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天生的免疫蛋白calprotectin消除了β-乳酸抗生素的杀菌活性
Amanda Z Velez1, Jana N Radin2, Emily N Kennedy1
1Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27559.
概括
主体蛋白质calprotectin (CP) 通过结合而导致抗生素耐受性,使必要的细菌酶失活. 这种免疫机制在感染期间损害了β-lactam的有效性,突出的是.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 药理学 药理学是指药理学的学科.
背景情况:
- β-乳酸抗生素对于治疗细菌感染至关重要.
- 尽管没有遗传性耐药性,但治疗失败发生.
- 影响抗生素疗效的宿主因素需要进一步研究.
研究的目的:
- 识别导致抗生素耐受性的宿主衍生机制.
- 阐明calprotectin (CP) 在调节β-乳糖抗生素疗效中的作用.
- 了解的可用性如何影响抗生素治疗结果.
主要方法:
- 在实验室中研究了calprotectin (CP) 对*黄金葡萄球菌*的影响.
- 进行了CP与细菌自解的相互作用的机制研究.
- 在使用缺乏CP的小鼠的小鼠鼠感染模型中评估了牛素的疗效.
主要成果:
- 通过结合并使自身lysins无活化,CP诱导对β-乳糖抗生素的耐受性.
- 具体来说,CP 抑制了 *S. aureus* Atl. 的依赖的自溶活性.
- 在缺乏CP的小鼠中,西林的疗效显著增强,体现了CP的体内损害.
结论:
- 卡尔蛋白蛋白 (CP) 通过封存调解一种新的免疫驱动抗生素耐受性的形式.
- 感染部位的可用性对于β-乳酸抗生素的疗效至关重要.
- 针对宿主金属封存可能提供改善抗生素治疗结果的策略.
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