%0 Journal Article %A YOSHIDA, KANAKO %A MATSUMOTO, TETSUYA %A TATEDA, KAZUHIRO %A UCHIDA, KOU %A TSUJIMOTO, SHIRO %A IWAKURA, YOICHIRO %A YAMAGUCHI, KEIZO %T Protection against pulmonary infection with Klebsiella pneumoniae in mice by interferon-γ through activation of phagocytic cells and stimulation of production of other cytokines %D 2001 %J Journal of Medical Microbiology, %V 50 %N 11 %P 959-964 %@ 1473-5644 %R https://doi.org/10.1099/0022-1317-50-11-959 %I Microbiology Society, %X 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. %U https://www.microbiologyresearch.org/content/journal/jmm/10.1099/0022-1317-50-11-959