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发热、体温过高与肺部:一切都与背景和时机有关。

Fever, hyperthermia, and the lung: it's all about context and timing.

作者信息

Hasday Jeffrey D, Shah Nirav, Mackowiak Phillip A, Tulapurkar Mohan, Nagarsekar Ashish, Singh Ishwar

机构信息

University of Maryland School of Medicine, Health Science Facility-II, Rm. S347, 20 Penn Street, Baltimore, MD 21201, USA.

出版信息

Trans Am Clin Climatol Assoc. 2011;122:34-47.

PMID:21686207
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3116334/
Abstract

Although body temperature is tightly regulated in humans, elevated temperatures are frequently encountered during febrile illnesses and exertional and environmental hyperthermia. Such temperature increases exert profound effects on cell signaling and gene expression patterns, which have important consequences for innate immune function and cell injury, apoptosis, and recovery. The lung offers a framework for understanding how these effects can either benefit or harm the host. We present data demonstrating that exposure to febrile-range hyperthermia (∼39.5 °C) exerts multiple biologic effects that converge on enhanced neutrophil recruitment to the lung, and describe the consequences of these effects for pathogen clearance and collateral tissue injury. We also discuss the influence of temperature on apoptosis in lung epithelium. Collectively, the data presented identify body temperature as a modifiable factor that exerts profound influence on the outcome of infection and injury.

摘要

尽管人体体温受到严格调节,但在发热性疾病、运动性和环境性体温过高期间,体温升高的情况却经常出现。这种体温升高会对细胞信号传导和基因表达模式产生深远影响,而这对先天免疫功能以及细胞损伤、凋亡和恢复具有重要影响。肺为理解这些影响如何对宿主产生利弊提供了一个框架。我们展示的数据表明,暴露于发热范围的高温(约39.5°C)会产生多种生物学效应,这些效应共同作用于增强中性粒细胞向肺的募集,并描述了这些效应对于病原体清除和附带组织损伤的后果。我们还讨论了温度对肺上皮细胞凋亡的影响。总体而言,所展示的数据表明体温是一个可调节的因素,对感染和损伤的结果具有深远影响。

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本文引用的文献

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Response of mice to continuous 5-day passive hyperthermia resembles human heat acclimation.小鼠对连续 5 天被动性过热的反应类似于人类的热适应。
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Febrile-range hyperthermia augments lipopolysaccharide-induced lung injury by a mechanism of enhanced alveolar epithelial apoptosis.发热范围性高热通过增强肺泡上皮细胞凋亡的机制增强脂多糖诱导的肺损伤。
J Immunol. 2010 Apr 1;184(7):3801-13. doi: 10.4049/jimmunol.0903191. Epub 2010 Mar 3.
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G-CSF, but not corticosterone, mediates circulating neutrophilia induced by febrile-range hyperthermia.粒细胞集落刺激因子(G-CSF)而非皮质酮介导了发热范围高温诱导的循环中性粒细胞增多。
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