|Institution||School of Medicine and Dentistry|
|Department||Microbiology and Immunology in the Center for Oral Biology|
|Address||University of Rochester Medical Center|
School of Medicine and Dentistry
601 Elmwood Ave, Box 611
Rochester NY 14642
Research: Molecular Genetics and Physiology of the Response to Stresses by Streptococci and Enterococci.
The research in my laboratory is focused on characterization of the stress responses by streptococci and enterococci. To accomplish our goals, we use a variety of state-of-the-art molecular and biochemical techniques, that include physiologic, enzymatic, genomic and proteomic approaches. The specific projects in the laboratory are divided in two major areas; (i) the role of the Streptococcus mutans stress regulon in biofilm formation, persistence and virulence, and (ii) characterization of the stringent response of Enterococcus faecalis.
1. Streptococcus mutans
Streptococcus mutans, a common inhabitant of dental biofilms, is recognized as a major etiologic agent of human dental caries. Despite significant progress in treatment and prevention, dental caries remains among the most common infectious diseases afflicting humans and results in an enormous health and economic burden worldwide. The virulence of S. mutans resides in three core attributes; its abilities to adhere and form biofilms on tooth surfaces, to produce large quantities of organic acids from a wide range of carbohydrates, and to tolerate environmental stresses, particularly low pH. Because stress tolerance is intertwined with S. mutans virulence, the dissection of the mechanisms that allow these bacteria to thrive in oral biofilms during stressful conditions is central for a complete understanding of the pathogenesis of dental caries. Our current efforts focus on the characterization of the Spx global regulator, and its role in controlling stress response and biofilm formation in S. mutans.
2. Enterococcus faecalis
The opportunistic pathogen Enterococus faecalis, a natural inhabitant of the human intestinal flora, is one of the leading causes of hospital-acquired infections, including endocarditis, bacteremia, and urinary tract and soft tissue infections. This organism has a remarkable ability to thrive in a variety of adverse environments, including an innate and acquired resistance to multiple antibiotics. Recently, we found that the stringent response, a key bacterial system for adaptation to changing environments, plays a key role in the ability of E. faecalis to tolerate the human host defenses and antimicrobial therapies. The objective of this study is to fully understand how, and to what extent, the stringent response controls the expression of virulence factors, and of antibiotic tolerance in E. faecalis.
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