Influenza Virus Primes Mice for Pneumonia From Staphylococcus aureus
Influenza Virus Primes Mice for Pneumonia From Staphylococcus aureus
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DOI：
10.1093/infdis/jiq113
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发表时间：
2011-03-15
影响因子：
6.4
通讯作者：
McCullers, Jonathan A.
中科院分区：
文献类型：
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作者：
Iverson, Amy R.;Boyd, Kelli L.;McCullers, Jonathan A.
流感后金黄色葡萄球菌的重复感染越来越受到关注。我们在小鼠流感病毒共感染模型中评估了几种实验室和临床毒株。一个耐甲氧西林的USA 300克隆和几个最近的临床菌株从病人坏死性肺炎引起高死亡率的流感病毒感染小鼠。与单一感染相比，合并感染期间肺部病毒和细菌滴度均增强。然而，滴度的差异并不对应于疾病结果的差异，从高致病性菌株与那些从致病性差的菌株的重叠感染的比较。然而，这些菌株在Panton-Valentine杀白细胞素的表达和各自产生的炎性肺损伤程度方面确实存在差异。病毒细胞毒素PB 1-F2导致阴性结果。这些数据表明，需要进一步研究参与合并感染过程中炎症和肺损伤发病机制的特定细菌毒力因子。
Superinfections from Staphylococcus aureus following influenza are an increasing concern. We assessed several laboratory and clinical strains in a mouse coinfection model with influenza virus. A methicillin-resistant USA300 clone and several recent clinical strains from patients with necrotizing pneumonia caused high mortality following influenza virus infection in mice. Both viral and bacterial lung titers were enhanced during coinfections compared with single infections. However, differences in titers did not correspond with differences in disease outcomes in a comparison of superinfections from a highly pathogenic strain with those from a poorly pathogenic strain. These strains did differ, however, in expression of Panton-Valentine leukocidin and in the degree of inflammatory lung damage each engendered. The viral cytotoxin PB1-F2 contributed to the negative outcomes. These data suggest that additional study of specific bacterial virulence factors involved in the pathogenesis of inflammation and lung damage during coinfections is needed.