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臭氧诱导的气道高反应性和上皮损伤模型。

Ozone-Induced Models of Airway Hyperreactivity and Epithelial Injury.

机构信息

Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University Medical Center, Durham, NC, USA.

出版信息

Methods Mol Biol. 2022;2506:67-81. doi: 10.1007/978-1-0716-2364-0_5.

DOI:10.1007/978-1-0716-2364-0_5
PMID:35771464
Abstract

Ozone (O), a criterion air pollutant produced as a product of internal combustion, generates increased inflammation, lung permeability, and airway hyperreactivity when exposed to rodents in laboratory settings. Airway hyperreactivity is defined as an exaggerated acute obstructive response of the airways to one or more nonspecific stimuli. Lung permeability is a measure of barrier functions that separate internal and external environments to limit access of pathogens and other noxious material. By modeling in vivo O exposure in rodents, this allows investigators to explore pulmonary and nonpulmonary O effects as a means of understanding its impact on human health and lung function. Furthermore, direct effects of O on epithelial permeability can be defined using in vitro exposures to airway epithelial cells. This chapter will focus on methods of generating O and then exposing rodents and cultured epithelial cells in laboratory settings.

摘要

臭氧(O)是一种作为内燃机产物的空气污染物,当暴露于实验室环境中的啮齿动物时,会引起炎症、肺通透性和气道高反应性增加。气道高反应性定义为气道对一种或多种非特异性刺激物的急性阻塞性反应过度。肺通透性是一种衡量分隔内外环境的屏障功能的指标,以限制病原体和其他有害物质的进入。通过在啮齿动物中模拟体内臭氧暴露,可以让研究人员探索肺部和非肺部臭氧的影响,以此了解其对人类健康和肺功能的影响。此外,还可以使用气道上皮细胞的体外暴露来定义臭氧对上皮通透性的直接影响。本章将重点介绍生成臭氧的方法,然后在实验室环境中暴露于啮齿动物和培养的上皮细胞。

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Ozone-Induced Models of Airway Hyperreactivity and Epithelial Injury.臭氧诱导的气道高反应性和上皮损伤模型。
Methods Mol Biol. 2022;2506:67-81. doi: 10.1007/978-1-0716-2364-0_5.
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Ozone Inhalation Attenuated the Effects of Budesonide on -Induced Airway Inflammation and Hyperreactivity in Mice.臭氧吸入减弱布地奈德对 - 诱导的气道炎症和小鼠气道高反应性的影响。
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Mechanisms of response to ozone exposure: the role of mast cells in mice.对臭氧暴露的反应机制:肥大细胞在小鼠中的作用。
Res Rep Health Eff Inst. 1999 Apr(85):1-30; discussion 31-6.
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Hypoxia-induced pulmonary arterial hypertension augments lung injury and airway reactivity caused by ozone exposure.缺氧诱导的肺动脉高压会加剧臭氧暴露所致的肺损伤和气道反应性。
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Chemokine (C-C Motif) Receptor-Like 2 is not essential for lung injury, lung inflammation, or airway hyperresponsiveness induced by acute exposure to ozone.趋化因子(C-C基序)受体样2对于急性暴露于臭氧引起的肺损伤、肺部炎症或气道高反应性并非必不可少。
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Progress in assessing air pollutant risks from in vitro exposures: matching ozone dose and effect in human airway cells.体外暴露评估空气污染物风险的进展:匹配人类气道细胞中的臭氧剂量与效应
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The influence of polymorphonuclear leukocytes on altered pulmonary epithelial permeability during ozone exposure.多形核白细胞对臭氧暴露期间肺上皮通透性改变的影响。
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Acute ozone-induced change in airway permeability: role of infiltrating leukocytes.急性臭氧诱导的气道通透性变化:浸润白细胞的作用。
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Physiol Rep. 2025 Feb;13(4):e70253. doi: 10.14814/phy2.70253.
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De-Epithelization of the Human Amniotic Membrane Using a System Involving Ozonated Water and Ultrasound.使用包含臭氧水和超声的系统对人羊膜进行去上皮处理。
Bioengineering (Basel). 2024 Sep 29;11(10):987. doi: 10.3390/bioengineering11100987.
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Minimum information for reporting on the TEER (trans-epithelial/endothelial electrical resistance) assay (MIRTA).

本文引用的文献

1
Tracheal permeability in rats exposed to ozone. An electron microscopic and autoradiographic analysis of the transport pathway.暴露于臭氧环境下大鼠的气管通透性。对转运途径的电子显微镜及放射自显影分析。
Am Rev Respir Dis. 1986 Sep;134(3):572-9. doi: 10.1164/arrd.1986.134.3.572.
跨上皮/内皮电阻(TEER)检测报告的最低信息要求(MIRTA)
Arch Toxicol. 2025 Jan;99(1):57-66. doi: 10.1007/s00204-024-03879-z. Epub 2024 Oct 4.
4
Aconitate decarboxylase 1 mediates the acute airway inflammatory response to environmental exposures.顺乌头酸酶 1 介导环境暴露引起的急性气道炎症反应。
Front Immunol. 2024 Sep 16;15:1432334. doi: 10.3389/fimmu.2024.1432334. eCollection 2024.
5
Tissue-Resident Alveolar Macrophages Reduce Ozone-induced Inflammation via MerTK-mediated Efferocytosis.组织驻留肺泡巨噬细胞通过 MerTK 介导的吞噬作用减少臭氧诱导的炎症。
Am J Respir Cell Mol Biol. 2024 Jun;70(6):493-506. doi: 10.1165/rcmb.2023-0390OC.
6
Tissue-resident alveolar macrophages reduce O-induced inflammation via MerTK mediated efferocytosis.组织驻留肺泡巨噬细胞通过MerTK介导的胞葬作用减轻氧诱导的炎症。
bioRxiv. 2023 Nov 6:2023.11.06.565865. doi: 10.1101/2023.11.06.565865.