Claudia J. Stocks

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

This paper shows bosutinib enhances macrophage phagocytosis and bacterial killing, reducing infection in mice.