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首页> 外文期刊>Infection and immunity >Aerobactin Mediates Virulence and Accounts for Increased Siderophore Production under Iron-Limiting Conditions by Hypervirulent (Hypermucoviscous) Klebsiella pneumoniae
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Aerobactin Mediates Virulence and Accounts for Increased Siderophore Production under Iron-Limiting Conditions by Hypervirulent (Hypermucoviscous) Klebsiella pneumoniae

机译：航空杆菌素介导毒力，并解释了铁限制条件下高毒性（超粘膜粘液）肺炎克雷伯菌的铁载体产量增加

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Hypervirulent (hypermucoviscous) Klebsiella pneumoniae (hvKP) strains are an emerging variant of “classical” K. pneumoniae (cKP) that cause organ and life-threatening infection in healthy individuals. An understanding of hvKP-specific virulence mechanisms that enabled evolution from cKP is limited. Observations by our group and previously published molecular epidemiologic data led us to hypothesize that hvKP strains produced more siderophores than cKP strains and that this trait enhanced hvKP virulence. Quantitative analysis of 12 hvKP strains in iron-poor minimal medium or human ascites fluid showed a significant and distinguishing 6- to 10-fold increase in siderophore production compared to that for 14 cKP strains. Surprisingly, high-pressure liquid chromatography (HPLC)-mass spectrometry and characterization of the hvKP strains hvKP1, A1142, and A1365 and their isogenic aerobactin-deficient (ΔiucA) derivatives established that aerobactin accounted for the overwhelming majority of increased siderophore production and that this was not due to gene copy number. Further, aerobactin was the primary factor in conditioned medium that enhanced the growth/survival of hvKP1 in human ascites fluid. Importantly the ex vivo growth/survival of hvKP1 ΔiucA was significantly less than that of hvKP1 in human ascites fluid, and the survival of outbred CD1 mice challenged subcutaneously or intraperitoneally with hvKP1 was significantly less than that of mice challenged with hvKP1 ΔiucA. The lowest subcutaneous and intraperitoneal challenge inocula of 3 × 102 and 3.2 × 101 CFU, respectively, resulted in 100% mortality, demonstrating the virulence of hvKP1 and its ability to cause infection at a low dose. These data strongly support that aerobactin accounts for increased siderophore production in hvKP compared to cKP (a potential defining trait) and is an important virulence factor.
机译：高毒力（高粘膜粘液）肺炎克雷伯菌（hvKP）菌株是“经典”肺炎克雷伯菌（cKP）的新兴变异，会导致健康个体的器官感染和危及生命的感染。对hvKP特异毒力机制的认识使从cKP进化成为可能是有限的。我们小组的观察和先前发表的分子流行病学数据使我们假设hvKP菌株比cKP菌株产生更多的铁载体，并且该特性增强了hvKP毒力。定量分析铁缺乏的中等培养基或人腹水中的12 hvKP菌株，与14 cKP菌株相比，铁载体的产量显着提高了6至10倍。令人惊讶的是，高压液相色谱（HPLC）质谱分析和鉴定hvKP菌株hvKP1，A1142和A1365及其等基因气杆菌素缺陷（Δ iucA ）衍生物，表明气菌素占了压倒性优势铁载体产生的大多数增加，这不是由于基因拷贝数。此外，航空细菌素是条件培养基中增加hvKP1在人腹水中生长/存活的主要因素。重要的是，在人腹水中，hvKP1Δ iucA 的离体生长/存活率显着低于hvKP1，而近亲CD1小鼠的存活率则通过hvKP1皮下或腹膜内攻击明显低于用hvKP1Δ iucA 攻击的小鼠。最低的皮下和腹膜内挑战接种量分别为3×10 2 和3.2×10 1 CFU，可导致100％的死亡率，证明hvKP1的毒力及其低剂量引起感染。这些数据有力地证明，与cKP（潜在的定义性状）相比，hbacK产生的铁载体产生的原因是航空杆菌素，这是重要的毒力因子。

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