Kévin Pethe

This study examines how tRNA reprogramming and codon bias link translation to metabolic state in Enterococcus faecalis across growth phases.

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 shows the mycobacterial ATP burst is an experimental artifact caused by cell lysis, not a biological response, and presents it as a tool for screening cell wall-disrupting drugs.

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.