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

• Published in: Journal of medical microbiology Vol. 50; no. 11; p. 959
• Main Authors: YOSHIDA, KANAKO, MATSUMOTO, TETSUYA, TATEDA, KAZUHIRO, UCHIDA, KOU, TSUJIMOTO, SHIRO, IWAKURA, YOICHIRO, YAMAGUCHI, KEIZO
• Format: Journal Article
• Language: English
• Published: Soc General Microbiol 01-11-2001
• ISSN: 0022-2615; 1473-5644

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.