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The Role of Interleukin-18 in Vesicular Stomatitis Virus Infection of the CNS
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The Role of Interleukin-18 in Vesicular Stomatitis Virus Infection of the CNS
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Journal Article
The Role of Interleukin-18 in Vesicular Stomatitis Virus Infection of the CNS
2001
Overview
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.
Publisher
Mary Ann Liebert, Inc,SAGE Publications
Subject
/ Central Nervous System Viral Diseases - etiology
/ interleukin 1^b-converting enzyme
/ Interleukin-18 - therapeutic use
/ Male
/ Mice
/ Rats
/ Rhabdoviridae Infections - drug therapy
/ Rhabdoviridae Infections - etiology
/ Rhabdoviridae Infections - mortality
/ Vesicular stomatitis Indiana virus - isolation & purification
