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细胞吸收和细胞毒性Clostridium perfringens的IOTA-毒素

Masahiro Nagahama¹, Masaya Takehara¹, Soshi Seike²

¹Department of Microbiology, Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Yamashiro-cho, Tokushima 770-8514, Japan.

|December 22, 2023

概括

克洛斯特里迪亚透毒素 (Clostridium perfringens iota-toxin) 使用宿主细胞修复途径进入. 毒素的结合蛋白本身就会通过破坏细胞膜导致细胞死亡.

科学领域:

微生物学和分子生物学
细胞生物学和生物化学

背景情况:

克洛斯特里透的IOTA毒素包括结合性 (Ib) 和催化性 (Ia) 蛋白质.
一种形成孔隙的毒素 (PFT) Ib 结合了宿主细胞上的脂解刺激的脂蛋白受体 (LSR).
它具有ADP-ribosyltransferase活性,破坏了行为细胞骨架.

研究的目的:

为了阐明Clostridium perfringens iota-toxin的细胞吸收机制.
为了研究结合蛋白 (Ib) 在毒素细胞毒性的作用.
为了探索宿主细胞对毒素诱导的膜损伤的反应.

主要方法:

关于Clostridium perfringens iota-toxin结构和功能的现有文献的审查.
分析Ib,LSR和宿主细胞等离子体膜之间的相互作用.
检查Ia的催化活性及其对actin细胞骨的影响.

主要成果:

结合LSR的IB触发了脂质中的寡合化,促进了Ia的进入.
通过Ia介导的G-actin的ADP-ribosylation会导致actin细胞骨的破坏,细胞的圆化和死亡.
仅IB就会导致敏感细胞的膜破坏和细胞毒性.
宿主细胞表现出一种Ca2+依赖的血修复通路,以抵消IB诱导的孔隙形成.

结论:

细胞吸收毒素利用宿主细胞等离子体膜修复途径.
结合蛋白 (Ib) 足以诱导细胞毒性,独立于催化子单元 (Ia).
了解这种机制,可以了解细菌毒素的致病性和宿主细胞防御.

关键词:

克洛斯特里会产生毒素 - - 毒素.细胞内的形成细胞内的形成在内部化,内化.膜修复膜修复膜修复

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