Research
Pseudomonas aeruginosa
Pseudomonas aeruginosa is a ubiquitous Gram-negative bacterium that can act as an opportunistic human pathogen, causing infections in individuals with compromised immune systems and burn wound patients. P. aeruginosa infections are especially common in individuals with the heritable disease Cystic Fibrosis (CF), of which it is the primary cause of morbidity and mortality. In addition, P. aeruginosa is used as a model organism for studying quorum sensing, or bacterial cell-cell communication, which is the use of small signaling molecules to control gene expression in a cell density-dependent manner.
We are interested in numerous aspects of the P. aeruginosa lifestyle, which include pathogenesis, nutrition, cell-cell communication, evolution, and the development of therapeutics. Some significant findings from our lab have demonstrated that nutrition in the host CF lung is important for cuing bacterial production of virulence factors and that unlike other bacteria, P. aeruginosa packages a cell-cell communication signal, the Pseudomonas Quinolone Signal (PQS), in outer membrane vesicles, which are spherical, bilayered structures that serve to traffic the signal. Ongoing research is aimed at further characterizing P. aeruginosa carbon preference in the CF lung, developing nutritional-based therapeutics, the formation and fusion of outer membrane vesicles, and research into the basic aspects of quorum sensing.
Aggregatibacter actinomycetemcomitans
Aggregatibacter actinomycetemcomitans (Aa) is a Gram-negative opportunistic pathogen that colonizes the mouths of approximately 50% of the population in the United States. Aa is one of the causative agents of localized aggressive periodontitis, which is an inflammatory disease that leads to the destruction of alveolar bone and tooth loss. Incidences of periodontal disease leave an individual at greater risk to develop endocardial infections, from which Aa has been isolated.
Our laboratory seeks to understand key aspects of Aa pathogenesis in the human host as well as how it relates to the microbial ecology of the mouth. In the mouth, Aa is in constant contact with numerous bacterial species (predominantly Streptococcus spp.) that compose the normal flora. Because of these constant interactions, we hypothesize that Aa my utilize numerous methods of communication, competition and cooperation with other bacteria.
Our studies to date have demonstrated that Aa utilizes novel means to regulate carbon source preference and innate immune response evasion. These studies are centered around the metabolites, ie. lactate and hydrogen peroxide that Aa encounters in the presence of the Streptococcus spp. containing microbial flora. These studies have demonstrated that Aa senses and responds to the physiological activity of the normal flora as well as the host and that these responses may impact Aa during its transition from a quiescent inhabitant of the mouth to an aggressive pathogen.
