Regulation of Salmonella-host cell interactions via the ubiquitin system
Regulation of Salmonella-host cell interactions via the ubiquitin system
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DOI：
10.1016/j.ijmm.2017.11.003
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发表时间：
2018-01-01
影响因子：
4.1
通讯作者：
Dikic, Ivan
中科院分区：
文献类型：
--
作者：
Herhaus, Lina;Dikic, Ivan
沙门氏菌感染通过分泌到宿主胞浆中的细菌效应蛋白的作用引起急性肠道炎症反应。这些蛋白通过解除对宿主固有免疫系统的调控和干扰宿主细胞泛素化信号来促进沙门氏菌的存活。本文综述了病原体感染过程中宿主泛素体的动态变化，细菌效应蛋白如何调节宿主泛素系统，以及宿主固有免疫系统如何利用这些病原体作为信号平台来发起免疫反应来对抗沙门氏菌的入侵。
Salmonella infections cause acute intestinal inflammatory responses through the action of bacterial effector proteins secreted into the host cytosol. These proteins promote Salmonella survival, amongst others, by deregulating the host innate immune system and interfering with host cell ubiquitylation signaling. This review describes the recent findings of dynamic changes of the host ubiquitinome during pathogen infection, how bacterial effector proteins modulate the host ubiquitin system and how the host innate immune system counteracts Salmonella invasion by using these pathogens as signaling platforms to initiate immune responses.