Elucidation of the molecular basis of Staphylococcus aureus exclusion via autophagy

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K11039
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Functional basic dentistry
• Research Institution: Kagoshima University (2016-2017); Hiroshima University (2015)
• Principal Investigator: HARADA Kae 鹿児島大学, 医歯学域歯学系, 助教 (60432663)
• Co-Investigator(Kenkyū-buntansha): 兼松 隆 広島大学, 医歯薬保健学研究科(歯), 教授 (10264053)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: オートファジー

Outline of Final Research Achievements

Autophagy is an intrinsic host defense system that recognizes and eliminates invading bacterial pathogens. We have identified microtubule-associated protein 1 light chain 3 (LC3), a marker protein of autophagy, as a binding partner of phospholipase C-related catalytically inactive protein (PRIP). To disclose the molecular mechanisms of bacterial elimination by autophagic pathway, we here examined by using a Salmonella Typhimurium infection assay.　In mouse embryonic fibroblasts (MEFs) infected with Salmonella, the number of intracellular Salmonella and Salmonella in LC3-positive autophagosome-like vacuoles (SCVs: Salmonella containing vacuoles) were both increased in Prip-knockout (KO) MEFs. In addition, we analyzed autophagic flux, and autophagic flux in Prip-KO MEFs was impaired. Altogether, impaired acidification in SCVs of Prip-KO MEFs may induce abnormality in antibacterial autophagy, resulting in remarkable Salmonella proliferation.

Free Research Field

歯科薬理学