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肠道病毒71型脑干脑炎的细胞因子免疫发病机制

Cytokine immunopathogenesis of enterovirus 71 brain stem encephalitis.

作者信息

Wang Shih-Min, Lei Huan-Yao, Liu Ching-Chuan

机构信息

Department of Emergency Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 70428, Taiwan.

出版信息

Clin Dev Immunol. 2012;2012:876241. doi: 10.1155/2012/876241. Epub 2012 Aug 23.

DOI:10.1155/2012/876241
PMID:22956971
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3432373/
Abstract

Enterovirus 71 (EV71) is one of the most important causes of herpangina and hand, foot, and mouth disease. It can also cause severe complications of the central nervous system (CNS). Brain stem encephalitis with pulmonary edema is the severe complication that can lead to death. EV71 replicates in leukocytes, endothelial cells, and dendritic cells resulting in the production of immune and inflammatory mediators that shape innate and acquired immune responses and the complications of disease. Cytokines, as a part of innate immunity, favor the development of antiviral and Th1 immune responses. Cytokines and chemokines play an important role in the pathogenesis EV71 brain stem encephalitis. Both the CNS and the systemic inflammatory responses to infection play important, but distinctly different, roles in the pathogenesis of EV71 pulmonary edema. Administration of intravenous immunoglobulin and milrinone, a phosphodiesterase inhibitor, has been shown to modulate inflammation, to reduce sympathetic overactivity, and to improve survival in patients with EV71 autonomic nervous system dysregulation and pulmonary edema.

摘要

肠道病毒71型(EV71)是疱疹性咽峡炎和手足口病的最重要病因之一。它还可引起中枢神经系统(CNS)的严重并发症。脑干脑炎伴肺水肿是可导致死亡的严重并发症。EV71在白细胞、内皮细胞和树突状细胞中复制,导致产生免疫和炎症介质,这些介质塑造先天性和获得性免疫反应以及疾病的并发症。细胞因子作为先天性免疫的一部分,有利于抗病毒和Th1免疫反应的发展。细胞因子和趋化因子在EV71脑干脑炎的发病机制中起重要作用。中枢神经系统和对感染的全身炎症反应在EV71肺水肿的发病机制中都起重要但明显不同的作用。静脉注射免疫球蛋白和磷酸二酯酶抑制剂米力农已被证明可调节炎症、减少交感神经过度活动,并改善EV71自主神经系统失调和肺水肿患者的生存率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746e/3432373/e7bd4c2527f1/CDI2012-876241.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746e/3432373/e7bd4c2527f1/CDI2012-876241.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746e/3432373/e7bd4c2527f1/CDI2012-876241.001.jpg

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Exogenous interleukin-6, interleukin-13, and interferon-γ provoke pulmonary abnormality with mild edema in enterovirus 71-infected mice.外源性白细胞介素-6、白细胞介素-13 和干扰素-γ 可诱发感染肠道病毒 71 的小鼠肺部异常,伴有轻度水肿。
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Seasonal Testing, Results, and Effect of the Pandemic on Coxsackievirus Serum Studies.
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Microorganisms. 2024 Feb 10;12(2):367. doi: 10.3390/microorganisms12020367.
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