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dc.contributor.authorStapels, Daphne A C*
dc.contributor.authorHill, Peter W S*
dc.contributor.authorWestermann, Alexander J*
dc.contributor.authorFisher, Robert A*
dc.contributor.authorThurston, Teresa L*
dc.contributor.authorSaliba, Antoine-Emmanuel*
dc.contributor.authorBlommestein, Isabelle*
dc.contributor.authorVogel, Jörg*
dc.contributor.authorHelaine, Sophie*
dc.date.accessioned2019-04-10T07:56:27Z
dc.date.available2019-04-10T07:56:27Z
dc.date.issued2018-12-07
dc.identifier.citationScience. 2018 Dec 7;362(6419):1156-1160. doi: 10.1126/science.aat7148.en_US
dc.identifier.issn1095-9203
dc.identifier.pmid30523110
dc.identifier.doi10.1126/science.aat7148
dc.identifier.urihttp://hdl.handle.net/10033/621741
dc.description.abstractMany bacterial infections are hard to treat and tend to relapse, possibly due to the presence of antibiotic-tolerant persisters. In vitro, persister cells appear to be dormant. After uptake of Salmonella species by macrophages, nongrowing persisters also occur, but their physiological state is poorly understood. In this work, we show that Salmonella persisters arising during macrophage infection maintain a metabolically active state. Persisters reprogram macrophages by means of effectors secreted by the Salmonella pathogenicity island 2 type 3 secretion system. These effectors dampened proinflammatory innate immune responses and induced anti-inflammatory macrophage polarization. Such reprogramming allowed nongrowing Salmonella cells to survive for extended periods in their host. Persisters undermining host immune defenses might confer an advantage to the pathogen during relapse once antibiotic pressure is relieved.en_US
dc.language.isoenen_US
dc.publisherAmerican Association for the Advancement of Scienceen_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleSalmonella persisters undermine host immune defenses during antibiotic treatment.en_US
dc.typeArticleen_US
dc.contributor.departmentHIRI, Helmholtz-Institut für RNA-basierte Infektionsforschung, Josef-Shneider Strasse 2, 97080 Würzburg, Germany.en_US
dc.identifier.journalScienceen_US
refterms.dateFOA2019-04-10T07:56:27Z
dc.source.journaltitleScience (New York, N.Y.)


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