Drake T A, Pang M
Department of Pathology, UCLA School of Medicine 90024-1732.
J Infect Dis. 1988 Apr;157(4):749-56. doi: 10.1093/infdis/157.4.749.
In vitro infection of cultured human cardiac valve endothelium (HCVE) with Staphylococcus aureus was used as a model to study potential mechanisms of vegetation formation in infective endocarditis. S. aureus was observed to adhere to and be ingested by HCVE. Infection for 8 h resulted in increased levels of procoagulant activity in HCVE, shown to be tissue factor by a specific assay. Mean activity in infected HCVE was 662 +/- 149 (mU/10(5) HCVE +/- 1 SD) versus 221 +/- 78 in control HCVE; surface-expressed activity was 57 +/- 25 in infected monolayers and undetectable (less than or equal to 10) in controls. Bacteria alone had no activity. These results suggest that endothelium may have a functional role in the pathogenesis of S. aureus endocarditis and may provide one potential mechanism for activating coagulation to initiate vegetation formation on a colonized cardiac valve.
用金黄色葡萄球菌对培养的人心脏瓣膜内皮细胞（HCVE）进行体外感染，以此作为研究感染性心内膜炎中赘生物形成潜在机制的模型。观察到金黄色葡萄球菌可黏附并被HCVE摄取。感染8小时导致HCVE中促凝血活性水平升高，通过特定检测显示其为组织因子。感染的HCVE中的平均活性为662±149（mU/10⁵ HCVE±1 SD），而对照HCVE中的为221±78；感染单层细胞表面表达的活性为57±25，而对照中检测不到（≤10）。单独的细菌没有活性。这些结果表明，内皮细胞可能在金黄色葡萄球菌性心内膜炎的发病机制中起功能性作用，并且可能为激活凝血以在定植的心脏瓣膜上启动赘生物形成提供一种潜在机制。
