ArticleInfection and immunity2014
Enterococcus faecalis infection activates phosphatidylinositol 3-kinase signaling to block apoptotic cell death in macrophages.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 54 citations in OpenAlex.
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- Dual role mechanisms of regulated cell death in apical periodontitis: from pathogenic destruction to therapeutic potential.Cell death discovery · 2025Review
- Biological characteristics of SARS-CoV-2 resistant populations by integrated gut microbiota sequencing, metabolomics, and proteomics: a cohort comparison study.Frontiers in medicine · 2025Article
- Role of necroptosis in pulpitis: integration of bacterial infection, immune imbalance, and oxidative stress.PeerJ · 2025Review
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- Enterococcal-host interactions in the gastrointestinal tract and beyond.FEMS microbes · 2024Review
- Breaking the cellular defense: the role of autophagy evasion inFrontiers in cellular and infection microbiology · 2024Article
- Apoptosis and its pathways as targets for intracellular pathogens to persist in cells.Parasitology research · 2023Review
- Role ofJournal of oral microbiology · 2023Review
- Caspase-1 Inhibition Reduces Occurrence of PANoptosis in Macrophages Infected byJournal of clinical medicine · 2022Article
- Enterococcus faecalis alters endo-lysosomal trafficking to replicate and persist within mammalian cells.PLoS pathogens · 2022Article
- Aloe-Emodin-Mediated Photodynamic Therapy Attenuates Sepsis-Associated Toxins in Selected Gram-Positive Bacteria In Vitro.Journal of microbiology and biotechnology · 2021Article
- Cardiac Microlesions Form During Severe Bacteremic Enterococcus faecalis Infection.The Journal of infectious diseases · 2021Article
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- Real-Time Induction of Macrophage Apoptosis, Pyroptosis, and Necroptosis byFrontiers in cellular and infection microbiology · 2021Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis is an intrinsic immune defense mechanism in the host response to microbial infection. Not surprisingly, many pathogens have evolved various strategies to manipulate this important pathway to benefit their own survival and dissemination in the host during infection. To our knowledge, no attempts have been made to explore the host cell survival signals modulated by the bacterium Enterococcus faecalis. Here, we show for the first time that during early stages of infection, internalized enterococci can prevent host cell (RAW264.7 cells, primary macrophages, and mouse embryonic fibroblasts [MEFs]) apoptosis induced by a wide spectrum of proapoptotic stimuli. Activation of caspase 3 and cleavage of the caspase 3 substrate poly(ADP-ribose) polymerase were inhibited in E. faecalis-infected cells, indicating that E. faecalis protects macrophages from apoptosis by inhibiting caspase 3 activation. This antiapoptotic activity in E. faecalis-infected cells was dependent on the activation of the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway, which resulted in the increased expression of the antiapoptotic factor Bcl-2 and decreased expression of the proapoptotic factor Bax. Further analysis revealed that active E. faecalis physiology was important for inhibition of host cell apoptosis, and this feature seemed to be a strain-independent trait among E. faecalis isolates. Employing a mouse peritonitis model, we also determined that cells collected from the peritoneal lavage fluid of E. faecalis-infected mice showed reduced levels of apoptosis compared to cells from uninfected mice. These results show early modulation of apoptosis during infection and have important implications for enterococcal pathogenesis.
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