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甲型流感病毒通过 I 型干扰素受体依赖途径损害对结核分枝杆菌共感染的控制。

Influenza A virus impairs control of Mycobacterium tuberculosis coinfection through a type I interferon receptor-dependent pathway.

机构信息

Division of Immunoregulation, Medical Research Council National Institute for Medical Research, The Ridgeway, Mill Hill, London.

出版信息

J Infect Dis. 2014 Jan 15;209(2):270-4. doi: 10.1093/infdis/jit424. Epub 2013 Aug 9.

Abstract

Influenza followed by severe acute bacterial pneumonia is a major cause of mortality worldwide. Several mechanisms account for this enhanced susceptibility, including increased production of type I interferon (IFN). In individuals infected with Mycobacterium tuberculosis, the influence of acute viral infections on tuberculosis progression is unclear. We show that prior exposure of mice to influenza A virus, followed by M. tuberculosis infection, leads to enhanced mycobacterial growth and decreased survival. Following M. tuberculosis/influenza virus coinfection, mycobacterial growth is enhanced by a type I IFN signaling pathway. Our findings highlight the detrimental influence influenza virus infection can have before or during M. tuberculosis infection.

摘要

流感后继发严重急性细菌性肺炎是全球范围内导致死亡的主要原因之一。多种机制导致了这种易感性的增强,包括Ⅰ型干扰素(IFN)的产生增加。在感染结核分枝杆菌的个体中,急性病毒感染对结核病进展的影响尚不清楚。我们发现,小鼠先前感染甲型流感病毒,然后再感染结核分枝杆菌,会导致分枝杆菌生长加速和存活率下降。在结核分枝杆菌/流感病毒混合感染后,分枝杆菌的生长受到Ⅰ型 IFN 信号通路的增强。我们的研究结果强调了流感病毒感染在结核分枝杆菌感染之前或感染期间可能产生的有害影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e0e/3873785/c01c1e4a68af/jit42401.jpg

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