title: The protective effects of interleukin-18 and interferon-γ on neuronal damages in the rat hippocampus following status epilepticus.
abstract: To elucidate whether interleukin-18 (IL-18) or interferon-γ (IFN-γ) participates in neurodegeneartion, we investigated the changes in IL-18 and IFN-γ systems within the rat hippocampus following status epilepticus (SE). In non-SE induced animals, IL-18, IL-18 receptor α (IL-18Rα), IFN-γ and IFN-γ receptor α (IFN-γRα) 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/macrophages. IL-18Rα immunoreactivity was detected in astrocytes and microglia/macrophages. IFN-γ immunoreactivity was detected only in astrocytes within all regions of the hippocampus. IFN-γRα immunoreactivity was increased in neurons as well as astrocytes. Intracerebroventricular infusions of recombinant rat IL-18 or IFN-γ alleviated SE-induced neuronal damages, while neutralization of IL-18, IFN-γ or their receptors aggravated them, as compared to saline-infused animals. These findings suggest that astroglial-mediated IFN-γ pathway in response to IL-18 induction may play an important role in alleviation of SE-induced neuronal damages.
authors.affiliation: Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chunchon, Kangwon-DO 200-702, South Korea.
authors.forename: H J
authors.initials: HJ
authors.lastname: Ryu
authors.forename: J-E
authors.initials: JE
authors.lastname: Kim
authors.forename: M-J
authors.initials: MJ
authors.lastname: Kim
authors.forename: H-J
authors.initials: HJ
authors.lastname: Kwon
authors.forename: S W
authors.initials: SW
authors.lastname: Suh
authors.forename: H-K
authors.initials: HK
authors.lastname: Song
authors.forename: T-C
authors.initials: TC
authors.lastname: Kang
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism; D004195:Disease Models, Animal; D006624:Hippocampus / Q000187:drug effects* / Q000473:pathology; D057967:Infusions, Intraventricular; D007371:Interferon-gamma / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D020382:Interleukin-18 / Q000008:administration & dosage / Q000378:metabolism; D053727:Interleukin-18 Receptor alpha Subunit / Q000378:metabolism; D008297:Male; D017628:Microglia / Q000378:metabolism; D009410:Nerve Degeneration / Q000378:metabolism / Q000517:prevention & control*; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D010862:Pilocarpine; D051381:Rats; D017207:Rats, Sprague-Dawley; D017471:Receptors, Interferon / Q000378:metabolism; D011994:Recombinant Proteins; D013226:Status Epilepticus / Q000139:chemically induced / Q000473:pathology*; D015854:Up-Regulation; D000096743:Interferon gamma Receptor
chemical_list: D007371:Interferon-gamma; D020382:Interleukin-18; D053727:Interleukin-18 Receptor alpha Subunit; D010862:Pilocarpine; D017471:Receptors, Interferon; D011994:Recombinant Proteins; D000096743:Interferon gamma Receptor