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Biofilm and planktonic Enterococcus faecalis elicit different responses from host phagocytes in vitro.
An AraC-type transcriptional regulator encoded on the Enterococcus faecalis pathogenicity island contributes to pathogenesis and intracellular macrophage survival.
Enterococcus faecalis infection activates phosphatidylinositol 3-kinase signaling to block apoptotic cell death in macrophages.
Roles of TLR/MyD88/MAPK/NF-?B Signaling Pathways in the Regulation of Phagocytosis and Proinflammatory Cytokine Expression in Response to E. faecalis Infection.
Surface protein Esp enhances pro-inflammatory cytokine expression through NF-?B activation during enterococcal infection.
The opportunistic pathogen Enterococcus faecalis resists phagosome acidification and autophagy to promote intracellular survival in macrophages.