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首页> 外文期刊>Infection and immunity >Loss of Sigma Factor RpoN Increases Intestinal Colonization of Vibrio parahaemolyticus in an Adult Mouse Model
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Loss of Sigma Factor RpoN Increases Intestinal Colonization of Vibrio parahaemolyticus in an Adult Mouse Model

机译：Sigma因子RpoN的损失增加成年小鼠模型中副溶血性弧菌的肠道定殖

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Vibrio parahaemolyticus is the leading cause of bacterial seafood-borne gastroenteritis worldwide, yet little is known about how this pathogen colonizes the human intestine. The alternative sigma factor RpoN/sigma-54 is a global regulator that controls flagellar synthesis, as well as a wide range of nonflagellar genes. We constructed an in-frame deletion mutation in rpoN (VP2670) in V. parahaemolyticus RIMD2210633, a clinical serogroup O3:K6 isolate, and examined the effects in vivo using a streptomycin-treated mouse model of colonization. We confirmed that deletion of rpoN rendered V. parahaemolyticus nonmotile, and it caused reduced biofilm formation and an apparent defect in glutamine synthetase production. In in vivo competition assays between the rpoN mutant and a wild-type RIMD2210633 strain marked with the β-galactosidase gene lacZ (WBWlacZ), the mutant colonized significantly more proficiently. Intestinal persistence competition assays also demonstrated that the rpoN mutant had enhanced fitness and outcompeted WBWlacZ. Mutants defective in the polar flagellum biosynthesis FliAP sigma factor also outcompeted WBWlacZ but not to the same level as the rpoN mutant, which suggested that lack of motility is not the sole cause of the fitness effect. In an in vitro growth competition assay in mouse intestinal mucus, the rpoN mutant also outcompeted the wild type and exhibited faster doubling times when grown in mucus and on individual components of mucus. Genes in the pathways for the catabolism of mucus sugars also had significantly higher expression levels in a ΔrpoN mutant than in the wild type. These data suggest that in V. parahaemolyticus, RpoN plays an important role in carbon utilization regulation, which may significantly affect host colonization.
机译：副溶血性弧菌是全世界细菌性海鲜引起的肠胃炎的主要原因，但对于这种病原体如何在人的肠道中定植却知之甚少。替代的sigma因子RpoN / sigma-54是控制鞭毛合成以及各种非鞭毛基因的全局调节剂。我们在溶血性弧菌RIMD2210633（一种临床血清型O3：K6分离株）中的rpoN（VP2670）中构建了一个框内缺失突变，并使用链霉素处理的小鼠定居模型研究了其体内作用。我们证实rpoN的删除使副溶血性弧菌失去了运动能力，并导致生物膜形成减少和谷氨酰胺合成酶生产中的明显缺陷。在rpoN突变体与标记有β-半乳糖苷酶基因lacZ（WBWlacZ）的野生型RIMD2210633菌株之间的体内竞争分析中，该突变体的定殖能力明显提高。肠持久性竞争试验还表明，rpoN突变体具有增强的适应性并且胜过WBWlacZ。极鞭毛生物合成FliAP sigma因子中有缺陷的突变体也胜过WBWlacZ，但与rpoN突变体的竞争水平不同，这表明缺乏运动性不是适应性作用的唯一原因。在小鼠肠道粘液的体外生长竞争试验中，rpoN突变体还胜过野生型，并且在粘液中和粘液的单个成分上生长时表现出更快的倍增时间。粘液糖分解代谢途径中的基因在ΔrpoN突变体中的表达水平也显着高于野生型。这些数据表明，在副溶血性弧菌中，RpoN在碳利用调节中起重要作用，这可能会显着影响宿主定殖。

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