Current Research in Microbial Sciences最新文献

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IF 5.8 Q1 MICROBIOLOGY

Current Research in Microbial Sciences

Pub Date : 2026-01-01

引用次数: 0

IF 5.8 Q1 MICROBIOLOGY

Current Research in Microbial Sciences

Pub Date : 2026-01-01

引用次数: 0

Comparative analysis of Borrelia’s Defence mechanisms and their impact on genetic manipulation of low-passage isolates of Borrelia afzelii and Borrelia garinii 阿氏疏螺旋体和加里氏疏螺旋体低传代分离株防御机制的比较分析及其对遗传操作的影响

IF 5.8 Q1 MICROBIOLOGY

Current Research in Microbial Sciences

Pub Date : 2026-01-01 DOI: 10.1016/j.crmicr.2025.100543

Margarida Ruivo, Anna-Margarita Schötta, Theresa Stelzer, Michael Reiter, Michiel Wijnveld

Borrelia, a highly prevalent tick-borne pathogen, has a genome with a linear chromosome and numerous linear and circular plasmids. There are three groups of Borrelia: Lyme borreliosis, relapsing fever, and Echidna-reptile. In Europe, Borrelia afzelii and Borrelia garinii are the main causative agents of Lyme borreliosis.

The primary defence mechanism of bacteria against bacteriophages and other invading DNA elements is the restriction-modification system (RMS), which discriminates between native and foreign DNA based on their distinct methylation patterns.

This present study compares the RMS of all the Borrelia species available in the REBASE database. Additionally, it investigates the effect of the RMS on the transformation efficiency of low-passage B. afzelii and B. garinii isolates.

Upon comparing the RMS of 18 Borrelia species, differences in the number, location and characteristics of genes were observed between groups. Given that Lyme borreliosis species exhibit higher genomic plasticity, we hypothesise that they possess a greater number of RMS genes to ensure functionality of the RMS even if some plasmids are lost.

In this study, we demonstrate a large increase in transformation efficiency of low-passage strains by using an in vitro methylated shuttle vector, confirming our hypothesis that the RMS of Borrelia recognises pre-methylated vectors as native DNA.

The knowledge gained in this study contributes to the understanding of Borrelia defence mechanisms and provides possible explanations for the relatively low transformation efficiency observed in previous studies. Consequently, in vitro methylation can serve as a valuable tool for facilitating studies involving genetic manipulation of Borrelia.

疏螺旋体是一种高度流行的蜱传病原体，其基因组具有线性染色体和许多线性和圆形质粒。伯氏疏螺旋体有三组：莱姆病、回归热和针鼹-爬行动物。在欧洲，阿氏疏螺旋体和加里氏疏螺旋体是莱姆病的主要病原体。细菌对噬菌体和其他入侵DNA元件的主要防御机制是限制性修饰系统（RMS），该系统根据不同的甲基化模式区分原生和外来DNA。本研究比较了REBASE数据库中所有伯氏疏螺旋体的RMS。此外，还研究了RMS对低传代B. afzelii和B. garinii菌株转化效率的影响。通过比较18种疏螺旋体的RMS，观察了不同组间基因数量、位置和特征的差异。鉴于莱姆病物种表现出更高的基因组可塑性，我们假设它们拥有更多的RMS基因，即使一些质粒丢失，也能确保RMS的功能。在本研究中，我们通过体外甲基化穿梭载体证明了低传代菌株的转化效率大大提高，证实了我们的假设，即伯氏疏螺旋体的RMS将预甲基化载体识别为天然DNA。本研究获得的知识有助于理解疏螺旋体防御机制，并为以往研究中观察到的相对较低的转化效率提供了可能的解释。因此，体外甲基化可以作为一个有价值的工具，促进研究涉及遗传操作伯氏疏螺旋体。

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引用次数: 0

Activation of the envelope stress-responsive two-component system AmgRS compensates for depletion of the essential lipoprotein signal peptidase LspA in Pseudomonas aeruginosa 在铜绿假单胞菌中，包膜应激响应双组分系统AmgRS的激活补偿了必需脂蛋白信号肽酶LspA的损耗

