Publikationsdatenbank

Phage regulation and persister cell formation upon ciprofloxacin treatment via the toxin TisB in Salmonella Typhimurium (2024)

Art

Vortrag

Autoren

Braetz, S. (WE 7)

Schwerk, P. (WE 7)

Figueroa-Bossi, N.

Tedin, K. (WE 7)

Fulde, M. (WE 7)

Kongress

DGHM & VAAM 2024 : 7th Joint Microbiology & Infection Conference

Würzburg, 02. – 05.06.2024

Quelle

DGHM & VAAM 2024 : 7th Joint Microbiology & Infection Conference – Abstracts — Deutsche Gesellschaft für Hygiene und Mikrobiologie (DGHM) e. V. - German Society for Hygiene and Microbiology, Vereinigung für Allgemeine und Angewandte Mikrobiologie (VAAM) e.V. - Association for General and Applied Microbiology (Hrsg.)

1. Auflage

Jena: Conventus Congressmanagement & Marketing GmbH, 2024 — S. 29

ISBN: 978-3-948023-39-3

Sprache

Englisch

Verweise

URL (Volltext): https://d-nb.info/1349629189/34

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

Introduction
Persisters are drug-tolerant cells that survive bactericidal concentrations of antibiotics, therefore playing an important role in clinical therapy failure [1]. Mechanisms influencing bacterial survival during treatment with antibiotics include the activity of bacterial toxins, induction of prophages, and activation of stress responses [2, 3].

Material/method
We examined the effects of a tisB toxin deletion mutant in Salmonella Typhimurium on the ATP concentrations during treatment with four-fold the MIC of ciprofloxacin. Furthermore, we also examined the TisB-dependent induction of the prophages and their impact on persister cell formation comparing a phage-free variant of the wild type strain in a ∆tisB background.

Results
Deletion of tisB significantly increased ATP concentration and SOS response when exposed to ciprofloxacin, with a reduction in the formation of persistent cells. Interestingly, a 90-fold reduction in bacterial survival was observed four hours after challenging the phage-carrying ∆tisB strain with
ciprofloxacin. In contrast, deletion of all prophages in the tisB background slowed initial killing and had a less significant impact on drug persistence.

Discussion
The SOS response is controlled by RecA, which requires ATP for its activity. We suggest that TisB inhibits ATP formation, and interferes with DNA repair responses. This significantly reduces the SOS response-dependent prophage induction and thus increases persister cell formation.