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Role of interferon-gamma in inflammatory responses in murine respiratory infection with Legionella pneumophila

YOKO SHINOZAWA, TETSUYA MATSUMOTO^*, KOU UCHIDA, SHIRO TSUJIMOTO, YOICHIRO IWAKURA and KEIZO YAMAGUCHI^*

Second Department of Internal Medicine, *Department of Microbiology and Department of Hospital Pathology, Toho University School of Medicine, 5-21-16 Omori-Nishi, Ota-ku, Tokyo, 143-8540 and Laboratory Animal Research Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan

Corresponding author: Dr Y. Shinozawa (e-mail: shinozaw{at}med.toho-u.ac.jp).

Received 26 March 2001: revised version received 20 Aug. 2001; accepted 4 Sept. 2001.

Abstract

The role of interferon (IFN)- in host inflammatory responses, including inflammatory cytokine production, in experimental pneumonia with Legionella pneumophila was examined in IFN- knockout (IFN-^-/-) mice. IFN-^-/- mice and wild-type BALB/cA mice were inoculated intranasally with L. pneumophila strain KC. The survival rate of IFN-^-/- mice was significantly lower than that of control mice. Viable bacterial counts in lungs and blood showed a rapid and continuous increase in IFN-^-/- mice, in contrast to a gradual decrease in the lungs and an intermittent bacteraemia in control mice. Histopathological analysis of L. pneumophila-infected lung tissues demonstrated mild pneumonia in control mice, whereas severe pneumonia was shown in IFN-^-/- mice. During the late stages of infection, the number of total bronchoalveolar lavage (BAL) cells was significantly higher in IFN-^-/- than in control mice. The concentrations of tumour necrosis factor- and interleukin-1ß in sera of IFN-^-/- mice were significantly lower in control mice during the early stages of infection, suggesting suppressed production of inflammatory cytokines in IFN-^-/- mice. In contrast, during the late stages of infection, the levels of these cytokines were significantly higher in sera of IFN-^-/- mice than in control mice, suggesting severe and systemic infection in IFN-^-/- mice. The findings suggest that retardation of host immune responses, including inflammatory cytokine production caused by deficiency of IFN-, might allow the bacteria to grow and cause fulminant pneumonia.

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