IF 5.8 Q1 MICROBIOLOGY

Current Research in Microbial Sciences

Pub Date : 2026-01-01 DOI: 10.1016/j.crmicr.2026.100565

Davide Sposato , Giorgia Molesini , Christopher Riccardi , Jessica Mercolino , Luisa Torrini , Ilaria Varone , Manuela Cipolletti , Filippo Acconcia , Giordano Rampioni , Livia Leoni , Paolo Visca , Marco Fondi , Francesco Imperi

Bacterial lipoproteins play crucial roles in cell envelope biogenesis, signaling, transport, and virulence, making the enzymes responsible for their maturation attractive targets for antibacterial drug development. Among these, the type II signal peptidase LspA is a particularly promising candidate, as several LspA inhibitors have been identified that exert potent antibacterial effects in some Gram-negative species. However, despite predictions that LspA is essential in Pseudomonas aeruginosa, these inhibitors show poor or no activity against this Gram-negative pathogen. To assess the essentiality of P. aeruginosa LspA and its potential as a drug target, here we generated and characterized an arabinose-dependent lspA conditional mutant. LspA depletion completely inhibited bacterial growth, progressively reduced cell viability, and caused severe defects in outer membrane integrity, leading to increased susceptibility to multiple antibiotics, including those that are normally inactive against P. aeruginosa. Selection of revertant clones, whole genome sequencing, and allelic replacement mutagenesis revealed that a gain-of-function mutation in amgS, encoding the sensor kinase of the envelope stress-responsive two-component system AmgRS, can support growth under LspA-limiting conditions and partially restore membrane integrity and antibiotic resistance. Functional analyses further showed that the AmgRS-regulated inner membrane proteins HtpX and YccA are required for this compensatory effect, although the underlying mechanism remains unclear. Together, these findings confirm the essentiality of LspA in P. aeruginosa, establish it as a promising antibacterial target, and uncover a role for the AmgRS-mediated stress response in mitigating the consequences of defective lipoprotein maturation.

细菌脂蛋白在细胞包膜生物发生、信号传导、运输和毒力中起着至关重要的作用，这使得负责它们成熟的酶成为抗菌药物开发的有吸引力的靶点。其中，II型信号肽酶LspA是一个特别有希望的候选者，因为几种LspA抑制剂已经被发现对一些革兰氏阴性菌具有有效的抗菌作用。然而，尽管预测LspA对铜绿假单胞菌至关重要，但这些抑制剂对这种革兰氏阴性病原体的活性很差或没有活性。为了评估铜绿假单胞菌LspA的重要性及其作为药物靶点的潜力，我们产生并鉴定了一个阿拉伯糖依赖性LspA条件突变体。LspA耗尽完全抑制细菌生长，逐渐降低细胞活力，并导致外膜完整性严重缺陷，导致对多种抗生素的敏感性增加，包括那些通常对铜绿假单胞菌无效的抗生素。逆转录克隆的选择、全基因组测序和等位基因置换突变表明，编码包膜应激响应双组分系统AmgRS的传感器激酶的amgS的功能获得突变可以支持lspa限制条件下的生长，并部分恢复膜完整性和抗生素耐药性。功能分析进一步表明，amgrs调控的内膜蛋白HtpX和YccA是这种代偿作用所必需的，尽管其潜在机制尚不清楚。总之，这些发现证实了LspA在P. aeruginosa中的重要性，确立了它作为一个有希望的抗菌靶点，并揭示了amgrs介导的应激反应在减轻缺陷脂蛋白成熟的后果中的作用。

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引用次数: 0

Extreme temperature exposure induces lung-gut dysbiosis in healthy mice 极端温度暴露诱导健康小鼠肺-肠生态失调

