FIBRINOGEN ACTS AS A BRIDGING MOLECULE IN THE ADHERENCE OF STAPHYLOCOCCUS-AUREUS TO CULTURED HUMAN ENDOTHELIAL-CELLS
FIBRINOGEN ACTS AS A BRIDGING MOLECULE IN THE ADHERENCE OF STAPHYLOCOCCUS-AUREUS TO CULTURED HUMAN ENDOTHELIAL-CELLS
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DOI：
10.1172/jci115259
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发表时间：
1991-06-01
影响因子：
15.9
通讯作者：
FISCHETTI, VA
中科院分区：
文献类型：
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作者：
CHEUNG, AL;KRISHNAN, M;FISCHETTI, VA
金黄色葡萄球菌在短暂菌血症期间引起急性血管内感染的倾向知之甚少。为了检查导致葡萄球菌粘附于内皮的事件，开发了粘附测定法以研究血液因子在体外介导葡萄球菌粘附于培养的人脐静脉内皮中的作用。结果表明，S.金黄色葡萄球菌对内皮细胞的作用是由从血浆吸附到内皮表面的纤维蛋白原介导的。这种结合显然是特异性的，因为它可以被山羊抗人纤维蛋白原抗体以剂量依赖性方式阻断，而非免疫山羊IgG、小鼠抗AG-1单克隆抗体（内皮细胞表面发现的血小板抗原）、非特异性小鼠单克隆抗体和兔抗人玻连蛋白和纤连蛋白抗体不具有抑制作用。我们的数据还表明，纤维蛋白原是一个必要的，但不是唯一的血液成分在介导的结合S。金黄色葡萄球菌至内皮细胞。这一点得到以下发现的支持：单独的纤维蛋白原（浓度相当于血浆中的纤维蛋白原）并不像血浆那样增强葡萄球菌的粘附，而用纤维蛋白原重建的无纤维蛋白原血症血浆则如此。因为已知纤维蛋白原与内皮细胞结合，我们的数据与纤维蛋白原和其他血浆因子（可能在炎症过程中激活）促进葡萄球菌粘附于内皮细胞的假设一致。此外，S.还提出了金黄色葡萄球菌作为天然内皮的粘附因子。
The propensity of Staphylococcus aureus to cause acute endovascular infections during transient bacteremia is poorly understood. To examine the events leading to the attachment of staphylococci to endothelium, adherence assays were developed to study the role of blood factors in the mediation of staphylococcal adherence to cultured human umbilical vein endothelium in vitro. Results indicate that the preferential attachment of S. aureus to endothelial cells is mediated by fibrinogen adsorbed from plasma onto the endothelial surface. The binding is apparently specific because it could be blocked by goat anti-human fibrinogen antibody in a dose-dependent fashion while nonimmune goat IgG, mouse MAb against AG-1 (a platelet antigen found on the endothelial cell surface), nonspecific mouse MAb and rabbit antibodies to human vitronectin and fibronectin were not inhibitory. Our data also indicate that fibrinogen is a necessary but not the only blood constituent in the mediation of binding of S. aureus to endothelium. This was supported by the finding that fibrinogen alone, at a concentration equivalent to that in plasma, did not potentiate staphylococcal adherence as much as plasma while afibrinogenemic plasma reconstituted with fibrinogen did. Because fibrinogen is known to bind to endothelial cells, our data is consistent with the hypothesis that fibrinogen and additional plasma factor(s), possibly activated during inflammation, promote staphylococcal adherence to endothelium. In addition, the role of the fibrinogen binding receptor of S. aureus as an adherence factor to native endothelium is also suggested.