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The study was designed to determine the role of interferon (IFN)-γ in inflammatory responses against experimentally induced pneumonia caused by Klebsiella pneumoniae. The host immunological responses in IFN-γ gene knockout (IFN-γ−/−) mice and immunocompetent control mice were compared. K. pneumoniae strain T-113 was inoculated intranasally into anaesthetised mice to induce pneumonia. Infected control mice survived significantly longer than infected IFN-γ−/− mice. Viable bacterial counts in lungs and blood abruptly increased in IFN-γ−/− mice; in contrast, a gradual decrease in the number of bacteria was noted in control mice. During the early stages of infection, the concentrations of interleukin (IL)-1β and IL-6 in broncho-alveolar lavage fluid and IL-1β in serum of IFN-γ−/− mice were significantly lower than in control mice. During the late stage of infection, serum IL-6 level in IFN-γ−/− mice was significantly higher than in control mice. These results suggest that the defective immunological host response, including inflammatory cytokine production caused by deficiency of IFN-γ, is one of the mechanisms that allow the progression of pulmonary infection to systemic septicaemia.