甲菌 (Enterococcus faecalis) 抑制金黄色葡萄球菌 (Staphylococcus aureus) 诱导的NETosis,并在多微生物感染中促进细菌的生存
Patrick Hsien-Neng Kao1,2, Jun-Hong Ch'ng3,4,5,6, Kelvin K L Chong2
1School of Biological Sciences, Nanyang Technological University, Singapore 637551.
FEMS microbes
|October 30, 2023
概括
在多微生物感染期间,Enterococcus faecalis抑制了中性粒细胞外陷的形成 (NETosis),促进了Staphylococcus aureus的生存. 这种免疫规避突出了伤口感染中复杂的宿主反应.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 病变的发生和发病.
背景情况:
- 菌 (Enterococcus faecalis) 是一种机会性病原体,通常在伤口感染中与其他微生物一起发现.
- E. faecalis可以通过细菌间协同作用和免疫颠覆来增强共感染微生物的存活率.
- 通过E. faecalis介导的免疫抑制对共感染微生物的影响尚不清楚.
研究的目的:
- 调查E. faecalis是否在混合物种感染中减弱中性粒细胞介导反应.
- 确定E. faecalis对中性粒细胞外细胞陷形成 (NETosis) 在黄金葡萄球菌联合感染期间的影响.
- 阐明E. faecalis在多微生物感染中影响宿主免疫反应的机制.
主要方法:
- 在联合感染模型中研究了对E. faecalis和黄金葡萄球菌的中性粒细胞反应.
- 评估了细胞形成,反应性氧物种 (ROS) 生产,脱粒化和NETosis.
- 分析了E. faecalis在S. aureus诱导的NETosis期间对基因素林的作用.
主要成果:
- 中性粒细胞通过 fagocytosis,ROS生产和脱粒化控制E. faecalis,但不是NETosis.
- E. faecalis 通过干扰基因组氨化,积极抑制 S. aureus 诱导的 NETosis.
- E. faecalis 避开了与NET相关的杀死机制,与增加的S. aureus存活率相关联.
结论:
- 在多微生物感染中,E. faecalis积极抑制中性粒细胞外细胞陷形成 (NETosis).
- 这种通过E. faecalis抑制NETosis促进了S. aureus等共感染细菌的生存.
- 减弱的病原体特异性免疫反应有助于多微生物伤口感染的发病.
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