Our lab is interested in understanding the molecular mechanisms of calcium (Ca2+) signaling in bacteria and its regulatory role in human pathogens. Ca2+ regulates a number of essential processes in eukaryotes. Slight abnormalities in cellular Ca2+ homeostasis have been implicated in many human diseases, including diseases associated with bacterial infections, such as cystic fibrosis (CF) pulmonary infections and endocarditis.
Our primary model is Pseudomonas aeruginosa, a gram negative opportunistic human pathogen and a leading cause of severe acute and chronic infections. It is one of the primary organisms that contribute to airway blockage and cellular damage in patients with CF. Since Ca2+regulates a number of essential host processes including hyperinflamatory response to bacterial infection, and accumulates in airway epithelia, pulmonary and nasal liquids of CF patients, we think it serves as an environmental trigger of virulence in P. aeruginosa.
Over the years, we have observed that elevated external Ca2+ induces a number of virulence factors in P. aeruginosa, including biofilm formation, production of alginate, rhamnolipid, pyocyanin, pyoverdine, secreted proteases, and others. Our main goal is to elucidate the regulatory and/or signaling mechanisms controlling the pleiotropic effects of Ca2+ on P. aeruginosa virulence and its interactions with the host.