Pseudomonas aeruginosa is still a prominent causative organism of sepsis in patients following severe trauma resulting in a significant morbidity and mortality. This organism is also a principal agent of lethal infections in cystic fibrosis patients.

Trauma and concomitant infection is a leading cause of death in severely injured higher organisms. In mammals, following septic trauma both acute and sustained responses are induced to orchestrate tissue repair and control infection. However, the host defense signaling pathways involved at the early stages of infection, and their role in defeating pathogens at the site of injury remains largely elusive.

The Rahme Lab aims to understand P. aeruginosa pathogenesis using clinically relevant acute and chronic murine burn and lung infection models that allow us to correlate our findings with pathology observed in human patients. Current studies in our Lab aim the identification of key host functions that are specific to local or distant burn trauma.

Work in our lab has used non-vertebrate hosts to identify novel virulence-associated genes and small molecules of P. aeruginosa that can now be used in a murine burn or a lung infection model to study their role on the inflammatory response following burn or lung infection. We developed a murine model that permits assessment of gene products in virulence and compounds efficacy against persistent and recurring infections. These models are used both to examine specific immunological responses and also perform functional genomics resulting in a systematic genome-wide approach.

It is our hope that our studies would lead to new insights into immune dysfunction that accompany bacterial infections, and provide therapeutic targets to improve the treatment and outcome of infected patients.