In patients with cystic fibrosis, chronic lung infection by the bacterium Pseudomonas aeruginosa is a critical step in the evolution of the disease. This chronic infection is characterized by the persistence of P. aeruginosa and ultimately resistance against the major antibiotics used in treatment. New antibacterial strategies or methods of controlling the inflammatory response generated by this bacterium must be developed. Our preliminary study of toxins secreted by P. aeruginosa shows that loss of two enzymes function involved in lipid metabolism ( LipA and LOXA ) appear to be associated with a phenotype favoring the formation of a biofilm structure that would be able to favor chronic lung infection. The objective of our project is to establish that the loss of activity of LipA and LOXA affect the ability of P. aeruginosa to persist in the lungs and escape the immune response of the host. We will also study how the expression of these enzymes is regulated during lung infection and whether strains that colonize patients chronically lose these enzymatic activities. Ultimately, our project will provide new approaches for limiting chronic P. aeruginosa infections in patients with cystic fibrosis.