Frederick Reinhart Tanoto

This study uses a diabetic mouse model to show that Enterococcus faecium persists in wounds due to impaired clearance and altered immune responses compared to non-diabetic mice.

This study identifies gelatinase as a key factor enabling Enterococcus faecalis to transition from intracellular replication to extracellular egress during infection.

This study identifies the Fsr quorum sensing system in Enterococcus faecalis as a negative regulator of biofilm growth and inflammation in infective endocarditis.

This study uses scRNA-seq to analyze infected and uninfected wounds in mice, revealing transcriptional and metabolic changes linked to E. faecalis infection and its impact on wound healing.