title: Ultra violet-induced localized inflammatory hyperalgesia in awake rats and the role of sensory and sympathetic innervation of the skin.
abstract: Exposure to mid range ultrat violet radiations (UVBs) has been shown to produce systemic inflammation and hyperalgesia in mice [Saadé, N.E., Nasr, I.W., Massaad, C.A., Safieh-Garabedian, B., Jabbur, S.J., Kanaan, S.A., 2000. Modulation of ultraviolet-induced hyperalgesia and cytokine upregulation by interleukins 10 and 13. Br. J. Pharmacol. 131, 1317-1324]. Our aim was to characterize a new rat model of localized exposure to UVB and to determine the role of skin innervation in the observed hyperalgesia and cytokine upregulation. In several groups of rats one hindpaw was exposed to UVB (250-350 mJ/cm(2)) and this was followed by the application, to the plantar area of the paw, of either Von Frey hairs or a few acetone drops to measure tactile and cold allodynia, respectively. Thermal hyperalgesia was assessed by the paw withdrawal latency and duration. Cytokine levels were determined, by ELISA, in processed samples of skin tissue isolated from the exposed and non-exposed paws. UVB induced a biphasic thermal hyperalgesia and cold and tactile allodynia with an early phase that peaked at 3-6h and disappeared at 24h and a late phase with a peak at 48 h and recovery at 72-h post-exposure. Tumor necrosis factor, interleukins 1 beta, 6, 8, 10 and NGF levels were significantly increased following the same biphasic temporal pattern. Chemical ablation of capsaicin sensitive afferents and guanethidine injection produced significant alteration of the hyperalgesia and allodynia. The increase in cytokine levels by UVB was also altered by both treatments. The present study describes a new animal model for localized UVB-induced inflammatory hyperalgesia and provides evidence about the involvement of neurogenic mechanisms in the observed hyperalgesia and upregulation of proinflammatory mediators.
authors: Department of Human Morphology, Faculty of Medicine, American University of Beirut, Riad E1 Solh Beirut, Beirut 1107-2020, Lebanon. nesaade@aub.edu.lb
authors: Nayef E
authors: NE
authors: Saadé
authors: Omar
authors: O
authors: Farhat
authors: Omar
authors: O
authors: Rahal
authors: Bared
authors: B
authors: Safieh-Garabedian
authors: Daniel
authors: D
authors: Le Bars
authors: Suhayl J
authors: SJ
authors: Jabbur
mesh_terms: D000818:Animals; D016207:Cytokines / Q000378:metabolism; D003872:Dermatitis / Q000188:drug therapy / Q000276:immunology*; D004195:Disease Models, Animal; D006145:Guanethidine / Q000494:pharmacology; D006930:Hyperalgesia / Q000188:drug therapy / Q000276:immunology*; D020932:Nerve Growth Factor / Q000378:metabolism; D015213:Neuroimmunomodulation / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D009475:Neurons, Afferent / Q000502:physiology; D009619:Nociceptors / Q000502:physiology / Q000528:radiation effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012867:Skin / Q000276:immunology* / Q000294:innervation / Q000528:radiation effects; D013563:Sympathectomy, Chemical; D013564:Sympathetic Nervous System / Q000276:immunology*; D013565:Sympatholytics / Q000494:pharmacology; D014466:Ultraviolet Rays / Q000009:adverse effects; D014851:Wakefulness
chemical_list: D016207:Cytokines; D013565:Sympatholytics; D020932:Nerve Growth Factor; D006145:Guanethidine