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Staphylococcus aureus SaeRS impairs macrophage immune functions through bacterial clumps formation in the early stage of infection. 金黄色葡萄球菌 SaeRS 在感染早期通过细菌团块的形成损害巨噬细胞的免疫功能。
IF 7.8 1区 生物学 Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-10-06 DOI: 10.1038/s41522-024-00576-8
Mingzhang Li, Boyong Wang, Jiani Chen, Luhui Jiang, Yawen Zhou, Geyong Guo, Feng Jiang, Yujie Hu, Changming Wang, Yi Yang, Jin Tang, Pei Han, Jinlong Yu, Hao Shen

The Staphylococcus aureus (S. aureus) SaeRS two-component system (TCS) regulates over 20 virulence factors. While its impact on chronic infection has been thoroughly discussed, its role in the early stage of infection remains elusive. Since macrophages serve as the primary immune defenders at the onset of infection, this study investigates the influence of SaeRS on macrophage functions and elucidates the underlying mechanisms. Macrophage expression of inflammatory and chemotactic factors, phagocytosis, and bactericidal activity against S. aureus were assessed, along with the evaluation of cellular oxidative stress. SaeRS was found to impair macrophage function. Mechanistically, SaeRS inhibited NF-κB pathway activation via toll-like receptor 2 (TLR2). Its immune-modulating effect could partially be explained by the strengthened biofilm formation. More importantly, we found SaeRS compromised macrophage immune functions at early infection stages even prior to biofilm formation. These early immune evasion effects were dependent on bacterial clumping as cytokine secretion, phagocytosis, and bactericidal activity were repaired when clumping was inhibited. We speculate that the bacterial clumping-mediated antigen mask is responsible for SaeRS-mediated immune evasion at the early infection stage. In vivo, ΔsaeRS infection was cleared earlier, accompanied by early pro-inflammatory cytokines production, and increased tissue oxidative stress. Subsequently, macrophages transitioned to an anti-inflammatory state, thereby promoting tissue repair. In summary, our findings underscore the critical role of the SaeRS TCS in S. aureus pathogenicity, particularly during early infection, which is likely initiated by SaeRS-mediated bacterial clumping.

金黄色葡萄球菌(S. aureus)的 SaeRS 双组分系统(TCS)调控着 20 多种毒力因子。虽然人们已经深入讨论了它对慢性感染的影响,但它在感染早期阶段的作用却仍然难以捉摸。由于巨噬细胞是感染初期的主要免疫防御者,本研究探讨了 SaeRS 对巨噬细胞功能的影响,并阐明了其潜在机制。研究评估了巨噬细胞炎症因子和趋化因子的表达、吞噬能力、对金黄色葡萄球菌的杀菌活性以及细胞氧化应激。研究发现,SaeRS 会损害巨噬细胞的功能。从机理上讲,SaeRS 通过类收费受体 2(TLR2)抑制了 NF-κB 通路的激活。其免疫调节作用可部分归因于生物膜形成的加强。更重要的是,我们发现 SaeRS 在早期感染阶段甚至在生物膜形成之前就损害了巨噬细胞的免疫功能。这些早期免疫逃避效应依赖于细菌的凝集,因为当凝集受到抑制时,细胞因子分泌、吞噬和杀菌活性都会得到修复。我们推测,细菌凝集介导的抗原屏蔽是 SaeRS 介导的早期感染阶段免疫逃避的原因。在体内,ΔsaeRS 感染较早被清除,伴随着早期促炎细胞因子的产生和组织氧化应激的增加。随后,巨噬细胞过渡到抗炎状态,从而促进了组织修复。总之,我们的研究结果强调了 SaeRS TCS 在金黄色葡萄球菌致病性中的关键作用,尤其是在早期感染期间,这很可能是由 SaeRS 介导的细菌凝集开始的。
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引用次数: 0
Adaptation of a methanogen to Fe0 corrosion via direct contact. 甲烷发生器通过直接接触适应 Fe0 腐蚀。
IF 7.8 1区 生物学 Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-10-04 DOI: 10.1038/s41522-024-00574-w
Satoshi Kawaichi, Rhitu Kotoky, Jacek Fiutowski, Amelia-Elena Rotaru

Due to unique genomic adaptations, Methanococcus maripaludis Mic1c10 is highly corrosive when in direct contact with Fe0. A critical adaptation involves increased glycosylation of an extracellular [NiFe]-hydrogenase, facilitating its anchoring to cell surface proteins. Corrosive strains adapt to the constructed environment via horizontal gene transfer while retaining ancestral genes important for intraspecies competition and surface attachment. This calls for a reevaluation of how the built environment impacts methane cycling.

