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Article: Spinal interleukin-17 promotes thermal hyperalgesia and NMDA NR1 phosphorylation in an inflammatory pain rat model

TitleSpinal interleukin-17 promotes thermal hyperalgesia and NMDA NR1 phosphorylation in an inflammatory pain rat model
Authors
Issue Date2013
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/pain
Citation
Pain, 2013, v. 154 n. 2, p. 294-305 How to Cite?
AbstractIt is known that interleukin-17 (IL-17) is associated with autoimmune disorders and that peripheral IL-17 plays a role in arthritis and neuropathic pain. The present study investigated the possibility of spinal cell expression of IL-17 during inflammatory pain and possible IL-17 involvement in such pain. Hyperalgesia was induced by injecting complete Freund adjuvant (CFA, 0.08 mL, 40 μg Mycobacterium tuberculosis) into one hind paw of the rat. Paw withdrawal latency (PWL) was tested before (-48 h) and 2 and 24 h after CFA injection to assess hyperalgesia. IL-17 antibody (0.2-2 μg/rat) was given intrathecally (i.t.) 24 h before CFA to block the action of basal IL-17 and 2 h before each of 2 PWL tests to block CFA-induced IL-17. I.t. recombinant IL-17 (10-400 ng per rat) was administered to naive rats to determine its effects on PWL and phosphorylated NR1 (p-NR1). p-NR1 modulates N-methyl-d-aspartate receptor (NMDAR) activity to facilitate pain. Spinal cords were removed for IL-17 immunostaining, double immunostaining of IL-17/cell markers and IL-17 receptor A (IL-17RA)/NR1, for Western blot testing of IL-17, p-NR1, IL-17RA, and GFAP, for in situ IL-17RA hybridization, and for real time polymerase chain reaction of IL-17RA. The data reveal that IL-17 is up-regulated in activated and nonactivated astrocytes; that IL-17RA is localized in NR1-immunoreactive neurons and up-regulated; and that IL-17 antibody at 2 μg/rat significantly increased PWL (P <.05) and decreased p-NR1 and IL-17RA compared to control in CFA- and IL-17-injected rats. The results suggest that spinal IL-17 is produced by astrocytes and enhances p-NR1 to facilitate pain. © 2012 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/188660
ISSN
2015 Impact Factor: 5.557
2015 SCImago Journal Rankings: 3.007
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMeng, Xen_US
dc.contributor.authorZhang, Yen_US
dc.contributor.authorLao, Len_US
dc.contributor.authorSaito, Ren_US
dc.contributor.authorLi, Aen_US
dc.contributor.authorBäckman, CMen_US
dc.contributor.authorBerman, BMen_US
dc.contributor.authorRen, Ken_US
dc.contributor.authorWei, PKen_US
dc.contributor.authorZhang, RXen_US
dc.date.accessioned2013-09-03T04:10:54Z-
dc.date.available2013-09-03T04:10:54Z-
dc.date.issued2013en_US
dc.identifier.citationPain, 2013, v. 154 n. 2, p. 294-305en_US
dc.identifier.issn0304-3959en_US
dc.identifier.urihttp://hdl.handle.net/10722/188660-
dc.description.abstractIt is known that interleukin-17 (IL-17) is associated with autoimmune disorders and that peripheral IL-17 plays a role in arthritis and neuropathic pain. The present study investigated the possibility of spinal cell expression of IL-17 during inflammatory pain and possible IL-17 involvement in such pain. Hyperalgesia was induced by injecting complete Freund adjuvant (CFA, 0.08 mL, 40 μg Mycobacterium tuberculosis) into one hind paw of the rat. Paw withdrawal latency (PWL) was tested before (-48 h) and 2 and 24 h after CFA injection to assess hyperalgesia. IL-17 antibody (0.2-2 μg/rat) was given intrathecally (i.t.) 24 h before CFA to block the action of basal IL-17 and 2 h before each of 2 PWL tests to block CFA-induced IL-17. I.t. recombinant IL-17 (10-400 ng per rat) was administered to naive rats to determine its effects on PWL and phosphorylated NR1 (p-NR1). p-NR1 modulates N-methyl-d-aspartate receptor (NMDAR) activity to facilitate pain. Spinal cords were removed for IL-17 immunostaining, double immunostaining of IL-17/cell markers and IL-17 receptor A (IL-17RA)/NR1, for Western blot testing of IL-17, p-NR1, IL-17RA, and GFAP, for in situ IL-17RA hybridization, and for real time polymerase chain reaction of IL-17RA. The data reveal that IL-17 is up-regulated in activated and nonactivated astrocytes; that IL-17RA is localized in NR1-immunoreactive neurons and up-regulated; and that IL-17 antibody at 2 μg/rat significantly increased PWL (P <.05) and decreased p-NR1 and IL-17RA compared to control in CFA- and IL-17-injected rats. The results suggest that spinal IL-17 is produced by astrocytes and enhances p-NR1 to facilitate pain. © 2012 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/painen_US
dc.relation.ispartofPainen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntibodies - Pharmacologyen_US
dc.subject.meshFreund's Adjuvanten_US
dc.subject.meshHot Temperatureen_US
dc.subject.meshHyperalgesia - Chemically Induced - Metabolismen_US
dc.subject.meshInflammation - Chemically Induced - Metabolismen_US
dc.subject.meshInterleukin-17 - Genetics - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshNeurons - Drug Effects - Metabolismen_US
dc.subject.meshPain Measurementen_US
dc.subject.meshPain Threshold - Drug Effectsen_US
dc.subject.meshPhosphorylation - Drug Effectsen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptors, Interleukin-17 - Genetics - Metabolismen_US
dc.subject.meshReceptors, N-Methyl-D-Aspartate - Genetics - Metabolismen_US
dc.subject.meshSpinal Cord - Drug Effects - Metabolismen_US
dc.titleSpinal interleukin-17 promotes thermal hyperalgesia and NMDA NR1 phosphorylation in an inflammatory pain rat modelen_US
dc.typeArticleen_US
dc.identifier.emailLao, L: lxlao1@hku.hken_US
dc.identifier.authorityLao, L=rp01784en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.pain.2012.10.022en_US
dc.identifier.pmid23246025-
dc.identifier.scopuseid_2-s2.0-84872685685en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84872685685&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume154en_US
dc.identifier.issue2en_US
dc.identifier.spage294en_US
dc.identifier.epage305en_US
dc.identifier.isiWOS:000313740700019-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridMeng, X=53064279800en_US
dc.identifier.scopusauthoridZhang, Y=55316213200en_US
dc.identifier.scopusauthoridLao, L=7005681883en_US
dc.identifier.scopusauthoridSaito, R=55515037600en_US
dc.identifier.scopusauthoridLi, A=16245342100en_US
dc.identifier.scopusauthoridBäckman, CM=55514761800en_US
dc.identifier.scopusauthoridBerman, BM=35458606800en_US
dc.identifier.scopusauthoridRen, K=7102272533en_US
dc.identifier.scopusauthoridWei, PK=8976704400en_US
dc.identifier.scopusauthoridZhang, RX=7404864527en_US

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