2013 Fiscal Year Final Research Report
Mechanism of intracellular persistence of Staphylococcus aureus by novel function of toxic shock syndrome toxin-1
| Project/Area Number |
23790467
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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 |
Bacteriology (including Mycology)
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| Research Institution | Hirosaki University |
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Principal Investigator |
ASANO Krisana 弘前大学, 医学(系)研究科(研究院), 助教 (70598622)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 黄色ブドウ球菌 / TSST-1 / オートファジー |
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| 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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