期刊
JOURNAL OF INFECTIOUS DISEASES
卷 206, 期 3, 页码 352-356出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jis192
关键词
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资金
- Departments of Pediatrics and Microbiology at the University of Chicago
- Region V Great Lakes Regional Center of Excellence (National Institutes of Health) [2-U54-AI-057153]
- National Institutes of Health [T32 GM007183]
Staphylococcus aureus is a leading cause of bacteremia and sepsis. The interaction of S. aureus with the endothelium is central to bloodstream infection pathophysiology yet remains ill-understood. We show herein that staphylococcal alpha-hemolysin, a pore-forming cytotoxin, is required for full virulence in a murine sepsis model. The alpha-hemolysin binding to its receptor A-disintegrin and metalloprotease 10 (ADAM10) upregulates the receptor's metalloprotease activity on endothelial cells, causing vascular endothelial-cadherin cleavage and concomitant loss of endothelial barrier function. These cellular injuries and sepsis severity can be mitigated by ADAM10 inhibition. This study therefore provides mechanistic insight into toxin-mediated endothelial injury and suggests new therapeutic approaches for staphylococcal sepsis.
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