超大·维勒布兰德因子纤维在剪切应力下调解光线黄金葡萄球菌粘附到完整的内皮细胞层
Karin I Pappelbaum1, Christian Gorzelanny, Sandra Grässle
1Experimental Dermatology, Department of Dermatology, Medical Faculty Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany.
Circulation
|May 31, 2013
概括
超大·威尔布兰德因子 (ULVWF) 调解了黄金葡萄球菌最初粘附于健康的心脏组织,这是传染性内心炎的一个关键步骤. 针对ULVWF形成的疗法显示出预防这种感染的希望.
科学领域:
- 心血管生物学 心血管生物学
- 微生物学 微生物学
- 血液学 血液学 血液学
背景情况:
- 黄金葡萄球菌感染性内心炎通常发生在没有先前存在的心脏病的情况下.
- 初始细菌粘附于完好无损的内心脏的机制尚不清楚.
研究的目的:
- 阐明最初黄金葡萄球菌粘附于形态完整的内心脏的分子机制.
- 调查超大威尔布兰德因子 (ULVWF) 在调解细菌粘附中的作用.
主要方法:
- 在高剪切条件下,在体外输注激活的人体内皮细胞与光黄金色S. aureus.
- 使用VWF删除突变体和肝素的流体实验.
- 对细菌删除突变体对粘附因子的分析.
- 在野生类型和VWF淘汰赛小鼠的体内静脉内显微镜.
主要成果:
- ULVWF调解了95%的S. aureus附着在内皮细胞上的情况.
- VWF的A型域和细菌壁中的铁酸都参与了结合.
- 血小板和血清增强了ULVWF介导的粘附性.
- 虽然ADAMTS13减少了细菌的结合,但ULVWF仍然可以结合细菌.
- 在体内,VWF淘汰赛小鼠的细菌粘附率显著降低.
结论:
- 在完整的内皮上,S. aureus内心炎的最初病原性步骤中,ULVWF至关重要.
- 用肝素或ADAMTS13准ULVWF形成提供了潜在的治疗策略.
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