由于独特的基因组适应性,海洋梅氏球菌 Mic1c10 在与 Fe0 直接接触时具有很强的腐蚀性。一个关键的适应包括增加细胞外[NiFe]-氢化酶的糖基化,促进其与细胞表面蛋白的锚定。腐蚀性菌株通过水平基因转移适应构建环境,同时保留了对种内竞争和表面附着非常重要的祖先基因。这就需要重新评估建筑环境对甲烷循环的影响。
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引用次数: 0
Bacillus subtilis EpsA-O: A novel exopolysaccharide structure acting as an efficient adhesive in biofilms. 枯草杆菌 EpsA-O:一种新型外多糖结构可作为生物膜中的高效粘合剂。
IF 7.8 1区 生物学 Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-10-02 DOI: 10.1038/s41522-024-00555-z
Iztok Dogsa, Barbara Bellich, Mojca Blaznik, Cristina Lagatolla, Neil Ravenscroft, Roberto Rizzo, David Stopar, Paola Cescutti

Extracellular polysaccharides are crucial components for biofilm development. Although Bacillus subtilis is one of the most characterized Gram-positive biofilm model system, the structure-function of its exopolysaccharide, EpsA-O, remains to be elucidated. By combining chemical analysis, NMR spectroscopy, rheology, and molecular modeling, high-resolution data of EpsA-O structure from atom to supramolecular scale was obtained. The repeating unit is composed of the trisaccharide backbone [→3)-β-D-QuipNAc4NAc-(1→3)-β-D-GalpNAc-(1→3)-α-D-GlcpNAc-(1]n, and the side chain β-D-Galp(3,4-S-Pyr)-(1→6)-β-D-Galp(3,4-S-Pyr)-(1→6)-α-D-Galp-(1→ linked to C4 of GalNAc. Close agreement between the primary structure and rheological behavior allowed us to model EpsA-O macromolecular and supramolecular solution structure, which can span the intercellular space forming a gel that leads to a complex 3D biofilm network as corroborated by a mutant strain with impaired ability to produce EpsA-O. This is a comprehensive structure-function investigation of the essential biofilm adhesive exopolysaccharide that will serve as a useful guide for future studies in biofilm architecture formation.

胞外多糖是生物膜形成的关键成分。虽然枯草芽孢杆菌是特征最明显的革兰氏阳性生物膜模型系统之一,但其外多糖 EpsA-O 的结构-功能仍有待阐明。通过结合化学分析、核磁共振光谱、流变学和分子建模,获得了从原子到超分子尺度的 EpsA-O 结构的高分辨率数据。其重复单元由三糖骨架[→3)-β-D-QuipNAc4NAc-(1→3)-β-D-GalpNAc-(1→3)-α-D-GlcpNAc-(1]n和与GalNAc的C4相连的侧链β-D-Galp(3,4-S-Pyr)-(1→6)-β-D-Galp(3,4-S-Pyr)-(1→6)-α-D-Galp-(1→)组成。一级结构与流变学行为之间的密切吻合使我们能够建立 EpsA-O 的大分子和超分子溶液结构模型,该结构可跨越细胞间隙形成凝胶,从而形成复杂的三维生物膜网络,这一点已被产生 EpsA-O 能力受损的突变株所证实。这是对生物膜粘合剂外多糖的全面结构-功能研究,将为未来生物膜结构形成的研究提供有益的指导。
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引用次数: 0
Colon or semicolon: gut sampling microdevices for omics insights. 结肠还是分号:肠道取样微型设备,用于omics洞察。
IF 7.8 1区 生物学 Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-10-02 DOI: 10.1038/s41522-024-00536-2
Sunil Nagpal, Sarvesh Kumar Srivastava

Ingestible microdevices represent a breakthrough in non-invasive sampling of the human gastrointestinal (GI) tract. By capturing the native spatiotemporal microbiome and intricate biochemical gradients, these devices allow a non-invasive multi-omic access to the unperturbed host-microbiota crosstalk, immune/nutritional landscapes and gut-organ connections. We present the current progress of GI sampling microdevices towards personalized metabolism and fostering collaboration among clinicians, engineers, and data scientists.

