Analysis of evasion mechanisms of neutrophil killing by V. vulnificus.
| Project/Area Number |
18H02350
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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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| Review Section |
Basic Section 42020:Veterinary medical science-related
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥13,000,000 (Direct Cost: ¥10,000,000、Indirect Cost: ¥3,000,000)
Fiscal Year 2021: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2020: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2019: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2018: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | ビブリオ / バルニフィカス / 敗血症 / 好中球 / 新規治療法 / リン脂質 / 感染モデル / 新規病原遺伝子同定法 / 人食いバクテリア / 好中球逃避機構 / 網羅的同定 / 人喰いバクテリア |
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| Outline of Final Research Achievements |
We have developed the novel method named ISLAP that comprehensively identifies the V. vulnificus genes required to evade neutrophils. Among 40 identified genes, VV1_0055 and VV1_0056 were involved in a protein transport system from inner membrane to outer membrane in periplasm. 0055 binds Enoyl-[acyl-carrier-protein] reductase [NADH] 2, which is the enzyme for Acyl ACP synthesis. Interestingly, 0058, 0059, 0060 and 0061 were found on the same pathway for Acyl ACP. Thus, the acylated proteins modified by 0055 and 0056 are involved in ability of evading neutrophils.
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| Academic Significance and Societal Importance of the Research Achievements |
V. vulnificusは、感染者を短時間内に死に至らしめるため、人食いバクテリアと呼ばれ恐れられている。しかし、どのような機構で短時間内における感染者体内での増殖を可能にしているかは明らかでない。本研究成果により、V. vulnificusが生体内で好中球から逃避し、増殖できる能力を証明できたと共に、それには菌体外膜に局在するタンパク質のアシル化が重要である可能性を示すことができた。本研究成果を発展させ、好中球逃避機構を担うアシル化修飾タンパク質を同定し、その働きを明らかにすることにより、人食いバクテリアの抗生物質に頼らない、新たな治療法が開発可能かもしれない。
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Report
(5 results)
Research Products
(14 results)
