Pseudomonas aeruginosa is a gram-negative, obligate respirer which is the most detrimental organism uniquely associated with morbidity and mortality in cystic fibrosis (CF) and is one of the most frequently encountered opportunistic pathogens. The organism generates a viscous exopolysaccharide called alginate within the CF lung that is harmful to the patient since it renders organisms resistant to drugs and phagocytosis. Our experiments are designed to elucidate the potential control of alginate production by endogenous oxidative stress and/or changes in the oxidation/reduction potential of the cell. We are also interested in how organisms growing as biofilms resist oxidative biocides and how a process known as quorum sensing (see figure) contributes to this process. Employing the disciplines of classical bacterial physiology and molecular biology, we are characterizing genes encoding the antioxidants superoxide dismutase, catalase and a structural protein called ankyrin in P. aeruginosa. Our studies are designed to determine if these proteins play a role in virulence and biofilm resistance to oxidizing biocides.

- (2005) Global analysis of cellular factors and responses involved in Pseudomonas aeruginosa resistance to arsenite. J Bacteriol, July, 187(14): 4853-64.
- (2006) Anaerobic killing of mucoid Pseudomonas aeruginosa by acidified nitrite derivatives under cystic fibrosis airway conditions. J Clin Invest, Feb, 116(2): 436-46.
- (2007) Two-pronged survival strategy for the major cystic fibrosis pathogen, Pseudomonas aeruginosa, lacking the capacity to degrade nitric oxide during anaerobic respiration. EMBO J, August 8, 26:(15): 3662-72.
- (2008) The peptidoglycan-associated lipoprotein OprL helps protect a Pseudomonas aeruginosa mutant devoid of the transactivator OxyR from hydrogen peroxide-mediated killing during planktonic and biofilm culture. J Bacteriol, May, 190(10): 3658-69.
- (2009) Pseudomonas aeruginosa hypoxic or naerobic biofilm infections within cystic fibrosis airways. Trends Microbiol, March, 17(3): 130-8.

