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Skin Injury Activates a Rapid TRPV1-Dependent Antiviral Protein Response
Journal article   Open access   Peer reviewed

Skin Injury Activates a Rapid TRPV1-Dependent Antiviral Protein Response

Vivian Lei, Chelsea Handfield, Jeffery T. Kwock, Stephen J. Kirchner, Min Jin Lee, Margaret Coates, Kaiyuan Wang, Qingjian Han, Zilong Wang, Jennifer G. Powers, …
Journal of investigative dermatology, Vol.142(8), pp.2249-2259.e9
08/01/2022
DOI: 10.1016/j.jid.2021.11.041
PMCID: PMC9259761
PMID: 35007556
url
https://doi.org/10.1016/j.jid.2021.11.041View
Published (Version of record) Open Access

Abstract

The skin serves as the interface between the body and the environment and plays a fundamental role in innate antimicrobial host immunity. Antiviral proteins (AVPs) are part of the innate host defense system and provide protection against viral pathogens. How breach of the skin barrier influences innate AVP production remains largely unknown. In this study, we characterized the induction and regulation of AVPs after skin injury and identified a key role of TRPV1 in this process. Transcriptional and phenotypic profiling of cutaneous wounds revealed that skin injury induces high levels of AVPs in both mice and humans. Remarkably, pharmacologic and genetic ablation of TRPV1-mediated nociception abrogated the induction of AVPs, including Oas2, Oasl2, and Isg15 after skin injury in mice. Conversely, stimulation of TRPV1 nociceptors was sufficient to induce AVP production involving the CD301b(+) cells.IL-27.mediated signaling pathway. Using IL-27 receptor.knockout mice, we show that IL-27 signaling is required in the induction of AVPs after skin injury. Finally, loss of TRPV1 signaling leads to increased viral infectivity of herpes simplex virus. Together, our data indicate that TRPV1 signaling ensures skin antiviral competence on wounding.
Dermatology Life Sciences & Biomedicine Science & Technology

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