Intimate host attachment: enteropathogenic and enterohaemorrhagic Escherichia coli.

Intimate host attachment: enteropathogenic and enterohaemorrhagic Escherichia coli.
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DOI:
10.1111/cmi.12179
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发表时间:
2013-11
影响因子:
3.4
通讯作者:
Frankel G
Frankel G
中科院分区:
生物学2区
文献类型:
--
作者:
Lai Y;Rosenshine I;Leong JM;Frankel G

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肠致病性和肠出血性大肠杆菌使用一种新的感染策略来定殖肠道上皮,包括通过III型分泌系统易位其自身的受体Tir,并随后形成附着和影响(A/E)病变。在整合到培养细胞的宿主细胞质膜中,并通过外膜粘附素intimin聚集后,Tir触发多个肌动蛋白聚合途径,所述多个肌动蛋白聚合途径涉及聚集在宿主Arp 2/3肌动蛋白成核剂上的宿主和细菌衔接蛋白。虽然最初被认为参与A/E病变的形成,但最近的数据表明,已知的TIR诱导的肌动蛋白聚合途径对这种活性是不利的,但可以在定植效率、体内适应性和全身性疾病中发挥其他主要作用。在这篇综述中,我们总结了路线图导致从发现的Tir,通过不同的肌动蛋白聚合途径,它触发,我们目前的理解他们的生理功能。
Enteropathogenic and enterohaemorrhagic Escherichia coli use a novel infection strategy to colonize the gut epithelium, involving translocation of their own receptor, Tir, via a type III secretion system and subsequent formation of attaching and effecting (A/E) lesions. Following integration into the host cell plasma membrane of cultured cells, and clustering by the outer membrane adhesin intimin, Tir triggers multiple actin polymerization pathways involving host and bacterial adaptor proteins that converge on the host Arp2/3 actin nucleator. Although initially thought to be involved in A/E lesion formation, recent data have shown that the known Tir-induced actin polymerization pathways are dispensable for this activity, but can play other major roles in colonization efficiency, in vivo fitness and systemic disease. In this review we summarize the roadmap leading from the discovery of Tir, through the different actin polymerization pathways it triggers, to our current understanding of their physiological functions.
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