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金黄色葡萄球菌侵袭培养的成骨细胞的机制。

Mechanisms of Staphylococcus aureus invasion of cultured osteoblasts.

作者信息

Ellington J K, Reilly S S, Ramp W K, Smeltzer M S, Kellam J F, Hudson M C

机构信息

Department of Biology, University of North Carolina at Charlotte, Charlotte, North Carolina 28223, USA.

出版信息

Microb Pathog. 1999 Jun;26(6):317-23. doi: 10.1006/mpat.1999.0272.

Abstract

Staphylococcus aureus is a bacterial pathogen causing approximately 80% of all cases of human osteomyelitis. This bacterium can adhere to and become internalized by osteoblasts and previous studies indicate that osteoblasts are active in the internalization process. In the current study, we examined the roles of microfilaments, microtubules and clathrin-dependent receptor-mediated endocytosis in the internalization of S. aureus by MC3T3-E1 mouse osteoblast cells. Microfilament and microtubule polymerization was inhibited with cytochalasin D and colchicine. Clathrin-coated pit formation was examined by using the transaminase inhibitor, monodanslycadaverine. The results of this study indicate that mouse osteoblasts utilize actin microfilaments, microtubules and clathrin-coated pits in the internalization of S. aureus; however, microfilaments seem to play the most significant role in the invasion process.

摘要

金黄色葡萄球菌是一种细菌病原体,约导致80%的人类骨髓炎病例。这种细菌可以粘附于成骨细胞并被其内化,先前的研究表明成骨细胞在该内化过程中具有活性。在本研究中,我们检测了微丝、微管和网格蛋白依赖性受体介导的内吞作用在MC3T3-E1小鼠成骨细胞内化金黄色葡萄球菌过程中的作用。用细胞松弛素D和秋水仙碱抑制微丝和微管聚合。通过使用转氨酶抑制剂单丹磺酰尸胺检测网格蛋白包被小窝的形成。本研究结果表明,小鼠成骨细胞在金黄色葡萄球菌内化过程中利用肌动蛋白微丝、微管和网格蛋白包被小窝;然而,微丝似乎在侵袭过程中发挥着最重要的作用。

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