Staphylococcal adaptations during stress and infection
My laboratory studies staphylococcal adaptations in response to weak acid stress. Staphylococci commonly encounter biological weak acids like lactate and acetate when residing on the human skin. While lactate is present in human sweat gland secretions, acetate is produced as a byproduct of staphylococcal glucose metabolism. Both lactate and acetate can inhibit growth and adversely affect staphylococcal survival under conditions of low pH, normally associated with human sweat. We are interested in determining metabolic and physiological adaptations that enhance staphylococcal resistance to weak acid stress. Current projects focus on the role and regulation of glucose and arginine catabolism in response to weak acid stress. We are also investigating how weak acids modulate biofilm development by this organism. Biofilms are surface attached bacterial communities that are encased in a matrix composed of proteins, DNA and carbohydrates. During biofilm development, a subpopulation of staphylococci undergo a ‘suicidal’ form of cell death and contribute to the build-up of the biofilm matrix, thus hastening the biofilm maturation process. Although we have recently demonstrated a role for acetate in potentiating cell death in staphylococcal populations, the mechanisms involved are not clear and therefore represent an active area of research in our lab. Our studies will not only help identify alternate targets for therapeutic intervention but also enhance our understanding on how staphylococci survive the harsh acidic environment of the skin.