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Interleukin-17 contributes to neuroinflammation and neuropathic pain following peripheral nerve injury in mice.
J Pain. 2011 Mar; 12(3):370-83.JP

Abstract

Cytokines, essential mediators of inflammatory and immune responses, play an important role in the pathophysiological processes associated with neuropathic pain following peripheral nerve injury. Recently, a novel proinflammatory cytokine, the interleukin (IL)-17, was found to orchestrate inflammatory responses in a wide range of inflammatory and autoimmune diseases of the nervous system. Here, we investigated the role of IL-17 in mediating neuroinflammation and pain hypersensitivity using the neuropathic pain model of partial ligation of the sciatic nerve in mice. Compared to wild-type, IL-17 knockout (KO) mice displayed significantly decreased mechanical pain hypersensitivity as well as decreased infiltration of T cells and macrophages to the injured sciatic nerves and the L3-L5 dorsal root ganglia and decreased activation of microglia and astrocytes in the L3-5 dorsal and ventral horns of the spinal cord. Further, intraplantar and intraneural injection of recombinant IL-17 into the hind paw and the sciatic nerve, respectively, induced both mechanical allodynia and thermal hyperalgesia, whereas intrathecal injection produced thermal hyperalgesia. IL-17 administration was associated with a significant increase in the numbers of infiltrating neutrophils and activated dendritic cells in the injected hind paws and infiltrating neutrophils in the injected sciatic nerves. Taken together, our results demonstrate that IL-17 contributes to the regulation of immune cell infiltration and glial activation after peripheral nerve injury and the ensuing neuropathic pain.

PERSPECTIVE

IL-17 is an important regulator of immune responses and is involved in inducing and mediating proinflammatory reactions. Using IL-17 KO mice, we have demonstrated that IL-17 contributes to neuroinflammatory responses and pain hypersensitivity following neuropathic injury. This work identifies IL-17 as a potential therapeutic target in neuropathic pain.

Authors+Show Affiliations

School of Medical Sciences, University of New South Wales, Sydney, Australia.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20889388

Citation

Kim, Cristina Fabiola, and Gila Moalem-Taylor. "Interleukin-17 Contributes to Neuroinflammation and Neuropathic Pain Following Peripheral Nerve Injury in Mice." The Journal of Pain : Official Journal of the American Pain Society, vol. 12, no. 3, 2011, pp. 370-83.
Kim CF, Moalem-Taylor G. Interleukin-17 contributes to neuroinflammation and neuropathic pain following peripheral nerve injury in mice. J Pain. 2011;12(3):370-83.
Kim, C. F., & Moalem-Taylor, G. (2011). Interleukin-17 contributes to neuroinflammation and neuropathic pain following peripheral nerve injury in mice. The Journal of Pain : Official Journal of the American Pain Society, 12(3), 370-83. https://doi.org/10.1016/j.jpain.2010.08.003
Kim CF, Moalem-Taylor G. Interleukin-17 Contributes to Neuroinflammation and Neuropathic Pain Following Peripheral Nerve Injury in Mice. J Pain. 2011;12(3):370-83. PubMed PMID: 20889388.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interleukin-17 contributes to neuroinflammation and neuropathic pain following peripheral nerve injury in mice. AU - Kim,Cristina Fabiola, AU - Moalem-Taylor,Gila, PY - 2010/03/31/received PY - 2010/07/08/revised PY - 2010/08/04/accepted PY - 2010/10/5/entrez PY - 2010/10/5/pubmed PY - 2011/7/2/medline SP - 370 EP - 83 JF - The journal of pain : official journal of the American Pain Society JO - J Pain VL - 12 IS - 3 N2 - UNLABELLED: Cytokines, essential mediators of inflammatory and immune responses, play an important role in the pathophysiological processes associated with neuropathic pain following peripheral nerve injury. Recently, a novel proinflammatory cytokine, the interleukin (IL)-17, was found to orchestrate inflammatory responses in a wide range of inflammatory and autoimmune diseases of the nervous system. Here, we investigated the role of IL-17 in mediating neuroinflammation and pain hypersensitivity using the neuropathic pain model of partial ligation of the sciatic nerve in mice. Compared to wild-type, IL-17 knockout (KO) mice displayed significantly decreased mechanical pain hypersensitivity as well as decreased infiltration of T cells and macrophages to the injured sciatic nerves and the L3-L5 dorsal root ganglia and decreased activation of microglia and astrocytes in the L3-5 dorsal and ventral horns of the spinal cord. Further, intraplantar and intraneural injection of recombinant IL-17 into the hind paw and the sciatic nerve, respectively, induced both mechanical allodynia and thermal hyperalgesia, whereas intrathecal injection produced thermal hyperalgesia. IL-17 administration was associated with a significant increase in the numbers of infiltrating neutrophils and activated dendritic cells in the injected hind paws and infiltrating neutrophils in the injected sciatic nerves. Taken together, our results demonstrate that IL-17 contributes to the regulation of immune cell infiltration and glial activation after peripheral nerve injury and the ensuing neuropathic pain. PERSPECTIVE: IL-17 is an important regulator of immune responses and is involved in inducing and mediating proinflammatory reactions. Using IL-17 KO mice, we have demonstrated that IL-17 contributes to neuroinflammatory responses and pain hypersensitivity following neuropathic injury. This work identifies IL-17 as a potential therapeutic target in neuropathic pain. SN - 1528-8447 UR - https://www.unboundmedicine.com/medline/citation/20889388/Interleukin_17_contributes_to_neuroinflammation_and_neuropathic_pain_following_peripheral_nerve_injury_in_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1526-5900(10)00694-2 DB - PRIME DP - Unbound Medicine ER -