在感染期间,Lawsonia intracellularis调节核因子-κB信号通路
Huan W Yang1, Tuanjun Hu2, Tahar Ait-Ali3
1Department of Biochemistry, The University of Illinois Champaign-Urbana, Champaign, IL, United States of America.
PloS one
|September 26, 2024
概括
劳森亚细胞内感染激活了核因子-kappaB (NF-κB) 免疫反应,增加了与细菌负载相关的信号. 这种免疫激活会影响受感染细胞中的细胞因子表达和细胞活力.
科学领域:
- 兽医免疫学 兽医免疫学
- 细胞微生物学 细胞微生物学
背景情况:
- 在哺乳动物中,Lawsonia intracellularis会引起增殖性肠病变 (PE).
- 对L. intracellularis感染的先天免疫反应尚不清楚.
研究的目的:
- 研究NF-κB调节的免疫反应对L.细胞内感染.
- 比较对临床菌株 (Dkp23) 和活衰减疫苗菌株 (Enterisol) 的反应.
主要方法:
- 用L. intracellularis菌株感染PK-15细胞.
- 对NF-κB激活的分析 (p65酸化和核转移).
- 对NF-κB基因 (TNF-α,IFN-γ,IL-6,IL-8) 和细菌负载的量化.
主要成果:
- 感染后5天 (dpi),NF-κB激活和基因表达 (IL-6,IFN-γ,IL-8) 增加,这与细菌负载的峰值相吻合.
- 增加的促炎性细胞因子表达与细胞活力下降相关,特别是在感染疫苗菌株的细胞中.
- 疫苗和Dkp23菌株之间NF-κB信号传递没有显著差异,与细菌负载相关的轻微基因表达变异.
结论:
- 在L. intracellularis感染期间诱导NF-κB信号,与PK-15细胞中的细菌负载相关.
- 由NF-κB介导的先天免疫反应会影响感染期间宿主细胞的活力.
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