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Nat Commun. 2017 Oct 30;8(1):980. doi: 10.1038/s41467-017-01056-8.

Sensory TRP channels contribute differentially to skin inflammation and persistent itch.

Author information

1
Department of Anesthesiology, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA.
2
Division of Dermatology, Department of Medicine, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA.
3
Department of Biophysics, Institute of Biology, Taras Shevchenko National University of Kyiv, Kyiv, 01601, Ukraine.
4
College of Pharmacy, South-Central University for Nationalities, Wuhan, 430074, China.
5
Department of Anesthesiology, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA. hongzhen.hu@wustl.edu.

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.

PMID:
29081531
PMCID:
PMC5661746
DOI:
10.1038/s41467-017-01056-8
[Indexed for MEDLINE]
Free PMC Article

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