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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

Authors Kim JH, Park JS, Park D

Received 10 March 2018

Accepted for publication 13 June 2018

Published 4 September 2018 Volume 2018:11 Pages 1729—1741

DOI https://doi.org/10.2147/JPR.S166624

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr E Alfonso Romero-Sandoval


Jong-Heon Kim,1 Jin-Sung Park,2 Donghwi Park3,4

1Department of Pharmacology, Brain Science and Engineering Institute, School of Medicine, Kyungpook National University, Daegu, Republic of Korea; 2Department of Neurology, School of Medicine, Kyungpook National University Chilgok Hospital, Daegu, Republic of Korea; 3Department of Rehabilitation Medicine, Daegu Fatima Hospital, Daegu, Republic of Korea; 4Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu, Republic of Korea

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.

Keywords: CRPS, IL-10, microglia, glial activation, NK1 receptor, substance P

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