Chronic wound infection is a major global public health issue, with diabetic foot ulcers (DFU) of particular concern. Enterococcus faecalis is one of the most commonly isolated pathogens from infected wounds, including DFU. Neutrophils are highly reactive, inherently short-lived immune cells that play a critical role in bacterial defence. The phagocytosis of most bacteria will rapidly drive neutrophil cell death (apoptosis); however, a very small number of intracellular bacteria have been found to block apoptosis and instead utilise this host cell as a niche for persistence. Currently, E. faecalis – neutrophil interactions are poorly understood. In a mouse model of wound infection, E. faecalis could colonise and persist in the wound out to 7 days post infection (p.i) despite an upregulated pro-inflammatory cytokine response and increased neutrophil recruitment. Unexpectedly, extended in vitro infection of neutrophils with E. faecalis did not induce host cell apoptosis. Rather, we observed that E. faecalis infection significantly prolongs both murine and human neutrophil lifespan even compared to uninfected controls. Assessment of infected cells under confocal microscopy and quantification of intracellular CFU demonstrated that bacteria were phagocytosed by neutrophils regardless of opsonisation and persisted intracellularly out to 24 h p.i. Using RADA, which incorporates into newly synthesised bacterial cell walls to monitor intracellular E. faecalis replication, we observed that E. faecalis actively replicates within murine neutrophils between 6-18 h post infection, followed by a predominately persistent phase between 18-24 h p.i. Investigations are currently underway to determine the role of key cell death enzymes (Caspase-3, -8 and -9) in mediating this cell death suppression and intracellular occupation.