Research Interests Pseudomonas aeruginosa, which usually resides in soil and water environments, can infect compromised hosts to cause significant morbidity and mortality. The pathogenesis of this organism in humans involves multiple virulence factors whose expression patterns are integrated with growth and replication. Virulence is mediated mainly by the expression of cell surface molecules, sensing and signal transduction systems, motility, chemotaxis and the ability to secrete a number of destructive enzymes including proteases, lipases, neuraminidase, toxins and capsular material. My long-term objective is to understand the interplay between host and bacterial factors that lead to life-threatening infections with P. aeruginosa. We have focused on the relationship between expression of toxins injected by the type III system and Pseudomonas pathogenesis in acute infection models. The local as well as the systemic delivery of toxins emphasize the pathogenic potential of the bacterium. Our hypothesis is that delivery of the type III toxins inhibits the uptake and destruction of P. aeruginosa during the initial stages of colonization, allowing multiplication past the point of resolution by innate immune mechanisms in compromised hosts. The outcome of infection is then determined by the extent of injury or compromised state of the host, the expression patterns of the various toxins, proteases and other destructive enzymes, and the host response.