Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/55259
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dc.contributor.authorOggioni, M.en
dc.contributor.authorTrappetti, C.en
dc.contributor.authorKadioglu, A.en
dc.contributor.authorCassone, M.en
dc.contributor.authorIannelli, F.en
dc.contributor.authorRicci, S.en
dc.contributor.authorAndrew, P.en
dc.contributor.authorPozzi, G.en
dc.date.issued2006en
dc.identifier.citationMolecular Microbiology, 2006; 61(5):1196-1210en
dc.identifier.issn0950-382Xen
dc.identifier.issn1365-2958en
dc.identifier.urihttp://hdl.handle.net/2440/55259-
dc.description.abstractTwo main patterns of gene expression of Streptococcus pneumoniae were observed during infection in the host by quantitative real time RT-PCR; one was characteristic of bacteria in blood and one of bacteria in tissue, such as brain and lung. Gene expression in blood was characterized by increased expression of pneumolysin, pspA and hrcA, while pneumococci in tissue infection showed increased expression of neuraminidases, metalloproteinases, oxidative stress and competence genes. In vitro situations with similar expression patterns were detected in liquid culture and in a newly developed pneumococcal model of biofilm respectively. The biofilm model was dependent on addition of synthetic competence stimulating peptide (CSP) and no biofilm was formed by CSP receptor mutants. As one of the differentially expressed gene sets in vivo were the competence genes, we exploited competence-specific tools to intervene on pneumococcal virulence during infection. Induction of the competence system by the quorum-sensing peptide, CSP, not only induced biofilm formation in vitro, but also increased virulence in pneumonia in vivo. In contrast, a mutant for the ComD receptor, which did not form biofilm, also showed reduced virulence in pneumonia. These results were opposite to those found in a bacteraemic sepsis model of infection, where the competence system was downregulated. When pneumococci in the different physiological states were used directly for challenge, sessile cells grown in a biofilm were more effective in inducing meningitis and pneumonia, while planktonic cells from liquid culture were more effective in inducing sepsis. Our data enable us, using in vivo gene expression and in vivo modulation of virulence, to postulate the distinction – from the pneumococcal point of view – between two main types of disease. During bacteraemic sepsis pneumococci resemble planktonic growth, while during tissue infection, such as pneumonia or meningitis, pneumococci are in a biofilm-like state.en
dc.description.statementofresponsibilityMarco R. Oggioni, Claudia Trappetti, Aras Kadioglu, Marco Cassone, Francesco Iannelli, Susanna Ricci, Peter W. Andrew and Gianni Pozzien
dc.language.isoenen
dc.publisherBlackwell Publishing Ltden
dc.subjectAnimals; Mice; Plankton; Biofilms; Streptococcus pneumoniae; Pneumococcal Infections; Sepsis; Pneumonia; Meningitis; Disease Models, Animal; Bacterial Proteins; RNA, Messenger; Survival Rate; Reverse Transcriptase Polymerase Chain Reaction; Virulence; Gene Expression Regulation, Bacterial; Time Factorsen
dc.titleSwitch from planktonic to sessile life: a major event in pneumococcal pathogenesisen
dc.typeJournal articleen
dc.identifier.rmid0020094303en
dc.identifier.doi10.1111/j.1365-2958.2006.05310.xen
dc.identifier.pubid36416-
pubs.library.collectionMolecular and Biomedical Science publicationsen
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidTrappetti, C. [0000-0001-8272-0068]en
Appears in Collections:Molecular and Biomedical Science publications

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