Staphylococcus aureus (SA) is an opportunistic pathogen responsible for difficult-to-treat infections, among which bone and joint infections (BJI). Three main factors that protect SA from the immune system and antibiotics are responsible for the large number (10-20%) of relapses observed during BJI treatments: biofilm formation, small colony variant phenotype and nonprofessional phagocyte cells invasion. SA inside osteoblasts have already been observed during a persistent case of BJI. Once internalized, SA is found in phago-endosomal vesicle where it can either persist or escape to induce cell death, notably due to mitochondria-dependent apoptosis. The response of mitochondria to an intracellular SA infection has been poorly studied so far. However, the few studies available suggest that SA can trigger oxida.ve damages together with mitochondria biogenesis and, in the case of a virulent strain, apoptosis. Our objective is to observe the mitochondrial behavior during the internalization of SA USA300 SF8300 (USA300) into osteoblasts, and compare it to the one triggered by the contact between the internalization-deficient mutant USA300 SF8300 ΔfnbPs (Δ) and osteoblasts.