RT explored potential oligomerization of FliI. JM coordinated

the work and edited the manuscript. All authors read and approved of the final manuscript.”
“Background Enterococci are part of the normal flora in human intestines and are also a leading cause of nosocomial infections [1, 2]. These organisms are somehow able to migrate from the gastrointestinal tract into the bloodstream and cause systemic infections such as bacteremia and even endocarditis [2–4]. Although many strains of enterococci seem to be harmless commensals, particular subgroups of Enterococcus faecalis and Enterococcus faecium predominate among Erastin chemical structure isolates from nosocomial enterococcal infections. In E. faecalis, numerous factors important for virulence have been characterized. For example, the Fsr system, a homologue of the staphylococcal Agr system, has been shown to be selleck products important for virulence due, at least in part, to its control of gelatinase and a serine protease expression via a quorum-sensing mechanism buy VX-689 [5–7]. Microarray studies also indicated that the Fsr system regulates other genes important for virulence [8], one of which is the locus encoding Ebp pili [8], whose subunits are encoded by the ebp

operon [9]. A non-piliated ebp mutant, producing much less biofilm than the parent strain, was shown to be attenuated in a rat model of endocarditis [9] and in a murine urinary tract infection model [10]. We previously described EbpR as an important activator of the ebpABC operon encoding the pili in E. faecalis OG1RF [11]. Although ebpR is not essential for ebpABC expression, we detected 100-fold less ebpABC mRNA in a ΔebpR mutant compared to the OG1RF parent strain. In addition, even in the presence of an intact ebpR gene, only 5-20% of the cells, grown aerobically in BHI or in TSBG, were found to produce pili (detected by electron microscopy or immunofluorescence) [9, 11]. These results imply that other regulatory

and/or environmental factors may affect pilus production. Bicarbonate is a major element of the mammalian body for reaching and maintaining homeostasis. In equilibrium with CO2, Ribonucleotide reductase H2CO2 and CO3 2-, depending on pH, temperature, and CO2 pressure, bicarbonate does not diffuse freely across the membrane and needs specific transporters [12]. In the stomach, HCO3 – is secreted by the surface mucus cells, where it gets trapped in the mucus and forms part of the mucus-HCO3 – barrier, thereby maintaining a pH gradient of pH 2 in the lumen to pH 7 at the mucosal epithelium interface. Interestingly, some microbial pathogens have been shown to respond in vivo to CO2 (from 5 to 20%) and/or HCO3 – (10-100 mM) by enhancing production of factors important for virulence (Staphyloccocus aureus [13], Vibrio cholerae [14], group A streptococcus [15], Bacillus anthracis [16, 17], Cryptococcus neoformans [18] and Citrobacter rodentium [19]). Regulatory proteins have been described which mediate the CO2/HCO3 – response at the transcriptional level in B.