沙门氏菌Pullorum效应剂SteE通过触发抑制NF-κB激活的STAT3/SOCS3途径来调节Th1/Th2细胞因子的表达,从而抑制NF-κB激活
Zhike Liu1, Li Wang2, Pei Gao2
1College of Animal Science and Veterinary Medicine, Henan Institute of Science and Technology, Xinxiang 453003, China; Faculty of Veterinary Medicine, Sumy National Agrarian University, Sumy 40021, Ukraine.
Veterinary microbiology
|June 22, 2023
概括
沙门氏菌Pullorum效应剂SteE通过调节STAT3/SOCS3和NF-κB通路来抑制Th1免疫力并促进Th2免疫力,为沙门氏菌提供了潜在的治疗点.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 分子生物学分子生物学
背景情况:
- 沙门氏菌 (Salmonella enterica serovar Pullorum (S. Pullorum)) 使用像SteE这样的效应物来逃避宿主免疫力并建立持久感染.
- 效应因子SteE在沙门氏菌对巨细胞的系统感染中发挥作用,影响宿主免疫反应.
- 了解T助手类型1 (Th1) 和T助手类型2 (Th2) 细胞因子的调节对于理解沙门氏菌的免疫逃避策略至关重要.
研究的目的:
- 研究S. Pullorum效应体SteE对Th1/Th2细胞因子平衡的影响.
- 阐明STAT3/SOCS3通路和NF-κB P65激活在SteE介导免疫调节中的作用.
- 评估SteE在细胞 (HD-11细胞) 和体内 (模型) 系统中的影响.
主要方法:
- 在S. Pullorum感染的HD-11细胞和模型中分析Th1 (IFN-γ,IL-12) 和Th2 (IL-4,IL-10) 细胞因子表达.
- 调查STAT3/SOCS3信号通路,包括SOCS3沉默的影响.
- 对NF-κB P65激活和核转移的评估.
主要成果:
- SteE显著减少了Th1细胞因子表达,同时促进了Th2细胞因子表达在受感染的细胞和中.
- 沉默SOCS3扭转了SteE的影响,突出了SOCS3在调解SteE功能中的关键作用.
- 发现SteE激活STAT3,导致SOCS3表达增加,这反过来又抑制了NF-κB P65激活和核转位.
结论:
- SteE通过STAT3/SOCS3和NF-κB信号通路调节Th1/Th2细胞因子的表达.
- 这种SteE对细胞因子平衡的调节可能会在S. Pullorum感染期间影响Th1/Th2细胞分化.
- 通过SteE介导的途径代表了一种潜在的新型治疗点,用于对抗沙门氏菌病.
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