ApoD调解了与年龄相关的流感病毒感染脆弱性增加
Zhimin Jiang1, Wenliang Pan1, Yu Chen1
1National Key Laboratory of Veterinary Public Health and Safety, Key Laboratory for Prevention and Control of Avian Influenza and Other Major Poultry Diseases of the Ministry of Agriculture and Rural Affairs, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
老龄化通过高的Apolipoprotein D (ApoD) 增加了流感A病毒 (IAV) 的严重程度,这驱动了线粒并削弱了老年人的天生的免疫反应.
科学领域:
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
- 老年学是指老年学的学科.
背景情况:
- 甲型流感病毒 (IAV) 对老年人构成重大健康风险,但与年龄相关的严重程度的潜在分子机制尚未完全理解.
- 衰老与免疫功能下降和对感染易感性增加有关.
研究的目的:
- 阐明将衰老,IAV感染严重程度和先天免疫反应联系在一起的分子机制.
- 研究Apolipoprotein D (ApoD) 在与年龄相关的IAV病变发生中的作用.
主要方法:
- 在衰老的人类细胞和老年小鼠模型中分析了线粒,Apolipoprotein D (ApoD) 水平和先天免疫反应.
- 在IAV感染期间调查ApoD与线粒体和LC3B的相互作用.
- 利用ApoD缺乏的小鼠和老化化合物 (ABT-263) 来评估它们对IAV感染的影响.
主要成果:
- 在IAV感染期间,在衰老细胞和老年小鼠中观察到线粒的增加和ApoD水平的升高.
- 局部化到线粒体的ApoD与LC3B相互作用,独立于PINK1通路诱导线粒细胞衰变,减弱I型干扰素反应,并促进病毒复制.
- ApoD 缺乏或老化治疗保护了老年小鼠免受严重流感,改善了生存率,并恢复了先天免疫抗病毒反应.
结论:
- 年龄诱导的Apolipoprotein D (ApoD) 在流感A病毒感染期间驱动线粒,在老年人中加剧了疾病的严重程度.
- 准ApoD或衰老细胞是一个潜在的治疗策略,可以改善患有流感的老年人的治疗结果.
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