Skin thymic stromal lymphopoietin promotes airway sensitization to inhalant house dust mites leading to allergic asthma in mice

Authors

  • H. Jiang,

    1. Institut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique/Institut National de la Santé́ et de la Recherche Médicale/Université́ de Strasbourg, Illkirch Cedex, France
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  • P. Hener,

    1. Institut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique/Institut National de la Santé́ et de la Recherche Médicale/Université́ de Strasbourg, Illkirch Cedex, France
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  • J. Li,

    1. Institut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique/Institut National de la Santé́ et de la Recherche Médicale/Université́ de Strasbourg, Illkirch Cedex, France
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  • M. Li

    Corresponding author
    • Institut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique/Institut National de la Santé́ et de la Recherche Médicale/Université́ de Strasbourg, Illkirch Cedex, France
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  • Edited by: Hans- Uwe Simon

Correspondence

Mei Li, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch Cedex 67404, France.

Tel.: +33 3 88 65 34 68

Fax: +33 3 88 65 32 01

E-mail: mei@igbmc.fr

Abstract

Asthma is often preceded by atopic dermatitis (AD), a phenomenon known as ‘atopic march’. It has been suggested that sensitization to common inhalant allergens, which is developed in a majority of patients with AD and often during the course of AD, may play a critical role in triggering the atopic march. Yet, what signal(s) delivered by AD skin could promote sensitization to inhalant allergens remains elusive. Here, by employing an experimental mouse asthma protocol, which is induced by airway sensitization and challenge to inhalant house dust mite (HDM), we demonstrate that the overproduction of cytokine thymic stromal lymphopoietin (TSLP) by AD skin promotes airway sensitization to HDM, thereby triggering subsequently an allergic asthma. Together, this study provides, for the first time, the experimental proof that TSLP represents an AD skin-delivered signal to promote sensitization to inhalant aeroallergen, which may account for one mechanism underlying the ‘atopic march’.

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