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发育肺中的卤素暴露损伤。

Halogen exposure injury in the developing lung.

机构信息

Department of Anesthesiology and Perioperative Medicine, the University of Alabama at Birmingham School of Medicine, Birmingham, Alabama.

Division of Molecular and Translational Biomedicine, Pulmonary Injury and Repair Center, the University of Alabama at Birmingham School of Medicine, Birmingham, Alabama.

出版信息

Ann N Y Acad Sci. 2020 Nov;1480(1):30-43. doi: 10.1111/nyas.14445. Epub 2020 Aug 1.

DOI:10.1111/nyas.14445
PMID:32738176
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9447934/
Abstract

Owing to a high-volume industrial usage of the halogens chlorine (Cl ) and bromine (Br ), they are stored and transported in abundance, creating a risk for accidental or malicious release to human populations. Despite extensive efforts to understand the mechanisms of toxicity upon halogen exposure and to develop specific treatments that could be used to treat exposed individuals or large populations, until recently, there has been little to no effort to determine whether there are specific features and or the mechanisms of halogen exposure injury in newborns or children. We established a model of neonatal halogen exposure and published our initial findings. In this review, we aim to contrast and compare the findings in neonatal mice exposed to Br with the findings published on adult mice exposed to Br and the neonatal murine models of bronchopulmonary dysplasia. Despite remarkable similarities across these models in overall alveolar architecture, there are distinct functional and apparent mechanistic differences that are characteristic of each model. Understanding the mechanistic and functional features that are characteristic of the injury process in neonatal mice exposed to halogens will allow us to develop countermeasures that are appropriate for, and effective in, this unique population.

摘要

由于卤素氯(Cl)和溴(Br)的大量工业用途,它们被大量储存和运输,这给人类群体带来了意外或恶意释放的风险。尽管人们已经做出了广泛的努力来了解卤素暴露后的毒性机制,并开发出可用于治疗暴露个体或大量人群的特定治疗方法,但直到最近,人们几乎没有努力去确定新生儿或儿童是否存在卤素暴露损伤的特定特征和/或机制。我们建立了一种新生儿卤素暴露模型,并发表了我们的初步发现。在这篇综述中,我们旨在对比和比较新生儿小鼠暴露于 Br 后的发现与成年小鼠暴露于 Br 后的发现以及新生儿支气管肺发育不良的小鼠模型。尽管这些模型在整体肺泡结构上存在显著的相似性,但每个模型都有独特的功能和明显的机制差异。了解新生儿小鼠暴露于卤素后损伤过程的特征性机制和功能特征,将使我们能够开发出针对这一独特人群的、合适的、有效的对策。

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本文引用的文献

1
Hyaluronan and halogen-induced airway hyperresponsiveness and lung injury.透明质酸和卤素诱导的气道高反应性和肺损伤。
Ann N Y Acad Sci. 2020 Nov;1479(1):29-43. doi: 10.1111/nyas.14415. Epub 2020 Jun 23.
2
Bronchopulmonary dysplasia.支气管肺发育不良。
Nat Rev Dis Primers. 2019 Nov 14;5(1):78. doi: 10.1038/s41572-019-0127-7.
3
Effects of hyperoxia on alveolar and pulmonary vascular development in germ-free mice.高氧对无菌小鼠肺泡和肺血管发育的影响。
Am J Physiol Lung Cell Mol Physiol. 2020 Feb 1;318(2):L421-L428. doi: 10.1152/ajplung.00316.2019. Epub 2019 Oct 23.
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Regulation of Macrophage Foam Cell Formation During Nitrogen Mustard (NM)-Induced Pulmonary Fibrosis by Lung Lipids.氮芥(NM)诱导的肺纤维化过程中肺部脂质对巨噬细胞泡沫细胞形成的调控。
Toxicol Sci. 2019 Dec 1;172(2):344-358. doi: 10.1093/toxsci/kfz187.
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Phosgene inhalation causes hemolysis and acute lung injury.光气吸入会导致溶血和急性肺损伤。
Toxicol Lett. 2019 Sep 15;312:204-213. doi: 10.1016/j.toxlet.2019.04.019. Epub 2019 Apr 30.
6
Loss of interleukin-6 enhances the inflammatory response associated with hyperoxia-induced lung injury in neonatal mice.白细胞介素-6缺失增强了新生小鼠高氧诱导肺损伤相关的炎症反应。
Exp Ther Med. 2019 Apr;17(4):3101-3107. doi: 10.3892/etm.2019.7315. Epub 2019 Feb 26.
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Heme scavenging reduces pulmonary endoplasmic reticulum stress, fibrosis, and emphysema.清除血红素可减轻肺内质网应激、纤维化和肺气肿。
JCI Insight. 2018 Nov 2;3(21):120694. doi: 10.1172/jci.insight.120694.
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Inhibition of chlorine-induced airway fibrosis by budesonide.布地奈德抑制氯诱导的气道纤维化。
Toxicol Appl Pharmacol. 2019 Jan 15;363:11-21. doi: 10.1016/j.taap.2018.08.024. Epub 2018 Sep 3.
9
Early airway microbial metagenomic and metabolomic signatures are associated with development of severe bronchopulmonary dysplasia.早期气道微生物宏基因组和代谢组学特征与严重支气管肺发育不良的发生有关。
Am J Physiol Lung Cell Mol Physiol. 2018 Nov 1;315(5):L810-L815. doi: 10.1152/ajplung.00085.2018. Epub 2018 Aug 16.
10
Resident alveolar macrophages are master regulators of arrested alveolarization in experimental bronchopulmonary dysplasia.驻留肺泡巨噬细胞是实验性支气管肺发育不良中肺泡化阻滞的主要调节者。
J Pathol. 2018 Jun;245(2):153-159. doi: 10.1002/path.5076. Epub 2018 Apr 18.