Staphylococcus aureus, including both MRSA and non-MRSA strains, represent a serious threat to global health being responsible for a range of infectious diseases, such as mild skin and soft tissue infections, infective endocarditis, osteomyelitis, bacteremia, and fatal pneumonia. It is commonly associated with significant morbidity, hospital mortality, length of stay and economic burden. The resistance rates of S. aureus infection and multidrug resistant strains are increasing, making the clinical anti-infective treatment more difficult. The development of new antimicrobial drugs has remained virtually stagnant over the past decade. The resulting prolonged hospitalizations and high mortality among patients with MRSA infections have substantially increased the medical costs.
Rates of S. aureus infections are particularly high in patients with diabetes, highlighting the ability of this pathogen to survive in the presence of high glucose concentration. This condition is generally detrimental for bacteria as it leads to excessive production of reactive oxygen species (ROS) that cause DNA and protein damages, interfere with oxidative phosphorylation and compromise envelope integrity and function. Little is known about how S. aureus adapts to glucose levels. Recently, I showed that ribosome hibernation, a widespread phenomenon among bacteria, is critical for S. aureus adaptation to glucose metabolism. Ribosome hibernation-deficient cells exhibit low viability in glucose rich condition.
The primary goal of my projects is to understand the molecular mechanisms underlying these adaptation processes mediated by ribosome hibernation. I believe that analyzing the molecular bases of S. aureus survival can help provide a basis for designing effective prevention and treatment measures against infections caused by S. aureus.