Abstract
BackgroundMechanisms underlying the transition from commensalism to virulence in Enterococcus faecalis are not fully understood. We previously identified the enterococcal leucine-rich protein A (ElrA) as a virulence factor of E. faecalis. The elrA gene is part of an operon that comprises four other ORFs encoding putative surface proteins of unknown function.ResultsIn this work, we compared the susceptibility to phagocytosis of three E. faecalis strains, including a wild-type (WT), a ΔelrA strain, and a strain overexpressing the whole elr operon in order to understand the role of this operon in E. faecalis virulence. While both WT and ΔelrA strains were efficiently phagocytized by RAW 264.7 mouse macrophages, the elr operon-overexpressing strain showed a decreased capability to be internalized by the phagocytic cells. Consistently, the strain overexpressing elr operon was less adherent to macrophages than the WT strain, suggesting that overexpression of the elr operon could confer E. faecalis with additional anti-adhesion properties. In addition, increased virulence of the elr operon-overexpressing strain was shown in a mouse peritonitis model.ConclusionsAltogether, our results indicate that overexpression of the elr operon facilitates the E. faecalis escape from host immune defenses.Electronic supplementary materialThe online version of this article (doi:10.1186/s12866-015-0448-y) contains supplementary material, which is available to authorized users.
Highlights
Mechanisms underlying the transition from commensalism to virulence in Enterococcus faecalis are not fully understood
Located immediately downstream of elrA in the five-gene elr operon, there is a gene encoding a small protein with an LPXTG anchor motif (ElrB), followed by two further proteins each possessing a carboxy-terminal WxL anchor motif (ElrC and ElrD), and a putative transmembrane protein (ElrE), a member of the DUF916 protein family [4]
Overexpression of elr operon impairs phagocytosis We explored the effect of elr operon overexpression on the E. faecalis interaction with macrophages by monitoring phagocytosis of green-fluorescent protein (GFP)-labeled E. faecalis strains by RAW cells using flow cytometry analysis
Summary
Mechanisms underlying the transition from commensalism to virulence in Enterococcus faecalis are not fully understood. While our current understanding of the mechanisms that lead to the lifestyle shift from commensalism to virulence in enterococci remains an emerging area of research, the pathogenesis of E. faecalis is clearly a complex multifactorial process that currently remains poorly understood. In this regard, we have previously identified the enterococcal leucine-rich protein A (ElrA), a protein that possesses a leucine-rich repeat (LRR) domain and Cortes-Perez et al BMC Microbiology (2015) 15:112 modulation, by stimulating host immune cells to counteract E. faecalis infection [4]. Capsular polysaccharide serotypes C and D contribute to complement evasion [12, 13] and rhamnopolysaccharide Epa protects from phagocytic killing [13, 14], most likely by preventing uptake by macrophages as we recently showed in zebrafish model [15]
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