Pseudomonas aeruginosa is a Gram-negative bacterium regarded as an opportunistic pathogen. It infects immunocompromised patients, and is the second leading cause of nosocomial diseases. This bacterium has numerous virulence factors, adapts quickly to new environments, and requires a few nutrients to survive. All of these mechanisms will generate a host response. The fastest immune response is neutrophil recruitment, followed by phagocytosis and degranulation. There is another mechanism to fight bacteria called NET formation, which is the formation of a neutrophil extracellular network. NET is formed through a process called NETosis where the release of the cell nuclear material can hold and destroy pathogens. The nuclear receptor peroxisome proliferator-activated receptor PPARγ, besides lipid and glucose metabolism, is involved in the inflammatory response modulation, being considered a potential target for the study of new therapies for inflammatory and infectious diseases. We therefore aim to investigate the involvement of PPARγ in lung injury caused by P. aeruginosa using an agonist of this receptor, rosiglitazone.