Mutual reprogramming of Yersinia and host responses during infection
Sprecher: Petra Dersch (Universität Münster) & Effie Bastounis (CMFI)
Gastgeber: Andreas Peschel (CMFI)
Datum & Uhrzeit: 08.01.2026 | 12:30–15:00 Uhr
Ort: Hörsaal 3M07, GUZ
Öffentliche Veranstaltung. Keine Anmeldung erforderlich. Nach den Vorträgen und der Diskussion findet ein kleiner Empfang in der EIngangshalle des GUZ statt.
Abstract:
Oral infections with Yersinia pseudotuberculosis lead to bacterial invasion of the gut-associated lymphoid tissues and deeper organs. During transcytosis, (i) the number of bacteria entering from the gut into the underlying lymphoid tissues is drastically reduced. However, even a small number of bacteria can efficiently replicate and (ii) trigger a strong recruitment of innate immune cells, primarily neutrophils, to the various sites of infection. This results in severe inflammation and extensive tissue damage. To understand the progression of the infection and the resulting disease outcome, we investigated the mutual reprogramming of bacteria and neutrophils both in vitro and in vivo throughout the infection process. We observed a complex spatiotemporal remodeling of neutrophils, particularly in the spleen and liver, which evolves over the course of the infection due to the secretion of toxins and the active injection of Yersinia effector proteins into the neutrophils.
Flash Talk: Bacterially infected macrophages promote biomechanical alterations in endothelial monolayers for transmigration
Abstract: Intracellular pathogens, like Listeria monocytogenes, manipulate host cells to spread from the initial infection site to distant organs through the bloodstream. For that, Listeria hijacks mononuclear phagocytes to traverse vascular endothelial cell (EC) linings, but how transmigration is regulated by EC is poorly understood. Here, we show that EC biomechanical responses to macrophages (ΜΦ) differ markedly with infection, decisively impacting their transmigration. Videomicroscopy reveals that MΦ exposure increases EC polarization and alignment while reducing migration speed. However, only uninfected MΦ-exposed EC increase their traction forces, monolayer stresses, and barrier integrity; responses significantly attenuated during infection. We show that TNF-α secretion during infection compromises EC barrier integrity and, combined with increased MΦ-EC adhesion, facilitates MΦ transmigration. Using zebrafish, we find that infection increases endothelial permeability, enhancing phagocyte extravasation in vivo. Thus, infection overrides MΦ-induced EC barrier strengthening for pathogen spread, remarkable feature that could be harnessed for infection control.