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Fungal-bacterial endosymbiosis: Recreating an ancient symbiotic relationship 真菌-细菌内共生:重建古老的共生关系
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2024-12-11 DOI: 10.1016/j.chom.2024.10.018
Paola Bonfante
Fungal-bacterial endosymbioses, the most intimate typology of symbioses, have been described in different taxa of Mucoromycota, an early diverging group of Fungi. In a recent issue of Nature, Giger and colleagues describe how they implanted a Burkolderia-related microbe inside a Mucoromycota fungus, giving rise to a functional and stable endosymbiosis.
真菌-细菌内共生是最亲密的共生类型,已在真菌早期分化类群——毛霉科的不同分类群中被描述。在最近一期的《自然》杂志上,吉格尔和他的同事描述了他们如何将一种与伯克氏菌有关的微生物植入一种Mucoromycota真菌中,从而产生一种功能稳定的内共生关系。
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引用次数: 0
Selenium nanoboosting of plant-beneficial microbiome 硒对植物有益微生物群的纳米促进作用
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2024-12-11 DOI: 10.1016/j.chom.2024.11.004
Miaomiao Ding, Ivie Sonia Osayande, Kenichi Tsuda
In the dynamic theater of plant-microbe interactions, a new conductor has emerged: selenium nanoparticles. As unveiled by Sun et al. in this issue of Cell Host & Microbe, these microbially synthesized nanoparticles recruit plant growth-promoting microbes, orchestrating a synergy between plants and the rhizosphere microbiome.
在植物与微生物相互作用的动态舞台上,出现了一种新的导体:硒纳米颗粒。Sun等人在本期《细胞宿主》(Cell Host &;微生物,这些微生物合成的纳米颗粒招募植物生长促进微生物,协调植物和根际微生物组之间的协同作用。
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引用次数: 0
Guilds as guides for health vs. disease 公会作为健康与疾病的指南
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2024-12-11 DOI: 10.1016/j.chom.2024.11.010
Antonio L.C. Gomes, Robert R. Jenq
In a recent Cell paper, Wu et al. identified microbiome guilds based on bacterial co-occurrence among type 2 diabetes patients. Two competing guilds, associated with high-fiber vs. control diets, correlated with healthy biomarkers. The potential of this approach was further verified across 15 diseases in 26 studies.
在最近的一篇Cell论文中,Wu等人根据2型糖尿病患者的细菌共发情况确定了微生物组行会。两个相互竞争的行会,与高纤维饮食和控制饮食相关,与健康的生物标志物相关。在26项研究中对15种疾病进一步验证了这种方法的潜力。
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引用次数: 0
HAMpering infection: Helicase ratcheting emerges as a phage-sensing mechanism 阻碍感染:解旋酶棘轮作为噬菌体感应机制出现
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2024-12-11 DOI: 10.1016/j.chom.2024.11.009
Zhifeng Zeng, Wenyuan Han
The sensing of pathogens is the first step for any immune response. A recent paper in Cell reveals that the bacterial Hachiman anti-phage defense system deploys a helicase subunit to sense phage invasion via 3′ DNA recognition and subsequent domain rotation to enable nuclease activation.
对病原体的感知是任何免疫反应的第一步。最近发表在Cell上的一篇论文揭示了细菌Hachiman抗噬菌体防御系统部署一个解旋酶亚基,通过3 ' DNA识别和随后的结构域旋转来感知噬菌体的入侵,从而激活核酸酶。
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引用次数: 0
The bad neighbor: Prophage competition in Salmonella during macrophage infection 坏邻居:巨噬细胞感染时沙门氏菌的前噬菌体竞争
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2024-12-11 DOI: 10.1016/j.chom.2024.11.011
Zoe Netter
Sargen and Helaine discover a prophage competition element in Salmonella that inhibits the lytic cycle of co-resident prophages by cleaving a subset of cellular tRNAs. During Salmonella pathogenesis in macrophages, a persister subset experiences prophage induction and competition, reducing release of immunogenic cellular components and altering macrophage response to infection.
