克拉米迪亚肺炎感染在循环的人类单细胞中是耐抗生素治疗的耐药性
J Gieffers1, H Füllgraf, J Jahn
1Institute of Medical Microbiology and Hygiene, Medical University of Lübeck, Lübeck, Germany.
Circulation
|February 7, 2001
概括
冠状病毒肺炎使用单细胞传播,成为持久性和耐药性抗生素,如阿兹菌素. 这挑战了预防血管感染和动脉样硬化的抗生素治疗.
科学领域:
- 传染性疾病 传染性疾病
- 心血管研究研究心血管研究
- 微生物学 微生物学
背景情况:
- 克拉米迪亚肺炎感染动脉样硬化斑块刺激了对冠状动脉疾病的抗菌疗法的研究.
- 单细胞参与了克拉米迪亚肺炎从呼吸道输送到血管壁的过程.
研究的目的:
- 评估抗生素治疗在消除和预防由Chlamydia pneumoniae引起的血管感染方面的疗效.
- 检查克拉米迪亚肺炎在循环的人类单细胞中的抗生素敏感性,在体外和体内.
主要方法:
- 从健康的志愿者获得的单细胞被注射了Chlamydia pneumoniae,并用阿齐思罗米或里法培养.
- 使用免疫黄金标记和mRNA检测评估了克拉米迪亚活力和感染进展.
- 来自治疗冠状动脉疾病的阿齐思罗米患者的循环单细胞被分析为克拉米迪亚肺炎感染.
主要成果:
- 抗生素没有抑制单细胞内Chlamydia pneumoniae的生长;形成了包容体,mRNA合成持续了10天.
- 电子显微镜证实了克拉米迪亚结合体的发展.
- 在接受阿齐思罗米治疗的患者的循环单细胞中找到了可活的克拉米迪亚肺炎,这表明体内持久性.
结论:
- 冠状病毒肺炎利用单细胞进行全身传播,并进入一种耐标准抗冠状病毒治疗的持久性状态.
- 预防血管感染的抗克拉米迪治疗可能是无效的,因为单细胞内存在持久性病原体.
- 单细胞介导的病原体运输和降低的抗菌素敏感性可以通过促炎媒介促进再感染和动脉样硬化.
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