In Vivo Antiviral Effect of Interleukin 18 in a Mouse Model of Vaccinia Virus Infection

Author： Tanaka-Kataoka M. Kunikata T. Takayama S. Iwaki K. Ohashi K. Ikeda M. Kurimoto M.

ISSN： 1043-4666

Source： Cytokine, Vol.11, Iss.8, 1999-08, pp. : 593-599

Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.

Previous Menu Next

Abstract

Interleukin-18 (IL-18), originally called interferon-γ (IFN-γ)-inducing factor is a novel cytokine which exhibits pleiotropic immunomodulatory activities such as the activation of natural killer (NK) cells and cytotoxic T lymphocytes (CTL). In this study, the efficacy of IL-18 on viral infection in mice was investigated. IL-18 treatment significantly suppressed pock formation on the tails of BALB/c mice inoculated intravenously with vaccinia virus when the cytokine was administered intraperitoneally on days 0, 2 and 4 after infection. Sequentially, NK and CTL activity of the infected mice were significantly augmented by IL-18 injection. The in vivo anti-vaccinia virus activity of IL-18 was only partially inhibited by treating the infected mice with anti-asialo GM1 antibody. When infected mice were injected with anti-IFN-γ antibody only, severe deterioration of health and significant body weight loss were observed, suggesting that IFN-γ is very important in protecting mice against vaccinia virus infection. Interestingly, IL-18 injection visibly improved the severe vaccinia virus-induced symptoms in mice treated with anti-IFN-γ antibody, even though a pivotal involvement of IFN-γ in IL-18-mediated anti-vaccinia virus effect is not yet determined. Taken together, these results indicate that the IL-18-elicited anti-vaccinia virus effect in the acute phase of infection would be raised by the sum of various host defence mechanisms including NK cells and CTL, and not from a specific immunocompetent cell population or effector molecule.