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Updated: Aug 19, 2026

Invasion of Human Cells by a Bacterial Pathogen
Published on: March 21, 2011
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
Abstract:
Enterococcus faecalis is responsible for a large variety of nosocomial infections. The intestinal barrier is thought to be one of the preferential portals of entry of enterococci, and the ability of E. faecalis to survive within peritoneal macrophages may contribute to spreading to distant sites. We examined the ability of a polysaccharide-expressing (biofilm-positive) E. faecalis strain and an isogenic biofilm-negative mutant to enter and survive within professional and nonprofessional phagocytes. Biofilm-positive bacteria survived longer in all cell systems than did biofilm-negative bacteria, through a process of receptor-mediated endocytosis that is dependent on functional reorganization of microtubules and polymerization of microfilament and on activation of protein kinases but not ATPases or protein phosphatases. We suggest that glycosaminoglycans--specifically heparin, heparan sulfate, and chondroitin sulfate A--are the host receptors for enterococci on professional and, possibly, nonprofessional phagocytes, allowing entry of enterococci into cell compartments where killing mechanisms are inhibited.
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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