{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T21:56:00Z","timestamp":1792706160988,"version":"4.5.0"},"reference-count":63,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2006,8,1]],"date-time":"2006-08-01T00:00:00Z","timestamp":1154390400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Microbiology"],"published-print":{"date-parts":[[2006,9]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Two main patterns of gene expression of <jats:italic>Streptococcus pneumoniae<\/jats:italic> were observed during infection in the host by quantitative real time RT\u2010PCR; 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, <jats:italic>pspA<\/jats:italic> and <jats:italic>hrcA<\/jats:italic>, while pneumococci in tissue infection showed increased expression of neuraminidases, metalloproteinases, oxidative stress and competence genes. <jats:italic>In vitro<\/jats:italic> 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 <jats:italic>in vivo<\/jats:italic> were the competence genes, we exploited competence\u2010specific tools to intervene on pneumococcal virulence during infection. Induction of the competence system by the quorum\u2010sensing peptide, CSP, not only induced biofilm formation <jats:italic>in vitro<\/jats:italic>, but also increased virulence in pneumonia <jats:italic>in vivo<\/jats:italic>. 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 <jats:italic>in vivo<\/jats:italic> gene expression and <jats:italic>in vivo<\/jats:italic> modulation of virulence, to postulate the distinction \u2013 from the pneumococcal point of view \u2013 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\u2010like state.<\/jats:p>","DOI":"10.1111\/j.1365-2958.2006.05310.x","type":"journal-article","created":{"date-parts":[[2006,8,2]],"date-time":"2006-08-02T14:14:46Z","timestamp":1154528086000},"page":"1196-1210","source":"Crossref","is-referenced-by-count":226,"title":["Switch from planktonic to sessile life: a major event in pneumococcal pathogenesis"],"prefix":"10.1111","volume":"61","author":[{"given":"Marco 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