| Project/Area Number |
08670274
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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 |
寄生虫学(含医用動物学)
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| Research Institution | AKITA UNIVERSITY |
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Principal Investigator |
YOSHIMURA Kentaro Akita University, School of Medicine, Professor, 医学部, 教授 (90053058)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMADA Hiroko (SUGAYA H) Akita University, School of Medicine, Research Associate, 医学部, 助手 (30235626)
ISHIDA Kazuto Akita University, School of Medicine, Research Associate, 医学部, 助手 (60006731)
ABE Tatsuya Akita University, School of Medicine, Associate Professor, 医学部, 教授 (80128363)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1997: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1996: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Angiostrongylus cantonensis / eosinophil / IL-5 transgenic mice / C.B-17 scid / BALB / c nu / nu / diffusion chamber / IgA / CD4^+T cell / 広東住血線虫 / IL-5 transgenic mouse / C.B.-17 scid / diffusion chamber / CD8^+T細胞 / 髄液 / major basic protein / eosinophil peroxidase / eosinophil cationic protein / eosinophil-derived neurotoxin |
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| Research Abstract |
This study demonstrated : 1. Angiostrongylus cantonensis worms in the subarachnoid spaces of IL-5 transgenic mice (IL-5 Tg) were surrounded by numerous eosinophils which degranulated and discharged lysosomal materials on to the worms, leading to worm killing. 2. Antigen-specific serum and cerebrospinal fluid (CSF) IgA antibodies were detectable on days 5 and 7 postinfection onward, respectively, in both IL-5 Tg and C3H/HeN mice, although the antibody level was higher in IL-5 Tg mice. 3. Anti-CD4 antibody treatment interfered with worm killing in BALB/c mice and improved host morbidity, whereas anti-CD8 antibody treatment failed to improve the morbidity. 4. Tumor necrosis factor-alpha does not cause morbidity of infected mice. 5. Anti-IL-5 antibody treatment blocked worm killing but failed to improve host morbidity. 6. Crude eosinophil basic proteins from IL-5 Tg was helminthotoxic to day 20 worms in vitro. 7. Both infected C.B-17 +/+ (+/+) and BALB/c nu/+ (nu/+) showed high morbidity,
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while both C.B-17 scid (SCID) and BALB/c nu/nu (nu/nu) failed to do so. 8. Intracranial worm recovery was markedly higher in +/+, SCID and nu/nu mice than in nu/+ and C57BL/6 mice. The former three strains, especially SCID and nu/nu, failed to show significant CSF eosinophilia. 9. Both SCID and nu/nu mice failed to produce a significant amount of antigen specific serum IgA and IgG1.10. Infected SCID mice previously transferred with peritoneal eosinophils from IL-5 Tg and also with serum IgA from infected IL-5 Tg yielded almost the same worm recovery as those transferred with eosinophils and the normal serum. This indicated that the accumulation of eosinophils in CSF occurs in nu/nu but not in SCID.11. When naive IL-5 Tg and C3H/HeN were implanted with a diffusion chamber (DC) containing infective third stage larvae (L3), cellular migration occurred in a DC with 2mum filter membrane, and the migration was more prominent in IL-5 Tg than in C3H/HeN.L3 larvae survived better in a DC with 0.1mum filter membrane than in a DC with 2mum membrane. Less
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