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调节生物膜分散和从定植到侵袭性疾病的转变。

Modulates Biofilm Dispersion and the Transition from Colonization to Invasive Disease.

机构信息

Department of Microbiology and Immunology, State University of New York at Buffalo, Buffalo, New York, USA.

Department of Translational Medicine, Lund University, Lund, Skåne, Sweden.

出版信息

mBio. 2018 Jan 9;9(1):e02089-17. doi: 10.1128/mBio.02089-17.

DOI:10.1128/mBio.02089-17
PMID:29317512
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5760742/
Abstract

and are ubiquitous upper respiratory opportunistic pathogens. Individually, these Gram-positive microbes are two of the most common causative agents of secondary bacterial pneumonia following influenza A virus infection, and they constitute a significant source of morbidity and mortality. Since the introduction of the pneumococcal conjugate vaccine, rates of cocolonization with both of these bacterial species have increased, despite the traditional view that they are antagonistic and mutually exclusive. The interactions between and in the context of colonization and the transition to invasive disease have not been characterized. In this report, we show that and form stable dual-species biofilms on epithelial cells When these biofilms are exposed to physiological changes associated with viral infection, disperses from the biofilm, whereas dispersal is inhibited. These findings were supported by results of an study in which we used a novel mouse cocolonization model. In these experiments, mice cocolonized in the nares with both bacterial species were subsequently infected with influenza A virus. The coinfected mice almost exclusively developed pneumococcal pneumonia. These results indicate that despite our previous report that disseminates into the lungs of mice stably colonized with these bacteria following influenza A virus infection, cocolonization with and inhibits dispersal and transition to disease. This study provides novel insight into both the interactions between and during carriage and the transition from colonization to secondary bacterial pneumonia. In this study, we demonstrate that can modulate the pathogenic potential of in a model of secondary bacterial pneumonia. We report that host physiological signals related to viral infection cease to elicit a dispersal response from while in a dual-species setting with , in direct contrast to results of previous studies with each species individually. This study underscores the importance of studying polymicrobial communities and their implications in disease states.

摘要

和 是普遍存在的上呼吸道机会性病原体。单独来看,这两种革兰氏阳性微生物是甲型流感病毒感染后继发细菌性肺炎的最常见病原体之一,也是发病率和死亡率的重要来源。自肺炎球菌结合疫苗问世以来,尽管传统观点认为它们是拮抗和互斥的,但这两种细菌的共定植率有所上升。在定植和向侵袭性疾病转变的背景下, 与 之间的相互作用尚未得到描述。在本报告中,我们表明 与 可在上皮细胞上形成稳定的双物种生物膜。当这些生物膜暴露于与病毒感染相关的生理变化时, 从生物膜中分散出来,而 则被抑制。这些发现得到了一项 研究的支持,在该研究中,我们使用了一种新型的小鼠共定植模型。在这些实验中,鼻腔中同时定植了这两种细菌的小鼠随后感染了甲型流感病毒。受感染的小鼠几乎仅发展为肺炎球菌肺炎。这些结果表明,尽管我们之前的报告指出,甲型流感病毒感染后, 会在稳定定植于这些细菌的小鼠肺部传播,但 与 共定植会抑制 分散和向疾病的转变。这项研究为 与 携带期间的相互作用以及从定植向继发性细菌性肺炎的转变提供了新的见解。在这项研究中,我们证明了 在继发性细菌性肺炎模型中可以调节 的致病潜力。我们报告说,与病毒感染相关的宿主生理信号不再引发 从双物种环境中分散出来的反应,这与之前对每种物种单独进行的研究结果形成直接对比。这项研究强调了研究多微生物群落及其在疾病状态中的意义的重要性。

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