Temperate Prophages Increase Bacterial Adhesin Expression and Virulence in an Experimental Model of Endocarditis Due to Staphylococcus aureus From the CC398 Lineage.

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Version: Final published version
License: CC BY 4.0
Serval ID
serval:BIB_D201DDAB1F0B
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Temperate Prophages Increase Bacterial Adhesin Expression and Virulence in an Experimental Model of Endocarditis Due to Staphylococcus aureus From the CC398 Lineage.
Journal
Frontiers in microbiology
Author(s)
Laumay F., Corvaglia A.R., Diene S.M., Girard M., Oechslin F., van der Mee-Marquet N., Entenza J.M., François P.
ISSN
1664-302X (Print)
ISSN-L
1664-302X
Publication state
Published
Issued date
2019
Peer-reviewed
Oui
Volume
10
Pages
742
Language
english
Notes
Publication types: Journal Article
Publication Status: epublish
Abstract
Until 2007, Staphylococcus aureus from clonal complex 398 (CC398) was exclusively associated with livestock species and companion animals. Recently, several studies described the emergence of S. aureus CC398 as etiologies of severe infections in humans living in an animal-free environment. Recent sequencing efforts showed that the mobile genetic elements found in CC398 isolates were specific for each population and enabled differentiation of strains responsible for asymptomatic colonization from strains involved in bloodstream infections. We mobilized prophages from a human CC398 isolate and introduced them into two naïve ancestral isolates devoid of prophages that exclusively colonize animals. These lysogenized ancestral CC398 isolates acquired features related to virulence, such as an increased capacity to adhere to human extracellular matrix proteins and the ability to invade and survive within non-phagocytic cells. Pathogenicity of several clinical isolates from the CC398 lineage as well as ancestral and in vitro lysogenized ancestral counterparts was assessed in a model of infectious endocarditis in rats. Natural and artificial lysogens were not only more invasive than their prophage-free parent but also showed an increased capacity to multiply within aortic vegetations. This study identified prophages as mediators of bacterial virulence in a model of infectious endocarditis, probably through promotion of interaction with extracellular matrix components. Further studies are needed to identify mechanisms leading to promotion of intrinsic virulence.
Keywords
Staphylococcus aureus, bacteriophages (phages), virulence, infection, adhesion, internalization, endocarditis (infectious), lysogeny
Pubmed
Web of science
Open Access
Yes
Create date
06/05/2019 12:41
Last modification date
20/08/2019 16:52
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