可摄入微型装置是人类胃肠道(GI)无创采样的一大突破。通过捕捉原生时空微生物群和复杂的生化梯度,这些设备能够以非侵入性的多组学方式访问未受干扰的宿主-微生物群串联、免疫/营养景观和肠道器官连接。我们将介绍消化道采样微型设备在实现个性化代谢以及促进临床医生、工程师和数据科学家之间合作方面的最新进展。
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引用次数: 0
Metabolic interactions shape emergent biofilm structures in a conceptual model of gut mucosal bacterial communities. 在肠道粘膜细菌群落的概念模型中,代谢相互作用形成了新出现的生物膜结构。
IF 7.8 1区 生物学 Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-10-02 DOI: 10.1038/s41522-024-00572-y
Amin Valiei, Andrew Dickson, Javad Aminian-Dehkordi, Mohammad R K Mofrad

The gut microbiome plays a major role in human health; however, little is known about the structural arrangement of microbes and factors governing their distribution. In this work, we present an in silico agent-based model (ABM) to conceptually simulate the dynamics of gut mucosal bacterial communities. We explored how various types of metabolic interactions, including competition, neutralism, commensalism, and mutualism, affect community structure, through nutrient consumption and metabolite exchange. Results showed that, across scenarios with different initial species abundances, cross-feeding promotes species coexistence. Morphologically, competition and neutralism resulted in segregation, while mutualism and commensalism fostered high intermixing. In addition, cooperative relations resulted in community properties with little sensitivity to the selective uptake of metabolites produced by the host. Moreover, metabolic interactions strongly influenced colonization success following the invasion of newcomer species. These results provide important insights into the utility of ABM in deciphering complex microbiome patterns.

肠道微生物群对人类健康起着重要作用;然而,人们对微生物的结构排列及其分布因素知之甚少。在这项工作中,我们提出了一个基于代理的硅学模型(ABM),从概念上模拟肠道粘膜细菌群落的动态。我们探讨了各种类型的代谢相互作用(包括竞争、中性、共生和互生)如何通过营养消耗和代谢物交换影响群落结构。结果表明,在初始物种丰度不同的情况下,交叉取食会促进物种共存。从形态上看,竞争和中性导致了隔离,而互利和共生则促进了高度混杂。此外,合作关系产生的群落特性对宿主产生的代谢物的选择性吸收几乎不敏感。此外,代谢相互作用对新物种入侵后的定殖成功率有很大影响。这些结果提供了重要的见解,使人们了解到 ABM 在解读复杂的微生物群模式方面的实用性。
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引用次数: 0
A population-scale analysis of 36 gut microbiome studies reveals universal species signatures for common diseases. 对 36 项肠道微生物组研究进行的群体规模分析揭示了常见疾病的普遍物种特征。
IF 7.8 1区 生物学 Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-10-01 DOI: 10.1038/s41522-024-00567-9
Wen Sun, Yue Zhang, Ruochun Guo, Shanshan Sha, Changming Chen, Hayan Ullah, Yan Zhang, Jie Ma, Wei You, Jinxin Meng, Qingbo Lv, Lin Cheng, Shao Fan, Rui Li, Xiaohong Mu, Shenghui Li, Qiulong Yan

The gut microbiome has been implicated in various human diseases, though findings across studies have shown considerable variability. In this study, we reanalyzed 6314 publicly available fecal metagenomes from 36 case-control studies on different diseases to investigate microbial diversity and disease-shared signatures. Using a unified analysis pipeline, we observed reduced microbial diversity in many diseases, while some exhibited increased diversity. Significant alterations in microbial communities were detected across most diseases. A meta-analysis identified 277 disease-associated gut species, including numerous opportunistic pathogens enriched in patients and a depletion of beneficial microbes. A random forest classifier based on these signatures achieved high accuracy in distinguishing diseased individuals from controls (AUC = 0.776) and high-risk patients from controls (AUC = 0.825), and it also performed well in external cohorts. These results offer insights into the gut microbiome's role in common diseases in the Chinese population and will guide personalized disease management strategies.

