| Project/Area Number |
10470065
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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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) |
MATSUDA Shinji Akita University, School of Medicine, Associate Professor, 医学部, 助教授 (70199800)
SHIMADA Hiroko (SUGAYA,HIROKO) 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, 助教授 (80128363)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥10,900,000 (Direct Cost: ¥10,900,000)
Fiscal Year 2000: ¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1999: ¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1998: ¥6,100,000 (Direct Cost: ¥6,100,000)
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| Keywords | Angiostrongylus cantonensis / chimeric mice / C57BL / 6 / BALB / c / C.B-17 / IFN-γ knockout mouse / B10 congenic mice / Genetics / 好酸球 / T細胞キメラ / T cell blot / 抗IL-4モノクローナル抗体 / 骨髄キメラマウス / T細胞キメラマウス / 好酸球増多 / 病態 / X線照射 / Angiostrongylus cantonensis / H-2 / B10 コンジェニックマウス / IFN-γ欠損マウス / サイトカイン / IL-4 / IL-10 |
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| Research Abstract |
The results obtained are as follows : 1. A study using B10 congenic mice indicated that murine morbidity and susceptibility to Angiostrongylus cantonensis infection are not linked to the H-2 complex but rather to non-H-2 background genes and also that there is no significant relationship between antigen-specific antibody responses and murine susceptibility or morbidity to A.cantonensis infection. 2. A study using INF-γ knockout mice suggested that INF-γ itself did not affect the outcome of A.cantonensis infection in mice. 3. C.B-17 strain mice have the defective eosinopoiesis and are thereby incapable of killing intracranial worms of A.cantonensis. This is probably due to the impaired expression of β-chain mRNA in bone marrow cells of C.B-17 strain. 4. A study using bone marrow chimeric mice between C.B-17 and C57BL/6 mice suggests that the bone marrow derived cells are primarily involved in the expression of morbidity in A.cantonensis infected C.B-17 mice but non-bone marrow derived c
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ell types are also concerned partly. 5. T cell-chimeric mice were produced by the procedure that BALB/c-nu/nu mice which had been irradiated with sublethal dose of X ray and additionally treated with anti-Thy-1.2 antibody were reconstituted with homologous bone marrow cells and then transferred with thymus cells derived from C57BL/6 or BALB/c. A majority of BALB/c-T cell-chimeric mice died before A.cantonensis infection and the infected BALB/c-T cell-chimeric mice also died soon after infection. Sham chimeric mice showed the impaired worm development when compared with nu/nu mice, and also exhibited marked body weight loss and high mortality after A.cantonensis infection although they yielded a similar level of worm burdens as nu/nu or +/+ mice. These data suggest that T cells of BALB/c are associated with morbidity after infection whereas T cells from C57BL/6 contribute to improving morbidity. 6. F1, F2 and back-cross progenies between C.B-17 and C57BL/6 mice were examined for susceptibility, eosinophil responses and morbidity. These responses were found to be controlled by multiple genes, and a weak positive correlation was recognized between worm recovery and the level of eosinophils in cerebrospinal fluid. 7. Splenic CD4^+T cells from infected BALB/c mice showed a proliferative response against several protein antigens ranging from 22 to 56 kD.This suggests that these responses by CD4^+T cells are responsible for inducing morbidity. Less
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