Project/Area Number |
18KK0451
|
Research Category |
Fund for the Promotion of Joint International Research (Fostering Joint International Research (A))
|
Allocation Type | Multi-year Fund |
Research Field |
Parasitology (including sanitary zoology)
|
Research Institution | Nagasaki University |
Principal Investigator |
Kato Kentaro 長崎大学, 熱帯医学研究所, 助教 (50508885)
|
Project Period (FY) |
2019 – 2023
|
Project Status |
Completed (Fiscal Year 2023)
|
Budget Amount *help |
¥14,820,000 (Direct Cost: ¥11,400,000、Indirect Cost: ¥3,420,000)
|
Keywords | 赤痢アメーバ / Entamoeba histolytica / レクチン / Iglサブユニット / Hglサブユニット / エクソソーム / 寄生虫学 / 糖鎖生物学 / 糖鎖アレイ |
Outline of Final Research Achievements |
In this project, I tried to identify virulence factors that interact with Entamoeba histolytica Igl lectin subunits. The virulence factors that interacted with Igl could not be identified due to the amount even though an interaction between Igl and another lectin subunit, Hgl, was confirmed by western blotting. In the process, I found that Igl fragments were in exosome fractions from E. histolytica culture supernatant and Igl had three regions for its hemolytic and cytotoxic activities. Igl is known to have a very weak affinities toward glycans. Therefore, I tried to identify the glycans recognized by Igl by using "Cell-based glycan array". As the results, Igl showed non-specific binding to the cells that had different glycans on the cell surfaces and I could not clarify the glycans that specifically recognized by Igl. I found that rare sugars could inhibit the growth of E. histolytica trophozoites in vitro.
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Academic Significance and Societal Importance of the Research Achievements |
赤痢アメーバIglレクチンサブユニットと相互作用する病原性因子の存在がわかり、この病原性因子を明らかにすることで、赤痢アメーバが病原性を発現する機構が明らかとなる。Iglの断片がエクソソーム中に存在することが示唆され、赤痢アメーバの病原性発現へのIglの関与が考えられる。Iglには溶血および細胞傷害性を有する領域が複数あり、Iglの活性を抑制するためには、すべての領域を阻害する必要があることを示せた。 Iglは細胞への非特異的吸着が強く、Iglの糖鎖親和性を明らかにするには別の方法が必要であることが示された。 赤痢アメーバの増殖を希少糖が抑制し、このことは赤痢アメーバ症への新薬開発に繋がる。
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