肠道微生物组与多种人类疾病有关,但不同研究的结果显示出相当大的差异。在这项研究中,我们重新分析了来自 36 项不同疾病病例对照研究的 6314 个公开的粪便元基因组,以研究微生物多样性和疾病共享特征。利用统一的分析管道,我们观察到许多疾病的微生物多样性降低了,而有些疾病的微生物多样性增加了。在大多数疾病中都发现了微生物群落的显著变化。一项荟萃分析确定了 277 种与疾病相关的肠道物种,其中包括患者体内富集的大量机会性病原体以及有益微生物的减少。基于这些特征的随机森林分类器在区分患病个体与对照组(AUC = 0.776)和高危患者与对照组(AUC = 0.825)方面具有很高的准确性,而且在外部队列中也表现良好。这些结果有助于深入了解肠道微生物组在中国人群常见疾病中的作用,并将为个性化疾病管理策略提供指导。
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引用次数: 0
Microbiome-derived antimicrobial peptides show therapeutic activity against the critically important priority pathogen, Acinetobacter baumannii. 微生物衍生的抗菌肽对极为重要的重点病原体鲍曼不动杆菌具有治疗活性。
IF 7.8 1区 生物学 Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-09-30 DOI: 10.1038/s41522-024-00560-2
P J Alexander, L B Oyama, H Olleik, F Godoy Santos, S O'Brien, A Cookson, S A Cochrane, B F Gilmore, M Maresca, S A Huws

Acinetobacter baumannii is designated by the World Health Organisation as a critical priority pathogen. Previously we discovered antimicrobial peptides (AMPs), namely Lynronne-1, -2 and -3, with efficacy against bacterial pathogens, such as Staphylococcus aureus and Pseudomonas aeruginosa. Here we assessed Lynronne-1, -2 and -3 structure by circular dichroism and efficacy against clinical strains of A. baumannii. All Lynronne AMPs demonstrated alpha-helical secondary structures and had antimicrobial activity towards all tested strains of A. baumannii (Minimum Inhibitory Concentrations 2-128 μg/ml), whilst also having anti-biofilm activity. Lynronne-2 and -3 demonstrated additive effects with amoxicillin and erythromycin, and synergy with gentamicin. The AMPs demonstrated little toxicity towards mammalian cell lines or Galleria mellonella. Fluorescence-based assay data demonstrated that Lynronne-1 and -3 had higher membrane-destabilising action against A. baumannii in comparison with Lynronne-2, which was corroborated by transcriptomic analysis. For the first time, we demonstrate the therapeutic activity of Lynronne AMPs against A. baumannii.

鲍曼不动杆菌被世界卫生组织指定为重要的优先病原体。在此之前,我们发现了抗菌肽(AMPs),即 Lynronne-1、-2 和 -3,它们对金黄色葡萄球菌和铜绿假单胞菌等细菌病原体具有疗效。在这里,我们通过圆二色性评估了 Lynronne-1、-2 和 -3 的结构以及对鲍曼尼杆菌临床菌株的疗效。所有 Lynronne AMP 均显示出α-螺旋二级结构,对所有测试的鲍曼不动杆菌菌株均具有抗菌活性(最低抑菌浓度为 2-128 μg/ml),同时还具有抗生物膜活性。Lynronne-2和-3与阿莫西林和红霉素具有相加作用,与庆大霉素具有协同作用。这两种 AMP 对哺乳动物细胞系或鼠瘿蚊的毒性很小。基于荧光的检测数据表明,与 Lynronne-2 相比,Lynronne-1 和 Lynronne-3 对鲍曼不动杆菌具有更强的膜破坏作用,转录组分析也证实了这一点。我们首次证明了 Lynronne AMPs 对鲍曼尼氏菌的治疗活性。
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引用次数: 0
Preventing bacterial adhesion to skin by altering their physicochemical cell surface properties specifically. 通过改变细菌细胞表面的物理化学特性,防止细菌粘附在皮肤上。
IF 7.8 1区 生物学 Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-09-30 DOI: 10.1038/s41522-024-00568-8
Xavier Janvier, Severine Jansen, Charleyne Prenom, Nabiha Khodabux, Francesca Zuttion, Cécile Duclairoir-Poc, Sylvie Cupferman, Ahmad Khodr

