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1,2Department of Microbiology1 and Department of Pathology2, Omori Hospital, Toho University School of Medicine, 5-21-16 Omori-nishi, Ota-ku Tokyo, Japan 3Department of Bacteriology, Hirosaki University School of Medicine, Hirosaki, Japan 4Laboratory Animal Research Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan
Correspondence Tetsuya Matsumoto tetsu{at}med.toho-u.ac.jp
Received May 7, 2004
Accepted September 21, 2004
This study was designed to determine the role of interleukin (IL)-1 in the inflammatory response against experimentally induced pneumonia caused by Klebsiella pneumoniae. The host immune responses of IL-1 gene knockout (IL-1 KO) mice and immunocompetent wild-type (WT) mice were compared after pulmonary infection with K. pneumoniae. There were no significant differences between the survival rates and viable bacterial counts in lungs and blood of IL-1 KO and WT mice after pulmonary infections under different conditions. Histopathological analysis showed a similar inflammatory response in both groups of mice. However, in the early stage of infection, the level of tumour necrosis factor alpha (TNF-
) in homogenized lungs of IL-1 KO mice was significantly higher than in WT mice. To determine the role of endogenous TNF- in the recovery of the defence mechanism in IL-1 KO mice, mice were treated with an anti-TNF- mAb before infection with K. pneumoniae. The results revealed a significantly lower survival rate of anti-TNF- mAb-treated IL-1 KO mice than BSA-treated IL-1 KO mice. The data suggest that compensatory production of TNF- in IL-1 KO mice contributes to the host defence against K. pneumoniae infection.
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