Glycosaminoglycans mediate invasion and survival of Enterococcus faecalis into macrophages

Lucilla Baldassarri1, Lucia Bertuccini, Roberta Creti

  • 1Dipartimento di Malattie Infettive, Parassitarie ed Immunomediate, Istituto Superiore di Sanità, Rome, Italy. lucilla.baldassarri@iss.it

Insights

Enterococcus faecalis biofilm-positive strains survive longer in phagocytes than biofilm-negative mutants. This enhanced survival is mediated by host glycosaminoglycans, facilitating bacterial entry and inhibiting killing mechanisms.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Enterococcus faecalis is a significant cause of hospital-acquired infections.
  • The intestinal barrier is a primary entry point for enterococci.
  • E. faecalis survival within macrophages aids systemic spread.

Purpose of the Study:

  • To investigate the mechanisms of E. faecalis entry and survival in phagocytes.
  • To compare the behavior of biofilm-positive and biofilm-negative strains within immune cells.

Main Methods:

  • Utilized polysaccharide-expressing (biofilm-positive) E. faecalis and an isogenic biofilm-negative mutant.
  • Examined bacterial entry and survival within professional and nonprofessional phagocytes.
  • Investigated the role of cytoskeletal elements and signaling pathways in bacterial uptake.

Main Results:

  • Biofilm-positive E. faecalis demonstrated enhanced survival in all tested phagocyte systems compared to biofilm-negative mutants.
  • Bacterial entry involved receptor-mediated endocytosis, dependent on microtubule reorganization and microfilament polymerization.
  • Protein kinase activation, but not ATPase or phosphatase activity, was crucial for bacterial survival.

Conclusions:

  • Glycosaminoglycans (heparin, heparan sulfate, chondroitin sulfate A) are identified as host receptors for E. faecalis on phagocytes.
  • These interactions facilitate bacterial entry into cellular compartments where intracellular killing is impaired.
  • This mechanism contributes to the pathogenesis and dissemination of E. faecalis infections.

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