Lowy F D, Fant J, Higgins L L, Ogawa S K, Hatcher V B
Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10467.
J Ultrastruct Mol Struct Res. 1988 Feb;98(2):137-46. doi: 10.1016/s0889-1605(88)80906-6.
Staphylococcus aureus is an invasive pathogen capable of causing life-threatening disease. A major component of this pathogen's virulence is its ability to invade normal endovascular tissue. We examined the interaction of S. aureus with cultured human endothelial cells and with human and rabbit endovascular tissue. Our ultrastructural study demonstrated a sequence of steps which occurred with staphylococcal invasion of human endothelial cells; adhesion, endocytosis, and intracellular replication. Ultimately, this resulted in cell disruption and death. Cytochemical staining of lysosomes demonstrated lysosomal fusion with both viable and killed intracellular bacteria without evidence of staphylococcal degradation. Quantitative studies using an in vitro infection assay demonstrated comparable rates of adhesion by viable and ultraviolet-killed bacteria, phagocytosis at a slower rate, and intracellular replication. The present study demonstrates an active role for the endothelial cell in the development and spread of endovascular staphylococcal infections. It also supports the use of this in vitro tissue culture system as a model for the study of bacterial invasion of the endothelium.
金黄色葡萄球菌是一种能够引发危及生命疾病的侵袭性病原体。该病原体毒力的一个主要组成部分是其侵入正常血管内组织的能力。我们研究了金黄色葡萄球菌与培养的人内皮细胞以及人与兔血管内组织之间的相互作用。我们的超微结构研究表明，金黄色葡萄球菌侵入人内皮细胞会发生一系列步骤：黏附、内吞和细胞内复制。最终，这导致细胞破裂和死亡。溶酶体的细胞化学染色显示，溶酶体与存活和死亡的细胞内细菌融合，但没有金黄色葡萄球菌降解的证据。使用体外感染试验的定量研究表明，存活细菌和紫外线灭活细菌的黏附率相当，吞噬作用速率较慢，且存在细胞内复制。本研究证明了内皮细胞在血管内葡萄球菌感染的发生和传播中发挥的积极作用。它还支持将这种体外组织培养系统用作研究细菌侵袭内皮的模型。
