| Project/Area Number |
15K18950
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Medical pharmacy
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| Research Institution | National Institutes of Biomedical Innovation, Health and Nutrition |
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Principal Investigator |
Suzuki Hidehiko 国立研究開発法人医薬基盤・健康・栄養研究所, 医薬基盤研究所 ワクチンマテリアルプロジェクト, プロジェクト研究員 (10710296)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 粘膜免疫 / ワクチン / 粘液 / 粘膜ワクチン |
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| Outline of Final Research Achievements |
Nasal physical barrier (ex. mucus) prevents the entry of exogenous materials. Nasal vaccine is probably affected by nasal physical barrier, but it remains unknown. In this study, I used Ttll1 kockout (KO) mice, which showed accumulation of nasal mucus, to check whether claudin-4-targeting vaccine (PspA-C-CPE) was affected by nasal physical barrier.
Ttll1 KO mice showed accumulation of nasal mucus around NALT, which was an immune induction site in nose. PspA-C-CPE was trapped by nasal mucus, and PspA-C-CPE could not effectively bind to NALT. Furthermore, PspA-specific nasal IgA was impaired with decrease of germinal center formation in Ttll1 KO mice. Thus, insufficient binding of PspA-C-CPE to NALT led to the impaired PspA-specific nasal IgA responses. Ttll1 KO mice treated with mucus remover showed recover of immune induction of PspA-specific nasal IgA. These findings indicated that accumulation of nasal mucus is an interfering factor in claudin-4-targeting nasal vaccine.
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