| Project/Area Number |
14207012
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Bacteriology (including Mycology)
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| Research Institution | Ehime University |
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Principal Investigator |
ASANO Yoshihiro Ehime University, School of Medicine, Professor, 医学部, 教授 (70114353)
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| Co-Investigator(Kenkyū-buntansha) |
SHINOMIYA Hiroto Ehime University, School of Medicine, Associate Professor, 医学部, 助教授 (80162618)
KANOH Makoto Ehime University, School of Medicine, Lecturer, 医学部, 講師 (10116923)
MATSUMOTO Akira Ehime University, School of Medicine, Lecturer, 医学部, 講師 (90363233)
MARUYAMA Saho Ehime University, School of Medicine, Research Assistant, 医学部, 教務職員 (10301326)
角田 恒輔 愛媛大学, 医学部, 助手 (20281454)
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| Project Period (FY) |
2002 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥38,870,000 (Direct Cost: ¥29,900,000、Indirect Cost: ¥8,970,000)
Fiscal Year 2005: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2004: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2003: ¥9,490,000 (Direct Cost: ¥7,300,000、Indirect Cost: ¥2,190,000)
Fiscal Year 2002: ¥17,940,000 (Direct Cost: ¥13,800,000、Indirect Cost: ¥4,140,000)
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| Keywords | Listeria monocytogenes / Innate immunity / Adaptive immunity / Cytokines / T cell subsets |
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| Research Abstract |
Pathogenic infections lead to activation of innate immunity followed by induction of a Th1 T cell subset. However, the mechanism in this shift has not been clarified. We used DO 11.10 OVA-specific TCR-TG mouse T cell and the intracellular infectious pathogen Listeria monocytogenes (Lm) to evaluate the effect of pathogenic infections. We investigated genes that involved in the host-pathogen interaction and is required for the initiation of T cell subset differentiation in the early phase of pathogen infection. We show in this report that toll like receptor (TLR)-2, TLR-4 and MyD88 molecules are not essentially required for the induction of Th1 differentiation during Lm infection. It is also shown that genes involved in the expression of the pathogenicity of Lm are not required for the induction of Th1. We checked the mutant strain of Lm which were disrupted gene by insertion of transposon or temperature sensitive plasmid. We evaluated the mutant for determining gene(s) responsible for inducing T cell shift. We found the mutants of Lm lost either the ability of Th1 induction or the inhibition of Th2 induction, suggesting that the induction of Th1 subset and the inhibition of Th2 subset induction are separate phenomenon and are influenced by distinct genes carried by Lm genome.
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