Subpopulations of primary nociceptors (C- and Aδ-fibers), express the TRPV1 receptor for heat and capsaicin. During cutaneous inflammation, these afferents may become sensitized, leading to primary hyperalgesia. It is known that TRPV1⁺ nociceptors are involved in heat hyperalgesia; however, their involvement in mechanical hyperalgesia is unclear. This study explored the contribution of capsaicin-sensitive nociceptors in the development of mechanical and heat hyperalgesia in humans following ultraviolet-B (UVB) irradiation. Skin areas in 18 healthy volunteers were randomized to treatment with 8% capsaicin/vehicle patches for 24 h. After patches removal, one capsaicin-treated area and one vehicle area were irradiated with 2xMED (minimal erythema dose) of UVB. 1, 3 and 7 days post-UVB exposure, tests were performed to evaluate the development of UVB-induced cutaneous hyperalgesia: thermal detection and pain thresholds, pain sensitivity to supra-threshold heat stimuli, mechanical pain threshold and sensitivity, touch pleasantness, trans-epidermal water loss (TEWL), inflammatory response, pigmentation and micro-vascular reactivity. Capsaicin pre-treatment, in the UVB-irradiated area (Capsaicin + UVB area), increased heat pain thresholds (P < 0.05), and decreased supra-threshold heat pain sensitivity (P < 0.05) 1, 3 and 7 days post-UVB irradiation, while mechanical hyperalgesia resulted unchanged (P > 0.2). No effects of capsaicin were reported on touch pleasantness (P = 1), TEWL (P = 0.31), inflammatory response and pigmentation (P > 0.3) or micro-vascular reactivity (P > 0.8) in response to the UVB irradiation. 8% capsaicin ablation predominantly defunctionalizes TRPV1⁺-expressing cutaneous nociceptors responsible for heat pain transduction, suggesting that sensitization of these fibers is required for development of heat hyperalgesia following cutaneous UVB-induced inflammation but they are likely only partially necessary for the establishment of robust primary mechanical hyperalgesia.

初级伤害感受器（C 和 Aδ 纤维）的亚群表达了热和辣椒素的 TRPV1 受体。在皮肤炎症期间，这些传入神经可能变得敏感，导致原发性痛觉过敏。据了解，TRPV1 ⁺伤害感受器参与热痛觉过敏；然而，它们与机械痛觉过敏的关系尚不清楚。本研究探讨了辣椒素敏感的伤害感受器在紫外线-B (UVB) 照射后人类机械和热痛觉过敏的发展中的作用。18 名健康志愿者的皮肤区域随机接受 8% 辣椒素/载体贴剂治疗 24 小时。去除贴剂后，用 2xMED（最小红斑剂量）UVB 照射一个辣椒素处理区域和一个载体区域。在 UVB 暴露后 1、3 和 7 天，进行测试以评估 UVB 诱导的皮肤痛觉过敏的发展：热检测和痛阈、对超阈值热刺激的疼痛敏感性、机械痛阈和敏感性、触摸愉悦度、反式- 表皮失水 (TEWL)，炎症反应、色素沉着和微血管反应性。辣椒素预处理，在UVB照射区（辣椒素+UVB区），增加热痛阈值（P  < 0.05），并且 在 UVB 照射后 1、3 和 7 天降低超阈值热痛敏感性（P < 0.05），而机械痛觉过敏没有变化（P  > 0.2）。未报告辣椒素 对 UVB 照射的触感愉悦度 ( P  = 1)、TEWL ( P  = 0.31)、炎症反应和色素沉着 ( P  > 0.3) 或微血管反应性 ( P > 0.8) 的影响。8% 辣椒素消融主要使 TRPV1 ^{+ 去功能化}- 表达负责热痛转导的皮肤伤害感受器，表明这些纤维的敏化是皮肤 UVB 诱导的炎症后热痛觉过敏的发展所必需的，但它们可能只是建立强大的原发性机械痛觉过敏的部分必要条件。