ArticlePLoS pathogens2022
Enterococcus faecalis alters endo-lysosomal trafficking to replicate and persist within mammalian cells.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- Select intratumoral riboflavin-auxotrophicProceedings of the National Academy of Sciences of the United States of America · 2026Article
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- Extracellular vesicles derived from Enterococcus faecalis: inflammatory activation does not require internalization.Cell communication and signaling : CCS · 2026Article
- Characterization of a novel cell wall-associated nucleotidase of Enterococcus faecalis that degrades extracellular c-di-AMP.PLoS pathogens · 2026Article
- Gelatinase regulates the egress of intracellular replicating populations during Enterococcus faecalis infection.PLoS pathogens · 2026Article
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- Identification of candidate nucleomodulins in ESKAPE bacteria -Frontiers in cellular and infection microbiology · 2026Article
- Nucleomodulins from gut bacteria: diverse mechanisms of translocation and interaction with host nuclear processes.Applied and environmental microbiology · 2025Review
- Interaction BetweenMicroorganisms · 2025Article
- Insights into ecology, pathogenesis, and biofilm formation ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Invasion of pancreatic ductal epithelial cells by Enterococcus faecalis is mediated by fibronectin and enterococcal fibronectin-binding protein A.Scientific reports · 2025Article
- Review
- Role of Rab GTPases in Bacteria Escaping from Vesicle Trafficking of Host Cells.Journal of microbiology (Seoul, Korea) · 2024Review
- Exploring the role of E. faecalis enterococcal polysaccharide antigen (EPA) and lipoproteins in evasion of phagocytosis.Molecular microbiology · 2024Article
- Article
- Bosutinib Stimulates Macrophage Survival, Phagocytosis, and Intracellular Killing of Bacteria.ACS infectious diseases · 2024Article
- Enterococcal-host interactions in the gastrointestinal tract and beyond.FEMS microbes · 2024Review
- Distribution Patterns and Antibiotic Resistance Profiles of Bacterial Pathogens Among Patients with Wound Infections in the Jiaxing Region from 2021 to 2023.Infection and drug resistance · 2024Article
- Mitoxantrone targets both host and bacteria to overcome vancomycin resistance inScience advances · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterococcus faecalis is a frequent opportunistic pathogen of wounds, whose infections are associated with biofilm formation, persistence, and recalcitrance toward treatment. We have previously shown that E. faecalis wound infection persists for at least 7 days. Here we report that viable E. faecalis are present within both immune and non-immune cells at the wound site up to 5 days after infection, raising the prospect that intracellular persistence contributes to chronic E. faecalis infection. Using in vitro keratinocyte and macrophage infection models, we show that E. faecalis becomes internalized and a subpopulation of bacteria can survive and replicate intracellularly. E. faecalis are internalized into keratinocytes primarily via macropinocytosis into single membrane-bound compartments and can persist in late endosomes up to 24 h after infection in the absence of colocalization with the lysosomal protease Cathepsin D or apparent fusion with the lysosome, suggesting that E. faecalis blocks endosomal maturation. Indeed, intracellular E. faecalis infection results in heterotypic intracellular trafficking with partial or absent labelling of E. faecalis-containing compartments with Rab5 and Rab7, small GTPases required for the endosome-lysosome trafficking. In addition, E. faecalis infection results in marked reduction of Rab5 and Rab7 protein levels which may also contribute to attenuated Rab incorporation into E. faecalis-containing compartments. Finally, we demonstrate that intracellular E. faecalis derived from infected keratinocytes are significantly more efficient in reinfecting new keratinocytes. Together, these data suggest that intracellular proliferation of E. faecalis may contribute to its persistence in the face of a robust immune response, providing a primed reservoir of bacteria for subsequent reinfection.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.