2003 Fiscal Year Final Research Report Summary
Functional Analysis of NODI Gene Related with Proliferation, Apoptosis, and Innate Immune Response Using Knockout Mice
| Project/Area Number |
14570177
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Akita University |
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Principal Investigator |
HORIE Yasuo Akita University, School of Medicine, Assistant, 医学部, 助手 (30282164)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Sumio Akita University, School of Medicine, Professor, 医学部, 教授 (20138225)
SUZUKI Akira Akita University, School of Medicine, Professor, 医学部, 教授 (10311565)
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| Project Period (FY) |
2002 – 2003
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| Keywords | NOD1 / proliferation / apoptosis / innate immune response / knockout mice |
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| Research Abstract |
Sensitivity to apoptotic stimuli in many kinds of cells derived from NOD1 deficient mice
While NOD1 deficient ES cells were more sensitive than wild-type ES cells to apoptotic stimuli such as anisomycin, cisplatin and ultraviolet irradiation, NOD1 deficient thymic and peripheral activated T cells were as sensitive as wild-type T cells to various kinds of apoptotic stimuli. It was suggested that NOD1 was the anti-apoptotic molecule in ES cells.
Proliferation ability of many kinds of cells derived from NOD1 deficient mice
The uptake of ^3H-thymedine to wild-type, heterozygous and homozygous NOD1 mutant ES cells cultured in the media containing 10% fetal bovine serum and ^3H-thymedine was more in this order. When wild-type, heterozygous and homozygous NOD1 mutant ES cells were transplanted subcutaneously in nude mice to measure the difference of growth rate, bigger teratomas were formed in this order. On the other hand, the uptake of ^3H-thymedine to wild-type and homozygous NOD1 mutant T ce
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lls or B cells under various kinds of proliferation stimuli was not different. It was suggested that NOD1 was the molecule to promote proliferation of ES cells but not T cells and B cells.
Sensitivity to bacterial infection of NOD1 deficient mice
When wild-type and NOD1 deficient mice were injected staphylococcus aureus via tail vein, accumulated survival rate of NOD1 deficient mice was statistically lower than that of wild-type mice. On the other hand, IL2 concentration in culture media of peripheral T cells under various kinds of proliferation stimuli was not different between wild-type and NOD1 deficient mice. Serum IgG1, IgG2a and IgG2b concentration as well as T cell dependent or independent antibody production was also not different between wild-type and NOD1 deficient mice. Moreover, NO production of macrophage to lipopolysaccharide, peptidoglycan and lipoteichoic acid stimuli was not different between wild-type and NOD1 deficient mice. Although we clarified that NOD1 deficient mice were easy to be infected with bacteria, we did no find the background of the abnormality of innate or acquired immune response in NOD1 deficient mice. We need to clarify the mechanism to be easily infected with bacteria in NOD1 deficient mice. Less
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Research Products
(3 results)
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[Publications] Mathias Chamaillard, Masahito Hashimoto, Yasuo Horie (equal contribution to first author), Junya Masumoto, Su Qiu, Lisa Saab, Yasunori Ogura, Akiko Kawasaki, Koichi Fukase, Shoichi Kusumoto, Miguel A Valvano, Simon J Foster, Tak W Mak, Gabriel Nunez, Naohiro Inohara: "An essential role for NOD1 in host recognition of bacterial peptidoglycan containing diaminopimelic acid"Nat Immunol. 4. 702-707 (2003)
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