由NDV诱导的自会通过NLRP3/Caspase-1炎症体和p38/MAPK通路增强炎症
Juncheng Cai1,2,3,4, Siyuan Wang1,2,3,4, Haoyun Du1,2,3,4
1College of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China.
Veterinary research
|June 5, 2023
概括
纽卡斯尔病病毒 (NDV) 感染会在家禽细胞中触发自,促进病毒复制和炎症. 这种自增强了通过NLRP3炎症体和p38/MAPK信号的炎症性细胞因子表达.
科学领域:
- 兽医病毒学 兽医病毒学
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
背景情况:
- 纽卡斯尔病 (ND) 是一种严重的家禽疾病,由纽卡斯尔病病毒 (NDV) 引起.
- NDV感染诱导宿主细胞的自和炎症,但它们的相互作用尚未完全理解.
- 众所周知,自和炎症在细胞过程中相互调节.
研究的目的:
- 调查自在NDV感染中的作用.
- 阐明NDV诱导的自和炎症反应之间的关系.
- 为了确定参与NDV诱导的自和炎症的分子途径.
主要方法:
- 在NDV感染实验中利用了DF-1细胞系.
- 量化病毒复制和细胞病变效应.
- 评估了自标志物,炎症性细胞因子mRNA水平 (IL-1β,IL-8,IL-18,CCL-5,TNF-α).
- 分析了NLRP3炎症组分,Caspase-1活性和p38/MAPK通路激活.
- 检查了线粒体损伤,线粒体,活性氧物种 (ROS) 和线粒体DNA (mtDNA) 泄漏.
主要成果:
- NDV感染诱导了DF-1细胞的自,增强了病毒复制和细胞病变效应.
- NDV诱导的自与炎症性细胞因子 (IL-1β,IL-8,IL-18,CCL-5,TNF-α) 的mRNA水平增加正相关.
- 自激活与NLRP3炎症酶激活 (NLRP3,Caspase-1) 和p38/MAPK通路酸化有关.
- 发生了线粒体损伤和线粒体,但没有导致显著的ROS或mtDNA释放,这表明在这种情况下它们不会导致炎症.
结论:
- 由NDV诱导的自促进禽类细胞中的病毒复制和炎症.
- NLRP3/Caspase-1炎症体和p38/MAPK通路介导NDV感染期间自的亲炎症效应.
- 线粒体损伤和线粒体并不是NDV感染的DF-1细胞中炎症的主要驱动因素.
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