2003 Fiscal Year Final Research Report Summary
Analysis of immunopahtological mechanisms induced by virus infected macrophages.
| Project/Area Number |
14560246
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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 |
Basic veterinary science/Basic zootechnical science
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| Research Institution | Tokyo University Agriculture And Technology |
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Principal Investigator |
TANIGUCHI Takahide Tokyo University Agriculture And Technology, Faculty of Agriculture, Associate Professor, 農学部, 講師 (70282803)
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| Project Period (FY) |
2002 – 2003
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| Keywords | Macrophage / Coronavirus / Mouse Hepatitis Virus / TNF α / Cytokine / Chemokine |
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| Research Abstract |
There are many viral disease that are mediated by host immune response to infection. Some of these viruses target at macrophages. Infected macrophages migrate and spread viruses systemically. Moreover, these macrophages secrete massive inflammatory cytokines and chemokines, and are able to cause sever and fatal pathologic consequences.
Mouse hepatitis virus (MHV) infection lead to acute and fulmiant hepatitis, chronic hepatitis. acute encephalitis and demyelination in mice. Our previous studies using TNF a deficient mice indicated that TNFa play a important role on the arising of fulminant hepatitis.
In this study, we investigated the effect of MHV infection to peritoneal macrophages on production of inflammatory cytokines and chemokines. The mRNA expression of IL-1 a and b of TNF a deficient mice were decreased than that of wild type C57BL/6J mice. It suggested that TNF a affected to the secretion of IL-1.
To investigate the role of TNFa on MHV induced encephalitis, we attempted to evaluate its role in acute encephalitis induced MHV-JHM strain infection of TNFa deficient B6 mice(TNFa-/-mice). Our results indicated the possibility that TNF-α did not affect JHM-induced acute lethal encephalomyelitis and two chemokines (RANTES and Crg-2) mRNA expression.
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