IF 5.8 Q1 MICROBIOLOGY

Current Research in Microbial Sciences

Pub Date : 2026-01-01 DOI: 10.1016/j.crmicr.2026.100564

Abubakar Zakari , Syue-Wei Peng , Chia-Li Han , Shu-Yun Wang , Shu-Chi Lan , Yu-S yuan Shih , Zih-An Liao , Ta-Chih Hsiao , Feng-Ming Yang , Yuan-Hung Wang , Shu-Chuan Ho , Kang-Yun Lee , Marc Chadeau-Hyam , Kian Fan Chung , Kin-Fai Ho , Kai-Jen Chuang , Jer-Hwa Chang , Hsiao-Chi Chuang

Climate change has a strong effect on respiratory health, the effects of extreme temperatures on the lung-gut axis remains unclear. This study investigates the impact of extreme temperatures on the lung-gut microbiome and its associated biological pathways in mice. B6.Sftpc^CreERT2/+ ROSA26Sor^CAG-tdTomato mice were exposed to normal (22 °C), low (10 °C), high (40 °C), or fluctuating (40 °C 2 hrs to 10 °C 2 hrs; 40–10 °C) temperatures at 65 % relative humidity, 4hrs/day for 7days. Lung and gut microbiota were analyzed by 16S rDNA sequencing, short-chain fatty acids (SCFAs) were quantified using gas chromatography-mass spectrometry. Intestinal LDH, IL-6, and KC levels were measured. Liquid chromatography-tandem mass spectrometry was used to characterized proteins. Significant beta diversity was observed among groups in the both lung and gut microbiomes. In the lung, Deferribacterota and Desulfobacterota increased at 10 °C and 40–10 °C, while Firmicutes and Verrucomicrobiota decreased under the same conditions. Desulfobacterota and Patescibacteria were enriched at 40–10 °C, whereas Verrucomicrobiota and Firmicutes increased at 40 °C and 10 °C in mice stool, respectively. 40 °C elevated intestinal KC levels, while 10 °C reduced serum butyric and pentanoic acids in mice serum. Significant correlations between lung and stool microbiota, SCFAs, inflammatory markers, and LDH were observed. Proteomic profiling makes available unique temperature-dependent expression patterns, involving: metabolic regulation, immune response, cellular stress, and injury pathways. Extreme temperature exposure induced lung-gut dysbiosis, intestinal inflammation, Serum SCFAs imbalance, and proteomic alterations in mice. These findings revealed the adverse effects of extreme temperature events in disrupting the host-microbiome homeostasis, which potentially increase the susceptibility to temperature-sensitive adverse health outcomes.

气候变化对呼吸系统健康有强烈影响，极端温度对肺肠轴的影响尚不清楚。本研究探讨了极端温度对小鼠肺-肠道微生物组及其相关生物学途径的影响。B6。SftpcCreERT2/+ ROSA26SorCAG-tdTomato小鼠暴露于正常（22°C）、低（10°C）、高（40°C）或波动（40°C 2小时至10°C 2小时；40 - 10°C）温度下，相对湿度为65%，每天4小时，持续7天。肺和肠道菌群采用16S rDNA测序，短链脂肪酸（SCFAs）采用气相色谱-质谱法定量。测定肠道LDH、IL-6、KC水平。采用液相色谱-串联质谱法对蛋白质进行了表征。在肺和肠道微生物组中观察到显著的β多样性。在肺中，在10℃和40-10℃条件下，脱铁菌群和脱硫菌群增加，而厚壁菌群和Verrucomicrobiota在相同条件下减少。40 - 10°C时，小鼠粪便中Desulfobacterota和Patescibacteria富集，而40°C和10°C时，Verrucomicrobiota和Firmicutes分别增加。40°C升高小鼠肠道KC水平，而10°C降低血清丁酸和戊酸。观察到肺和粪便微生物群、SCFAs、炎症标志物和LDH之间存在显著相关性。蛋白质组学分析提供了独特的温度依赖性表达模式，包括：代谢调节、免疫反应、细胞应激和损伤途径。极端温度暴露诱导小鼠肺-肠生态失调、肠道炎症、血清SCFAs失衡和蛋白质组学改变。这些发现揭示了极端温度事件在破坏宿主-微生物组稳态方面的不利影响，这可能会增加对温度敏感的不良健康结果的易感性。

