Veltrop Marcel H A M, Beekhuizen Henry
Department of Infectious Diseases, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands.
J Infect Dis. 2002 Oct 15;186(8):1145-54. doi: 10.1086/344231. Epub 2002 Sep 25.
Intravascular infection with Staphylococcus aureus, Staphylococcus epidermidis, or Streptococcus sanguis can initiate fibrin formation on endocardial tissue, causing bacterial endocarditis. The ability of these bacteria to injure intact endothelial cells (ECs) and to aggravate tissue factor (TF)-dependent coagulation in the presence of blood leukocytes was investigated. Cytolysis of ECs occurred after infection with S. aureus and, with membrane-bound monocytes or granulocytes present, also after infection with S. sanguis or S. epidermidis. Monocytes that subsequently bound to the resultant bacteria-infected subcellular EC matrix (ECM) elicited TF mRNA, TF antigen, and TF activity (TFA). This was most pronounced in ECM prepared after the cytolysis of ECs by infection with S. aureus or S. epidermidis. We demonstrate that monocytes continue and intensify fibrin formation after lysis of bacteria-infected ECs, which suggests that, during the course of intravascular infection, early fibrin formation shifts from being mediated by EC-derived TFA to being mediated by TFA of monocytes bound to bacteria-infected ECM.
金黄色葡萄球菌、表皮葡萄球菌或血链球菌的血管内感染可在心内膜组织上引发纤维蛋白形成，导致细菌性心内膜炎。研究了这些细菌损伤完整内皮细胞（ECs）以及在血液白细胞存在的情况下加重组织因子（TF）依赖性凝血的能力。金黄色葡萄球菌感染后会发生内皮细胞溶解，在存在膜结合单核细胞或粒细胞的情况下，血链球菌或表皮葡萄球菌感染后也会发生内皮细胞溶解。随后与产生的细菌感染的亚细胞内皮细胞基质（ECM）结合的单核细胞会引发TF mRNA、TF抗原和TF活性（TFA）。这在金黄色葡萄球菌或表皮葡萄球菌感染导致内皮细胞溶解后制备的ECM中最为明显。我们证明，单核细胞在细菌感染的内皮细胞裂解后会继续并加剧纤维蛋白形成，这表明，在血管内感染过程中，早期纤维蛋白形成从由内皮细胞衍生的TFA介导转变为由与细菌感染的ECM结合的单核细胞的TFA介导。
