Ultraviolet-B induced inflammation of human skin: Characterisation and comparison with traditional models of hyperlagesia

被引:74
作者
Bishop, Thomas [1 ]
Ballard, Angela [1 ]
Holmes, Helen [1 ]
Young, Antony R. [2 ]
McMahon, Stephen B. [1 ]
机构
[1] Kings Coll London, Neurorestorat Grp, Wolfson Ctr Age Related Dis, Wolfson Wing, London SE1 1UL, England
[2] Kings Coll London, St Johns Inst Dermatol, Div Genet & Mol Med, Guys Hosp, London SE1 9RT, England
关键词
Primary hyperalgesia; Secondary hyperalgesia; Sunburn; Ultraviolet-B; Nociceptor sensitisation; BRADYKININ B-1 RECEPTOR; HUMAN LUNG FIBROBLASTS; SECONDARY HYPERALGESIA; MECHANICAL HYPERALGESIA; SUBSTANCE-P; PAIN MODEL; PERIPHERAL INFLAMMATION; CUTANEOUS HYPERALGESIA; CENTRAL SENSITIZATION; NERVE-FIBERS;
D O I
10.1016/j.ejpain.2008.06.006
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
The effect on human skin of over-exposure to solar ultraviolet radiation (UVR) has been well described. The erythema produced is commonly referred to as 'sunburn'. Recently UVR induced inflammation has been Utilised as a human model of sub-acute pain. Our aim was to characterise the sensory phenotype of UVB inflammation in human volunteers. We delivered UVB to small areas of volar forearm skin in healthy volunteers and found that the degree of inflammation and concomitant increase in sensitivity to cutaneous stimuli were UVB dose and time dependant. We directly compared UVB induced inflammation and the more established thermal burn and topical capsaicin pain models. UVB inflammation produced precisely demarcated erythematous lesions without secondary flare. Both thermal burns and topical capsaicin produced large areas of flare, indistinguishable in character from the primary lesions. Moreover, UVB inflammation induced large reductions in mechanical pain threshold restricted to the primary lesion site, whereas the more established inflammatory pain models produced not only primary hypersensitivity but also significant areas of secondary mechanical hypersensitivity. Taken together these findings suggest that UVB inflammation, at least using moderate doses produces sensory changes primarily by sensitising peripheral pain Processing in the relative absence of alterations in central pain processing. (C) 2008 Published by Elsevier Ltd on behalf of European Federation of Chapters of the International Association for the Study of Pain.
引用
收藏
页码:524 / 532
页数:9
相关论文
共 57 条
[1]   Secondary hyperalgesia to mechanical but not heat stimuli following a capsaicin injection in hairy skin [J].
Ali, Z ;
Meyer, RA ;
Campbell, JN .
PAIN, 1996, 68 (2-3) :401-411
[2]   Mechanical and heat sensitization of cutaneous nociceptors after peripheral inflammation in the rat [J].
Andrew, D ;
Greenspan, JD .
JOURNAL OF NEUROPHYSIOLOGY, 1999, 82 (05) :2649-2656
[3]  
BENRATH J, 1995, EUR J PHARM-ENVIRON, V293, P87
[4]   Differential time courses of skin blood flow and hyperalgesia in the human sunburn reaction following ultraviolet irradiation of the skin [J].
Benrath, J ;
Gillardon, F ;
Zimmermann, M .
EUROPEAN JOURNAL OF PAIN, 2001, 5 (02) :155-167
[5]   Effects of antihyperalgesic drugs on experimentally induced hyperalgesia in man [J].
Bickel, A ;
Dorfs, S ;
Schmelz, M ;
Forster, C ;
Uhl, W ;
Handwerker, HO .
PAIN, 1998, 76 (03) :317-325
[6]   Differences in the performance of commercially available 10-g monofilaments [J].
Booth, J ;
Young, MJ .
DIABETES CARE, 2000, 23 (07) :984-988
[7]   Mechanical sensory threshold testing using nylon monofilaments: The pain field's "Tin Standard" [J].
Bove, Geoffrey .
PAIN, 2006, 124 (1-2) :13-17
[8]  
Charlton E, 1995, Pain, V63, P277, DOI 10.1016/0304-3959(95)90040-3
[9]   Ultraviolet B irradiation-enhanced interleukin (IL)-6 production and mRNA expression are mediated by IL-1 alpha in cultured human keratinocytes [J].
Chung, JH ;
Youn, SH ;
Koh, WS ;
Eun, HC ;
Cho, KH ;
Park, KC ;
Youn, JI .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1996, 106 (04) :715-720
[10]   Ultraviolet light induced injury: Immunological and inflammatory effects [J].
Clydesdale, GJ ;
Dandie, GW ;
Muller, HK .
IMMUNOLOGY AND CELL BIOLOGY, 2001, 79 (06) :547-568