TY - JOUR
T1 - ace, Which encodes an adhesin in Enterococcus faecalis, is regulated by Ers and is involved in virulence
AU - Lebreton, Francois
AU - Riboulet-Bisson, Eliette
AU - Serror, Pascale
AU - Sanguinetti, Maurizio
AU - Posteraro, Brunella
AU - Torelli, Riccardo
AU - Hartke, Axel
AU - Auffray, Yanick
AU - Giard, Jean-Christophe
PY - 2009
Y1 - 2009
N2 - Enterococcus faecalis is an opportunistic pathogen that causes numerous infectious diseases in humans and is a major agent of nosocomial infections. In this work, we showed that the recently identified transcriptional regulator Ers (PrfA like), known to be involved in the cellular metabolism and the virulence of E. faecalis, acts as a repressor of ace, which encodes a collagen-binding protein. We characterized the promoter region of ace, and transcriptional analysis by reverse transcription-quantitative PCR and mobility shift protein-DNA binding assays revealed that Ers directly regulates the expression of ace. Transcription of ace appeared to be induced by the presence of bile salts, probably via the deregulation of ers. Moreover, with an ace deletion mutant and the complemented strain and by using an insect (Galleria mellonella) virulence model, as well as in vivo-in vitro murine macrophage models, we demonstrated for the first time that Ace can be considered a virulence factor for E. faecalis. Furthermore, animal experiments revealed that Ace is also involved in urinary tract infection by E. faecalis.
AB - Enterococcus faecalis is an opportunistic pathogen that causes numerous infectious diseases in humans and is a major agent of nosocomial infections. In this work, we showed that the recently identified transcriptional regulator Ers (PrfA like), known to be involved in the cellular metabolism and the virulence of E. faecalis, acts as a repressor of ace, which encodes a collagen-binding protein. We characterized the promoter region of ace, and transcriptional analysis by reverse transcription-quantitative PCR and mobility shift protein-DNA binding assays revealed that Ers directly regulates the expression of ace. Transcription of ace appeared to be induced by the presence of bile salts, probably via the deregulation of ers. Moreover, with an ace deletion mutant and the complemented strain and by using an insect (Galleria mellonella) virulence model, as well as in vivo-in vitro murine macrophage models, we demonstrated for the first time that Ace can be considered a virulence factor for E. faecalis. Furthermore, animal experiments revealed that Ace is also involved in urinary tract infection by E. faecalis.
KW - enterococcus
KW - enterococcus
UR - http://hdl.handle.net/10807/1605
U2 - 10.1128/IAI.01218-08
DO - 10.1128/IAI.01218-08
M3 - Article
SN - 0019-9567
VL - 77
SP - 2832
EP - 2839
JO - Infection and Immunity
JF - Infection and Immunity
ER -