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引用次数: 0

Vegetation composition shapes denitrifier community structure and enhances nitrogen removal in estuarine wetlands: evidence from Reed-Willow Mix promoting nirK-dominated guilds 植被组成塑造了河口湿地反硝化菌群落结构并增强了氮的去除：来自芦苇-柳树混合群落促进以nirk为主的行会的证据

IF 5.8 Q1 MICROBIOLOGY

Current Research in Microbial Sciences

Pub Date : 2026-01-01 DOI: 10.1016/j.crmicr.2026.100546

Shengni Tian , Dan Huang , Guokai Yuan, Yupeng Chen, Penghui Zhang, Mingzhu Zhang

Estuarine wetlands are critical biogeochemical hotspots where vegetation and soil properties jointly regulate microbial processes such as denitrification. This study investigated soil physicochemical properties and denitrifying bacterial communities (harboring nirS and nirK genes) across different vegetation types (Reed, Zhongshanshan, and Reed-Willow Mix) and soil depths (0–20 cm, 20–40 cm, and 40–60 cm) in the mudflat of the Paihe River estuary, Chaohu Lake. Soil nutrient availability and pH varied significantly with vegetation, with mixed vegetation supporting higher organic matter, nitrate, and total phosphorus levels. Proteobacteria dominated both nirS and nirK-type communities, but nirS assemblages exhibited greater compositional richness and stronger depth-related shifts. Environmental drivers differed between groups, nirS communities correlated mainly with pH, total nitrogen, and C/N, whereas nirK communities were more responsive to pH, total phosphorus, and nitrate. Co-occurrence network analysis revealed vegetation and depth-dependent structural complexity, with mixed vegetation showing increased network complexity with depth. Denitrification rates declined with depth and ranked Reed-Willow Mix > Reed > Zhongshanshan. nirK taxa explained more rate variation than nirS, with Bradyrhizobium, Sinorhizobium, and Mesorhizobium most influential; regression implicated Brucella and Achromobacter positively and Bosea negatively. Mixed vegetation thus enhances denitrification by improving soil conditions and selecting nirK-dominated guilds in the active layer. The findings provide novel evidence that vegetation composition shapes both the structure and function of denitrifying microbial communities, with Reed-Willow Mix enhancing microbial diversity, interaction complexity, and denitrification efficiency. These results underscore the importance of vegetation management in sustaining nitrogen removal capacity and ecosystem functioning in estuarine wetlands.

河口湿地是重要的生物地球化学热点，植被和土壤特性共同调节反硝化等微生物过程。研究了巢湖排河河口泥滩不同植被类型（芦苇、中山山、芦苇-柳叶混合）和土壤深度（0-20 cm、20-40 cm和40-60 cm）土壤理化性质和含nirS和nirK基因的反硝化细菌群落。土壤养分有效性和pH值随植被变化显著，混合植被支持较高的有机质、硝酸盐和全磷水平。变形菌门在nirS和nirk型群落中均占主导地位，但nirS组合表现出更大的成分丰富度和更强的深度相关变化。不同群落间环境驱动因素存在差异，近红外群落主要与pH、总氮和C/N相关，而近红外群落对pH、总磷和硝态氮的响应更大。共生网络分析揭示了植被和深度相关的结构复杂性，混合植被的网络复杂性随深度增加而增加。反硝化率随深度的增加而下降，排在芦苇-柳树混合芦苇和中山山的排在第二位。nirK分类群比nirS解释了更多的速率变化，其中慢根瘤菌、中根瘤菌和中根瘤菌影响最大；回归显示布鲁氏菌和无色杆菌阳性，Bosea阴性。因此，混合植被通过改善土壤条件和选择活性层中以nirk为主的行当来增强反硝化作用。这些发现为植被组成决定反硝化微生物群落的结构和功能提供了新的证据，芦苇-柳树混合可以提高微生物的多样性、相互作用的复杂性和反硝化效率。这些结果强调了植被管理在维持河口湿地氮去除能力和生态系统功能中的重要性。