The adhesion of bacteria to surfaces is associated with physicochemical and biological interactions. The present investigations provide new results about the differential adhesion levels of skin bacteria using a representative 3D skin model which mainly relies on the different physicochemical properties of the respective surfaces. Modulation of the adhesion of bacteria and thus their colonization, may occur by adjusting the physicochemical properties of the epidermal and bacterial surfaces. Lewis acid and hydrophobicity were the most strongly correlated parameters with the antiadhesion properties of the tested compounds. Modulation of physicochemical properties appears to be the primary driver of reduced Staphylococcus aureus adhesion in this study, with no significant changes observed in the expression of genes associated with classical adhesion pathways.

细菌对表面的粘附与物理化学和生物相互作用有关。本研究利用具有代表性的三维皮肤模型提供了有关皮肤细菌不同粘附水平的新结果,这主要依赖于各自表面的不同理化特性。通过调整表皮和细菌表面的理化特性,可以改变细菌的粘附性,进而改变细菌的定植。路易斯酸和疏水性是与测试化合物的抗粘附性最密切相关的参数。在本研究中,理化性质的改变似乎是降低金黄色葡萄球菌粘附性的主要驱动因素,而在与经典粘附途径相关的基因表达中没有观察到明显的变化。
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引用次数: 0
Stress triggers gut dysbiosis via CRH-CRHR1-mitochondria pathway. 压力通过 CRH-CRHR1 线粒体途径引发肠道菌群失调。
IF 7.8 1区 生物学 Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-09-30 DOI: 10.1038/s41522-024-00571-z
Yiming Zhang, Xiaoang Li, Siqi Lu, Huaizhu Guo, Zhuangyi Zhang, Haonan Zheng, Cunzheng Zhang, Jindong Zhang, Kun Wang, Fei Pei, Liping Duan

Stress can lead to gut dysbiosis in brain-gut axis disordered diseases as irritable bowel syndrome (IBS), yet the mechanisms how stress transfer from the brain to the gut and disrupt gut microbiota remain elusive. Here we describe a stress-responsive brain-to-gut axis which impairs colonocytes' mitochondria to trigger gut dysbiosis. Patients with IBS exhibit significantly increased facultative anaerobes and decreased obligate anaerobes, related to increased serum corticotropin-releasing hormone (CRH) level and defected colonocytes' mitochondria ultrastructure. Mice exposed to acute stress experienced enhanced CRH-CRH receptor type 1 (CRHR1) signaling, which impaired mitochondria and epithelium hypoxia in the colon, subsequently triggered gut dysbiosis. Antagonizing CRHR1 expression to inhibit cAMP/Ras/MAPK signaling or activating mitochondria respiration conferred resilience against stress-induced mitochondria damaging and epithelium hypoxia impairment, ultimately improving gut dysbiosis. These results suggest that the CRH-CRHR1-mitochondria pathway plays a pivotal role in stress-induced gut dysbiosis that could be therapeutically targeted for stress-induced gastrointestinal diseases. Yiming Zhang et.al report that psychological stress activated Corticotropin-releasing hormone (CRH)-CRH receptor type 1 (CRHR1)-mitochondria pathway to trigger gut dysbiosis and reveal CRHR1 upregulation damages mitochondria via cAMP/Ras/MAPK signaling in colonocytes.

