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首页> 外文期刊>Infection and immunity >Role of NleH, a Type III Secreted Effector from Attaching and Effacing Pathogens, in Colonization of the Bovine, Ovine, and Murine Gut
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Role of NleH, a Type III Secreted Effector from Attaching and Effacing Pathogens, in Colonization of the Bovine, Ovine, and Murine Gut

机译：NleH，一种III型分泌效应物，来自于附着和暴露的病原体，在牛，羊和鼠肠内定植中的作用

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The human pathogen enterohemorrhagic Escherichia coli (EHEC) O157:H7 colonizes human and animal gut via formation of attaching and effacing lesions. EHEC strains use a type III secretion system to translocate a battery of effector proteins into the mammalian host cell, which subvert diverse signal transduction pathways implicated in actin dynamics, phagocytosis, and innate immunity. The genomes of sequenced EHEC O157:H7 strains contain two copies of the effector protein gene nleH, which share 49% sequence similarity with the gene for the Shigella effector OspG, recently implicated in inhibition of migration of the transcriptional regulator NF-κB to the nucleus. In this study we investigated the role of NleH during EHEC O157:H7 infection of calves and lambs. We found that while EHEC ΔnleH colonized the bovine gut more efficiently than the wild-type strain, in lambs the wild-type strain exhibited a competitive advantage over the mutant during mixed infection. Using the mouse pathogen Citrobacter rodentium, which shares many virulence factors with EHEC O157:H7, including NleH, we observed that the wild-type strain exhibited a competitive advantage over the mutant during mixed infection. We found no measurable differences in T-cell infiltration or hyperplasia in colons of mice inoculated with the wild-type or the nleH mutant strain. Using NF-κB reporter mice carrying a transgene containing a luciferase reporter driven by three NF-κB response elements, we found that NleH causes an increase in NF-κB activity in the colonic mucosa. Consistent with this, we found that the nleH mutant triggered a significantly lower tumor necrosis factor alpha response than the wild-type strain.
机译：人类病原体肠出血性大肠杆菌（EHEC）O157：H7通过附着和消失的损伤形成在人和动物肠道中定殖。 EHEC菌株使用III型分泌系统将一系列效应蛋白转运到哺乳动物宿主细胞中，从而破坏了肌动蛋白动力学，吞噬作用和先天免疫所涉及的多种信号转导途径。测序的EHEC O157：H7菌株的基因组包含两个拷贝的效应蛋白基因 nleH ，与最近感染的 Shigella 效应子OspG的基因具有49％的序列相似性。抑制转录调节因子NF-κB向核的迁移。在这项研究中，我们调查了NleH在EHEC O157：H7犊牛和羔羊感染中的作用。我们发现，尽管EHECΔ nleH 比野生型菌株更有效地定居在牛肠道中，但在羔羊中，野生型菌株在混合感染过程中表现出比突变体更强的竞争优势。使用与EHEC O157：H7具有许多毒力因子（包括NleH）的小鼠病原体 Centrobacter rodentium ，我们观察到野生型菌株在混合感染过程中显示出比突变体更具竞争优势。我们发现在接种野生型或 nleH 突变株的小鼠结肠中T细胞浸润或增生没有可测量的差异。使用携带转基因的NF-κB报告基因小鼠，该转基因包含由三个NF-κB反应元件驱动的荧光素酶报告基因，我们发现NleH导致结肠粘膜中NF-κB活性增加。与此相符，我们发现 nleH 突变体引发的肿瘤坏死因子α反应明显低于野生型菌株。

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