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伤寒毒素劫持Wnt5a以确定宿主衰老和沙门氏菌感染

Mohamed ElGhazaly¹, Mark O Collins¹, Angela E M Ibler¹

¹School of Biosciences, University of Sheffield, Sheffield, South Yorkshire S10 2TN, UK.

|October 4, 2023

概括

沙门氏菌利用细胞衰老,癌症防御机制,通过劫持关键信号分子,如Wnt5a. 这使得病原体能够引起感染,并在宿主体内传播损伤.

科学领域:

细胞生物学细胞生物学
微生物学微生物学
免疫学免疫学免疫学

背景情况:

细胞衰老是一种不可逆转的增长停止状态,由细胞损伤引发,作为瘤抑制机制.
衰老细胞释放一种与衰老相关的分泌表型 (SASP),影响周围细胞.
沙门氏菌利用细胞衰老,特别是通过其伤寒毒素,促进细胞内感染.

研究的目的:

为了确定毒素诱导衰老细胞 (TxSCs) 的秘密体内的特定因素,Salmonella enterica劫持.
阐明这些已识别的因素在调解沙门氏菌感染和影响细胞衰老中的作用.
了解沙门氏菌如何选择宿主防御机制来进行自身传播.

主要方法:

毒素诱导衰老细胞 (TxSCs) 的转录学分析.
来自TxSCs的分泌体的蛋白质组学分析.
在纤维细胞中进行功能性测试,以评估自身隐性和副隐性衰老.
在肠道环境中进行体内研究,以评估已识别的因素在感染中的作用.

主要成果:

确定了Wnt5a,INHBA和GDF15作为由沙门氏菌的伤寒毒素夺的关键因素.
Wnt5a形成了一个正反循环,上调INHBA和GDF15.
Wnt5a和INHBA都会诱导自身隐性衰老和副隐性衰老.
Wnt5a和GDF15协同增强了沙门氏菌的入侵.
Wnt5a对于建立肠道TxSCs至关重要,防止细胞亡.

结论:

沙门氏菌通过劫持Wnt5a,INHBA和GDF15来利用细胞衰老.
这种劫持促进了细胞内感染,并促进了病原体的传播.
这项研究揭示了一种机制,即细菌病原体利用宿主的先天抗癌防御以造福自身.

关键词:

CP: 免疫学免疫学对DNA损伤的反应反应主体-病原体相互作用感染的感染感染.具有天生的免疫力.衰老是一种老化.毒素毒素是一种毒素.毒性因子是毒性因子.

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