Sargen和Helaine在沙门氏菌中发现了一种噬菌体竞争因子,它通过切割细胞trna的一个子集来抑制共同居住的噬菌体的分解周期。在沙门氏菌在巨噬细胞中的发病过程中,一个持久亚群经历了噬菌体诱导和竞争,减少了免疫原性细胞成分的释放,改变了巨噬细胞对感染的反应。
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引用次数: 0
Exploring the early life gut microbiome with MAGIC 用MAGIC探索生命早期肠道微生物群
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2024-12-11 DOI: 10.1016/j.chom.2024.10.019
Edoardo Pasolli
In this issue of Cell Host & Microbe, Peng et al. provide the MAGIC catalog as a resource for studying bacterial and viral diversity of the global gut microbiome in early life. By addressing gaps in geographic and age representation, this database enhances our understanding of early microbiome dynamics.
在本期《细胞宿主》杂志中;微生物,Peng等人提供了MAGIC目录,作为研究生命早期全球肠道微生物组细菌和病毒多样性的资源。通过解决地理和年龄代表性的差距,该数据库增强了我们对早期微生物组动力学的理解。
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引用次数: 0
Type I IFN-mediated NET release promotes Mycobacterium tuberculosis replication and is associated with granuloma caseation I型ifn介导的NET释放促进结核分枝杆菌复制并与肉芽肿干酪化有关
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2024-12-04 DOI: 10.1016/j.chom.2024.11.008
Chanchal Sur Chowdhury, Rachel L. Kinsella, Michael E. McNehlan, Sumanta K. Naik, Daniel S. Lane, Priyanka Talukdar, Asya Smirnov, Neha Dubey, Ananda N. Rankin, Samuel R. McKee, Reilly Woodson, Abigail Hii, Sthefany M. Chavez, Darren Kreamalmeyer, Wandy Beatty, Joshua T. Mattila, Christina L. Stallings
Neutrophils are the most abundant cell type in the airways of tuberculosis patients. Mycobacterium tuberculosis (Mtb) infection induces the release of neutrophil extracellular traps (NETs); however, the molecular regulation and impact of NET release on Mtb pathogenesis are unknown. We find that during Mtb infection in neutrophils, PAD4 citrullinates histones to decondense chromatin that gets released as NETs in a manner that can maintain neutrophil viability and promote Mtb replication. Type I interferon promotes the formation of chromatin-containing vesicles that allow NET release without compromising plasma membrane integrity. Analysis of nonhuman primate granulomas supports a model where neutrophils are exposed to type I interferon from macrophages as they migrate into the granuloma, thereby enabling the release of NETs associated with necrosis and caseation. Our data reveal NET release as a promising target to inhibit Mtb pathogenesis.
嗜中性粒细胞是肺结核患者气道中最丰富的细胞类型。结核分枝杆菌(Mtb)感染诱导中性粒细胞胞外陷阱(NETs)的释放;然而,NET释放对结核分枝杆菌发病机制的分子调控和影响尚不清楚。我们发现,在中性粒细胞感染Mtb期间,PAD4瓜氨酸化组蛋白去致密染色质,以net的方式释放,可以维持中性粒细胞活力并促进Mtb复制。I型干扰素促进含染色质囊泡的形成,使NET释放而不损害质膜的完整性。对非人灵长类动物肉芽肿的分析支持一种模型,即当巨噬细胞迁移到肉芽肿时,中性粒细胞暴露于来自巨噬细胞的I型干扰素,从而使与坏死和干酪化相关的NETs释放。我们的数据显示,NET释放是抑制结核分枝杆菌发病机制的一个有希望的靶点。
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引用次数: 0
Cas10 relieves host growth arrest to facilitate spacer retention during type III-A CRISPR-Cas immunity 在III-A型CRISPR-Cas免疫过程中,Cas10缓解宿主生长停滞,促进间隔物保留
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2024-12-02 DOI: 10.1016/j.chom.2024.11.005
Naama Aviram, Amanda K. Shilton, Nia G. Lyn, Bernardo S. Reis, Amir Brivanlou, Luciano A. Marraffini
Cells from all kingdoms of life can enter growth arrest in unfavorable environmental conditions. Key to this process are mechanisms enabling recovery from this state. Staphylococcal type III-A CRISPR-Cas loci encode the Cas10 complex that uses a guide RNA to locate complementary viral transcripts and start an immune response. When the target sequence is expressed late in the viral lytic cycle, defense requires the activity of Csm6, a non-specific RNase that inhibits the growth of the infected cell. How Csm6 protects from infection and whether growth can be restored is not known. Here, we show that growth arrest provides immunity at the population level, preventing viral replication and allowing uninfected cells to propagate. In addition, the ssDNase activity of Cas10 is required for the regrowth of a subset of the arrested cells and the recovery of the infected host, presumably ending the immune response through degradation of the viral DNA.
