菌根PE12蛋白通过抑制细胞亡来促进细菌的生存
Ahui Xu1, Ke Yang1, Jinxia Xu1
1Key Laboratory of Applied Technology on Green-Eco-Healthy Animal Husbandry of Zhejiang Province, Zhejiang Provincial Engineering Research Center for Animal Health Diagnostics & Advanced Technology, Zhejiang International Science and Technology Cooperation Base for Veterinary Medicine and Health Management, China-Australia Joint Laboratory for Animal Health Big Data Analytics, College of Animal Science and Technology & College of Veterinary Medicine of Zhejiang A&F University, 666 Wusu Street, Lin'an District, Hangzhou, Zhejiang Province 311300, China.
在感染期间,Mycobacterium bovis PE12蛋白质增强了细菌的存活率,并抑制了宿主细胞的亡. 这种蛋白质对于了解M. bovis.病原机制至关重要.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 菌根菌的PE_PGRS蛋白家族对于病原体与宿主相互作用至关重要.
- 大多数PE_PGRS蛋白的特定功能尚未被理解.
- 杆菌 (M. bovis) 对动物和人类健康构成重大威胁.
研究的目的:
- 调查M. bovis PE12在细菌生存和宿主细胞亡中的作用.
- 分析PE12在M. smegmatis感染期间对宿主细胞基因表达的影响.
- 为了阐明PE12对M. bovis.病原性的贡献.
主要方法:
- 表达M. bovis PE12 (Ms_PE12) 和一个控制载体 (Ms_Vec) 的M. smegmatis的特征.
- 评估细菌生长,生存率和宿主细胞 (THP-1) 亡.
- 感染 Ms_PE12 和 Ms_Vec 的 THP-1 细胞的转录组测序 (RNA-Seq).
主要成果:
- M. bovis PE12没有影响M. smegmatis. 的殖民地形态.
- 与Ms_Vec相比,Ms_PE12的生存率显著更高.
- 在THP-1细胞中,PE12抑制了M. smegmatis诱导的亡,并抑制了前炎性细胞因子反应.
- 转录组分析显示,Ms_PE12感染细胞中的70个下调基因,富含与细胞粘附,细胞化和炎症反应相关的途径.
结论:
- M. bovis PE12在增强细菌生存和逃避宿主免疫反应方面发挥着作用.
- PE12抑制宿主细胞的亡,并调节炎性细胞因子的产生.
- 这些发现表明PE12参与巨细胞化和亡,为M. bovis的发病过程提供了洞察力.
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