The elaboration of interleukin (IL)-36γ in the alveolar space was observed not only in mice during P. aeruginosa pulmonary infection but also patients with pneumonia due to P. aeruginosa. In murine P. aeruginosa lung infection, deletion of IL-36γ or its receptor resulted in improved bacterial clearance associated with reduced prostaglandin E2 production, and attenuated lung injury independent of changes in leukocyte influx. The gene discussed is IL36G; the disease is susceptibility to pneumonia measurement.