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dc.contributor.authorPustelny, Christian
dc.contributor.authorKomor, Uliana
dc.contributor.authorPawar, Vinay
dc.contributor.authorLorenz, Anne
dc.contributor.authorBielecka, Agata
dc.contributor.authorMoter, Annette
dc.contributor.authorGocht, Benjamin
dc.contributor.authorEckweiler, Denitsa
dc.contributor.authorMüsken, Mathias
dc.contributor.authorGrothe, Claudia
dc.contributor.authorLünsdorf, Heinrich
dc.contributor.authorWeiss, Siegfried
dc.contributor.authorHäussler, Susanne
dc.date.accessioned2015-02-24T15:27:08Zen
dc.date.available2015-02-24T15:27:08Zen
dc.date.issued2015-01en
dc.identifier.citationContribution of Veillonella parvula to Pseudomonas aeruginosa-mediated pathogenicity in a murine tumor model system. 2015, 83 (1):417-29 Infect. Immun.en
dc.identifier.issn1098-5522en
dc.identifier.pmid25385800en
dc.identifier.doi10.1128/IAI.02234-14en
dc.identifier.urihttp://hdl.handle.net/10033/345168en
dc.description.abstractThe recent finding that high numbers of strict anaerobes are present in the respiratory tract of cystic fibrosis (CF) patients has drawn attention to the pathogenic contribution of the CF microbiome to airway disease. In this study, we investigated the specific interactions of the most dominant bacterial CF pathogen, Pseudomonas aeruginosa, with the anaerobic bacterium Veillonella parvula, which has been recovered at comparable cell numbers from the respiratory tract of CF patients. In addition to growth competition experiments, transcriptional profiling, and analyses of biofilm formation by in vitro studies, we used our recently established in vivo murine tumor model to investigate mutual influences of the two pathogens during a biofilm-associated infection process. We found that P. aeruginosa and V. parvula colonized distinct niches within the tumor. Interestingly, significantly higher cell numbers of P. aeruginosa could be recovered from the tumor tissue when mice were coinfected with both bacterial species than when mice were monoinfected with P. aeruginosa. Concordantly, the results of in vivo transcriptional profiling implied that the presence of V. parvula supports P. aeruginosa growth at the site of infection in the host, and the higher P. aeruginosa load correlated with clinical deterioration of the host. Although many challenges must be overcome to dissect the specific interactions of coinfecting bacteria during an infection process, our findings exemplarily demonstrate that the complex interrelations between coinfecting microorganisms and the immune responses determine clinical outcome to a much greater extent than previously anticipated.
dc.language.isoenen
dc.relationinfo:eu-repo/grantAgreement/EC/FP7/260276en
dc.rightsopenAccessen
dc.titleContribution of Veillonella parvula to Pseudomonas aeruginosa-mediated pathogenicity in a murine tumor model system.en
dc.typeArticleen
dc.contributor.departmentHelmholtz Centre for infection research, Inhoffenstr. 7, 38124 Braunschweig, Germany.en
dc.identifier.journalInfection and immunityen
refterms.dateFOA2018-06-13T01:35:07Z
html.description.abstractThe recent finding that high numbers of strict anaerobes are present in the respiratory tract of cystic fibrosis (CF) patients has drawn attention to the pathogenic contribution of the CF microbiome to airway disease. In this study, we investigated the specific interactions of the most dominant bacterial CF pathogen, Pseudomonas aeruginosa, with the anaerobic bacterium Veillonella parvula, which has been recovered at comparable cell numbers from the respiratory tract of CF patients. In addition to growth competition experiments, transcriptional profiling, and analyses of biofilm formation by in vitro studies, we used our recently established in vivo murine tumor model to investigate mutual influences of the two pathogens during a biofilm-associated infection process. We found that P. aeruginosa and V. parvula colonized distinct niches within the tumor. Interestingly, significantly higher cell numbers of P. aeruginosa could be recovered from the tumor tissue when mice were coinfected with both bacterial species than when mice were monoinfected with P. aeruginosa. Concordantly, the results of in vivo transcriptional profiling implied that the presence of V. parvula supports P. aeruginosa growth at the site of infection in the host, and the higher P. aeruginosa load correlated with clinical deterioration of the host. Although many challenges must be overcome to dissect the specific interactions of coinfecting bacteria during an infection process, our findings exemplarily demonstrate that the complex interrelations between coinfecting microorganisms and the immune responses determine clinical outcome to a much greater extent than previously anticipated.


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