IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v8y2017i1d10.1038_s41467-017-01056-8.html
   My bibliography  Save this article

Sensory TRP channels contribute differentially to skin inflammation and persistent itch

Author

Listed:
  • 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
    Institute of Biology, Taras Shevchenko National University of Kyiv)

  • 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
    College of Pharmacy, South-Central University for Nationalities)

  • 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)

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.

Suggested Citation

  • 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 & Hongzhen Hu, 2017. "Sensory TRP channels contribute differentially to skin inflammation and persistent itch," Nature Communications, Nature, vol. 8(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01056-8
    DOI: 10.1038/s41467-017-01056-8
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-017-01056-8
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/s41467-017-01056-8?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01056-8. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.