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炭病致死毒素和瘤亡因子-α在肠道上皮上协同作用,诱导小鼠死亡

Xinhe Gao¹, Teng Teng¹, Yifei Liu¹

¹State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen 361102, China.

|October 19, 2023

概括

炭杆菌致命毒素 (LT) 和瘤亡因子-α (TNF-α) 通过破坏肠道上皮细胞 (IEC) 协同导致致命的炭. 在IEC中,LT抑制p38α MAPK信号传递促进TNF-α诱导的细胞死亡,导致器官损伤和致死.

科学领域:

病原体与宿主相互作用
细胞和分子生物学是细胞和分子生物学.
免疫学免疫学免疫学

背景情况:

炭杆菌致命毒素 (LT) 对于炭病的致命性至关重要,它会影响髓状细胞和心血管系统.
瘤亡因子-α (TNF-α) 是一种在B. anthracis感染期间积累的促炎性细胞因子.
在炭病原发生过程中,LT,TNF-α和宿主反应之间的相互作用需要进一步阐明.

研究的目的:

调查LT和TNF-α对宿主致死性的联合作用,模仿体内炭病感染条件.
确定特定的宿主细胞和负责LT + TNF-α诱导死亡的分子机制.
通过了解肠道上皮细胞损伤的作用来探索炭病的潜在治疗点.

主要方法:

在小鼠中使用LT和TNF-α的同时治疗模型.
采用骨髓移植和基因工程小鼠来区分细胞特异性贡献.
研究了p38α基因激活蛋白激酶 (MAPK) 在肠上皮细胞 (IECs) 中信号传递的作用.
使用人类结肠上皮细胞HT-29的验证结果.

主要成果:

LT + TNF-α诱导的致死性主要是通过肠上皮细胞 (IEC) 的死亡,而不是造血细胞.
在IEC中,LT抑制了p38α MAPK信号传递.
这种抑制促进了TNF-α诱导的IEC中的亡和亡,导致肠道损伤和死亡.
LT诱导的p38α抑制增强了TNF-α介导的人体结肠上皮细胞中的细胞死亡.

结论:

由LT抑制p38αMAPK信号传递和随后的TNF-α诱导的细胞死亡驱动的肠上皮细胞损伤是LT + TNF-α联合暴露的致命性关键机制.
这一发现强调了肠道损伤是炭病原发生的关键因素,也是潜在的治疗点.

关键词:

这就是TNF TNF.细胞死亡是细胞死亡.肠道上皮细胞是肠道上皮细胞这是一种致命的毒素毒素.在p38α中使用.

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