Sunburn—A human inflammatory pain model for primary and secondary hyperalgesia

Sunburn—A human inflammatory pain model for primary and secondary hyperalgesia In this issue of the Scandinavian Journal of Pain, Rössler et al. describe an experimental model that confirms the central origin of pin prick hyperalgesia in the human sunburn model [1]. UV-irradiation has been used extensively as a translational model for inflammatory pain and hyperalgesia using rodents [2,3], pigs [4] and human volunteers [5,6]. The time course of hyperalgesia development is similar in different species, with an onset latency of 3–6 h and a peak responsiveness 24–48 h after irradiation, thus representing a useful experimental model for drug testing. Upon irradiation of small skin patches (about 1cm2), only primary hyperalgesia has been detected in human and rodents [2,3]. As a multitude of mediators are being released upon UV-irradiation of the skin, including eicosanoids (e.g. PGE2, PGD2, PGF2a, LTB-4, 12-HETE), cytokines (e.g. IL-1, IL-6, IL-8, TNF-alpha), growth factors (e.g. TGF-beta, VEGF, NGF) vasoactive amines and neuropeptides (e.g.histamine, bradykinin, CGRP), researchers have mainly focused on the primary hyperalgesia that is evident in the inflamed skin. Some of these can be accounted for the in flammatory UV-induced responses, such as erythema (i.e. CGRP) or heat hyperalgesia (e.g. PGE2, bradykinin) and sensitization of heat-sensing ion channels (e.g. TRPV1). Another cardinal symptom of UV-inflammation http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Scandinavian Journal of Pain de Gruyter

Sunburn—A human inflammatory pain model for primary and secondary hyperalgesia

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Publisher
de Gruyter
Copyright
© 2012 Scandinavian Association for the Study of Pain
ISSN
1877-8860
eISSN
1877-8879
D.O.I.
10.1016/j.sjpain.2012.11.006
Publisher site
See Article on Publisher Site

Abstract

In this issue of the Scandinavian Journal of Pain, Rössler et al. describe an experimental model that confirms the central origin of pin prick hyperalgesia in the human sunburn model [1]. UV-irradiation has been used extensively as a translational model for inflammatory pain and hyperalgesia using rodents [2,3], pigs [4] and human volunteers [5,6]. The time course of hyperalgesia development is similar in different species, with an onset latency of 3–6 h and a peak responsiveness 24–48 h after irradiation, thus representing a useful experimental model for drug testing. Upon irradiation of small skin patches (about 1cm2), only primary hyperalgesia has been detected in human and rodents [2,3]. As a multitude of mediators are being released upon UV-irradiation of the skin, including eicosanoids (e.g. PGE2, PGD2, PGF2a, LTB-4, 12-HETE), cytokines (e.g. IL-1, IL-6, IL-8, TNF-alpha), growth factors (e.g. TGF-beta, VEGF, NGF) vasoactive amines and neuropeptides (e.g.histamine, bradykinin, CGRP), researchers have mainly focused on the primary hyperalgesia that is evident in the inflamed skin. Some of these can be accounted for the in flammatory UV-induced responses, such as erythema (i.e. CGRP) or heat hyperalgesia (e.g. PGE2, bradykinin) and sensitization of heat-sensing ion channels (e.g. TRPV1). Another cardinal symptom of UV-inflammation

Journal

Scandinavian Journal of Painde Gruyter

Published: Jan 1, 2013

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