Abstract
Background Enterococcus faecalis plays a dual role in human ecology, predominantly existing as a commensal in the alimentary canal, but also as an opportunistic pathogen that frequently causes nosocomial infections like bacteremia. A number of virulence factors that contribute to the pathogenic potential of E. faecalis have been established. However, the process in which E. faecalis gains access to the bloodstream and establishes a persistent infection is not well understood.Methodology/Principal FindingsTo enhance our understanding of how this commensal bacterium adapts during a bloodstream infection and to examine the interplay between genes we designed an in vitro experiment using genome-wide microarrays to investigate what effects the presence of and growth in blood have on the transcriptome of E. faecalis strain V583. We showed that growth in both 2xYT supplemented with 10% blood and in 100% blood had a great impact on the transcription of many genes in the V583 genome. We identified several immediate changes signifying cellular processes that might contribute to adaptation and growth in blood. These include modulation of membrane fatty acid composition, oxidative and lytic stress protection, acquisition of new available substrates, transport functions including heme/iron transporters and genes associated with virulence in E. faecalis.Conclusions/SignificanceThe results presented here reveal that cultivation of E. faecalis in blood in vitro has a profound impact on its transcriptome, which includes a number of virulence traits. Observed regulation of genes and pathways revealed new insight into physiological features and metabolic capacities which enable E. faecalis to adapt and grow in blood. A number of the regulated genes might potentially be useful candidates for development of new therapeutic approaches for treatment of E. faecalis infections.
Highlights
Enterococcus faecalis is a common resident of the gastrointestinal tract of humans [1]
Since E. faecalis is known to sense and respond to target cells such as erythrocytes, e.g. by expressing virulence factors like the toxin cytolysin [23], we decided to use whole blood rather than serum or plasma to mimic the in vivo environment and to examine other responses possibly modulated by erythrocytes
In order to obtain reliable colony forming units (CFU) counts, gentle sonication was applied to break up aggregates and long chains of V583 cells
Summary
Enterococcus faecalis is a common resident of the gastrointestinal tract of humans [1]. E. faecalis V583 (referred to as V583 hereafter) originates from a patient suffering from a persistent bloodstream infection, and it was the first vancomycin-resistant clinical isolate reported in the United States [6]. It has been acknowledged that E. faecalis acquires genetic traits by horizontal gene transfer, which includes virulence and antibiotic resistance determinants, to survive and persist in complex environments such as different infection sites (reviewed in [14]). E. faecalis pathogenesis most likely involves an orchestrated interplay between the regulation of virulence factors and multiple genetic traits that govern adaptation of the bacterial cell physiology during the process of infection. Enterococcus faecalis plays a dual role in human ecology, predominantly existing as a commensal in the alimentary canal, and as an opportunistic pathogen that frequently causes nosocomial infections like bacteremia. The process in which E. faecalis gains access to the bloodstream and establishes a persistent infection is not well understood
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