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    E. coli Nissle 1917 Affects Salmonella adhesion to porcine intestinal epithelial cells (2011)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Schierack, Peter
    Kleta, Sylvia
    Tedin, Karsten
    Babila, Julius Tachu
    Oswald, Sibylle
    Oelschlaeger, Tobias A
    Hiemann, Rico
    Paetzold, Susanne
    Wieler, Lothar H
    Quelle
    PLOS ONE
    Bandzählung: 6
    Heftzählung: 2
    Seiten: e14712
    ISSN: 1932-6203
    Sprache
    Englisch
    Verweise
    URL (Volltext): http://edocs.fu-berlin.de/docs/receive/FUDOCS_document_000000017265
    DOI: 10.1371/journal.pone.0014712
    Pubmed: 21379575
    Kontakt
    Institut für Mikrobiologie und Tierseuchen

    Robert-von-Ostertag-Str. 7-13
    14163 Berlin
    +49 30 838 51843 / 66949
    mikrobiologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    The probiotic Escherichia coli strain Nissle 1917 (EcN) has been shown to interfere in a human in vitro model with the invasion of several bacterial pathogens into epithelial cells, but the underlying molecular mechanisms are not known.

    In this study, we investigated the inhibitory effects of EcN on Salmonella Typhimurium invasion of porcine intestinal epithelial cells, focusing on EcN effects on the various stages of Salmonella infection including intracellular and extracellular Salmonella growth rates, virulence gene regulation, and adhesion. We show that EcN affects the initial Salmonella invasion steps by modulating Salmonella virulence gene regulation and Salmonella SiiE-mediated adhesion, but not extra- and intracellular Salmonella growth. However, the inhibitory activity of EcN against Salmonella invasion always correlated with EcN adhesion capacities. EcN mutants defective in the expression of F1C fimbriae and flagellae were less adherent and less inhibitory toward Salmonella invasion. Another E. coli strain expressing F1C fimbriae was also adherent to IPEC-J2 cells, and was similarly inhibitory against Salmonella invasion like EcN.

    We propose that EcN affects Salmonella adhesion through secretory components. This mechanism appears to be common to many E. coli strains, with strong adherence being a prerequisite for an effective reduction of SiiE-mediated Salmonella adhesion.