1996 Fiscal Year Final Research Report Summary
Immunological and genetic regulations of innate immunity against cutaneous leishmaniasis in mice
| Project/Area Number |
06454202
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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 | Jikei University School of Medicine |
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Principal Investigator |
OHTOMO Hiroshi Jikei University School of Medicine, Department of Tropical Medicine, Professor, 医学部, 教授 (80072916)
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| Co-Investigator(Kenkyū-buntansha) |
SAITO Saburo Jikei University School of Medicine, Institute of DNA medicine, Lecturer, 医学部, 講師 (10186934)
MAKIOKA Asao Jikei University School of Medicine, Department of Tropical Medicine, Lecturer, 医学部, 講師 (90119850)
KATAKURA Ken Jikei University School of Medicine, Department of Tropical Medicine, Lecturer, 医学部, 講師 (10130155)
WATANABE Naohiro Jikei University School of Medicine, Department of Tropical Medicine, Associate, 医学部, 助教授 (00057019)
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| Project Period (FY) |
1994 – 1996
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| Keywords | cutaneous leishmaniasis / Leishmania amazonensis / innate immunity / resistant gene to infection / gene mapping / mouse / immunology / cytokines |
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| Research Abstract |
This study was aimed to understand mechanisms of innate immunity against cutaneous leishmaniasis by examining immunological and genetic regulations in mice infected with Leishmania amazonensis, a pathogen of cutaneous leishmaniasis in the South America. Different strains of mice were subcutaneously inoculated with L.amazonensis promastigotes at the tail base and the size of the skin lesions was measured. Almost all strains of mice such as BALB/c and C57BL/6 exhibited susceptible phenotype to the infection, but SJL/J mice showed strong resistant phenotype without visual lesions. In crossing experiments, both male and female mice of (BALB/c x SJL/J) F1 produced intermediate lesions in size and the backcrossed mice (N2) exhibited susceptible and resistant phenotype at a ratio of approximately 1 : 1, suggesting that the onset of cutaneous lesion is regulated by a single autosomal gene. Mapping of the resistant gene was attempted by analyzing microsatellite DNA polymorphisms in a total of seventy-two N2 mice. The linkage analysis indicated that resistance phenotype of the N2 mice was not linked to Scl1, Scl2 and Lsh/Bcg/Ita gene, which have been reported as the disease control genes for L.major, L.mexicana and L.donovani infection, respectively. The experiments of immunological regulation using mast cell-deficient W/W^V mice, gene-targeted gamma/delta T cell-deficient mice and anti-asialo GM1-inoculated mice suggested that the natural resistance against L.amazonensis infection may be regulated by natural killer cells and gamma/delta T lymphocytes but not by mast cells. Furthermore, intracellular survival of Leishmania in macrophages might be controlled by nerve growth factor, a cytokine involving in inflammatory reactions.
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[Publications] Saito, S., Hamada, A., Watanabe, N., Obata, T., Katakura, K.and Ohtomo, H: "Eosinophil chemotactic activity in Leishmania amazonensis promastigotes" Parasitol Res. 82. 485-489 (1996)
Description
「研究成果報告書概要(欧文)」より
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[Publications] Susaki, Y., Shimizu, S., Katakura, K., Watanabe, N., Kawamoto, K., Matsumoto, M., Tsudzuki, M., Furusaka, T., Kitamura, Y.and Matsuda, H: "Functional properties of murine macrophages promoted by nerve growth factor" Blood. 88. 4630-4637 (1996)
Description
「研究成果報告書概要(欧文)」より
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