AbstractAimsItch often occurs in cutaneous conditions characterized by some degree of inflammation, e.g. atopic dermatitis, psoriasis or urticaria. It is unclear to which extent cutaneous inflammation causes sensitization of pruriceptive primary afferent C-fibers. The aim of this study was to explore if inflammation induced by UVB (B-ultraviolet rays) modify neurogenic inflammation and itch associated with experimental itch provocations.MethodsTwenty healthy volunteers (10F/10M, 26.2 ± 1.6 years) were included. Eight circles (diameter=2cm), four on each volar forearm were studied. Two spots were irradiated with 0.5 × Minimal Erythema Dose (MED), two with 1× MED and two with 2× MED, and two acted as controls. Itch provocations were conducted using histamine (1%) percutaneously introduced and 35–45 cowhage spicules (non-histaminergic itch). The duration and intensity of itch and pain, sensitivity to touch-evoked itch (STI), mechanical pain thresholds (MPT) and sensitivity (MPS), and superficial blood perfusion where measured in UVB-irradiated- and control areas 24-h after UVB-irradiation and following each itch provocation.ResultsUVB induced dose-dependent hyperalgesia validated by decreased MPT, increased MPS and neurogenic inflammation (all P < 0.01). UVB-induced inflammation did not increase the magnitude of itch reported following any itch provocation. However, cowhage was associated with more pain in UVB-irradiated areas and the proportional ratings of the mixed itch and pain sensation was shifted towards increased pain dominance (P < 0.01). Itch provocations did not increase the mechanical hyperalgesia induced by UVB, whereas it provoked an increase in superficial blood perfusion compared to UVB alone (P < 0.05).Conclusions(1) The UVB model induces sensitization to pain but not itch stimuli and independently increases the nociceptive sensations associated with non-histaminergic itch provocation. (2) The inflammatory UVB-perturbation does not mimic the sensitization associated with inflammatory dermatoses where lesioned skin is more receptive to pruritogens, suggesting that more specific or prolonged inflammatory processes are involved in clinical itch conditions.