Staphylococcus aureus and Influenza A Virus: Partners in Coinfection.

Staphylococcus aureus and Influenza A Virus: Partners in Coinfection.
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金黄色葡萄球菌和流感病毒:共同感染的伴侣。

DOI:
10.1128/mbio.02068-16
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发表时间:
2016-12-13
期刊:
影响因子:
6.4
通讯作者:
McLoughlin RM
McLoughlin RM
中科院分区:
生物学1区
文献类型:
--
作者:
Mulcahy ME;McLoughlin RM

文献摘要

被引文献

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在甲型流感病毒(IAV)感染的宿主中,鼻腔携带金黄色葡萄球菌是继发性葡萄球菌肺炎的重要危险因素。然而,很少有研究已经进行了定义的环境和生理变化,导致金黄色葡萄球菌转变为致病生物体在这种情况下。Reddinger等人在最近的一项研究中探索了病毒驱动的危险信号导致金黄色葡萄球菌从败血症转变为肺部感染的能力。M. Reddinger,N. R. Luke-Marshall,A. P. Hakansson和A. A. Campagnari,mBio 7(6):e01235-16,2016,http://dx.doi.org/10.1128/mBio.01235-16。作者报告说,生理宿主变化,包括发热温度和宿主应激反应信号的组合,导致金黄色葡萄球菌生物膜从鼻腔环境中分散并引起活动性肺部感染。本文根据目前对葡萄球菌与IAV合并感染机制的理解,讨论了这一新发现。此外,它认为在这个模型中的葡萄球菌扩散背后的机制。总的来说,这项研究表明,IAV感染后可能会发生界间信号传导,这可能有助于使IAV感染的宿主对继发性葡萄球菌肺炎敏感。
Nasal carriage of Staphylococcus aureus is a significant risk factor for secondary staphylococcal pneumonia in influenza A virus (IAV)-infected hosts. However, little research has been undertaken to define the environmental and physiological changes that cause S. aureus to shift from commensal to pathogenic organism in this setting. The ability of virus-driven danger signals to cause S. aureus to transition from commensalism to pulmonary infection was explored in a recent study by Reddinger et al. R. M. Reddinger, N. R. Luke-Marshall, A. P. Hakansson, and A. A. Campagnari, mBio 7(6):e01235-16, 2016, http://dx.doi.org/10.1128/mBio.01235-16. The authors report that physiological host changes, including febrile temperature and a combination of host stress response signals, caused S. aureus biofilms to disperse from the nasal environment and cause active pulmonary infection. This commentary discusses the new finding in light of the current understanding of the mechanisms behind staphylococcal coinfection with IAV. In addition, it considers the mechanisms behind staphylococcal dispersal in this model. Overall, the study indicates that interkingdom signaling may occur following IAV infection and this likely contributes to sensitizing the IAV-infected host to secondary staphylococcal pneumonia.