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Skin Injury Activates a Rapid TRPV1-Dependent Antiviral Protein Response.

Publication ,  Journal Article
Lei, V; Handfield, C; Kwock, JT; Kirchner, SJ; Lee, MJ; Coates, M; Wang, K; Han, Q; Wang, Z; Powers, JG; Wolfe, S; Corcoran, DL; Fanelli, B ...
Published in: J Invest Dermatol
August 2022

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.

Duke Scholars

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Published In

J Invest Dermatol

DOI

EISSN

1523-1747

Publication Date

August 2022

Volume

142

Issue

8

Start / End Page

2249 / 2259.e9

Location

United States

Related Subject Headings

  • TRPV Cation Channels
  • Skin
  • Nociceptors
  • Mice
  • Interleukin-27
  • Immunity, Innate
  • Humans
  • Herpes Simplex
  • Dermatology & Venereal Diseases
  • Antiviral Restriction Factors
 

Citation

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MLA
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Lei, V., Handfield, C., Kwock, J. T., Kirchner, S. J., Lee, M. J., Coates, M., … MacLeod, A. S. (2022). Skin Injury Activates a Rapid TRPV1-Dependent Antiviral Protein Response. J Invest Dermatol, 142(8), 2249-2259.e9. https://doi.org/10.1016/j.jid.2021.11.041
Lei, Vivian, Chelsea Handfield, Jeffery T. Kwock, Stephen J. Kirchner, Min Jin Lee, Margaret Coates, Kaiyuan Wang, et al. “Skin Injury Activates a Rapid TRPV1-Dependent Antiviral Protein Response.J Invest Dermatol 142, no. 8 (August 2022): 2249-2259.e9. https://doi.org/10.1016/j.jid.2021.11.041.
Lei V, Handfield C, Kwock JT, Kirchner SJ, Lee MJ, Coates M, et al. Skin Injury Activates a Rapid TRPV1-Dependent Antiviral Protein Response. J Invest Dermatol. 2022 Aug;142(8):2249-2259.e9.
Lei, Vivian, et al. “Skin Injury Activates a Rapid TRPV1-Dependent Antiviral Protein Response.J Invest Dermatol, vol. 142, no. 8, Aug. 2022, pp. 2249-2259.e9. Pubmed, doi:10.1016/j.jid.2021.11.041.
Lei V, Handfield C, Kwock JT, Kirchner SJ, Lee MJ, Coates M, Wang K, Han Q, Wang Z, Powers JG, Wolfe S, Corcoran DL, Fanelli B, Dadlani M, Ji R-R, Zhang JY, MacLeod AS. Skin Injury Activates a Rapid TRPV1-Dependent Antiviral Protein Response. J Invest Dermatol. 2022 Aug;142(8):2249-2259.e9.
Journal cover image

Published In

J Invest Dermatol

DOI

EISSN

1523-1747

Publication Date

August 2022

Volume

142

Issue

8

Start / End Page

2249 / 2259.e9

Location

United States

Related Subject Headings

  • TRPV Cation Channels
  • Skin
  • Nociceptors
  • Mice
  • Interleukin-27
  • Immunity, Innate
  • Humans
  • Herpes Simplex
  • Dermatology & Venereal Diseases
  • Antiviral Restriction Factors