IL-1 is an essential pro-inflammatory factor in inflammation response. The effect of IL-1 is through binding to the IL-1 receptor that triggers the following signal transduction pathway. To study the role of IL-1 receptor-mediated signal pathway in inflammatory response, injecting P. aeruginosa into trachea of wild-type (WT) and type-1 IL-1 receptor knock-out (IL-1R1-/-) mice was used as the experimental model. Injecting bacterium into trachea of mice will induce pneumonia which increases accumulation of neutrophils, production of nitric oxide, expression of intercellular adhesion molecule-1 as well as many kinds of cytokines and causes the lung damage. The pneumonia-induced lung damage and inflammation at 24 hr after injecting P. aeruginosa into trachea were more severe in knock-out than in WT mice, as demonstrated by increases in extravasations of Evans blue dye (EBD), myeloperoxidase (MPO) activity, expression of iNOS, IL-1 beta and ICAM-1, and higher mortality of knock-out mice. The cause of the high mortality in knock-out mice was further investigated by culturing the lung and blood samples for bacterial counts. The bacterial counts of lung and blood of IL-1R1-/- mice were all higher than that of WT mice in 8 to 24 hr after injection of bacterium. Finally, chimeric mice (WT ¡÷ WT, IL1R1-/- ¡÷IL1R1-/-, WT ¡÷ IL1R1-/-, IL1R1-/- ¡÷ WT) were generated and used to determine the role of PMN cells of blood. Suggesting that increased amounts of bacteria in lung and blood is related to the higher mortality in knock-out mice and the type-1 IL-1 receptor is essential for mice to against pneumonia in this model.