Strategy of Staphylococcus aureus infection by pressure of staphylococcal enterotoxin family

2014 Fiscal Year Final Research Report

• Project/Area Number: 23390100
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Immunology
• Research Institution: Hirosaki University
• Principal Investigator: NAKANE AKIO 弘前大学, 医学(系)研究科(研究院), 教授 (30164239)
• Co-Investigator(Renkei-kenkyūsha): HU Dong-Liang 北里大学, 獣医学部 (10333733) ; NARITA Kouji 弘前大学, 医学(系)研究科(研究院) (30419220) ; ASANO Krisana 弘前大学, 医学(系)研究科(研究院) (70598622)
• Project Period (FY): 2011-04-01 – 2015-03-31
• Keywords: 黄色ブドウ球菌 / TSST-1 / オートファジー / 上皮細胞 / ワクチン / スーパー抗原 / IL-17 / 感染

Outline of Final Research Achievements

We investigated the role of toxic shock syndrome toxin-1 (TSST-1), a superantigenic toxin produced by Staphylococcus aureus during infection.
(1) As the suppressive mechanism of autophagy by TSST-1, accumulation of LC3-II and the expression of LC3B were inhibited by TSST-1 in starvation-induced epithelial cells. (2) Suppression of autophagy by TSST-1 was independent of superantigenic activity. (3) The results of S. aureus infection in epithelial cells suggested that autophagy might be involved in intracellular survival and proliferation of S. aureus. (4) Vaccination of a superantigenic activity-deficient TSST-1 (mTSST-1) induced IL-17A-dependent protection against S. aureus infection in mice. On the other hand, long-term memory by vaccination was masked by IL-10.

Free Research Field

医歯薬学