Cell Biology of Enterococcal Infection

Cell Biology of Enterococcal Infection

Intracellular E. faecalis replicating within macrophages (right) and subsequently egressing following host cell lysis or other escape mechanisms (left). (F. Reinhart Tanoto)

Although traditionally viewed as an extracellular pathogen, Enterococcus faecalis is increasingly recognized for its ability to invade, persist, and even replicate within host cells. This intracellular phase of infection may play a critical role in immune evasion, chronic colonization, and relapse following antibiotic treatment. However, the cellular and molecular mechanisms that enable E. faecalis to engage with and exploit the intracellular environment remain largely underexplored.

Our lab investigates the cell biology of E. faecalis infection using a combination of mammalian cell culture, tissue explants, and in vivo models. We employ high-resolution and live-cell imaging techniques alongside genetic and molecular tools to study how E. faecalis enters non-phagocytic cells, traffics within host compartments, and subverts innate immune responses. Particular focus is placed on bacterial adaptations that facilitate intracellular survival, such as modulation of host signaling, nutrient acquisition, and resistance to oxidative stress.

We are also interested in the consequences of intracellular persistence on host cell physiology, as well as the role of intracellular reservoirs in recurrent or treatment-refractory infection. By defining the host–pathogen interactions that govern the intracellular lifestyle of E. faecalis, we aim to uncover novel mechanisms of persistence and identify therapeutic vulnerabilities not addressed by conventional antimicrobial strategies.