Abstracts

Rationale: Although Interleukin-18 (IL-18) and interferon-? (IFN-?) are involved in inflammatory responses under neuropathological conditions, the role of IL-18 and IFN-? in epilepsy is still controversial. Methods: To elucidate whether IL-18 participates in epilepsy-related events, we investigated the changes in IL-18 and INF-? systems within the rat hippocampus following status epilepticus (SE) Results: : In non-SE induced animals, IL-18, IL-18 receptor ? (IL-18R?), IL-18 binding protein (IL-18BP), IFN-? and IFN-? receptor ? (IFN-?R?) immunoreactivity was not detected in the hippocampus. Following SE, IL-18 immunoreactivity was increased in CA1-3 pyramidal cells as well as dentate granule cells. IL-18 immunoreactivity was also up-regulated in astrocytes and microglia. IL-18R? immunoreactivity was detected in astrocytes and microglia. IL-18BP immunoreactivity appeared in astrocytes and microglia. IFN-? immunoreactivity was detected only in astrocytes within all regions of the hippocampus. IFN-?R? immunoreactivity was increased in neurons as well as astrocytes. Intracerebroventricular infusions of recombinant rat IL-18 or INF-? alleviated SE-induced neuronal damages, while neutralization of IL-18, INF-? or their receptors aggravated them, as compared to saline-infused animals. Conclusions: These findings suggest that astroglial-mediated INF-? pathway in response to IL-18 induction may play an important role in alleviation of SE-induced neuronal damages.