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Phenol-Soluble Modulin Peptides Contribute to Influenza A Virus-Associated Staphylococcus aureus Pneumonia.酚溶性调节素肽促成甲型流感病毒相关的金黄色葡萄球菌肺炎。
Infect Immun. 2017 Nov 17;85(12). doi: 10.1128/IAI.00620-17. Print 2017 Dec.
2
Epic Immune Battles of History: Neutrophils vs. .历史上的史诗级免疫之战:中性粒细胞对决……
Front Cell Infect Microbiol. 2017 Jun 30;7:286. doi: 10.3389/fcimb.2017.00286. eCollection 2017.
3
Secondary Bacterial Infections Associated with Influenza Pandemics.与流感大流行相关的继发性细菌感染
Front Microbiol. 2017 Jun 23;8:1041. doi: 10.3389/fmicb.2017.01041. eCollection 2017.
4
Host Physiologic Changes Induced by Influenza A Virus Lead to Staphylococcus aureus Biofilm Dispersion and Transition from Asymptomatic Colonization to Invasive Disease.甲型流感病毒诱导的宿主生理变化导致金黄色葡萄球菌生物膜分散,并从无症状定植转变为侵袭性疾病。
mBio. 2016 Aug 9;7(4):e01235-16. doi: 10.1128/mBio.01235-16.
5
Deaths: Final Data for 2013.死亡情况:2013年最终数据。
Natl Vital Stat Rep. 2016 Feb 16;64(2):1-119.
6
The Lung Microbiome: New Principles for Respiratory Bacteriology in Health and Disease.肺部微生物群:健康与疾病中呼吸细菌学的新原理
PLoS Pathog. 2015 Jul 9;11(7):e1004923. doi: 10.1371/journal.ppat.1004923. eCollection 2015 Jul.
7
Toxin-induced necroptosis is a major mechanism of Staphylococcus aureus lung damage.毒素诱导的坏死性凋亡是金黄色葡萄球菌肺损伤的主要机制。
PLoS Pathog. 2015 Apr 16;11(4):e1004820. doi: 10.1371/journal.ppat.1004820. eCollection 2015 Apr.
8
The co-pathogenesis of influenza viruses with bacteria in the lung.流感病毒与肺部细菌的共同发病机制。
Nat Rev Microbiol. 2014 Apr;12(4):252-62. doi: 10.1038/nrmicro3231. Epub 2014 Mar 3.
9
Vaccination against Staphylococcus aureus pneumonia.金黄色葡萄球菌肺炎的疫苗接种。
J Infect Dis. 2014 Jun 15;209(12):1955-62. doi: 10.1093/infdis/jit823. Epub 2013 Dec 19.
10
The role of innate immunity in promoting SaeR/S-mediated virulence in Staphylococcus aureus.天然免疫在促进金黄色葡萄球菌中SaeR/S介导的毒力方面的作用。
J Innate Immun. 2014;6(1):21-30. doi: 10.1159/000351200. Epub 2013 Jun 29.

金黄色葡萄球菌继发于甲型流感感染的继发性细菌性肺炎与 SaeR/S 相关。

Secondary Bacterial Pneumonia by Staphylococcus aureus Following Influenza A Infection Is SaeR/S Dependent.

机构信息

Department of Microbiology and Immunology, Montana State University, Bozeman.

Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire.

出版信息

J Infect Dis. 2018 Jul 24;218(5):809-813. doi: 10.1093/infdis/jiy210.

DOI:10.1093/infdis/jiy210
PMID:29668950
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6057542/
Abstract

Staphylococcus aureus is a predominant cause of fatal pneumonia following influenza A virus (IAV) infection. Herein we investigate the influence of antecedent IAV infection on S. aureus virulence gene expression. Using a murine model, comparing the USA300 and USA300ΔsaeR/S strains, we demonstrate that S. aureus pathogenesis following IAV infection is SaeR/S dependent. Furthermore, we show that IAV modulates the lung environment to rapidly up-regulate S. aureus virulence factors containing the SaeR-binding domain. Data demonstrate that the pathogen response to IAV infection impacts host outcome and provides evidence that the ability of S. aureus to sense and respond to the lung environment determines severity of pneumonia.

摘要

金黄色葡萄球菌是甲型流感病毒(IAV)感染后导致致命性肺炎的主要病原体。在此,我们研究了先前 IAV 感染对金黄色葡萄球菌毒力基因表达的影响。通过使用一种鼠模型,比较 USA300 和 USA300ΔsaeR/S 两种菌株,我们证明了金黄色葡萄球菌在 IAV 感染后的发病机制依赖于 SaeR/S。此外,我们表明 IAV 可调节肺部环境,从而快速上调含有 SaeR 结合域的金黄色葡萄球菌毒力因子。研究数据表明,病原体对 IAV 感染的反应会影响宿主的结果,并提供了证据表明金黄色葡萄球菌感知和响应肺部环境的能力决定了肺炎的严重程度。