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Autoinducer-2 plays a crucial role in gut colonization and probiotic functionality of Bifidobacterium breve UCC2003

机译:Autoinducer-2在短双歧杆菌UCC2003的肠道定植和益生菌功能中起关键作用

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摘要

In the present study we show that luxS of Bifidobacterium breve UCC2003 is involved in the production of the interspecies signaling molecule autoinducer-2 (AI-2), and that this gene is essential for gastrointestinal colonization of a murine host, while it is also involved in providing protection against Salmonella infection in Caenorhabditis elegans. We demonstrate that a B. breve luxS-insertion mutant is significantly more susceptible to iron chelators than the WT strain and that this sensitivity can be partially reverted in the presence of the AI-2 precursor DPD. Furthermore, we show that several genes of an iron starvation-induced gene cluster, which are downregulated in the luxS-insertion mutant and which encodes a presumed iron-uptake system, are transcriptionally upregulated under in vivo conditions. Mutation of two genes of this cluster in B. breve UCC2003 renders the derived mutant strains sensitive to iron chelators while deficient in their ability to confer gut pathogen protection to Salmonella-infected nematodes. Since a functional luxS gene is present in all tested members of the genus Bifidobacterium, we conclude that bifidobacteria operate a LuxS-mediated system for gut colonization and pathogen protection that is correlated with iron acquisition.
机译:在本研究中,我们表明短双歧杆菌UCC2003的luxS参与种间信号分子autoinducer-2(AI-2)的产生,并且该基因对于鼠宿主的胃肠道定殖是必不可少的。在预防秀丽隐杆线虫感染沙门氏菌的过程中发挥作用。我们证明,短双歧杆菌luxS插入突变体比WT菌株对铁螯合剂更敏感,并且在AI-2前体DPD存在下可以部分还原这种敏感性。此外,我们表明,在体内条件下,铁饥饿诱导的基因簇的几个基因在luxS-insertion突变体中被下调并编码一个假定的铁摄取系统,在转录上被上调。短双歧杆菌UCC2003中该簇的两个基因的突变使得衍生的突变株对铁螯合剂敏感,而它们缺乏赋予肠道病原体保护沙门氏菌感染的线虫的能力。由于双歧杆菌属的所有受试成员均存在功能性luxS基因,因此我们得出结论,双歧杆菌可通过LuxS介导的系统进行肠道定居和病原体保护,与铁的摄取有关。

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