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


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