| Project/Area Number |
15H06649
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Laboratory medicine
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| Research Institution | The University of Tokyo (2016-2017)
Nippon Medical School (2015) |
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Principal Investigator |
Ishida-Kuroki Kasumi 東京大学, 大学院農学生命科学研究科(農学部), 特任助教 (80760272)
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| Project Period (FY) |
2015-08-28 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | クラミジア / 慢性感染 / aberrant body / リソソーム融合 / エフェクター蛋白質 / III型分泌装置 / リソソーム / 異常な菌体 / 感染症 / 細菌 / 微生物 / 蛋白質 |
|---|
| Outline of Final Research Achievements |
One of causes for the chronic infection of Chlamydia trachomatis is the morphological change to aberrant body (AB). It is known that chlamydia could change into AB by various stresses such as the exposure to penicillin or IFN-γ, but the detail characteristics of AB is unclear. In this study, we showed that the expression of lysosomal marker was increased in penicillin-induced AB infected cells compared with normal chlamydia or IFN-γ-induced AB infected cells. In addition, penicillin-induced AB tended to show low viability compared with normal chlamydia or IFN-γ-induced AB. Furthermore, the expression of CT228, CT232, CT365 and CT849 which were predicted as chlamydial effector proteins of type III secretion system changed in penicillin-induced AB. These results suggested that CT228, CT232, CT365 and/or CT849 play some roles in the lysosomal fusion with chlamydial vacuoles and changes of the expression of these protein affected the viability of penicillin-induced AB.
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