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      Anti-allodynic effect of interleukin 10 in a mouse model of complex regional pain syndrome through reduction of NK1 receptor expression of microglia in the spinal cord

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          Abstract

          Background

          To date, there has been no study on the effects of interleukin-10 (IL-10) on complex regional pain syndrome (CRPS) rodent models, despite the anti-allodynic effect of IL-10 in previous studies. Thus, the aim of this study was to investigate the effect of IL-10 in a CRPS mouse model and find whether early inhibition of neuro-inflammation by IL-10 administration, which is considered to be one of the important mechanisms in the generation of central sensitization, could prevent the transition from the acute stage to the chronic stage of CRPS.

          Method

          A mouse model of CRPS (n=6/group) involving tibia fracture/cast immobilization to test the efficacy of intrathecal IL-10 (0.3 μg/5 μL −1 day −1 for 7 days) or vehicle during the acute (3 weeks after fracture) stage of CRPS.

          Results

          Intrathecal recombinant IL-10 (rIL-10) administration was anti-allodynic in the acute stage of the CRPS mouse model, and these anti-allodynic effects of IL-10 developed by modulating microglial activation and decreasing NK1 receptor expression in the spinal cord. However, intrathecal rIL-10 administration in the acute stage of the CRPS mouse model cannot prevent the transition to the chronic stage of CRPS in the acute stage of CRPS.

          Conclusion

          Collectively, these results demonstrate that intrathecally administered rIL-10 attenuates mechanical allodynia in the CRPS mouse model. However, this effect of IL-10 on allodynia in the acute stage of CRPS was not sufficient to prevent the transition to the chronic stage of CRPS. In the future, further studies about the mechanisms of central sensitization in CRPS will be necessary.

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          Most cited references 32

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          Inflammation in complex regional pain syndrome: a systematic review and meta-analysis.

          We conducted a systematic review of the literature with meta-analysis to determine whether complex regional pain syndrome (CRPS) is associated with a specific inflammatory profile and whether this is dependent on the duration of the condition. Comprehensive searches of the literature using MEDLINE, Embase, Scopus, Web of Science, and reference lists from published reviews identified articles that measured inflammatory factors in CRPS. Two independent investigators screened titles and abstracts, and performed data extraction and risk of bias assessments. Studies were subgrouped by medium (blood, blister fluid, and CSF) and duration (acute and chronic CRPS). Where possible, meta-analyses of inflammatory factor concentrations were performed and pooled effect sizes were calculated using random-effects models. Twenty-two studies were included in the systematic review and 15 in the meta-analysis. In acute CRPS, the concentrations of interleukin (IL)-8 and soluble tumor necrosis factor receptors I (sTNF-RI) and II (sTNF-RII) were significantly increased in blood. In chronic CRPS, significant increases were found in 1) TNFα, bradykinin, sIL-1RI, IL-1Ra, IL-2, sIL-2Ra, IL-4, IL-7, interferon-γ, monocyte chemoattractant protein-1 (MCP-1), and sRAGE (soluble receptor for advanced glycation end products) in blood; 2) IL-1Ra, MCP-1, MIP-1β, and IL-6 in blister fluid; and 3) IL-1β and IL-6 in CSF. Chronic CRPS was also associated with significantly decreased 1) substance P, sE-selectin, sL-selectin, sP-selectin, and sGP130 in blood; and 2) soluble intercellular adhesion molecule-1 (sICAM-1) in CSF. Most studies failed to meet 3 or more of our quality criteria. CRPS is associated with the presence of a proinflammatory state in the blood, blister fluid, and CSF. Different inflammatory profiles were found for acute and chronic cases.
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            Controlling neuropathic pain by adeno-associated virus driven production of the anti-inflammatory cytokine, interleukin-10

            Despite many decades of drug development, effective therapies for neuropathic pain remain elusive. The recent recognition of spinal cord glia and glial pro-inflammatory cytokines as important contributors to neuropathic pain suggests an alternative therapeutic strategy; that is, targeting glial activation or its downstream consequences. While several glial-selective drugs have been successful in controlling neuropathic pain in animal models, none are optimal for human use. Thus the aim of the present studies was to explore a novel approach for controlling neuropathic pain. Here, an adeno-associated viral (serotype II; AAV2) vector was created that encodes the anti-inflammatory cytokine, interleukin-10 (IL-10). This anti-inflammatory cytokine is known to suppress the production of pro-inflammatory cytokines. Upon intrathecal administration, this novel AAV2-IL-10 vector was successful in transiently preventing and reversing neuropathic pain. Intrathecal administration of an AAV2 vector encoding beta-galactosidase revealed that AAV2 preferentially infects meningeal cells surrounding the CSF space. Taken together, these data provide initial support that intrathecal gene therapy to drive the production of IL-10 may prove to be an efficacious treatment for neuropathic pain.
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              Long-term trans-synaptic glial responses in the human thalamus after peripheral nerve injury.

              Limb denervation leads to reorganization of the representational zones of the somatosensory cortex. Using [11C](R)-PK11195, a sensitive in vivo marker of glial cell activation, and PET, we provide first evidence that limb denervation induces a trans-synaptic increase in [11C](R)-PK11195 binding in the human thalamus but not somatosensory cortex: these brain structures appeared morphologically normal on magnetic resonance imaging (MRI). The increased thalamic signal was detectable many years after nerve injury, indicating persistent reorganization of the thalamus. This glial activation, beyond the first-order projection area of the injured neurons, may reflect continually altered afferent activity. Our findings support the view that long-term rearrangement of cortical representational maps is significantly determined within the thalamus.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                1178-7090
                2018
                04 September 2018
                : 11
                : 1729-1741
                Affiliations
                [1 ]Department of Pharmacology, Brain Science and Engineering Institute, School of Medicine, Kyungpook National University, Daegu, Republic of Korea
                [2 ]Department of Neurology, School of Medicine, Kyungpook National University Chilgok Hospital, Daegu, Republic of Korea
                [3 ]Department of Rehabilitation Medicine, Daegu Fatima Hospital, Daegu, Republic of Korea, bdome@ 123456hanmail.net
                [4 ]Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu, Republic of Korea, bdome@ 123456hanmail.net
                Author notes
                Correspondence: Donghwi Park, Department of Rehabilitation Medicine, Daegu Fatima Hospital, Ayangro 99, Dong gu, Daegu 41199, Republic of Korea, Tel +82 53 940 7821, Fax +82 53 954 7417, Email bdome@ 123456hanmail.net
                Article
                jpr-11-1729
                10.2147/JPR.S166624
                6129024
                © 2018 Kim et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Anesthesiology & Pain management

                substance p, nk1 receptor, glial activation, microglia, il-10, crps

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