| Project/Area Number |
62440020
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Applied veterinary science
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| Research Institution | Obihiro University |
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Principal Investigator |
SUZUKI Naoyoshi Obihiro Univ., Veterinary. Physiology, Prof., 畜産学部・家畜生理学講座, 教授 (10003071)
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| Co-Investigator(Kenkyū-buntansha) |
SATO Motoyoshi Obihiro Univ., Vet. Clinical Radiology, Assoc. Prof., 畜産学部・獣医放射線学講座, 助教授 (50003140)
MIKAMI Masayuki Obihiro Univ., Bio. Resource Sciences, Assoc. Prof., 畜産学部・生物資源利用学講座, 助教授 (40003107)
SAITO Atushi Obihiro Univ., Vet. Physiology, Assoc. Prof., 畜産学部・家畜生理学講座, 助教授 (10002263)
MIURA Hiroyuki Obihiro Univ., Bio. Resource Sciences, Prof., 畜産学部・生物資源利用学講座, 教授 (90003079)
HIROSE Tsuneo Obihiro Univ., Vet. Clinical Radiology, Prof., 畜産学部・獣医放射線学講座, 教授 (60003076)
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| Project Period (FY) |
1987 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥27,100,000 (Direct Cost: ¥27,100,000)
Fiscal Year 1990: ¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1989: ¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1988: ¥6,900,000 (Direct Cost: ¥6,900,000)
Fiscal Year 1987: ¥14,500,000 (Direct Cost: ¥14,500,000)
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| Keywords | Toxoplasma lysate antigen (TLA) / immunopotentiator / Protozoan parasites / Natural killer cells / Macrophages / LAK cells / FeLN resistance / Tumor inhibition / トキソプラズマ溶解抗原 / オビオアクチオ / 免疫賦活・調整物資 / Killer細胞 / 単核細胞誘導 / トキソプラズマ可溶性成分 / 免疫賦活物質 / BRM / -IFN誘導 / NK細胞活性誘導 / T-細胞誘導 / Meth A腫瘍 / オビオアクチン / 免疫調整物質 |
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| Research Abstract |
Toxoplasma gondii has been reported to stimulate non-specific resistance to rodent malaria and babesia diseases. Mice that were treated systemically with Toxoplasma lysate antigen (TLA) were highly resistant to infection with Plasmodium berghei and Babesia rodhaini. Consequently, studies of the behavior of lymphocytes and natural killer (NK) cells and lymphokines activated killer (LAK) cells from TLA sensitized animals may clarify the factors responsible for resistance to infection with protozoan parasites and with tumors.
When adult BALB/C mice were sensitized with two intramuscular injection of TLA at 2 week interval, the numbers of Sig(+), Thy-1(+), Lyt-2, 2(+), and asialo GM1(+) cells in the spleen, liver and peripheral blood increased by 2 to 4 times over those found in unsensitized mice of the same age. When TLA-sensitized and unsensitized mice were inoculated with Babesia, 4 of 10(40%) of the TLA-sensitized mice survived infection, while none of the unsensitized control mice live
… More
d longer than 14 days after infection. By contrast sensitization of nude mice with TLA has no effect on survival, and mice did not live more than 12 days. The number of thymic Thy-1, 2(+) cells decreased in TLA-sensitized and unsensitized BALA/c mice by almost 80% within 10 days after infection. During the same time, the numbers of B cells, T cells, and NK cells increased in the spleen, liver and peripheral blood of both sensitized and unsensitized mice. Especially notable were increases in the numbers of Lyt-2,2 cells in the spleen and blood and increases in numbers of NK cells in the spleen, liver and blood in both TLA-sensitized and unsensitized mice. When spleen cells from TLA-sensitized and unsensitized mice were cultured in the presence or absence of TLA for 6 days, assays for cytotoxicity using NK-insensitive P-815 target cells and NK-sensitive YAC-1 target cells demonstrated higher rates of cytotoxicity in cultures of TLA-sensitized spleen cells. The present results showed clearly that addition of TLA to cultures of TLA-sensitized spleen cells stimulates production of killer cells, such as lymphokine activated killer (LAK) cells and NK-like LAK and/or NK cells. Consequently, resistance of TLA sensitized mice to protozoan infection may be mediated not only by increases in the numbers of Thy-1, 2(+) and asialo GM1(+) cells, but also by quantitative and qualitative variations in these cell types. Less
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