Sensory TRP channels contribute differentially to skin inflammation and persistent itch

Jing Feng, Pu Yang, Madison R. Mack, Dariia Dryn, Jialie Luo, Xuan Gong, Shenbin Liu, Landon K. Oetjen, Alexander V. Zholos, Zhinan Mei, Shijin Yin, Brian S. Kim and Hongzhen Hu ()
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Jing Feng: The Center for the Study of Itch, Washington University School of Medicine
Pu Yang: The Center for the Study of Itch, Washington University School of Medicine
Madison R. Mack: The Center for the Study of Itch, Washington University School of Medicine
Dariia Dryn: The Center for the Study of Itch, Washington University School of Medicine
Jialie Luo: The Center for the Study of Itch, Washington University School of Medicine
Xuan Gong: The Center for the Study of Itch, Washington University School of Medicine
Shenbin Liu: The Center for the Study of Itch, Washington University School of Medicine
Landon K. Oetjen: The Center for the Study of Itch, Washington University School of Medicine
Alexander V. Zholos: Institute of Biology, Taras Shevchenko National University of Kyiv
Zhinan Mei: College of Pharmacy, South-Central University for Nationalities
Shijin Yin: College of Pharmacy, South-Central University for Nationalities
Brian S. Kim: The Center for the Study of Itch, Washington University School of Medicine
Hongzhen Hu: The Center for the Study of Itch, Washington University School of Medicine

Nature Communications, 2017, vol. 8, issue 1, 1-12

Abstract: Abstract Although both persistent itch and inflammation are commonly associated with allergic contact dermatitis (ACD), it is not known if they are mediated by shared or distinct signaling pathways. Here we show that both TRPA1 and TRPV1 channels are required for generating spontaneous scratching in a mouse model of ACD induced by squaric acid dibutylester (SADBE), a small molecule hapten, through directly promoting the excitability of pruriceptors. TRPV1 but not TRPA1 channels protect the skin inflammation, as genetic ablation of TRPV1 function or pharmacological ablation of TRPV1-positive sensory nerves promotes cutaneous inflammation in the SADBE-induced ACD. Our results demonstrate that persistent itch and inflammation are mediated by distinct cellular and molecular mechanisms in a mouse model of ACD. Identification of distinct roles of TRPA1 and TRPV1 in regulating itch and inflammation may provide new insights into the pathophysiology and treatment of chronic itch and inflammation in ACD patients.

Date: 2017
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DOI: 10.1038/s41467-017-01056-8

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