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Alt a 1 通过 TLR4-肺泡巨噬细胞促进变应性哮喘。

Alt a 1 Promotes Allergic Asthma Through TLR4-Alveolar Macrophages.

机构信息

Centre for Plant Biotechnology and Genomics Universidad Politécnica de Madrid, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, Consejo Superior de Investigaciones Cientificas (UPM -INIA/CSIC), Universidad Politécnica de Madrid, Madrid, Spain.

Department of Biotechnology-Plant Biology, Escuela Tecnica Superior de Ingeniería Agronómica, Alimentaria y de Biosistemas (ETSIAAB), Universidad Politécnica de Madrid, Madrid, Spain.

出版信息

Front Immunol. 2022 Jun 30;13:877383. doi: 10.3389/fimmu.2022.877383. eCollection 2022.

Abstract

The mold is one of the main sources of asthma exacerbation, being its major allergen, Alt a 1, indispensable for its development. The main objective of this work was to answer two main questions: 1) can Alt a 1 by itself (without any other context) induce an asthmatic profile ?; and 2) Which molecular mechanisms take place during this phenomenon? To answer both questions, we have developed a mouse model of allergic asthma using only Alt a 1 for mice sensitization. We also made use of cellular models and computational studies to support some aspects of our hypothesis. Our results showed that Alt a 1 can induce an asthmatic phenotype, promoting tissue remodeling and infiltration of CD45+ cells, especially eosinophils and macrophages (Siglec F+ and F4/80+). Also, we have found that Alt a 1 sensitization is mediated by the TLR4-macrophage axis.

摘要

霉菌是哮喘恶化的主要来源之一,其主要过敏原 Alt a 1 是其发展所必需的。这项工作的主要目的是回答两个主要问题:1)Alt a 1 本身(没有任何其他背景)是否可以诱导哮喘表型?2)在此现象过程中发生了哪些分子机制?为了回答这两个问题,我们仅使用 Alt a 1 对小鼠进行敏化,开发了一种过敏性哮喘的小鼠模型。我们还利用细胞模型和计算研究来支持我们假设的某些方面。我们的结果表明,Alt a 1 可以诱导哮喘表型,促进组织重塑和 CD45+细胞浸润,特别是嗜酸性粒细胞和巨噬细胞(Siglec F+ 和 F4/80+)。此外,我们发现 Alt a 1 致敏是由 TLR4-巨噬细胞轴介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/9280186/dc048cb02abd/fimmu-13-877383-g001.jpg

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