{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T03:11:40Z","timestamp":1793761900995,"version":"4.6.1"},"reference-count":38,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2012,4,24]],"date-time":"2012-04-24T00:00:00Z","timestamp":1335225600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European Journal of Pain"],"published-print":{"date-parts":[[2012,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Neuropathic pain is caused by neural damage or dysfunction and neuropathic pain\u2010related symptoms are resistant to conventional analgesics. Neuroinflammation due to the cytokine\u2010chemokine network may play a pivotal role in neuropathic pain. We demonstrate that macrophage inflammatory protein\u20101\u03b2 (<jats:styled-content style=\"fixed-case\">MIP<\/jats:styled-content>\u20101\u03b2) participates in neuropathic pain.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Mice received partial sciatic nerve ligation (<jats:styled-content style=\"fixed-case\">PSL<\/jats:styled-content>), and tactile allodynia and thermal hyperalgesia were assessed by von <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>rey test and <jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>argreaves test, respectively. Agents were administered into the region surrounding the sciatic nerve (<jats:styled-content style=\"fixed-case\">SCN<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Using reverse transcription polymerase chain reaction, the m<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> expressions of <jats:styled-content style=\"fixed-case\">MIP<\/jats:styled-content>\u20101\u03b2 and its receptor (<jats:styled-content style=\"fixed-case\">CC<\/jats:styled-content>\u2010chemokine receptor 5; <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>5) in the injured <jats:styled-content style=\"fixed-case\">SCN<\/jats:styled-content> were up\u2010regulated after <jats:styled-content style=\"fixed-case\">PSL<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">MIP<\/jats:styled-content>\u20101\u03b2 immunoreactivity was localized in macrophages and Schwann cells and increased in the injured <jats:styled-content style=\"fixed-case\">SCN<\/jats:styled-content> on day 1. <jats:styled-content style=\"fixed-case\">PSL<\/jats:styled-content>\u2010induced tactile allodynia on days 4 to 7 was prevented by the administration of <jats:styled-content style=\"fixed-case\">MIP<\/jats:styled-content>\u20101\u03b2 neutralizing antibody (anti\u2010<jats:styled-content style=\"fixed-case\">MIP<\/jats:styled-content>\u20101\u03b2; on days 0, 3 and 6). <jats:styled-content style=\"fixed-case\">PSL<\/jats:styled-content>\u2010induced up\u2010regulations of inflammatory cytokine\u2010chemokine m<jats:styled-content style=\"fixed-case\">RNAs<\/jats:styled-content> in the injured <jats:styled-content style=\"fixed-case\">SCN<\/jats:styled-content> were suppressed with anti\u2010<jats:styled-content style=\"fixed-case\">MIP<\/jats:styled-content>\u20101\u03b2 treatment on day 7. Administration of <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>5 antagonist, <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\u2010ala\u2010peptide <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010amide (on days 0, 3 and 6) prevented tactile allodynia and thermal hyperalgesia on days 4 to 14. Single administration of recombinant mouse <jats:styled-content style=\"fixed-case\">MIP<\/jats:styled-content>\u20101\u03b2 (rm<jats:styled-content style=\"fixed-case\">MIP<\/jats:styled-content>\u20101\u03b2) elicited tactile allodynia. Moreover, rm<jats:styled-content style=\"fixed-case\">MIP<\/jats:styled-content>\u20101\u03b2 increased the m<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> expression of inflammatory mediators in the <jats:styled-content style=\"fixed-case\">SCN<\/jats:styled-content> on day 1 after administration.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These results suggest that <jats:styled-content style=\"fixed-case\">MIP<\/jats:styled-content>\u20101\u03b2 is a novel key mediator, and the peripheral <jats:styled-content style=\"fixed-case\">MIP<\/jats:styled-content>\u20101\u03b2\u2010<jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>5 axis contributes to neuropathic pain. Therefore, investigation of this cascade might be a validated approach for the elucidation of neuropathic pain mechanisms.<\/jats:p><\/jats:sec>","DOI":"10.1002\/j.1532-2149.2012.00146.x","type":"journal-article","created":{"date-parts":[[2012,4,24]],"date-time":"2012-04-24T14:08:43Z","timestamp":1335276523000},"page":"1271-1280","source":"Crossref","is-referenced-by-count":87,"title":["<scp>CC<\/scp>\u2010chemokine ligand 4\/macrophage inflammatory protein\u20101\u03b2 participates in the induction of neuropathic pain after peripheral nerve injury"],"prefix":"10.1002","volume":"16","author":[{"given":"F.","family":"Saika","sequence":"first","affiliation":[{"name":"Department of Pharmacology Wakayama Medical University  Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N.","family":"Kiguchi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Wakayama Medical University  Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y.","family":"Kobayashi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Wakayama Medical University  Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y.","family":"Fukazawa","sequence":"additional","affiliation":[{"name":"Department of Anatomy Kansai University of Health Sciences  Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Kishioka","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Wakayama Medical University  Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,4,24]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1331358100"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1093\/bja\/87.1.12"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2006.09.021"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra052723"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1080\/13550280290101003"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0610811104"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(94)90960-1"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3959(88)90026-7"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(06)00055-8"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.111.187724"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neulet.2010.07.085"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.pain.2010.02.025"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2008.07.008"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2006.03856.x"},{"key":"e_1_2_7_16_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrn1700"},{"key":"e_1_2_7_17_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1359-6101(02)00045-X"},{"key":"e_1_2_7_18_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0166-2236(99)01408-3"},{"key":"e_1_2_7_19_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainresrev.2005.11.004"},{"key":"e_1_2_7_20_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V95.10.3032"},{"key":"e_1_2_7_21_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.21-14-05027.2001"},{"key":"e_1_2_7_22_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.pain.2011.09.022"},{"key":"e_1_2_7_23_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0707263"},{"key":"e_1_2_7_24_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.antiviral.2005.03.007"},{"key":"e_1_2_7_25_1","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2234"},{"key":"e_1_2_7_26_1","first-page":"1341","article-title":"Cellular localization of the chemokine receptor CCR5. 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