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皮肤胸腺基质淋巴细胞生成素促进对吸入性屋尘螨的气道致敏,导致小鼠发生变应性哮喘。

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

机构信息

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.

出版信息

Allergy. 2012 Aug;67(8):1078-82. doi: 10.1111/j.1398-9995.2012.02857.x. Epub 2012 Jun 12.

DOI:10.1111/j.1398-9995.2012.02857.x
PMID:22687045
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'.

摘要

哮喘通常先于特应性皮炎(AD),这种现象被称为“特应性进行曲”。有人提出,对常见吸入性过敏原的致敏作用,在大多数 AD 患者中发展,并且通常在 AD 过程中发展,可能在引发特应性进行曲方面发挥关键作用。然而,AD 皮肤发出的什么信号可以促进对吸入性过敏原的致敏作用仍然难以捉摸。在这里,通过使用一种实验性的哮喘小鼠模型,该模型通过气道致敏和吸入性屋尘螨(HDM)挑战来诱导,我们证明 AD 皮肤中细胞因子胸腺基质淋巴细胞生成素(TSLP)的过度产生促进了对 HDM 的气道致敏作用,从而随后引发过敏性哮喘。总的来说,这项研究首次提供了实验证据,证明 TSLP 代表了 AD 皮肤发出的信号,以促进对吸入性变应原的致敏作用,这可能是“特应性进行曲”的一种机制。

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