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CXCL5 mediates UVB irradiation-induced pain

Dawes, JM; Calvo, M; Perkins, JR; Paterson, KJ; Kiesewetter, H; Hobbs, C; Kaan, TK; ... McMahon, SB; + view all (2011) CXCL5 mediates UVB irradiation-induced pain. Sci Transl Med , 3 (90) 90ra60+-90ra60+. 10.1126/scitranslmed.3002193%20%5Bdoi%5D.

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Abstract

Many persistent pain states (pain lasting for hours, days, or longer) are poorly treated because of the limitations of existing therapies. Analgesics such as nonsteroidal anti-inflammatory drugs and opioids often provide incomplete pain relief and prolonged use results in the development of severe side effects. Identification of the key mediators of various types of pain could improve such therapies. Here, we tested the hypothesis that hitherto unrecognized cytokines and chemokines might act as mediators in inflammatory pain. We used ultraviolet B (UVB) irradiation to induce persistent, abnormal sensitivity to pain in humans and rats. The expression of more than 90 different inflammatory mediators was measured in treated skin at the peak of UVB-induced hypersensitivity with custom-made polymerase chain reaction arrays. There was a significant positive correlation in the overall expression profiles between the two species. The expression of several genes [interleukin-1beta (IL-1beta), IL-6, and cyclooxygenase-2 (COX-2)], previously shown to contribute to pain hypersensitivity, was significantly increased after UVB exposure, and there was dysregulation of several chemokines (CCL2, CCL3, CCL4, CCL7, CCL11, CXCL1, CXCL2, CXCL4, CXCL7, and CXCL8). Among the genes measured, CXCL5 was induced to the greatest extent by UVB treatment in human skin; when injected into the skin of rats, CXCL5 recapitulated the mechanical hypersensitivity caused by UVB irradiation. This hypersensitivity was associated with the infiltration of neutrophils and macrophages into the dermis, and neutralizing the effects of CXCL5 attenuated the abnormal pain-like behavior. Our findings demonstrate that the chemokine CXCL5 is a peripheral mediator of UVB-induced inflammatory pain, likely in humans as well as rats.

Type: Article
Title: CXCL5 mediates UVB irradiation-induced pain
DOI: 10.1126/scitranslmed.3002193%20%5Bdoi%5D
Publisher version: http://dx.doi.org/10.1126/scitranslmed.3002193%20%...
Additional information: citeulike-article-id: 12411837 citeulike-linkout-0: http://dx.doi.org/10.1126/scitranslmed.3002193%20%5Bdoi%5D comment: eng —=note-separator=— Nlm —=note-separator=— Dawes, John M Calvo, Margarita Perkins, James R Paterson, Kathryn J Kiesewetter, Hannes Hobbs, Carl Kaan, Timothy K Y Orengo, Christine Bennett, David L H McMahon, Stephen B 083259/Wellcome Trust/United Kingdom Biotechnology and Biological Sciences Research Council/United Kingdom Wellcome Trust/United Kingdom Research Support, Non-U.S. Gov’t United States Science translational medicine Sci Transl Med. 2011 Jul 6;3(90):90ra60. doi: 10.1126/scitranslmed.3002193. —=note-separator=— CXCL5 mediates UVB irradiation-induced pain —=note-separator=— Jul 6 keywords: adverse, animals, calcium-metabolism, cell, cells, chemokine, cultured, cxcl5-, cytokines-immunology, effects, female, humans, immunology, immunology-, macrophages-cytology-immunology, male, measurement, movement-immunology, pain, pain-, physiopathology, radiation, rats, rays-, skin-cytology-immunology-, ultraviolet, wistar, *file-import-13-06-12 posted-at: 2013-06-12 22:01:26 priority: 2 bdsk-url-1: http://dx.doi.org/10.1126/scitranslmed.3002193%5C%20%5C%5Bdoi%5C%5D bdsk-url-2: http://dx.doi.org/10.1126/scitranslmed.3002193%5C%2520%5C%255Bdoi%5C%255D
UCL classification: UCL > School of Life and Medical Sciences
UCL > School of Life and Medical Sciences > Faculty of Life Sciences
UCL > School of Life and Medical Sciences > Faculty of Life Sciences > Biosciences (Division of) > Structural and Molecular Biology
URI: http://discovery.ucl.ac.uk/id/eprint/1396622
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