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用于研究病毒诱导的哮喘加重的模型:一个关键问题的简短综述

models to study viral-induced asthma exacerbation: a short review for a key issue.

作者信息

Pereira De Oliveira Rémi, Droillard Clément, Devouassoux Gilles, Rosa-Calatrava Manuel

机构信息

CIRI, Centre International de Recherche en Infectiologie, Team VirPath, Université de Lyon, Inserm, U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, ENS de Lyon, Lyon, France.

International Research Laboratory RESPIVIR France - Canada, Centre Hospitalier Universitaire de Québec- Université Laval, Québec, QC, Canada.

出版信息

Front Allergy. 2025 Mar 28;6:1530122. doi: 10.3389/falgy.2025.1530122. eCollection 2025.

DOI:10.3389/falgy.2025.1530122
PMID:40224321
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11987631/
Abstract

Asthma is a heterogenous inflammatory bronchial disease involving complex mechanisms, several inflammatory pathways, and multiples cell-type networks. Bronchial inflammation associated to asthma is consecutive to multiple aggressions on epithelium, such as microbiologic, pollutant, and antigenic agents, which are responsible for both T2 and non-T2 inflammatory responses and further airway remodeling. Because asthma physiopathology involves multiple crosstalk between several cell types from different origins (epithelial, mesenchymal, and immune cells) and numerous cellular effectors, no single and/or representative model is suitable to study the overall of this disease. In this short review, we present and discuss the advantages and limitations of different models to decipher different aspects of virus-related asthma physiopathology and exacerbation.

摘要

哮喘是一种异质性炎症性支气管疾病,涉及复杂机制、多种炎症途径和多细胞类型网络。与哮喘相关的支气管炎症是上皮受到多种侵害的结果,如微生物、污染物和抗原性物质,这些会引发2型和非2型炎症反应以及进一步的气道重塑。由于哮喘的病理生理学涉及来自不同来源的多种细胞类型(上皮细胞、间充质细胞和免疫细胞)之间的多次相互作用以及众多细胞效应器,因此没有单一的和/或代表性模型适合研究该疾病的全貌。在这篇简短的综述中,我们展示并讨论了不同模型在解读病毒相关哮喘病理生理学和加重的不同方面的优点和局限性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ee/11987631/6760d62e937b/falgy-06-1530122-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ee/11987631/6760d62e937b/falgy-06-1530122-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ee/11987631/6760d62e937b/falgy-06-1530122-g001.jpg

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本文引用的文献

1
Immune Response to Respiratory Viral Infections.呼吸道病毒感染的免疫反应。
Int J Mol Sci. 2024 Jun 4;25(11):6178. doi: 10.3390/ijms25116178.
2
Advances in non-type 2 severe asthma: from molecular insights to novel treatment strategies.非 2 型严重哮喘的研究进展:从分子认识到新的治疗策略。
Eur Respir J. 2024 Aug 15;64(2). doi: 10.1183/13993003.00826-2023. Print 2024 Aug.
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Human metapneumovirus infection of organoid-derived human bronchial epithelium represents cell tropism and cytopathology as observed in models.人类偏肺病毒感染类器官衍生的人支气管上皮细胞代表了在 模型中观察到的细胞嗜性和细胞病理学特征。
mSphere. 2024 Feb 28;9(2):e0074323. doi: 10.1128/msphere.00743-23. Epub 2024 Jan 24.
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Breaking Bad: Inflammasome Activation by Respiratory Viruses.《绝命毒师》:呼吸道病毒引发的炎性小体激活
Biology (Basel). 2023 Jul 1;12(7):943. doi: 10.3390/biology12070943.
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Natural killer cells in the lung: potential role in asthma and virus-induced exacerbation?肺部自然杀伤细胞:在哮喘和病毒诱发加重中的潜在作用?
Eur Respir Rev. 2023 Jul 12;32(169). doi: 10.1183/16000617.0036-2023. Print 2023 Sep 30.
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Front Pharmacol. 2023 Mar 6;14:1114739. doi: 10.3389/fphar.2023.1114739. eCollection 2023.
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SARS-CoV-2-Induced TSLP Is Associated with Duration of Hospital Stay in COVID-19 Patients.SARS-CoV-2 诱导的 TSLP 与 COVID-19 患者的住院时间有关。
Viruses. 2023 Feb 17;15(2):556. doi: 10.3390/v15020556.
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Advances of microfluidic lung chips for assessing atmospheric pollutants exposure.用于评估大气污染物暴露的微流控肺芯片的研究进展。
Environ Int. 2023 Feb;172:107801. doi: 10.1016/j.envint.2023.107801. Epub 2023 Feb 4.
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