2004 Fiscal Year Final Research Report Summary
EXPRESSION of CHEMOKINES and CYTOKINS in HERPESVIRUS INFECTION
Project/Area Number |
15592152
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Orthodontic/Pediatric dentistry
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Research Institution | TOHOKU university |
Principal Investigator |
MOMMA Yuko Tohoku University, Hospital, Instructor, 病院, 講師 (00191073)
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Co-Investigator(Kenkyū-buntansha) |
ENDO Yasuo Tohoku University, Graduate school of Dentistry, Associate professor, 大学院・歯学研究科, 助教授 (50005039)
MAYANAGI Hideaki Tohoku University, Graduate school of Dentistry, Professor, 大学院・歯学研究科, 教授 (60005098)
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Project Period (FY) |
2003 – 2004
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Keywords | Chemokine / Cytokine / Virus Infection / HDC revitalization |
Research Abstract |
The purpose of this study is to evaluate the chemokines and cytokines secretions in human oral epidermoid carcinoma cell (KB) and human gingival fibroblast cell (KD) following herpesvirus infection. The virus strains used in the experiments were HSV type 1 -F, -Miyama-GC+, KMY-986 (clinical divided strain) and HCMV-Towne strain. The cell culture supernatants were collected at each time course after the virus-infection. The amounts of chemokines and cytokines in the culture supernatants were determined by ELISA kits. In HCMV infection, the significant increase in IL-8, MCP-1, RANTES and IL-6 secretion were observed in HCMV infected KD cell, while the significant increase in IL-8 and IL-6 secretion were observed in KB cell. In HSV-infected KB cells, the significant increase in IL-8 secretion was observed at post-infection, while the significant decrease in RANTES, VEGF and IL-8 secretion were observed at 72 hrs post-infection. There were no detectable secretions of MCP-1 and GM-CSF in HSV infected KB cell. In contrast, there was no detectable secretion of chemokines and cytokines in both uninfected and HSV-infected KD cell. These studies demonstrate that herpesvirus infection induces differential secretion of chemokines and cytokines in the oral-derived cells. Therefore, the studies on oral host-cell-virus interactions may provide insight ways by which herpes virus modifiers host responses for immune evasion and/or pathogenesis.
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