在肠易激综合征(IBS)等脑-肠轴紊乱疾病中,压力可导致肠道菌群失调,但压力如何从大脑转移到肠道并破坏肠道微生物群的机制仍然难以捉摸。在这里,我们描述了一种应激反应性脑-肠轴,它损害了结肠细胞的线粒体,从而引发肠道菌群失调。肠易激综合征患者表现出明显的兼性厌氧菌增加和强制性厌氧菌减少,这与血清促肾上腺皮质激素释放激素(CRH)水平升高和结肠细胞线粒体超微结构受损有关。小鼠暴露于急性应激时,CRH-CRH 受体 1 型(CRHR1)信号传导增强,损害了线粒体和结肠上皮细胞缺氧,进而引发肠道菌群失调。拮抗CRHR1表达以抑制cAMP/Ras/MAPK信号或激活线粒体呼吸,可抵御应激引起的线粒体损伤和上皮细胞缺氧,最终改善肠道菌群失调。这些结果表明,CRH-CRHR1-线粒体通路在应激诱导的肠道菌群失调中起着关键作用,可作为应激诱导的胃肠道疾病的治疗靶点。张一鸣等人报告了心理应激激活促肾上腺皮质激素释放激素(CRH)-CRH受体1型(CRHR1)-线粒体通路引发肠道菌群失调,并揭示了CRHR1上调通过cAMP/Ras/MAPK信号转导损伤结肠细胞中的线粒体。
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引用次数: 0
Leptospira interrogans biofilm transcriptome highlights adaption to starvation and general stress while maintaining virulence. 讯号钩端螺旋体生物膜转录组突显了在保持毒性的同时对饥饿和一般压力的适应性。
IF 7.8 1区 生物学 Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Pub Date : 2024-09-30 DOI: 10.1038/s41522-024-00570-0
Grégoire Davignon, Natalia Pietrosemoli, Nadia Benaroudj, Marie-Estelle Soupé-Gilbert, Julie Cagliero, Élodie Turc, Mathieu Picardeau, Linda Guentas, Cyrille Goarant, Roman Thibeaux

Life-threatening Leptospira interrogans navigate a dual existence: surviving in the environment and infecting mammalian hosts. Biofilm formation is presumably an important survival strategy to achieve this process. Understanding the relation between biofilm and virulence might improve our comprehension of leptospirosis epidemiology. Our study focused on elucidating Leptospira's adaptations and regulations involved in such complex microenvironments. To determine the transcriptional profile of Leptospira in biofilm, we compared the transcriptomes in late biofilms and in exponential planktonic cultures. While genes for motility, energy production, and metabolism were downregulated, those governing general stress response, defense against metal stress, and redox homeostasis showed a significant upsurge, hinting at a tailored defensive strategy against stress. Further, despite a reduced metabolic state, biofilm disruption swiftly restored metabolic activity. Crucially, bacteria in late biofilms or resulting from biofilm disruption retained virulence in an animal model. In summary, our study highlights Leptospira's adaptive equilibrium in biofilms: minimizing energy expenditure, potentially aiding in withstanding stresses while maintaining pathogenicity. These insights are important for explaining the survival strategies of Leptospira, revealing that a biofilm lifestyle may confer an advantage in maintaining virulence, an understanding essential for managing leptospirosis across both environmental and mammalian reservoirs.

危及生命的钩端螺旋体有双重生存方式:在环境中生存和感染哺乳动物宿主。生物膜的形成可能是实现这一过程的重要生存策略。了解生物膜与毒力之间的关系可能会提高我们对钩端螺旋体流行病学的理解。我们的研究重点是阐明钩端螺旋体在这种复杂微环境中的适应性和相关调节。为了确定钩端螺旋体在生物膜中的转录特征,我们比较了晚期生物膜和指数浮游生物培养物中的转录组。虽然运动、能量产生和新陈代谢的基因下调,但那些管理一般应激反应、金属应激防御和氧化还原平衡的基因却显著增加,这暗示了一种针对应激的定制防御策略。此外,尽管新陈代谢状态有所降低,但生物膜的破坏能迅速恢复新陈代谢活动。最重要的是,在动物模型中,晚期生物膜中的细菌或生物膜破坏后产生的细菌仍具有毒性。总之,我们的研究强调了钩端螺旋体在生物膜中的适应平衡:最大限度地减少能量消耗,在保持致病性的同时可能有助于抵御压力。这些见解对于解释钩端螺旋体的生存策略非常重要,揭示了生物膜生活方式可能在保持致病性方面具有优势,而这种认识对于管理环境和哺乳动物体内的钩端螺旋体病至关重要。
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引用次数: 0
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npj Biofilms and Microbiomes
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