Haris Antypas

This study shows E. faecalis biofilms suppress neutrophil defenses by producing lactic acid and high bacterial density.

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 paper shows that E. faecalis uses lactic acid to suppress macrophage activation, enabling persistent and polymicrobial wound infections.

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 shows Enterococcus faecalis persists and replicates intracellularly within neutrophils, prolonging infection and inflammation in chronic wounds.