Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/78319
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Type: Journal article
Title: Low-dose endotoxin potentiates capsaicin-induced pain in man: evidence for a pain neuroimmune connection
Author: Hutchinson, M.
Bujis, M.
Tuke, S.
Kwok, Y.
Gentgall, M.
Williams, D.
Rolan, P.
Citation: Brain Behavior and Immunity, 2013; 30:3-11
Publisher: Academic Press Inc
Issue Date: 2013
ISSN: 0889-1591
1090-2139
Statement of
Responsibility: 
Mark R. Hutchinson, Mara Buijs, Jonathan Tuke, Yuen Hei Kwok, Melanie Gentgall, Desmond Williams, Paul Rolan
Abstract: Despite the wealth of evidence in animals that immune activation has a key role in the development and maintenance of chronic pain, evidence to support this in humans is scant. We have sought such evidence by examining the effect of a subtle immunological stimulus, low dose intravenous endotoxin, on the allodynia, hyperalgesia, flare and pain produced by intradermal capsaicin in healthy volunteers. Here we provide evidence of immune priming of this neuropathic-like pain response in humans. Specifically, in 12 healthy volunteers, activation of Toll-Like Receptor 4 by endotoxin (0.4ng/kg IV) caused significant 5.1-fold increase in the 90-min integral of areas of capsaicin-induced allodynia (95% CI 1.3-9.1), 2.2-fold increase in flare (95% CI 1.9-2.6) and 1.8-fold increase in hyperalgesia (95% CI 1.1-2.5) following 50μg intradermal capsaicin injected into the forearm 3.5h after endotoxin. These data demonstrate clinically a significant role for the neuroimmune pain connection in modifying pain, thus providing evidence that immune priming may produce pain enhancement in humans and hence offer a novel range of pharmacological targets for anti-allodynics and/or analgesics. Additionally, the simplicity of the model makes it suitable as a test-bed for novel immune-targeted pain therapeutics.
Keywords: Endotoxin; Capsaicin; Chronic pain; TLR4
Rights: Copyright © 2013 Elsevier Inc. All rights reserved.
RMID: 0020128127
DOI: 10.1016/j.bbi.2013.03.002
Appears in Collections:Pharmacology publications

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