Iron acquisition pathways and colonization of the inflamed intestine by Salmonella enterica serovar Typhimurium
Iron acquisition pathways and colonization of the inflamed intestine by Salmonella enterica serovar Typhimurium
复制标题
DOI：
10.1016/j.ijmm.2016.10.004
复制
发表时间：
2016-12-01
影响因子：
4.1
通讯作者：
Santos, Renato L.
中科院分区：
文献类型：
--
作者：
Costa, Luciana F.;Mol, Juliana P. S.;Santos, Renato L.
沙门氏菌肠道型伤寒型鼠伤寒可以通过尚未完全解决的机制在发炎的肠道内扩展。在这里，我们利用链霉素预处理的小鼠和硫酸钠（DSS）处理的小鼠研究鼠伤寒链霉菌采集的途径如何有助于发炎的肠道病原体的扩张。在链霉素预处理的小鼠中缺乏TONB FEOB，FEOB，TONB或铁缺乏TONB FEOB，FEOB，TONB或铁缺乏铁菌菌株的竞争感染和突变菌株表明，在发炎的肠道中，需要铁和Tonb在生长过程中具有适应性优势。但是，亚铁摄取机制赋予的健身优势与炎症无关，并且仅在正常的微生物群组成受到抗生素处理破坏的模型中才明显。 （c）2016 Elsevier GmbH。版权所有。
Salmonella enterica serotype Typhimurium is able to expand in the lumen of the inflamed intestine through mechanisms that have not been fully resolved. Here we utilized streptomycin-pretreated mice and dextran sodium sulfate (DSS)-treated mice to investigate how pathways for S. Typhimurium iron acquisition contribute to pathogen expansion in the inflamed intestine. Competitive infection with an iron uptake-proficient S. Typhimurium strain and mutant strains lacking tonB feoB, feoB, tonB or iroN in streptomycin pretreated mice demonstrated that ferric iron uptake requiring IroN and TonB conferred a fitness advantage during growth in the inflamed intestine. However, the fitness advantage conferred by ferrous iron uptake mechanisms was independent of inflammation and was only apparent in models where the normal microbiota composition had been disrupted by antibiotic treatment. (C) 2016 Elsevier GmbH. All rights reserved.