Mechanism of intracellular persistence of Staphylococcus aureus by novel function of toxic shock syndrome toxin-1
Project/Area Number |
23790467
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Bacteriology (including Mycology)
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Research Institution | Hirosaki University |
Principal Investigator |
ASANO Krisana 弘前大学, 医学(系)研究科(研究院), 助教 (70598622)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | 黄色ブドウ球菌 / TSST-1 / オートファジー / 感染症 / 細胞内寄生 |
Research Abstract |
Effect of toxic shock syndrome toxin-1 (TSST-1) on Staphylococcus aureus infection in the epithelial cells was investigated. TSST-1 did not alter the adhesion and invasion into the epithelial cells, HeLa 229, HEK293 and 407. However, TSST-1 reduced the accumulation of autophagosomes in nutrient starved cells or rapamycin-treated cells, suggesting that TSST-1 suppresses autophagy. In addition, this suppression did not require superantigenic activity and might be involved in the autophagosome formation process rather than autophagosome degradation. From day 5 after infection, intracellular bacterial number and cytotoxicity of TSST-1-producing S. aureus were deceased in comparison to non-producing strain, suggesting that TSST-1 may promote intracellular persistence of S. aureus in the epithelial cells.
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Report
(4 results)
Research Products
(14 results)