Publikationsdatenbank

Salmonella Pathogenicity Island 2 (SPI2) effectors facilitate enterocyte transmigration in neonatal non-typhoidal Salmonella infections (2023)

Art

Poster

Autoren

van Vorst, Kira (WE 7)

Zhang, Kaiyi

Repnik, Urska

Hensel, Michael

Valentin-Weigand, Peter

Hornef, Mathias Walter

Fulde, Marcus (WE 7)

Kongress

Zoonoses 2023 - International Symposium on Zoonoses Research

09. – 11.10.2023

Quelle

Zoonoses 2023 - International Symposium on Zoonoses Research : benefits and chances of one health research : program and abstracts — German Research Platform for Zoonoses (Hrsg.)

— S. 59

Sprache

Englisch

Verweise

URL (Volltext): https://evis.events/event/260/attachments/99/255/Zoonoses%202023%20-%20Book%20of%20Abstracts.pdf

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

Non-typhoidal Salmonella (NTS) belong to the most prevalent causes of infectious diarrheal disease in humans and pigs worldwide, but also contribute to invasive infections in infants. The pathogenicity of NTS is conferred by horizontally acquired chromosomal regions, called Salmonella pathogenicity islands (SPIs), encoding sets of effector proteins delivered into the host cell via specific type-three secretion systems. Several in vitro studies identified SPI2 as a requirement for the establishment of an intracellular compartment allowing bacterial survival and replication inside the host cell, the Salmonella containing vacuole (SCV).
We used our previously established neonatal mouse model to clarify the role of SPI2 in establishment and progression of systemic NTS infections in the neonate host.
Oral infection with wildtype and SPI2-deficient NTS resulted in similar bacterial loads of the gastrointestinal tract, whereas re-isolation rates of mutants from systemic organs were significantly decreased. In contrast to the general understanding of SPI2 as prerequisite for SCV formation in vitro, mutants
established and maintained SCVs and even grew to high numbers without harming the host cell. By evaluating isogenic SPI2 effector protein deficient Salmonella strains, we demonstrate that the effector SifA significantly contributes to the SPI2-dependent phenotype in vivo. Its absence prevents transmi-
gration of enterocytes and subsequent systemic dissemination.