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引用次数: 0

The lncRNA GAS5-encoded micropeptide facilitates influenza virus replication through modulation of the Wnt/β-catenin signaling pathway gas5编码的lncRNA微肽通过调节Wnt/β-catenin信号通路促进流感病毒复制

IF 5.8 Q1 MICROBIOLOGY

Current Research in Microbial Sciences

Pub Date : 2026-01-01 DOI: 10.1016/j.crmicr.2026.100559

Xinni Zhou , Xiaojuan Chi , Benqun Peng , Ming Gao , Ning Li , Lu Liu , Jie Zeng , Yuxin Li , Yuzhang Chen , Song Wang

Long non-coding RNAs (lncRNAs) have been implicated in various cellular processes, including the regulation of gene expression and cellular response to viral infections. Herein, our RNA-seq analysis revealed a significant increase in the expression of an annotated lncRNA, GAS5, following influenza A virus (IAV) infection. Stimulation of cells with type I interferon, type III interferon or IL-6 can also result in upregulation of GAS5 expression. Additionally, overexpression of GAS5 promoted IAV replication, while knockdown of GAS5 decreased viral titers. Notably, we identified a novel 50-amino acid micropeptide encoded by GAS5, named GAS5-P50, through ribosome profiling and mass spectrometry analysis. It was found that overexpression of GAS5-P50 alone could facilitate the replication of IAV; conversely, frameshift mutation-mediated silencing of GAS5-P50 diminished the capacity of GAS5 to promote IAV replication, implying that GAS5-P50 is essential for GAS5-mediated enhancement of viral replication. Moreover, synthetic GAS5-P50 was demonstrated to boost IAV propagation both in vitro and in vivo. Mechanistically, GAS5-P50 interacted with NOTUM, a negative regulator of Wnt signaling, leading to enhanced Wnt/β-catenin pathway activation, which facilitated viral replication. These findings uncover a previously unrecognized function of GAS5 as a proviral lncRNA that encodes a functional micropeptide, which modulates host Wnt/β-catenin signaling to support IAV infection. Our study not only expands the understanding of lncRNA-encoded micropeptides in viral pathogenesis but also highlights GAS5-P50 as a potential target for antiviral intervention.

长链非编码rna （lncRNAs）参与多种细胞过程，包括基因表达调控和细胞对病毒感染的反应。在此，我们的RNA-seq分析显示，在甲型流感病毒（IAV）感染后，加注释的lncRNA GAS5的表达显著增加。用I型干扰素、III型干扰素或IL-6刺激细胞也可导致GAS5表达上调。此外，GAS5的过表达促进了IAV的复制，而GAS5的敲低降低了病毒滴度。值得注意的是，通过核糖体分析和质谱分析，我们发现了一种新的由GAS5编码的50个氨基酸的微肽，命名为GAS5- p50。结果表明，单独过表达GAS5-P50可促进IAV的复制；相反，移码突变介导的GAS5- p50沉默降低了GAS5促进IAV复制的能力，这意味着GAS5- p50对GAS5介导的病毒复制增强至关重要。此外，合成的GAS5-P50被证明可以促进IAV在体外和体内的繁殖。从机制上讲，GAS5-P50与Wnt信号负调控因子NOTUM相互作用，导致Wnt/β-catenin通路激活增强，促进病毒复制。这些发现揭示了GAS5以前未被认识到的功能，GAS5是一种编码功能性微肽的前病毒lncRNA，其调节宿主Wnt/β-catenin信号以支持IAV感染。我们的研究不仅扩大了对lncrna编码的微肽在病毒发病机制中的理解，而且强调了GAS5-P50是抗病毒干预的潜在靶点。

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引用次数: 0

IF 5.8 Q1 MICROBIOLOGY

Current Research in Microbial Sciences

Pub Date : 2026-01-01

引用次数: 0

IF 5.8 Q1 MICROBIOLOGY

Current Research in Microbial Sciences

Pub Date : 2026-01-01

引用次数: 0

IF 5.8 Q1 MICROBIOLOGY

Current Research in Microbial Sciences

Pub Date : 2026-01-01

引用次数: 0

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