FN Archimer Export Format
PT J
TI Species-specific mechanisms of cytotoxicity toward immune cells determine the successful outcome of Vibrio infections
BT 
AF RUBIO, Tristan
   OYANEDEL, Daniel
   LABREUCHE, Yannick
   TOULZA, Eve
   LUO, Xing
   BRUTO, Maxime
   CHAPARRO, Cristian
   TORRES, Marta
   DE LORGERIL, Julien
   HAFFNER, Philippe
   VIDAL-DUPIOL, Jeremie
   LAGORCE, Arnaud
   PETTON, Bruno
   MITTA, Guillaume
   JACQ, Annick
   LE ROUX, Frederique
   CHARRIERE, Guillaume
   DESTOUMIEUX-GARZON, Delphine
AS 1:6;2:6;3:2,3;4:7;5:4;6:3;7:8;8:1,4,5;9:1;10:1;11:1;12:6;13:2;14:7;15:4;16:2,3;17:6;18:8;
FF 1:;2:;3:PDG-RBE-PFOM;4:;5:;6:PDG-RBE-PFOM;7:;8:;9:PDG-RBE-IHPE;10:PDG-RBE-IHPE;11:PDG-RBE-IHPE;12:;13:PDG-RBE-PFOM-LPI;14:;15:;16:PDG-RBE-PFOM;17:;18:;
C1 Univ Montpellier, IFREMER, IHPE, CNRS, Univ Perpignan Via Domitia, F-34090 Montpellier, France.
   IFREMER, Unite Physiol Fonct Organismes Marins, F-29280 Plouzane, France.
   Sorbonne Univ, Univ Pierre & Marie Curie Paris 06, Stn Biol Roscoff, UMR 8227,CNRS,Integrat Biol Marine Models, F-29688 Roscoff, France.
   Univ Paris Saclay, Univ Paris Sud, Inst Integrat Biol Cell Commissariat Energi Atom, CNRS, F-91198 Gif Sur Yvette, France.
   Univ Granada, Dept Microbiol, Fac Pharm, E-18071 Granada, Spain.
   Univ Montpellier, IFREMER, IHPE, CNRS, Univ Perpignan Via Domitia, F-34090 Montpellier, France.
   Univ Montpellier, IFREMER, IHPE, CNRS, Univ Perpignan Via Domitia, F-34090 Montpellier, France.
   Univ Montpellier, IFREMER, IHPE, CNRS, Univ Perpignan Via Domitia, F-34090 Montpellier, France.
C2 IFREMER, FRANCE
   IFREMER, FRANCE
   UNIV PARIS 06, FRANCE
   UNIV PARIS SACLAY, FRANCE
   UNIV GRANADA, SPAIN
   UNIV MONTPELLIER, FRANCE
   UNIV PERPIGNAN, FRANCE
   CNRS, FRANCE
SI ROSCOFF
   MONTPELLIER
   ARGENTON
SE PDG-RBE-PFOM
   PDG-RBE-IHPE
   PDG-RBE-PFOM-LPI
UM LEMAR
   IHPE
IN WOS Ifremer UPR
   WOS Ifremer UMR
   WOS Cotutelle UMR
   copubli-france
   copubli-europe
   copubli-univ-france
IF 9.412
TC 32
UR https://archimer.ifremer.fr/doc/00507/61837/65900.pdf
   https://archimer.ifremer.fr/doc/00507/61837/65901.pdf
   https://archimer.ifremer.fr/doc/00507/61837/65902.xlsx
   https://archimer.ifremer.fr/doc/00507/61837/65903.xlsx
   https://archimer.ifremer.fr/doc/00507/61837/65904.xlsx
   https://archimer.ifremer.fr/doc/00507/61837/65905.xlsx
LA English
DT Article
DE ;T6SS;toxin;dual RNA-seq;cytolysis;pathogenesis
AB Vibrio species cause infectious diseases in humans and animals, but they can also live as commensals within their host tissues. How Vibrio subverts the host defenses to mount a successful infection remains poorly understood, and this knowledge is critical for predicting and managing disease. Here, we have investigated the cellular and molecular mechanisms underpinning infection and colonization of 2 virulent Vibrio species in an ecologically relevant host model, oyster, to study interactions with marine Vibrio species. All Vibrio strains were recognized by the immune system, but only nonvirulent strains were controlled. We showed that virulent strains were cytotoxic to hemocytes, oyster immune cells. By analyzing host and bacterial transcriptional responses to infection, together with Vibrio gene knock-outs, we discovered that Vibrio crassostreae and Vibrio tasmaniensis use distinct mechanisms to cause hemocyte lysis. Whereas V. crassostreae cytotoxicity is dependent on a direct contact with hemocytes and requires an ancestral gene encoding a protein of unknown function, r5.7, V. tasmaniensis cytotoxicity is dependent on phagocytosis and requires intracellular secretion of T6SS effectors. We conclude that proliferation of commensal vibrios is controlled by the host immune system, preventing systemic infections in oysters, whereas the successful infection of virulent strains relies on Vibrio species-specific molecular determinants that converge to compromise host immune cell function, allowing evasion of the host immune system. 
PY 2019
PD JUN
SO Proceedings Of The National Academy Of Sciences Of The United States Of America
SN 0027-8424
PU Natl Acad Sciences
VL 116
IS 28
UT 000474535700081
BP 14238
EP 14247
DI 10.1073/pnas.1905747116
ID 61837
ER

EF