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dc.contributor.authorWeigel, W A
dc.contributor.authorDersch, P
dc.date.accessioned2018-05-03T10:31:54Z
dc.date.available2018-05-03T10:31:54Z
dc.date.issued2018-02-01
dc.identifier.citationPhenotypic heterogeneity: a bacterial virulence strategy. 2018 Microbes Infect.en
dc.identifier.issn1769-714X
dc.identifier.pmid29409898
dc.identifier.doi10.1016/j.micinf.2018.01.008
dc.identifier.urihttp://hdl.handle.net/10033/621363
dc.description.abstractGrowing knowledge of the complexity of the host-pathogen interactions during the course of an infection revealed an amazing variability of bacterial pathogens within the same host tissue site. This heterogeneity in bacterial populations is either the result of a different bacterial response to a slightly divergent tissue microenvironment or is caused by a genetic circuit in which small endogenous fluctuations in a small number of transcription factors drive gene expression in combination with a positive feedback loop. As a result host-pathogen encounters can have different outcomes in individual cells, which enables bet-hedging and/or a co-operative behavior that enhance bacterial fitness and virulence, drive different host responses and promote resistance of small subpopulations to antibiotic treatment. This has a strong impact on the progression and control of the infection, which must be considered for the development of successful antimicrobial therapies.
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titlePhenotypic heterogeneity: a bacterial virulence strategy.en
dc.typeArticleen
dc.contributor.departmentHelmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7, 38124 Braunschweig, Germany.en
dc.identifier.journalMicrobes and infectionen
refterms.dateFOA2019-02-01T00:00:00Z
html.description.abstractGrowing knowledge of the complexity of the host-pathogen interactions during the course of an infection revealed an amazing variability of bacterial pathogens within the same host tissue site. This heterogeneity in bacterial populations is either the result of a different bacterial response to a slightly divergent tissue microenvironment or is caused by a genetic circuit in which small endogenous fluctuations in a small number of transcription factors drive gene expression in combination with a positive feedback loop. As a result host-pathogen encounters can have different outcomes in individual cells, which enables bet-hedging and/or a co-operative behavior that enhance bacterial fitness and virulence, drive different host responses and promote resistance of small subpopulations to antibiotic treatment. This has a strong impact on the progression and control of the infection, which must be considered for the development of successful antimicrobial therapies.


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