Published November 11, 2015
| Version v1
Journal article
Switching Rho GTPase activation into effective antibacterial defenses requires the caspase-1/IL-1beta signaling axis
Creators
Contributors
Others:
- Toxines bactériennes dans la relation hôtes-pathogènes ; Université Nice Sophia Antipolis (1965 - 2019) (UNS) ; COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-IFR50-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA)
- Centre méditerranéen de médecine moléculaire (C3M) ; Université Nice Sophia Antipolis (1965 - 2019) (UNS) ; COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA)
- Université Nice Sophia Antipolis (1965 - 2019) (UNS) ; COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)
- Our laboratory is supported by INSERM, Ligue Nationale contre le Cancer, the French Government (National Research Agency, ANR) through the "Investments for the Future" LABEX SIGNALIFE ANR-11-LABX-0028–01 and ANR-11-BSV3–004–01, Fondation ARC pour la Recherche sur le Cancer (ARC 3800, RAC13006AAA).
- ANR-11-LABX-0028,SIGNALIFE,Réseau d'Innovation sur les Voies de Signalisation en Sciences de la Vie(2011)
Description
The monitoring of the activation state of Rho GTPases has emerged as a potent innate immune mechanism for detecting pathogens. In the March issue of PLOS Pathogens, we show that the activation of Rho GTPases by the CNF1 toxin during E. coli-triggered bacteremia leads to a GR1(+)cell-mediated efficient bacterial clearing and improves host survival. Host alarm requires the Caspase-1/IL-1beta signaling axis. Furthermore, we discover that pathogenic bacteria have the capacity to block immune responses via the expression of the α-hemolysin pore-forming toxin. In this commentary, we will comment on these findings and highlight the questions raised by this example of attack-defense mechanisms used alternatively by the pathogen and the host during blood infection.
Abstract
International audienceAdditional details
Identifiers
- URL
- https://hal-pasteur.archives-ouvertes.fr/pasteur-02448674
- URN
- urn:oai:HAL:pasteur-02448674v1
Origin repository
- Origin repository
- UNICA