抗病毒上皮细胞-巨细胞交叉允许二次细菌感染
Sidney Lane1, Tristan L A White2, Erin E Walsh1
1Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine , Pittsburgh, Pennsylvania, USA.
mBio
|September 29, 2023
概括
在病毒感染期间释放的表皮质衍生的细胞外囊泡 (EVs) 阻碍了巨细胞的抗菌功能. 这损害了细菌清除,改变了免疫信号,揭示了呼吸道 coinfections 免疫功能障碍的新机制.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 呼吸系统医学 呼吸系统医学
背景情况:
- 呼吸道病毒-细菌共感染导致严重疾病由于错误的免疫信号.
- 细胞外囊泡 (EVs) 是感染期间细胞间通信的关键媒介.
研究的目的:
- 调查表皮衍生的EVs在抗病毒反应期间调节巨细胞抗菌活性中的作用.
- 了解这些EVs对免疫信号和巨细胞代谢重编程的影响.
主要方法:
- 巨细胞暴露于在抗病毒反应期间收集的表皮衍生的EVs.
- 评估巨细胞对*黄金葡萄球菌*的细胞能力.
- 对暴露的巨细胞中炎症信号通路和代谢概况的分析.
主要成果:
- 来自抗病毒反应的表皮质衍生的EV显著降低了 * Staphylococcus aureus * 的巨细胞清除.
- 暴露于这些EV的巨体显示出改变的炎症信号.
- 在接受治疗的巨细胞中观察到抗炎代谢重编程的证据.
结论:
- 在病毒感染期间释放的表皮质衍生的EV破坏了巨细胞的抗菌功能.
- 这代表了一种新的表皮质-巨细胞杂交失调的途径,影响共感染结果.
- 这些发现为呼吸道 coinfections 中的免疫功能障碍机制提供了新的见解.
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