在Clostridium perfringensβ2毒素刺激期间,IPEC-J2细胞中JAK/STAT通路的分子特征和功能
Xiaoli Gao1, Pengfei Wang1, Zunqiang Yan1
1College of Animal Science and Technology, Gansu Agricultural University, Lanzhou, 730070, China.
Veterinary research communications
|July 12, 2023
概括
在小猪中,Clostridium perfringens感染会触发JAK/STAT通路. 阻断JAK2 / STAT3信号减少细胞损伤和炎症,为C. perfringens感染提供潜在的治疗点.
科学领域:
- 兽医医学 兽医医学 兽医医学
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 克洛斯特里迪亚 (Clostridium perfringens) 在小猪中引起腹爆发.
- 简氏激酶/信号转换器和转录激活器 (JAK/STAT) 途径调节细胞活动和炎症.
- 在猪肠上皮细胞 (IPEC-J2) 中的C. perfringens beta2 (CPB2) 感染中JAK/STAT的作用尚不清楚.
研究的目的:
- 在CPB2诱导时,研究IPEC-J2细胞中JAK/STAT通路组件的表达.
- 探索抑制JAK2/STAT3通路对CPB2诱导的细胞损伤的保护作用.
- 阐明JAK2/STAT3影响IPEC-J2细胞中亡,细胞毒性,氧化应激和炎症反应的机制.
主要方法:
- 定量实时PCR (qRT-PCR) 和西布洛特用于评估JAK/STAT基因和蛋白质表达.
- 用WP1066治疗CPB2诱导的IPEC-J2细胞,WP1066是一种JAK2/STAT3抑制剂.
- 对亡,细胞毒性,氧化应激标志物和炎症性细胞因子分泌 (IL-6,IL-1β,TNF-α) 的评估.
主要成果:
- 在IPEC-J2细胞中,CPB2诱导导致JAK2,JAK3,STAT1,STAT3,STAT5A和STAT6的高表达,其中STAT3表达最高.
- 使用WP1066抑制JAK2/STAT3,减弱了CPB2诱导的亡,细胞毒性和氧化应激.
- 在CPB2治疗的IPEC-J2细胞中,WP1066显著抑制了IL-6,IL-1β和TNF-α的分泌.
结论:
- 在C. perfringens感染猪肠细胞时,JAK2/STAT3通路被激活.
- 抑制JAK2/STAT3激活提供了对CPB2诱导的细胞损伤和炎症的保护作用.
- 准JAK2/STAT3通路为控制小猪中C. perfringens感染提供了一个潜在的治疗策略.
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