Global gene expression as a function of the iron status of the bacterial cell:: Influence of differentially expressed genes in the virulence of the human pathogen Vibrio vulnificus
Global gene expression as a function of the iron status of the bacterial cell:: Influence of differentially expressed genes in the virulence of the human pathogen Vibrio vulnificus
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DOI：
10.1128/iai.00208-08
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发表时间：
2008-09-01
影响因子：
3.1
通讯作者：
Crosa, Jorge H.
中科院分区：
文献类型：
--
作者：
Alice, Alejandro F.;Naka, Hiroaki;Crosa, Jorge H.
在铁超载的条件下，创伤弧菌在宿主组织中迅速繁殖。为了了解铁对该病原体生理学的影响，我们对在三种不同铁浓度下生长的创伤弧菌进行了全基因组转录分析，即铁限制性[含有1.5% NaCl (TSBS)加乙二胺-二(邻羟基苯乙酸)酸(EDDA)的胰蛋白酶大豆肉汤]、低铁(1μg Fe/ml；TSBS)和富铁(38μg) Fe/ml；TSBS 加柠檬酸铁铵）浓度。一些基因在后两种条件下上调，而一些基因仅在其中一种条件下表达差异。在这两种条件下上调的基因编码外膜孔蛋白 OmpH，而其他基因则与氨基糖的生物合成有关。 ompH 突变体对十二烷基硫酸钠 (SDS) 和多粘菌素 B 表现出敏感性，并且与铁超载小鼠中的野生型相比，竞争指数也降低。在铁限制条件下，两个参与伏尼巴汀转运的 TonB 系统被诱导。这些基因对于皮下接种的铁超载小鼠的毒力至关重要，强调了主动铁转运在感染中的重要性，即使在该动物模型的高铁条件下也是如此。此外，我们证明 RyhB 同源物对于铁超载小鼠的毒力也是至关重要的。这些关于铁限制下诱导的基因在铁超载小鼠模型中的作用的新信息，以及发现仅在富铁条件下表达的具有毒力推定作用的新基因的发现，揭示了该病原体在易感宿主中快速繁殖所使用的许多策略。
Vibrio vulnificus multiplies rapidly in host tissues under iron-overloaded conditions. To understand the effects of iron in the physiology of this pathogen, we performed a genome-wide transcriptional analysis of V. vulnificus growing at three different iron concentrations, i.e., iron-limiting [Trypticase soy broth with 1.5% NaCl (TSBS) plus ethylenediamine-di-(o-hydroxyphenylacetic) acid (EDDA)], low-iron (1 mu g Fe/ml; TSBS), and iron-rich (38 mu g Fe/ml; TSBS plus ferric ammonium citrate) concentrations. A few genes were upregulated under the last two conditions, while several genes were expressed differentially under only one of them. A gene upregulated under both conditions encodes the outer membrane porin, OmpH, while others are related to the biosynthesis of amino sugars. An ompH mutant showed sensitivity to sodium dodecyl sulfate (SDS) and polymyxin B and also had a reduced competitive index compared with the wild type in the iron-overloaded mice. Under iron-limiting conditions, two of the TonB systems involved in vulnibactin transport were induced. These genes were essential for virulence in the iron-overloaded mice inoculated subcutaneously, underscoring the importance of active iron transport in infection, even under the high-iron conditions of this animal model. Furthermore, we demonstrated that a RyhB homologue is also essential for virulence in the iron-overloaded mouse. This novel information on the role of genes induced under iron limitation in the iron-overloaded mouse model and the finding of new genes with putative roles in virulence that are expressed only under iron-rich conditions shed light on the many strategies used by this pathogen to multiply rapidly in the susceptible host.