金属化和抑制组织的细菌生长
Brian D Corbin1, Erin H Seeley, Andrea Raab
1Department of Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Science (New York, N.Y.)
|February 16, 2008
概括
由中性粒细胞释放的宿主蛋白calprotectin通过和等必需金属的化来阻止腹内的细菌生长. 这种金属耗尽阻碍了黄金葡萄球菌的增殖,突出显示了calprotectin.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 生物化学 生物化学
背景情况:
- 细菌感染通常会导致组织,作为宿主-病原体相互作用的关键地点.
- 天生的免疫系统在中的反应对于感染控制至关重要.
研究的目的:
- 为了识别影响细菌生长的黄金葡萄球菌腹中的宿主因素.
- 研究宿主蛋白质calprotectin在对形成的先天免疫反应中的作用.
主要方法:
- 在S. aureus中识别宿主蛋白质.
- 在体外和体内对calprotectin对S. aureus生长的影响的评估.
- 对细菌基因表达变化的分析,以应对calprotectin.
- 野生类型和calprotectin缺乏的小鼠的金属含量分析.
主要成果:
- 核蛋白蛋白质是一种依赖于中性粒细胞的蛋白质,在金黄色中表达.
- 来自中性粒细胞的calprotectin通过结合 (Mn2+) 和 (Zn2+) 来抑制金黄色细菌的生长.
- 通过calprotectin介导的金属化导致细菌转录组重编程.
- 在calprotectin缺乏的小鼠中,缺失显示金属含量增加和S. aureus增强的扩散.
结论:
- 蛋白是一种关键的先天性免疫因子,在中活跃.
- 通过calprotectin进行金属化是一种重要的抗微生物战略.
- 准金属的可用性是一种潜在的治疗方法,可以对抗形成的细菌感染.
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