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Int. J. Mol. Sci. 2017, 18(11), 2296;

Pharmacological Regulation of Neuropathic Pain Driven by Inflammatory Macrophages

Department of Pharmacology, Wakayama Medical University, Wakayama 641-0012, Japan
Author to whom correspondence should be addressed.
Received: 19 October 2017 / Revised: 27 October 2017 / Accepted: 31 October 2017 / Published: 1 November 2017
(This article belongs to the Special Issue Macrophages in Inflammation)
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Neuropathic pain can have a major effect on quality of life but current therapies are often inadequate. Growing evidence suggests that neuropathic pain induced by nerve damage is caused by chronic inflammation. Upon nerve injury, damaged cells secrete pro-inflammatory molecules that activate cells in the surrounding tissue and recruit circulating leukocytes to the site of injury. Among these, the most abundant cell type is macrophages, which produce several key molecules involved in pain enhancement, including cytokines and chemokines. Given their central role in the regulation of peripheral sensitization, macrophage-derived cytokines and chemokines could be useful targets for the development of novel therapeutics. Inhibition of key pro-inflammatory cytokines and chemokines prevents neuroinflammation and neuropathic pain; moreover, recent studies have demonstrated the effectiveness of pharmacological inhibition of inflammatory (M1) macrophages. Nicotinic acetylcholine receptor ligands and T helper type 2 cytokines that reduce M1 macrophages are able to relieve neuropathic pain. Future translational studies in non-human primates will be crucial for determining the regulatory mechanisms underlying neuroinflammation-associated neuropathic pain. In turn, this knowledge will assist in the development of novel pharmacotherapies targeting macrophage-driven neuroinflammation for the treatment of intractable neuropathic pain. View Full-Text
Keywords: cytokine; chemokine; leukocyte; neutrophil; neuroinflammation; allodynia; hyperalgesia; nicotinic acetylcholine receptor cytokine; chemokine; leukocyte; neutrophil; neuroinflammation; allodynia; hyperalgesia; nicotinic acetylcholine receptor

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Kiguchi, N.; Kobayashi, D.; Saika, F.; Matsuzaki, S.; Kishioka, S. Pharmacological Regulation of Neuropathic Pain Driven by Inflammatory Macrophages. Int. J. Mol. Sci. 2017, 18, 2296.

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