The role of interleukin-18 in vesicular stomatitis virus infection of the CNS

J. L. Hodges, D. D C Ireland, C. S. Reiss

Research output: Contribution to journalArticlepeer-review

Abstract

Intranasal application of vesicular stomatitis virus (VSV) results in the initial infection of the olfactory receptor neurons and a rapid progression of the virus through the mouse central nervous system (CNS). Interleukin-18 (IL-18) is an 18.3-kd cytokine that induces interferon gamma (IFN-γ) production in mice. IL-18 is synthesized as an inactive precursor that is cleaved and activated by caspase-1/interleukin-1β converting enzyme (ICE). IL-18 shares several biological properties with IL-12, including the ability to induce IFN-γ production in T lymphocytes and natural killer (NK) cells. In the CNS, microglia and astrocytes produce IL-18 and IL-12. We have previously shown that IL-12 promotes recovery from VSV encephalitis. This led us to examine the potential role of IL-18 in the pathogenesis of VSV encephalitis. We show that both IL-18 and caspase-1 mRNA are consistently present in the CNS of mice. The addition of exogenous IL-18 to cell cultures does not affect the production of VSV, and addition of exogenous IL-18 at the time of infection does not alter the morbidity or mortality of BALB/c mice. In vitro studies with neutralizing monoclonal antibody to IL-18 had no effect. From these results we conclude that in this system and under the experimental conditions used, unlike IL-12 and IFN-γ, IL-18 does not play a significant role in the host response to VSV infection.

Original languageEnglish (US)
Pages (from-to)181-191
Number of pages11
JournalViral Immunology
Volume14
Issue number2
DOIs
StatePublished - 2001

ASJC Scopus subject areas

  • Immunology
  • Molecular Medicine
  • Virology

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