Elucidation of autophagy regulation by TSST-1 integrated with its mechanism on chronic Staphylococcus aureus skin infection

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K08819
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Bacteriology (including mycology)
• Research Institution: Hirosaki University
• Principal Investigator: Krisana Asano 弘前大学, 医学研究科, 教授 (70598622)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: 黄色ブドウ球菌 / TSST-1 / オートファジー / 皮膚感染 / 慢性感染

Outline of Final Research Achievements

Toxic shock syndrome toxin-1 (TSST-1) produced by Staphylococcus aureus has been shown to suppress autophagy. Regarding this activity, details in mechanism and a role TSST-1 on chronic skin infection of S. aureus were studied. TSST-1 expression was temperature-dependently regulated by SarAB system. The autophagy suppression mechanism of this toxin was suggested to be mediated by a small GTPase, Septin 7. Live-imaging demonstrated that TSST-1 promotes bacterial number of S. aureus in the epithelial cells. Skin infection in mouse model showed that TSST-1 promotes tissue damage and invasion of S. aureus in the deep dermis layer. These results suggested that TSST-1 may involve in the persistence of S. aureus in the host cells and promote chronic skin infection.

Free Research Field

細菌学

Academic Significance and Societal Importance of the Research Achievements

黄色ブドウ球菌の慢性感染機序は明らかになっておらず、その解明が待たれている。本研究では、本菌の毒素TSST-1がオートファジー抑制を通して細胞内感染を促進する新しい機序を示すことで、慢性感染機序の一端を明らかにした。この成果は、MRSAをはじめとする多剤耐性黄色ブドウ球菌の感染症予防および治療法開発に貢献し、さらに薬剤耐性菌の原因となる抗生物質に代わる分子標的創薬にもつながる知見を提供する。