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Hypothermia protects brain mitochondrial function from hypoxemia in a murine model of sepsis.在脓毒症小鼠模型中,低温可保护脑线粒体功能免受低氧血症影响。
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Disease tolerance mediated by microbiome E. coli involves inflammasome and IGF-1 signaling.由微生物群大肠杆菌介导的疾病耐受性涉及炎性小体和胰岛素样生长因子-1信号传导。
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体温调节作为一种疾病耐受防御策略。

Thermoregulation as a disease tolerance defense strategy.

作者信息

Schieber Alexandria M Palaferri, Ayres Janelle S

机构信息

The Salk Institute for Biological Studies, Immunobiology and Microbial Pathogenesis, 10010 North Torrey Pines Road, San DIego CA, USA.

The Salk Institute for Biological Studies, Immunobiology and Microbial Pathogenesis, 10010 North Torrey Pines Road, San DIego CA, USA

出版信息

Pathog Dis. 2016 Dec;74(9). doi: 10.1093/femspd/ftw106. Epub 2016 Nov 3.

DOI:10.1093/femspd/ftw106
PMID:27815313
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5975229/
Abstract

Physiological responses that occur during infection are most often thought of in terms of effectors of microbial destruction through the execution of resistance mechanisms, due to a direct action of the microbe, or are maladaptive consequences of host-pathogen interplay. However, an examination of the cellular and organ-level consequences of one such response, thermoregulation that leads to fever or hypothermia, reveals that these actions cannot be readily explained within the traditional paradigms of microbial killing or maladaptive consequences of host-pathogen interactions. In this review, the concept of disease tolerance is applied to thermoregulation during infection, inflammation and trauma, and we discuss the physiological consequences of thermoregulation during disease including tissue susceptibility to damage, inflammation, behavior and toxin neutralization.

摘要

感染期间发生的生理反应通常被认为是通过执行抵抗机制来破坏微生物的效应器,这是由于微生物的直接作用,或者是宿主 - 病原体相互作用的适应不良后果。然而,对一种这样的反应(导致发热或体温过低的体温调节)的细胞和器官水平后果进行研究后发现,这些作用无法在传统的微生物杀灭范式或宿主 - 病原体相互作用的适应不良后果范式中轻易得到解释。在本综述中,疾病耐受性的概念被应用于感染、炎症和创伤期间的体温调节,并且我们讨论了疾病期间体温调节的生理后果,包括组织对损伤的易感性、炎症、行为和毒素中和。