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dc.contributor.authorVidigal, Pedrina G
dc.contributor.authorMüsken, Mathias
dc.contributor.authorBecker, Katrin A
dc.contributor.authorHäussler, Susanne
dc.contributor.authorWingender, Jost
dc.contributor.authorSteinmann, Eike
dc.contributor.authorKehrmann, Jan
dc.contributor.authorGulbins, Erich
dc.contributor.authorBuer, Jan
dc.contributor.authorRath, Peter Michael
dc.contributor.authorSteinmann, Jörg
dc.date.accessioned2014-05-23T13:53:16Z
dc.date.available2014-05-23T13:53:16Z
dc.date.issued2014
dc.identifier.citationEffects of green tea compound epigallocatechin-3-gallate against Stenotrophomonas maltophilia infection and biofilm. 2014, 9 (4):e92876 PLoS ONEen
dc.identifier.issn1932-6203
dc.identifier.pmid24690894
dc.identifier.doi10.1371/journal.pone.0092876
dc.identifier.urihttp://hdl.handle.net/10033/317387
dc.description.abstractWe investigated the in vitro and in vivo activities of epigallocatechin-3-gallate (EGCg), a green tea component, against Stenotrophomonas maltophilia (Sm) isolates from cystic fibrosis (CF) patients. In vitro effects of EGCg and the antibiotic colistin (COL) on growth inhibition, survival, and also against young and mature biofilms of S. maltophilia were determined. Qualitative and quantitative changes on the biofilms were assessed by confocal laser scanning microscopy (CLSM). Further, in vivo effects of nebulized EGCg in C57BL/6 and Cftr mutant mice during acute Sm lung infection were evaluated. Subinhibitory concentrations of EGCg significantly reduced not only biofilm formation, but also the quantity of viable cells in young and mature biofilms. CLSM showed that EGCg-exposed biofilms exhibited either a change in total biofilm biovolume or an increase of the fraction of dead cells contained within the biofilm in a dose depended manner. Sm infected wild-type and Cftr mutant mice treated with 1,024 mg/L EGCg by inhalation exhibited significantly lower bacterial counts than those undergoing no treatment or treated with COL. EGCg displayed promising inhibitory and anti-biofilm properties against CF Sm isolates in vitro and significantly reduced Sm bacterial counts in an acute infection model with wild type and CF mice. This natural compound may represent a novel therapeutic agent against Sm infection in CF.
dc.language.isoenen
dc.rightsArchived with thanks to PloS oneen
dc.titleEffects of green tea compound epigallocatechin-3-gallate against Stenotrophomonas maltophilia infection and biofilm.en
dc.typeArticleen
dc.contributor.departmentDepartment of Molecular Bacteriology, Helmholtz Center for Infection Research, Braunschweig, Germanyen
dc.identifier.journalPloS oneen
refterms.dateFOA2018-06-12T18:12:16Z
html.description.abstractWe investigated the in vitro and in vivo activities of epigallocatechin-3-gallate (EGCg), a green tea component, against Stenotrophomonas maltophilia (Sm) isolates from cystic fibrosis (CF) patients. In vitro effects of EGCg and the antibiotic colistin (COL) on growth inhibition, survival, and also against young and mature biofilms of S. maltophilia were determined. Qualitative and quantitative changes on the biofilms were assessed by confocal laser scanning microscopy (CLSM). Further, in vivo effects of nebulized EGCg in C57BL/6 and Cftr mutant mice during acute Sm lung infection were evaluated. Subinhibitory concentrations of EGCg significantly reduced not only biofilm formation, but also the quantity of viable cells in young and mature biofilms. CLSM showed that EGCg-exposed biofilms exhibited either a change in total biofilm biovolume or an increase of the fraction of dead cells contained within the biofilm in a dose depended manner. Sm infected wild-type and Cftr mutant mice treated with 1,024 mg/L EGCg by inhalation exhibited significantly lower bacterial counts than those undergoing no treatment or treated with COL. EGCg displayed promising inhibitory and anti-biofilm properties against CF Sm isolates in vitro and significantly reduced Sm bacterial counts in an acute infection model with wild type and CF mice. This natural compound may represent a novel therapeutic agent against Sm infection in CF.


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