TRPV1 and TRPA1 in cutaneous neurogenic and chronic inflammation： pro-inflammatory response induced by their activation and their sensitization

作     者：Olivier Gouin Killian L'Herondelle Nicolas Lebonvallet Christelle Le Gall-lanotto Mehdi Sakka Virginie Buhe Emmanuelle PIee-Gautier Jean-Luc Carre Luc Lefeuvre Laurent Misery~,Raphaele Le Garrec 

作者机构：Laboratory on Interaction Neurons-Keratinocytes (LINK) University of Western Brittany 29200 Brest France Uriage Dermatological Laboratories 92400 Courbevoie France 

出 版 物：《Protein & Cell》 (蛋白质与细胞（英文版）)

年 卷 期：2017年第8卷第9期

页      面：644-661页

核心收录：

学科分类：0710[理学-生物学] 071010[理学-生物化学与分子生物学] 081704[工学-应用化学] 07[理学] 08[工学] 0817[工学-化学工程与技术] 

基　　金：supported by the Uriage Dermatological Laboratories, Courbevoie, France research grants from Uriage research grants from Beiersdorf, Clarins, L'Oreal, Natura, Pierre Fabre research grants from BASF, Johnson & Johnson research grants from Almirall, BASF, Beiersdorf, Bioderma, Celgene, Clarins, Expanscience, Galderma, Johnson & Johnson, L'Oreal, Natura, Pierre Fabre, Sofibel, Solabia, Uriage 

主　　题：sensory nervenflammation inflammatory geneneurogenic skinregulation pruritus 

摘      要：Cutaneous neurogenic inflammation （CNI） is inflammation that is induced （or enhanced） in the skin by the release of neuropeptides from sensory nerve endings. Clinical manifestations are mainly sensory and vascular disorders such as pruritus and erythema. Transient receptor potential vanilloid 1 and ankyrin 1 （TRPV1 and TRPA1, respectively） are non-selective cation channels known to specifically participate in pain and CNI. Both TRPV1 and TRPA1 are co-expressed in a large subset of sensory nerves, where they integrate numerous noxious stimuli. It is now clear that the expression of both channels also extends far beyond the sensory nerves in the skin, occuring also in keratinocytes, mast cells, dendritic cells, and endothelial cells. In these non-neu- ronal cells, TRPV1 and TRPA1 also act as nociceptive sensors and potentiate the inflammatory process. This review discusses the role of TRPV1 and TRPA1 in the modulation of inflammatory genes that leads to or maintains CNI in sensory neurons and non-neuronal skin cells. In addition, this review provides a summary of current research on the intracellular sensitization pathways of both TRP channels by other endogenous inflammatory mediators that promote the self-maintenance of CNI.