Scholzen T E, Brzoska T, Kalden D H, O'Reilly F, Armstrong C A, Luger T A, Ansel J C
Department of Dermatology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
J Investig Dermatol Symp Proc. 1999 Sep;4(1):55-60. doi: 10.1038/sj.jidsp.5640182.
Ultraviolet (UV) irradiation of the skin causes both inflammation and alterations in the skin immune system. There is increasing experimental evidence that UV-induced skin inflammation is influenced by the sensory nervous system and the neuroendocrine system in the skin. The resulting complex network of cytokines, chemokines, neuropeptides, neuropeptide-degrading enzymes, neurohormones, and other inflammatory mediators mediate photodermatitis and cutaneous inflammation. Neuropeptides such as substance P (SP) and calcitonin gene-related peptide (CGRP) are released from sensory nerves innervating the skin upon UV exposure. In addition, a variety of cells in the skin produce increased neuroendocrine hormones such as proopiomelanocortin (POMC) peptides and their receptors as well as neurotrophins after UV exposure. Neuropeptides and neurohormones are capable of directly or indirectly mediating UV-induced cutaneous neurogenic inflammation by the induction of vasodilatation, plasma extravasation, and augmentation of UV-induced cytokine, chemokine, or cellular adhesion molecule expression required for activation and trafficking of inflammatory cells into the inflamed tissue. Neuropeptides and neurotrophins may also play a role in the repair of cutaneous UV injury. In addition to proinflammatory effects, UV-induced neuropeptides and neurohormones such as CGRP and alpha-melanocyte-stimulating hormone may have immunosuppressive effects in the skin. This review will focus on the role that SP, CGRP, POMC peptides, and their receptors may play in modulating UV-induced inflammation in the skin.
皮肤受到紫外线(UV)照射会引发炎症以及皮肤免疫系统的改变。越来越多的实验证据表明,紫外线诱导的皮肤炎症受皮肤中的感觉神经系统和神经内分泌系统影响。由此产生的由细胞因子、趋化因子、神经肽、神经肽降解酶、神经激素和其他炎症介质组成的复杂网络介导了光性皮炎和皮肤炎症。诸如P物质(SP)和降钙素基因相关肽(CGRP)等神经肽在紫外线照射后从支配皮肤的感觉神经中释放出来。此外,皮肤中的多种细胞在紫外线照射后会产生更多的神经内分泌激素,如阿片促黑素皮质素原(POMC)肽及其受体以及神经营养因子。神经肽和神经激素能够通过诱导血管舒张、血浆外渗以及增强紫外线诱导的细胞因子、趋化因子或细胞黏附分子的表达,直接或间接介导紫外线诱导的皮肤神经源性炎症,这些表达是炎症细胞激活和进入炎症组织所必需的。神经肽和神经营养因子也可能在皮肤紫外线损伤的修复中发挥作用。除了促炎作用外,紫外线诱导的神经肽和神经激素,如CGRP和α-黑素细胞刺激素,可能在皮肤中具有免疫抑制作用。本综述将聚焦于SP、CGRP、POMC肽及其受体在调节紫外线诱导的皮肤炎症中可能发挥的作用。