| Project/Area Number |
12670291
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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 |
Virology
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| Research Institution | Institute for Development Research, Aichi Human Service Center |
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Principal Investigator |
TAKIZAWA Takenori Institute for Development Research, Aichi Human Service Center, Dept. of Biochemistry, Section Head, 生化学部, 室長 (40192158)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | influenza virus / apoptosis / caspase / inflammatory cells / phagocyte / マクロファージ / 白血球 |
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| Research Abstract |
We have been analysing the mechanisms of apoptosis induced by influenza virus infection. We previously reported that the vims-infected HeLa cells were effectively engulfed when co-cultured with mouse peritoneal macrophages. Phagocytosis was effectively inhibited by caspase inhibitors, indicating that the event is dependent on apoptosis. Phosphatidyl serine (PS), one of the phospholipid in sell membrane is externalised during die virus-induced apoptosis. PS has been reported to be a maker recognised by phagocytes. We therefore examined the effect of an addition of PS-containing liposomes to culture medium on the phagocytosis, and found that PS treatment also inhibited phagocytosis. This indicated that PS plays an important role for the engulfnient of the virus-infected ceils. Since the extent of phagocytosis still progresses after the PS externalisation reached maximum level, other factors seemed to be required for efficient phagocytosis. To explore other factors, we used temperature sensitive mutant with neuraminidase (NA), since NA has been reported to implicate in the virus-induced apoptosis. Whereas the mutant virus did not show marked difference in the induction of apoptosis compared to the wild-type, phagocytosis was markedly retarded. Neuraminidase inhibitor also inhibited the phagocytosis of the virus-infected cells. These results suggested that NA plays a role for the efficient phagocytosis of the virus-infected cells.
We examined the effect of the co-culture of leukocyte with the virus-infected cells. However, mock-infected as well as the virus-infected cells showed cytopathic changes even though the former change was less severe. Therefore, experimental conditions must be examined to show the effect of leukocytes clear.
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