| Project/Area Number |
03660318
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Applied veterinary science
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| Research Institution | The Research Center for Protozoan Molecular Immunology, Obihiro University |
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Principal Investigator |
IGARASHI Ikuo Obihiro Univ., Res.Ctr.Protozoan Mol.Immunol., Assoc.Prof., 原虫病分子免疫研, 助教授 (80159582)
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| Co-Investigator(Kenkyū-buntansha) |
OMATA Yoshitaka Obihiro Univ., Vet.Physiol., Assoc.Prof., 畜産学部, 助教授 (10132987)
SAITO Atsushi Obihiro Univ., Vet.Physiol., Prof., 畜産学部, 教授 (10002263)
SUZUKI Naoyoshi Obihiro Univ., Res Ctr.Protozool.Mol.Immunol., Prof., 原虫病分子免疫研, 教授 (10003071)
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| Project Period (FY) |
1991 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1993: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1992: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1991: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | Murine Babesia / Protective immunity / CD4^+ T cells / Gamma interferon / Cross-reactive antigen / Renal pathology / Immunopathology / Nonspecific immunity / バベシア原虫 / 感染防御 / CD_4陽性細胞 / ガンア-インターフェロン / 赤血球内寄生原虫 / 感染防抑 / CD4^+細胞 / 感染防御免疫 |
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| Research Abstract |
Role of cell-mediated immunity in Babesia infection was investigated using mouse models in the present study. In lethal Babesia rodhaini infection, drug-cured mice showed 75% protection against challenge infection with B.rodhaini and a humoral immunity appears to be major role in the effector phase of immunity. Mice which were cured first infection with anti-Babesia durg and survived with challenge infection, showed 100% protection against B.radhaini infection, Lyt1^+ and Lyt2^+ T cells may contribute in controlling secondary infection.
In B.microti infection, while mice sufferd high parasitemia, but recovered naturally from their primary infection, nu/nu mice and SCID had a higher peak parasitemia and failed to clear the infection. These results demonstrated that T lymphocytes are necessary for the resolution of B.microti infection. Mice depleted of CD4^+ T cells with monoclonal antibody (mAb) had high parasitemia and failed to control the infection, while depletion of CD8^+ cells had
… More
no effect on the course of infection. Culture supernatants of spleen cells from control and CD8^+ cells depleted, but not from CD4^+ depleted mice, showed high concentration of IFN-gamma. Treatment of infected mice with anti-IFN-gamma mAb showed higher parasitemia than that of the control group. These results suggest that IFN-gamma produce by CD4^+ T cells, at least in part, is responsible for the control of acute infection with B.microti in mice.
Mab, recognizing 70,30 kDa antigens of B.microti and challenged with B.rodhaini, was produced from mice infected with B.microti and challenged with B.rodhaini. Administration of the mAb gave the delay of onset of parasitemias in mice. Mice which were exposed to oocysts of Isospora felis, showed absolute resistance against B.microti infection on 28th day post-exposure of oocysts. CD4^+ T cells induced by I.felis infection provides mice protection against B.microti.
Pathological changes were examined in the kidneys and liver of mice of two babesioses. Severe damages to kidneys and liver were observed in B.rodhaini infection rather than in B.microti infection. Electron-dense deposits were demonstrated in the mesangial matrix and along the glomerular basement membrane and these deposits were suggested as immune complexes by immunohistochemistry. Less
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