Background: Pseudomonas aeruginosa may cause severe or even fatal infection in hosts with immunodeficiency. Interleukin-17 (IL-17) is a newly discovered pro-inflammatory cytokine, which promotes the recruitment and activation of neutrophils in the respiratory tract by inducing release of chemokine C-X-C. Objective: This study was conducted to explore the role of IL-17 in host defense against acute pseudomonas aeruginosa infection in lungs. Methods: The expression of IL-17 and its downstream effectors (IL-1 beta, MIP-2 and G-CSF) were detected in mouse lungs with acute pseudomonas aeruginosa infection; 48 h after intratracheal administration of justice plasmid, mice were infected with pseudomonas aeruginosa again, and the bacterial clearance rate and the expression of downstream effectors of IL-17, as well as the mice death rate, were determined 6 h later. Results: The expression of IL-17 and its downstream effectors (IL-1 beta, MIP-2 and G-CSF) significantly increased in mouse lungs with acute pseudomonas aeruginosa infection. After intratracheal administration of justice plasmid expressing IL-17, the expression of IL-17 and its downstream effectors significantly increased, accompanied by increase in neutrophil count. The justice plasmid expressing IL-17 was intratracheally administered before acute pseudomonas aeruginosa lung infection, which significantly increased the expression of IL-17 and its downstream effectors (IL-1 beta, MIP-2 and G-CSF) in the respiratory tract, leading to increasing clearance rate of bacteria and survival rate. Conclusion: IL-17 may recruit neutrophil to the infected areas in the early phase of pseudomonas aeruginosa lung infection.