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铜绿假单胞菌可以通过产生铁载体来抑制链球菌属的生长。

Pseudomonas aeruginosa Can Inhibit Growth of Streptococcal Species via Siderophore Production.

机构信息

Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, USA.

School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China.

出版信息

J Bacteriol. 2019 Mar 26;201(8). doi: 10.1128/JB.00014-19. Print 2019 Apr 15.

DOI:10.1128/JB.00014-19
PMID:30718303
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6436353/
Abstract

Cystic fibrosis (CF) is a genetic disease that causes patients to accumulate thick, dehydrated mucus in the lung and develop chronic, polymicrobial infections due to reduced mucociliary clearance. These chronic polymicrobial infections and subsequent decline in lung function are significant factors in the morbidity and mortality of CF. and spp. are among the most prevalent organisms in the CF lung; the presence of correlates with lung function decline, and the group (SMG), a subgroup of the viridans streptococci, is associated with exacerbations in patients with CF. Here we characterized the interspecies interactions that occur between these two genera. We demonstrated that multiple laboratory strains and clinical CF isolates promote the growth of multiple SMG strains and oral streptococci in an coculture system. We investigated the mechanism by which enhances growth of streptococci by screening for mutants of PA14 that are unable to enhance growth, and we identified the ::Tn mutant, which failed to promote growth of and Characterization of the Δ mutant revealed that this strain cannot promote growth. Our genetic data and growth studies support a model whereby the Δ mutant overproduces siderophores and thus likely outcompetes for limited iron. We propose a model whereby competition for iron represents one important means of interaction between and spp. Cystic fibrosis (CF) lung infections are increasingly recognized for their polymicrobial nature. These polymicrobial infections may alter the biology of the organisms involved in CF-related infections, leading to changes in growth, virulence, and/or antibiotic tolerance, and could thereby affect patient health and response to treatment. In this study, we demonstrate interactions between and streptococci using a coculture model and show that one interaction between these microbes is likely competition for iron. Thus, these data indicate that one CF pathogen may influence the growth of another, and they add to our limited knowledge of polymicrobial interactions in the CF airway.

摘要

囊性纤维化 (CF) 是一种遗传性疾病,导致患者肺部积聚浓稠、脱水的黏液,由于黏液清除能力降低,导致慢性、多微生物感染。这些慢性多微生物感染和随后的肺功能下降是 CF 发病率和死亡率的重要因素。和 spp. 是 CF 肺部最常见的病原体之一;的存在与肺功能下降相关,而 组(SMG),是草绿色链球菌的一个亚群,与 CF 患者的恶化有关。在这里,我们描述了这两个属之间发生的种间相互作用。我们证明,多种 实验室菌株和临床 CF 分离株在共培养系统中促进多个 SMG 株和口腔链球菌的生长。我们通过筛选不能增强 生长的 PA14 突变体来研究 增强链球菌生长的机制,我们鉴定了 ::Tn 突变体,该突变体不能促进 和 的生长。对 Δ 突变体的特性分析表明,该菌株不能促进 生长。我们的遗传数据和生长研究支持这样一种模型,即 Δ 突变体过度产生铁载体,因此可能与 竞争有限的铁。我们提出了一种模型,即竞争铁代表了 和 之间相互作用的一种重要方式。囊性纤维化 (CF) 肺部感染因其多微生物性质而日益受到关注。这些多微生物感染可能改变与 CF 相关感染相关的生物体的生物学特性,导致生长、毒力和/或抗生素耐药性发生变化,从而影响患者的健康和对治疗的反应。在这项研究中,我们使用共培养模型证明了 和链球菌之间的相互作用,并表明这些微生物之间的一种相互作用可能是对铁的竞争。因此,这些数据表明,一种 CF 病原体可能会影响另一种病原体的生长,并且它们增加了我们对 CF 气道中多微生物相互作用的有限了解。

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本文引用的文献

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Sputum microbiota is predictive of long-term clinical outcomes in young adults with cystic fibrosis.痰液微生物组可预测年轻囊性纤维化患者的长期临床结局。
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Mixed Communities of Mucoid and Nonmucoid Exhibit Enhanced Resistance to Host Antimicrobials.黏液型和非黏液型混合群落表现出增强的宿主抗菌药物耐药性。
mBio. 2018 Mar 27;9(2):e00275-18. doi: 10.1128/mBio.00275-18.
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Cystic Fibrosis Airway Microbiome: Overturning the Old, Opening the Way for the New.囊性纤维化气道微生物组:颠覆旧观念,开拓新道路。
J Bacteriol. 2018 Jan 24;200(4). doi: 10.1128/JB.00561-17. Print 2018 Feb 15.
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Community Composition Determines Activity of Antibiotics against Multispecies Biofilms.群落组成决定抗生素对多物种生物膜活性的影响。
Antimicrob Agents Chemother. 2017 Aug 24;61(9). doi: 10.1128/AAC.00302-17. Print 2017 Sep.
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A commensal streptococcus hijacks a Pseudomonas aeruginosa exopolysaccharide to promote biofilm formation.一种共生链球菌利用铜绿假单胞菌的胞外多糖来促进生物膜形成。
PLoS Pathog. 2017 Apr 27;13(4):e1006300. doi: 10.1371/journal.ppat.1006300. eCollection 2017 Apr.
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