Grant: Operating Grant

Staphylococcus aureus is one of the leading causes of hospital-and community-acquired infections. This microorganism has a remarkable ability to rapidly adapt to antibiotic pressure and acquire resistance. Extensive use of beta-lactam antibiotics has invariably been followed by the development and spread of resistance in S. aureus. Methicillin, a beta-lactam antibiotic designed to circumvent beta-lactam-resistant S. aureus, encountered resistant strains soon after its introduction into clinics. Methicillin-resistant S. aureus (MRSA) strains pose a serious threat to public health as they have become resistant to almost all the clinically used antibiotics. Emergence of intermediate-vancomycin-resistant S. aureus strains has limited the options for treatment of MRSA infections. Given the recent development of this microorganism and the impact it has on human health we are undertaking research aimed at understanding the molecular mechanism of antibiotic resistance. In particular, we are interested in investigating the S. aureus response to antibiotics that inhibit cell wall peptidoglycan biosynthesis. Peptidoglycan is the main component of cell wall. It provides shape and mechanic strength to the cell wall, and it is unique to bacteria. Therefore, it is an important target for drug development. Studies have shown that many genes in S. aureus are regulated in response to cell wall damage caused by cell wall inhibitors. Elucidation of the roles these genes play in the S. aureus response to cell damage will have a great impact in the design of new strategies in treatment of Staphylococcal infections.