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    SPI2 T3SS effectors facilitate enterocyte apical to basolateral transmigration of Salmonella-containing vacuoles in vivo (2021)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Fulde, Marcus (WE 7)
    van Vorst, Kira (WE 7)
    Zhang, Kaiyi
    Westermann, Alexander J.
    Busche, Tobias
    Huei, Yong Chiun
    Welitschanski, Katharina
    Froh, Isabell
    Pägelow, Dennis (WE 7)
    Plendl, Johanna (WE 1)
    Pfarrer, Christiane
    Kalinowski, Jörn
    Vogel, Jörg
    Valentin-Weigand, Peter
    Hensel, Michael
    Tedin, Karsten (WE 7)
    Repnik, Urska
    Hornef, Mathias W.
    Quelle
    Gut microbes
    Bandzählung: 13
    Heftzählung: 1
    Seiten: Article: 1973836
    ISSN: 1949-0976
    Sprache
    Englisch
    Verweise
    URL (Volltext): https://www.tandfonline.com/doi/full/10.1080/19490976.2021.1973836
    DOI: 10.1080/19490976.2021.1973836
    Pubmed: 34542008
    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

    Salmonella pathogenicity island (SPI) 2 type three secretion system (T3SS)-mediated effector molecules facilitate bacterial survival in phagocytes but their role in the intestinal epithelium in vivo remains ill-defined. Using our neonatal murine infection model in combination with SPI2 reporter technology and RNA-Seq of sorted primary enterocytes, we demonstrate expression of SPI2 effector molecules by intraepithelial Salmonella Typhimurium (S. Typhimurium). Contrary to expectation, immunostaining revealed that infection with SPI2 T3SS-mutants resulted in significantly enlarged intraepithelial Salmonella-containing vacuoles (SCV) with altered cellular positioning, suggesting impaired apical to basolateral transmigration. Also, infection with isogenic tagged S. Typhimurium strains revealed a reduced spread of intraepithelial SPI2 T3SS mutant S. Typhimurium to systemic body sites. These results suggest that SPI2 T3SS effector molecules contribute to enterocyte apical to basolateral transmigration of the SCV during the early stage of the infection.