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dc.contributor.authorTuchscherr, Lorena
dc.contributor.authorMedina, Eva
dc.contributor.authorHussain, Muzaffar
dc.contributor.authorVölker, Wolfgang
dc.contributor.authorHeitmann, Vanessa
dc.contributor.authorNiemann, Silke
dc.contributor.authorHolzinger, Dirk
dc.contributor.authorRoth, Johannes
dc.contributor.authorProctor, Richard A
dc.contributor.authorBecker, Karsten
dc.contributor.authorPeters, Georg
dc.contributor.authorLöffler, Bettina
dc.date.accessioned2015-03-19T09:21:47Zen
dc.date.available2015-03-19T09:21:47Zen
dc.date.issued2011-03en
dc.identifier.citationStaphylococcus aureus phenotype switching: an effective bacterial strategy to escape host immune response and establish a chronic infection. 2011, 3 (3):129-41 EMBO Mol Meden
dc.identifier.issn1757-4684en
dc.identifier.pmid21268281en
dc.identifier.doi10.1002/emmm.201000115en
dc.identifier.urihttp://hdl.handle.net/10033/346878en
dc.description.abstractStaphylococcus aureus is a frequent cause for serious, chronic and therapy-refractive infections in spite of susceptibility to antibiotics in vitro. In chronic infections, altered bacterial phenotypes, such as small colony variants (SCVs), have been found. Yet, it is largely unclear whether the ability to interconvert from the wild-type to the SCV phenotype is only a rare clinical and/or just laboratory phenomenon or is essential to sustain an infection. Here, we performed different long-term in vitro and in vivo infection models with S. aureus and we show that viable bacteria can persist within host cells and/or tissues for several weeks. Persistence induced bacterial phenotypic diversity, including SCV phenotypes, accompanied by changes in virulence factor expression and auxotrophism. However, the recovered SCV phenotypes were highly dynamic and rapidly reverted to the fully virulent wild-type form when leaving the intracellular location and infecting new cells. Our findings demonstrate that bacterial phenotype switching is an integral part of the infection process that enables the bacteria to hide inside host cells, which can be a reservoir for chronic and therapy-refractive infections.
dc.language.isoenen
dc.subject.meshAnimalsen
dc.subject.meshCell Lineen
dc.subject.meshChronic Diseaseen
dc.subject.meshDisease Models, Animalen
dc.subject.meshEnergy Metabolismen
dc.subject.meshFemaleen
dc.subject.meshGene Expression Profilingen
dc.subject.meshHumansen
dc.subject.meshImmune Evasionen
dc.subject.meshMetabolic Networks and Pathwaysen
dc.subject.meshMiceen
dc.subject.meshMice, Inbred C57BLen
dc.subject.meshMicrobial Viabilityen
dc.subject.meshPhagocytesen
dc.subject.meshStaphylococcal Infectionsen
dc.subject.meshStaphylococcus aureusen
dc.subject.meshVirulence Factorsen
dc.titleStaphylococcus aureus phenotype switching: an effective bacterial strategy to escape host immune response and establish a chronic infection.en
dc.typeArticleen
dc.identifier.journalEMBO molecular medicineen
refterms.dateFOA2018-06-13T04:05:39Z
html.description.abstractStaphylococcus aureus is a frequent cause for serious, chronic and therapy-refractive infections in spite of susceptibility to antibiotics in vitro. In chronic infections, altered bacterial phenotypes, such as small colony variants (SCVs), have been found. Yet, it is largely unclear whether the ability to interconvert from the wild-type to the SCV phenotype is only a rare clinical and/or just laboratory phenomenon or is essential to sustain an infection. Here, we performed different long-term in vitro and in vivo infection models with S. aureus and we show that viable bacteria can persist within host cells and/or tissues for several weeks. Persistence induced bacterial phenotypic diversity, including SCV phenotypes, accompanied by changes in virulence factor expression and auxotrophism. However, the recovered SCV phenotypes were highly dynamic and rapidly reverted to the fully virulent wild-type form when leaving the intracellular location and infecting new cells. Our findings demonstrate that bacterial phenotype switching is an integral part of the infection process that enables the bacteria to hide inside host cells, which can be a reservoir for chronic and therapy-refractive infections.


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