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黏液纤毛防御:新兴的细胞、分子和动物模型。

Mucociliary Defense: Emerging Cellular, Molecular, and Animal Models.

机构信息

1 Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Denver School of Medicine, Aurora, Colorado.

2 Department of Bioengineering.

出版信息

Ann Am Thorac Soc. 2018 Nov;15(Suppl 3):S210-S215. doi: 10.1513/AnnalsATS.201806-439AW.

DOI:10.1513/AnnalsATS.201806-439AW
PMID:30431350
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6322027/
Abstract

Respiratory tissues are bombarded by billions of particles daily. If allowed to accumulate, these particles can cause injury, inflammation, or infection, and thus may significantly disrupt airflow and gas exchange. Mucociliary defense, a primary mechanism for protecting host tissues, operates through the coordinated functions of mucus and cilia that trap and eliminate inhaled materials. Mucociliary function is also required for the elimination of endogenous cells and debris. Although defense is necessarily robust, it is also tightly regulated to minimize physiologic disruption of the host. Indeed, mucociliary dysfunction contributes to the pathogenesis of many lung diseases-including asthma, chronic obstructive pulmonary disease, pulmonary fibrosis, and cystic fibrosis-in which airflow limitation, inflammation, persistent tissue injury, and structural remodeling occur. Here, we highlight recent advances in cilia and mucin biology, the importance of well-controlled mucociliary interactions, and the need to better understand how these regulate innate barrier and immune defense.

摘要

呼吸道组织每天都会受到数十亿个粒子的冲击。如果这些粒子得以积累,就可能导致损伤、炎症或感染,从而严重扰乱气流和气体交换。作为保护宿主组织的主要机制之一,黏液纤毛防御通过黏液和纤毛的协调功能发挥作用,纤毛捕获并清除吸入的物质。为了清除内源性细胞和碎片,也需要黏液纤毛功能。尽管防御机制必然是强大的,但它也受到严格的调控,以最大程度地减少对宿主的生理干扰。事实上,黏液纤毛功能障碍是许多肺部疾病(包括哮喘、慢性阻塞性肺疾病、肺纤维化和囊性纤维化)的发病机制之一,这些疾病会导致气流受限、炎症、持续的组织损伤和结构重塑。在这里,我们重点介绍纤毛和粘蛋白生物学的最新进展,强调良好控制的黏液纤毛相互作用的重要性,并需要更好地了解这些相互作用如何调节先天屏障和免疫防御。

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本文引用的文献

1
Airway Epithelial Differentiation and Mucociliary Clearance.气道上皮细胞分化和黏液纤毛清除功能。
Ann Am Thorac Soc. 2018 Nov;15(Suppl 3):S143-S148. doi: 10.1513/AnnalsATS.201802-128AW.
2
Primary ciliary dyskinesia: mechanisms and management.原发性纤毛运动障碍:机制与管理
Appl Clin Genet. 2017 Sep 19;10:67-74. doi: 10.2147/TACG.S127129. eCollection 2017.
3
Identification of sialic acid-binding function for the Middle East respiratory syndrome coronavirus spike glycoprotein.鉴定中东呼吸综合征冠状病毒刺突糖蛋白的唾液酸结合功能。
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Sialic acid-to-urea ratio as a measure of airway surface hydration.唾液酸与尿素的比值作为气道表面水合作用的一种度量指标。
Am J Physiol Lung Cell Mol Physiol. 2017 Mar 1;312(3):L398-L404. doi: 10.1152/ajplung.00398.2016. Epub 2017 Jan 6.
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Matched-Comparative Modeling of Normal and Diseased Human Airway Responses Using a Microengineered Breathing Lung Chip.利用微工程呼吸肺芯片对正常和患病人体气道反应进行匹配比较建模。
Cell Syst. 2016 Nov 23;3(5):456-466.e4. doi: 10.1016/j.cels.2016.10.003. Epub 2016 Oct 27.
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Cilia and Mucociliary Clearance.纤毛与黏液纤毛清除功能
Cold Spring Harb Perspect Biol. 2017 Apr 3;9(4):a028241. doi: 10.1101/cshperspect.a028241.
7
Idiopathic Pulmonary Fibrosis: A Genetic Disease That Involves Mucociliary Dysfunction of the Peripheral Airways.特发性肺纤维化:一种涉及外周气道黏液纤毛功能障碍的遗传性疾病。
Physiol Rev. 2016 Oct;96(4):1567-91. doi: 10.1152/physrev.00004.2016.
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Control of lung defence by mucins and macrophages: ancient defence mechanisms with modern functions.黏液和巨噬细胞对肺部防御的控制:具有现代功能的古老防御机制。
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Searching the Evolutionary Origin of Epithelial Mucus Protein Components-Mucins and FCGBP.探寻上皮黏液蛋白成分——黏蛋白和FCGBP的进化起源。
Mol Biol Evol. 2016 Aug;33(8):1921-36. doi: 10.1093/molbev/msw066. Epub 2016 Apr 4.