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Interleukin-18 improves the early defence system against influenza virus infection by augmenting natural killer cell-mediated cytotoxicity.

Authors
  • Liu, Beixing
  • Mori, Isamu
  • Hossain, Md Jaber
  • Dong, Li
  • Takeda, Kiyoshi
  • Kimura, Yoshinobu
Type
Published Article
Journal
The Journal of general virology
Publication Date
Feb 01, 2004
Volume
85
Issue
Pt 2
Pages
423–428
Identifiers
PMID: 14769900
Source
Medline
License
Unknown

Abstract

The role of interleukin (IL)-18 in the development of the host defence system against influenza virus infection was investigated. IL-18-deficient (IL-18(-/-)) C57BL/6 mice that were inoculated intranasally with the mouse-adapted strain of human influenza A/PR/8/34 (H1N1) virus showed an increased mortality with the occurrence of pathogenic changes in the lung for the first 3 days of infection, which included pronounced virus growth with massive infiltration of inflammatory cells and elevated nitric oxide production. The interferon-gamma (IFN-gamma) level induced in the respiratory tract of IL-18(-/-) mice in the first few days after virus infection was significantly lower but, in contrast, the IL-12 level was slightly higher than the corresponding levels in wild-type C57BL/6 mice. Natural killer (NK) cell-mediated cytotoxicity in the lung of IL-18(-/-) mice was poorly activated. Local immune responses in the lung such as specific cytotoxic T lymphocyte and antibody production were induced upon influenza virus infection equally well in both strains of mice. These results indicate that IL-18 is involved in controlling influenza virus replication in the lung, especially at an early stage of infection, through activation of the innate immune mechanisms such as IFN and NK cells.

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