| Project/Area Number |
62480193
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Mie University |
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Principal Investigator |
SUZUKI Shiro Mie Univ. Sch. Med. Int. Med. Professor, 医学部, 教授 (70027316)
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| Co-Investigator(Kenkyū-buntansha) |
BABA Masaru Mie Univ. Sch. Med. Int. Med. Lecturer, 医学部附属病院, 講師 (70118488)
WATANABE Shozoh Mie Univ. Sch. Med. Int. Med. Lecturer, 医学部附属病院, 講師 (20134934)
ITOH Yasuhiko Mie Univ. Sch. Med. Int. Med. Microbiology Professor, 医学部, 教授 (00022872)
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| Project Period (FY) |
1987 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1989: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1988: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1987: ¥4,700,000 (Direct Cost: ¥4,700,000)
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| Keywords | Type A Hepatitis / Liver cell damage / HAV / Electron microscopy / Crystalline array / NK cell activity / LAK cell activity / HAV / 肝細胞障害機序 / インタ-フェロン / 同種PBMC / NK細胞 / LAK細胞 |
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| Research Abstract |
Precise mechanisms of liver cell injury in type A hepatitis are not yet clear and host responses to viral infection including immune mechanisms were thought to be involved in the pathogenesis of liver cell damage in Hepatitis A.
To clarify the mechanisms, the electron microscopic observation of HAV infected cultured cell line was performed using JTC-12-P_3 cells derived from cynomolgus monkey kidney. Through this study, it was confirmed that cytopathic effect was not observed despite the propagation of HAV in JTC-12-P_3 cells. Furthermore crystalline array of HAV was observed in the cytoplasm which was not yet reported ever in HAV propagation.
Next, the role of NK or LAK cell activity in type A hepatitis was investigated.
Infected and non infected JTC-12-P_3 cell were labeled with ^<51>Cr, and then lymphocytes, treated and not treated with IL-2, from normal humans type A hepatitis patients and normal cynomolgus monkeys were incubated with these ^<51>Cr labeled cells. The release of ^<51>Cr in supernatant was assayed and the degree of cell damage was estimated.
When human lymphocytes were used, no significant difference of ^<51>Cr release was observed between infected and non infected JTC-12-P_3 cells even in the use of type A hepatitis patients lymphocytes. While, when cynomolgus monkey lymphocytes were used, significant increase of cell damage was observed in infected cultures.
Thus NK or LAK cell activity seemed to be involved, at least in some extent, in the liver cell damage of type A hepatitis, and this kind of non specific host response appeared to be effective in autologous or allogeneic relationships.
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