Singapore Centre for Environmental Life Science Engineering, Nanyang Technological University, Singapore.
School of Biological Sciences, Nanyang Technological University, Singapore.
mBio. 2018 Apr 10;9(2):e00626-17. doi: 10.1128/mBio.00626-17.
Enterococci are important human commensals and significant opportunistic pathogens. Biofilm-related enterococcal infections, such as endocarditis, urinary tract infections, wound and surgical site infections, and medical device-associated infections, often become chronic upon the formation of biofilm. The biofilm matrix establishes properties that distinguish this state from free-living bacterial cells and increase tolerance to antimicrobial interventions. The metabolic versatility of the enterococci is reflected in the diversity and complexity of environments and communities in which they thrive. Understanding metabolic factors governing colonization and persistence in different host niches can reveal factors influencing the transition to biofilm pathogenicity. Here, we report a form of iron-dependent metabolism for where, in the absence of heme, extracellular electron transfer (EET) and increased ATP production augment biofilm growth. We observe alterations in biofilm matrix depth and composition during iron-augmented biofilm growth. We show that the gene encoding l-lactate dehydrogenase is required for iron-augmented energy production and biofilm formation and promotes EET. Bacterial metabolic versatility can often influence the outcome of host-pathogen interactions, yet causes of metabolic shifts are difficult to resolve. The bacterial biofilm matrix provides the structural and functional support that distinguishes this state from free-living bacterial cells. Here, we show that the biofilm matrix can immobilize iron, providing access to this growth-promoting resource which is otherwise inaccessible in the planktonic state. Our data show that in the absence of heme, l-lactate dehydrogenase promotes EET and uses matrix-associated iron to carry out EET. Therefore, the presence of iron within the biofilm matrix leads to enhanced biofilm growth.
肠球菌是重要的人类共生菌，也是重要的机会性病原体。生物膜相关的肠球菌感染，如心内膜炎、尿路感染、伤口和手术部位感染以及与医疗设备相关的感染，在生物膜形成后往往会变为慢性感染。生物膜基质赋予了这种状态不同于游离细菌细胞的特性，并增加了对抗菌干预的耐受性。肠球菌的代谢多功能性反映在它们赖以生存的环境和群落的多样性和复杂性中。了解在不同宿主小生境中定植和持续存在的代谢因素，可以揭示影响生物膜致病性转变的因素。在这里，我们报告了一种铁依赖性代谢形式，即当缺乏血红素时，细胞外电子转移（EET）和增加的 ATP 产生会促进生物膜的生长。我们观察到在铁增强的生物膜生长过程中，生物膜基质的深度和组成发生了变化。我们表明，编码 l-乳酸脱氢酶的 基因对于铁增强的能量产生和生物膜形成以及促进 EET 是必需的。细菌的代谢多功能性通常会影响宿主-病原体相互作用的结果，但代谢转变的原因很难确定。细菌生物膜基质提供了区分这种状态与游离细菌细胞的结构和功能支持。在这里，我们表明生物膜基质可以固定铁，从而获得这种促进生长的资源，而在浮游状态下，这种资源是无法获得的。我们的数据表明，在缺乏血红素的情况下，l-乳酸脱氢酶促进 EET，并利用基质相关的铁进行 EET。因此，生物膜基质中存在铁会导致生物膜生长增强。
