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在HBMEC中,ARF6促进Streptococcus suis suilysin诱导的亡

Changsheng Jiang¹, Pei Zhou¹, Xiaoqian Zhang²

¹National Key Laboratory of Agricultural Microbiology, College of Animal Sciences and Veterinary Medicine, Huazhong Agricultural University, The Cooperative Innovation Center for Sustainable Pig Production, Wuhan 430070, China.

International journal of biological macromolecules

|April 25, 2024

概括

杆菌 suis suilysin (SLY) 与宿主细胞蛋白 ARF6 相互作用,增强了细菌的入侵和毒性. 这种ARF6-SLY相互作用激活了p38 MAPK通路,促进了亡并增加了小鼠的疾病严重程度.

科学领域:

微生物学微生物学
细胞生物学细胞生物学
病原发生和发病的过程.

背景情况:

瑞士白杆菌 (S. suis) 是一种致动物性病原体,在猪和人类中引起严重脑膜炎和败血症.
苏利辛 (SLY) 是一个关键的S. suis毒性因子,但其宿主细胞相互作用仍然不清楚.

研究的目的:

在人类大脑微血管内皮细胞 (HBMEC) 中识别与SLY相互作用的蛋白质.
阐明S. suis病原体中已识别的相互作用蛋白的作用.

主要方法:

使用TurboID介导的近距离标签来识别SLY相互作用的蛋白质.
在体外测试中评估了细菌入侵,亡和信号通路激活.
在C57BL/6小鼠的体内研究评估了SLY毒性.

主要成果:

确定了251种独特的蛋白质,包括血膜蛋白ARF6和PNN作为直接的SLY相互作用体.
在HBMEC中,ARF6显著增强了S. suis入侵和SLY诱导的p38 MAPK通路激活.
在HBMEC中,ARF6促进了SLY诱导的亡,在小鼠中增加了SLY的毒性.

结论:

ARF6是一个关键的宿主因子,调解SLY的致病作用.
通过p38 MAPK信号传递,ARF6-SLY相互作用有助于S. suis的毒性和疾病.
结果提供了关于S. suis病原体和潜在治疗点的见解.

关键词:

在ARF6中,ARF6是ARF6的代码.细胞灭亡 (apoptosis) 是一种死亡的过程.这是一种Streptococcus suis.苏利辛 (Suilysin) 是一种可怕的药物.通过TurboID介导的近距离标签.p38 MAPK信号通道的信号通道

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