Phage-mediated dispersal of biofilm and distribution of bacterial virulence genes is induced by quorum sensing.
Phage-mediated dispersal of biofilm and distribution of bacterial virulence genes is induced by quorum sensing.
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DOI：
10.1371/journal.ppat.1004653
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发表时间：
2015-02
期刊：
影响因子：
6.7
通讯作者：
Huebner J
中科院分区：
文献类型：
--
作者：
Rossmann FS;Racek T;Wobser D;Puchalka J;Rabener EM;Reiger M;Hendrickx AP;Diederich AK;Jung K;Klein C;Huebner J
人类肠道内的微生物组和噬菌体元基因组受到抗生素治疗的影响。确定一种新的机制，在这里，我们证明了细菌使用通用通讯分子AI-2诱导毒力基因，并通过噬菌体释放转移它们。高浓度（即100 μ M）的AI-2促进细菌从已经建立的生物膜中扩散，并与能够感染其他细菌的细菌的释放有关。粪肠球菌V583 Δ ABC基因组中含有7个原噬菌体，其中一个原噬菌体缺陷的突变体（即原噬菌体5）表现出生物膜扩散的显著降低。益生菌E.在用AI-2诱导后，不含裂解性前噬菌体的faecalis菌株与前噬菌体5的融合导致生物膜形成增加，并且也导致生物膜分散增加。益生菌E. faecalis菌株与通过AI-2从E. faecalis V583 Δ ABC对该菌株的致病性显著增强。多溶原性益生菌菌株在小鼠脓毒症模型和大鼠心内膜炎模型中也更具毒性。AI-2和环丙沙星均导致噬菌体释放，表明用抗生素治疗的住院患者的胃肠道中的状况可能导致毒力基因分布到非致病性肠球菌，并且还可能分布到其他益生菌或甚至有益的益生菌菌株。所有高等生物都生活在与细菌和病毒密切接触的直接环境中。我们肠道中的一些细菌可以在无害的寄生虫和导致严重甚至致命的感染之间转换。这涉及对最初定殖和随后伤害宿主所需的机制的严格调节。在这里，我们描述了一种新的机制，通过这种机制，细菌（即感染细菌的病毒）有助于肠道细菌的毒力。我们的研究结果表明，细菌通过一种称为群体感应的过程“感知”任何给定时刻存在的细菌数量，这为它们提供了评估感染过程中特定步骤所需的信息。在感染的晚期，细菌通常大量存在，此时会释放病毒，感染附近的细菌并转移引起感染所需的基因，从而使以前无害的细菌成为危险的病原体。
The microbiome and the phage meta-genome within the human gut are influenced by antibiotic treatments. Identifying a novel mechanism, here we demonstrate that bacteria use the universal communication molecule AI-2 to induce virulence genes and transfer them via phage release. High concentrations (i.e. 100 μM) of AI-2 promote dispersal of bacteria from already established biofilms, and is associated with release of phages capable of infecting other bacteria. Enterococcus faecalis V583ΔABC harbours 7 prophages in its genome, and a mutant deficient in one of these prophages (i.e. prophage 5) showed a greatly reduced dispersal of biofilm. Infection of a probiotic E. faecalis strain without lytic prophages with prophage 5 resulted in increased biofilm formation and also in biofilm dispersal upon induction with AI-2. Infection of the probiotic E. faecalis strain with phage-containing supernatants released through AI-2 from E. faecalis V583ΔABC resulted in a strong increase in pathogenicity of this strain. The polylysogenic probiotic strain was also more virulent in a mouse sepsis model and a rat endocarditis model. Both AI-2 and ciprofloxacin lead to phage release, indicating that conditions in the gastrointestinal tract of hospitalized patients treated with antibiotics might lead to distribution of virulence genes to apathogenic enterococci and possibly also to other commensals or even to beneficial probiotic strains. All higher organisms live in intimate contact with bacteria and viruses in their direct environment. Some of these bacteria in our gut can switch between being harmless commensals and causing severe and sometimes lethal infections. This involves a tight regulation of the mechanisms needed to initially colonize and later to harm the host. Here we describe a novel mechanism by which phages (i.e. viruses that infect bacteria) contribute to virulence in commensal gut bacteria. Our results show that bacteria "sense" the number of bacteria present at any given moment through a process called quorum sensing and this provides them with the information needed to assess the specific step during the infectious process. At late stages of infection bacteria are usually present in high numbers, and at this point release viruses that can infect nearby bacteria and transfer genes that are needed to cause infection, thereby enabling previously harmless bacteria to become dangerous pathogens.
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DOI：
10.1038/nrmicro2853
发表时间：
2012-09
期刊：
Nature reviews. Microbiology
影响因子：
--
作者：
通讯作者：
--
影响因子：
11
作者：
Goedeke, Julia;Paul, Kristina;Thormann, Kai M.
通讯作者：
Thormann, Kai M.
影响因子：
2.9
作者：
Rajamani, Sathish;Zhu, Jinge;Sayre, Richard
通讯作者：
Sayre, Richard
影响因子：
56.9
作者：
Paulsen, IT;Banerjei, L;Fraser, CM
通讯作者：
Fraser, CM
影响因子：
3.2
作者：
Doherty, N;Holden, MTG;Winzer, K
通讯作者：
Winzer, K