Exploration of the role of the virulence factor ElrA during Enterococcus faecalis cell infection

Sci Rep. 2018 Jan 29;8(1):1749. doi: 10.1038/s41598-018-20206-6.

Abstract

Enterococcus faecalis, an organism generally not pathogenic for healthy humans, has the potential to cause disease in susceptible hosts. While it seems to be equipped to interact with and circumvent host immune defense, most of the molecular and cellular mechanisms underlying the enterococcal infectious process remain elusive. Here, we investigated the role of the Enterococcal Leucine Rich protein A (ElrA), an internalin-like protein of E. faecalis also known as a virulence factor. ElrA was previously shown to prevent adhesion to macrophages. We show that ElrA does not inhibit the basic phagocytic process, but is able to prevent sensing and migration of macrophages toward E. faecalis. Presence or absence of FHL2, a eukaryotic partner of ElrA, does not affect the ElrA-dependent mechanism preventing macrophage migration. However, we highlight a partial contribution of FHL2 in ElrA-mediated virulence in vivo. Our results indicate that ElrA plays at least a dual role of which anti-phagocytic activity may contribute to dissemination of extracellular E. faecalis during infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bacterial Proteins / metabolism
  • Caco-2 Cells
  • Cell Line
  • Cell Line, Tumor
  • Enterococcus faecalis / metabolism*
  • Gram-Positive Bacterial Infections / microbiology*
  • HeLa Cells
  • Hep G2 Cells
  • Humans
  • Leucine / metabolism
  • Macrophages / metabolism
  • Macrophages / microbiology
  • Mice
  • RAW 264.7 Cells
  • Staphylococcal Protein A / metabolism*
  • Virulence / physiology*
  • Virulence Factors / metabolism*

Substances

  • Bacterial Proteins
  • Staphylococcal Protein A
  • Virulence Factors
  • Leucine