| Project/Area Number |
13670675
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Osaka Medical College |
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Principal Investigator |
NAKAJIMA Hideto Osaka Medical College Faculty of Medicine Research Associate, 医学部, 助手 (20330095)
|
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| Co-Investigator(Kenkyū-buntansha) |
FUKUDA Kazuhiro Osaka Medical College Faculty of Medicine Research Assistant, 医学部, 専攻医
|
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| Project Period (FY) |
2001 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 2002: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2001: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | herpes simplex virus / encephalomyelitis / chemokine / Th1 / Th2 cytokines / Th2サイトカン |
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| Research Abstract |
Th1/Th2 responses play an important role on the host defense against herpes simplex encephalomyelitis. Recently, some specific chemokines have been described as an initiator of Th1/Th2 responses. We investigated a role of monocyte chemoattractant protein (MCP)-1 in the pathogenesis of herpesvirus-induced encephalomyelitis (HSM). Anti-MCP-1 antibody greatly decreased HSM severity in mice infected with herpes simplex virus type 2 (HSM mice). HSM severity was markedly enhanced in mice previously treated with a mixture of interleukin (IL) 4 and -10. In response to stimulation with antigen, HSM mouse cells isolated from cerebrospinal fluids (CSF cells) produced IL-4 in culture fluids, however, IL-4 production decreased in CSF cells derived from HSM mice previously treated with anti-MCP-1 antibody. A macrophage population isolated in CSF cells from HSM mice (CSF-Mphi) produced MCP-1 in culture fluids. In response to stimulation with herpesvirus antigen, T cells isolated from CSF cells from HSM mice (CSF-T cells) produced IL-4 into their culture fluids, although MCP-1 was not produced by CSF-T cells. IL-4 production by CSF-T cells was markedly enhanced when they were stimulated with viral antigen in the presence of murine recombinant MCP-1 (rMCP-1). Furthermore, IL-4 was produced in naive splenic T cells cocultured with CSF-Mphi. These results indicate that the severity of HSM is influenced by MCP-1, which stimulates Th2 responses.
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