FN Archimer Export Format
PT J
TI Copper homeostasis at the host vibrio interface: lessons from intracellular vibrio transcriptomics
BT 
AF VANHOVE, Audrey
   RUBIO, Tristan
   NGUYEN, An N.
   LEMIRE, Astrid
   ROCHE, David
   NICOD, Julie
   VERGNES, Agnes
   POIRIER, Aurore
   DISCONZI, Elena
   BACHERE, Evelyne
   LE ROUX, Frederique
   JACQ, Annick
   CHARRIERE, Guillaume
   DESTOUMIEUX-GARZON, Delphine
AS 1:1;2:1;3:2;4:3,4;5:5,6;6:1;7:1;8:1;9:2;10:1;11:3,4;12:;13:1;14:1;
FF 1:;2:;3:;4:;5:;6:;7:PDG-RBE-IHPE;8:;9:;10:PDG-RBE-IHPE;11:PDG-RBE-PFOM;12:;13:;14:;
C1 Univ Montpellier, Univ Perpignan, CNRS, IFREMER,IHPE,UMR 5244, Via Domitia, F-34095 Montpellier, France.
   Univ Paris 11, CNRS, CEA, I2BC, F-91405 Orsay, France.
   IFREMER, Unite Physiol Fonct Organismes Marins, CS 10070, F-29280 Plouzane, France.
   Univ Paris 06, Sorbonne Univ, Integrat Biol Marine Models, Stn Biol Roscoff,UMR 8227,CS 90074,CNRS, F-29688 Roscoff, France.
   Commissariat Energie Atom & Energies Alternat CEA, DSV, Inst Genom, Genoscope, F-91057 Evry, France.
   CNRS, Lab Anal Bioinformat Genom & Metab LABGeM, UMR 8030, F-91057 Evry, France.
C2 UNIV MONTPELLIER, FRANCE
   UNIV PARIS 11, FRANCE
   IFREMER, FRANCE
   UNIV PARIS 06, FRANCE
   CEA, FRANCE
   CNRS, FRANCE
SI MONTPELLIER
   ROSCOFF
SE PDG-RBE-IHPE
   PDG-RBE-PFOM
UM IHPE
IN WOS Ifremer jusqu'en 2018
   copubli-france
   copubli-univ-france
IF 5.395
TC 29
UR https://archimer.ifremer.fr/doc/00301/41254/88202.pdf
LA English
DT Article
AB Recent studies revealed that several vibrio species have evolved the capacity to survive inside host cells. However, it is still often ignored if intracellular stages are required for pathogenicity. Virulence of Vibrio tasmaniensis LGP32, a strain pathogenic for Crassostrea gigas oysters, depends on entry into hemocytes, the oyster immune cells. We investigated here the mechanisms of LGP32 intracellular survival and their consequences on the host–pathogen interaction. Entry and survival inside hemocytes were required for LGP32-driven cytolysis of hemocytes, both in vivo and in vitro. LGP32 intracellular stages showed a profound boost in metabolic activity and a major transcription of antioxidant and copper detoxification genes, as revealed by RNA sequencing. LGP32 isogenic mutants showed that resistance to oxidative stress and copper efflux are two main functions required for vibrio intracellular stages and cytotoxicity to hemocytes. Copper efflux was also essential for host colonization and virulence in vivo. Altogether, our results identify copper resistance as a major mechanism to resist killing by phagocytes, induce cytolysis of immune cells and colonize oysters. Selection of such resistance traits could arise from vibrio interactions with copper-rich environmental niches including marine invertebrates, which favour the emergence of pathogenic vibrios resistant to intraphagosomal killing across animal species.
PY 2016
PD MAR
SO Environmental Microbiology
SN 1462-2912
PU Wiley-blackwell
VL 18
IS 3
UT 000372964800011
BP 875
EP 888
DI 10.1111/1462-2920.13083
ID 41254
ER

EF