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Background  We previously identified  ebpR , encoding a potential member of the AtxA/Mga transcriptional regulator family, and showed that it is important for transcriptional activation of the  Enterococcus faecalis   e ndocarditis and  b iofilm associated  p ilus operon,  ebpABC . Although  ebpR  is not absolutely essential for  ebpABC  expression (100-fold reduction), its deletion led to phenotypes similar to those of an  ebpABC  mutant such as absence of pili at the cell surface and, consequently, reduced biofilm formation. A non-piliated  ebpABC  mutant has been shown to be attenuated in a rat model of endocarditis and in a murine urinary tract infection model, indicating an important participation of the  ebpR-ebpABC  locus in virulence. However, there is no report relating to the environmental conditions that affect expression of the  ebpR-ebpABC  locus.    Results  In this study, we examined the effect of CO 2 /HCO 3  - , pH, and the Fsr system on the  ebpR-ebpABC  locus expression. The presence of 5% CO 2 /0.1 M HCO 3  -  increased  ebpR-ebpABC  expression, while the Fsr system was confirmed to be a weak repressor of this locus. The mechanism by which the Fsr system repressed the  ebpR-ebpABC  locus expression appears independent of the effects of CO 2  -  bicarbonate. Furthermore, by using an  ebpA :: lacZ  fusion as a reporter, we showed that addition of 0.1 M sodium bicarbonate to TSBG (buffered at pH 7.5), but not the presence of 5% CO 2 , induced  ebpA  expression in TSBG broth. In addition, using microarray analysis, we found 73 genes affected by the presence of sodium bicarbonate (abs(fold) > 2,  P  < 0.05), the majority of which belong to the PTS system and ABC transporter families. Finally, pilus production correlated with  ebpA  mRNA levels under the conditions tested.    Conclusions  This study reports that the  ebp  locus expression is enhanced by the presence of bicarbonate with a consequential increase in the number of cells producing pili. Although the molecular basis of the bicarbonate effect remains unclear, the pathway is independent of the Fsr system. In conclusion,  E. faecalis  joins the growing family of pathogens that regulates virulence gene expression in response to bicarbonate and/or CO 2 .

Bicarbonate enhances expression of the endocarditis and biofilm associated pilus locus, ebpR-ebpABC, in Enterococcus faecalis