Publikationsdatenbank

Minimal SPI1-T3SS effector requirement for Salmonella enterocyte invasion and intracellular proliferation in vivo (2018)

Art

Zeitschriftenartikel / wissenschaftlicher Beitrag

Autoren

Zhang, Kaiyi

Riba, Ambre

Nietschke, Monika

Torow, Natalia

Repnik, Urska

Pütz, Andreas

Fulde, Marcus (WE 7)

Dupont, Aline

Hensel, Michael

Hornef, Mathias

Quelle

PLoS pathogens

Bandzählung: 14

Heftzählung: 3

Seiten: e1006925

ISSN: 1553-7374

Sprache

Englisch

Verweise

DOI: 10.1371/journal.ppat.1006925

Pubmed: 29522566

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

Effector molecules translocated by the Salmonella pathogenicity island (SPI)1-encoded type 3 secretion system (T3SS) critically contribute to the pathogenesis of human Salmonella infection. They facilitate internalization by non-phagocytic enterocytes rendering the intestinal epithelium an entry site for infection. Their function in vivo has remained ill-defined due to the lack of a suitable animal model that allows visualization of intraepithelial Salmonella. Here, we took advantage of our novel neonatal mouse model and analyzed various bacterial mutants and reporter strains as well as gene deficient mice. Our results demonstrate the critical but redundant role of SopE2 and SipA for enterocyte invasion, prerequisite for transcriptional stimulation and mucosal translocation in vivo. In contrast, the generation of a replicative intraepithelial endosomal compartment required the cooperative action of SipA and SopE2 or SipA and SopB but was independent of SopA or host MyD88 signaling. Intraepithelial growth had no critical influence on systemic spread. Our results define the role of SPI1-T3SS effector molecules during enterocyte invasion and intraepithelial proliferation in vivo providing novel insight in the early course of Salmonella infection.