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Protection against pulmonary infection with Klebsiella pneumoniae in mice by interferon- through activation of phagocytic cells and stimulation of production of other cytokines

KANAKO YOSHIDA, TETSUYA MATSUMOTO^*, KAZUHIRO TATEDA^*, KOU UCHIDA, SHIRO TSUJIMOTO, YOICHIRO IWAKURA and KEIZO YAMAGUCHI^*

Departments of Internal Medicine II, *Microbiology and Hospital Pathology, Toho University School of Medicine, Omori-Hishi, Ota-ku, Tokyo and Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan

Corresponding author: Dr K. Yoshida (e-mail: kanako{at}med.tohu-u.ac.jp).

Received 22 Feb. 2001; revised version received 20 April 2001; accepted 20 April 2001.

Abstract

The study was designed to determine the role of interferon (IFN)- in inflammatory responses against experimentally induced pneumonia caused by Klebsiella pneumoniae. The host immunological responses in IFN- gene knockout (IFN-^-/-) 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-^-/- mice. Viable bacterial counts in lungs and blood abruptly increased in IFN-^-/- 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)-1ß and IL-6 in broncho-alveolar lavage fluid and IL-1ß in serum of IFN-^-/- mice were significantly lower than in control mice. During the late stage of infection, serum IL-6 level in IFN-^-/- 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-, is one of the mechanisms that allow the progression of pulmonary infection to systemic septicaemia.

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