuropathic Pain

β-Caryophyllene, a CB2-Receptor-Selective Phytocannabinoid, Suppresses Mechanical Allodynia in a Mouse Model of Antiretroviral-Induced Neuropathic Pain

Sensory Ganglia-Specific TNF Expression Is Associated With Persistent Nociception After Resolution of Inflammation

Understanding the Molecular Mechanisms Underlying the Pathogenesis of Arthritis Pain Using Animal Models

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