断奶小猪的细菌感染通过诱导NLRP3炎酶 - 热的途径促进腹
Jie Fu1,2, Zipeng Jiang1,2, Chaoyue Wen1,2
1Key Laboratory of Molecular Animal Nutrition, Ministry of Education, College of Animal Sciences, Zhejiang University, Hangzhou, 310063, China.
Science China. Life sciences
|July 7, 2025
概括
细菌感染通过NLRP3炎症酶和热灭激活引发了断奶小猪的腹. 种植 播种 种植 播种
科学领域:
- 兽医免疫学 兽医免疫学
- 微生物学 微生物学
- 胃肠病学 胃肠病学
背景情况:
- 断奶小猪腹是一个重要的经济和动物福利问题.
- 将细菌感染与腹联系在一起的确切机制尚不完全理解.
- NLRP3炎症酶和 pyroptosis 被涉及到粘膜免疫损伤.
研究的目的:
- 为了研究NLRP3炎酶 - 铁灭菌途径在断奶小猪的细菌诱导腹中的作用.
- 探索致病细菌,特别是ETEC K88和C. perfringens对肠道完整性和炎症的影响.
- 评估母猪母乳免疫球蛋白对这些炎症通路的保护作用.
主要方法:
- 对肠道微生物群和NLRP3炎症酶/炎症酶激活在健康和腹小猪中的比较分析.
- 使用肠毒性大肠杆菌 (ETEC) K88和Clostridium perfringens的实验性感染模型.
- 使用NLRP3淘汰赛小鼠来阐明机械路径.
- 评估血清细胞因子水平 (IL-1β,IL-18),肠道完整性标记物和炎症细胞透.
主要成果:
- 断奶后出现腹的小猪显示NLRP3炎症体和热的激活,肠道微生物群多样性的减少,以及Firmicutes/Bacteroidetes比率的增加.
- ETEC K88和C. perfringens的感染破坏了肠道完整性,增加了腹,增加了IL-1β和IL-18,并激活了NLRP3炎症酶-激素灭菌通路.
- 在受到病原体挑战后,NLRP3淘汰小鼠表现出减少的炎症和腹发病率.
- 母乳免疫球蛋白对病原体诱导的NLRP3炎症酶激活和腹具有保护作用.
结论:
- 断奶小猪的细菌感染激活了NLRP3炎症酶-激素灭菌通路,导致腹.
- 降低母猪母乳免疫球蛋白的水平会加剧这种炎症反应.
- 这项研究阐明了一种关键的炎症机制,导致小猪的断奶后腹.
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