所有生命体的细胞在不利的环境条件下都会进入生长停滞状态。此过程的关键是从该状态恢复的机制。葡萄球菌III-A型CRISPR-Cas基因座编码Cas10复合体,该复合体使用向导RNA定位互补的病毒转录物并启动免疫反应。当目标序列在病毒裂解周期的后期表达时,防御需要Csm6的活性,Csm6是一种抑制被感染细胞生长的非特异性RNase。目前尚不清楚Csm6是如何防止感染的,以及是否可以恢复生长。在这里,我们表明生长抑制在群体水平上提供免疫力,阻止病毒复制并允许未感染的细胞繁殖。此外,Cas10的ssDNase活性对于一部分被阻滞细胞的再生和被感染宿主的恢复是必需的,可能通过病毒DNA的降解来结束免疫反应。
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引用次数: 0
Campylobacter jejuni-derived cytolethal distending toxin promotes colorectal cancer metastasis 空肠弯曲杆菌衍生的细胞致死膨胀毒素促进结直肠癌转移
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2024-12-02 DOI: 10.1016/j.chom.2024.11.006
Zhen He, Jing Yu, Junli Gong, Jinjie Wu, Xuan Zong, Zhanhao Luo, Xiaowen He, Wai Ming Cheng, Yugeng Liu, Chen Liu, Qiang Zhang, Lei Dai, Tao Ding, Beile Gao, Raad Z. Gharaibeh, Jinlin Huang, Christian Jobin, Ping Lan
Various forms of solid tumors harbor intracellular bacteria, but the physiological consequences of these microorganisms are poorly understood. We show that Campylobacter is significantly enriched in primary colorectal cancer (CRC) lesions from patients with metastasis. Campylobacter jejuni-derived cytolethal distending toxin (CDT) promotes CRC metastasis through JAK2-STAT3-MMP9 signaling in liver or pulmonary metastatic mice models, as confirmed in C. jejuni-infected human colonic tissue and CDT-treated colonic tumoroids from patients. Genetic deletion of cdtB (ΔcdtB) or purified CdtB protein demonstrates that the genotoxin is essential for C. jejuni’s pro-metastatic property. In C.-jejuni-colonized mice, increased translocation of CDT-producing C. jejuni to extraintestinal implanted tumors potentially leads to accelerated metastasis of these tumors. Overall, these findings demonstrate that an intratumor-bacteria-derived genotoxin accelerates tumor metastasis, potentially opening a new diagnostic and therapeutic avenue for cancer management.
各种形式的实体肿瘤都有细胞内细菌,但这些微生物的生理后果尚不清楚。我们发现弯曲杆菌在转移患者的原发性结直肠癌(CRC)病变中显著富集。在肝或肺转移小鼠模型中,空肠弯曲杆菌衍生的细胞致死膨胀毒素(CDT)通过JAK2-STAT3-MMP9信号通路促进结直肠癌转移,这在空肠弯曲杆菌感染的人类结肠组织和CDT治疗的结肠类肿瘤患者中得到证实。cdtB基因缺失(ΔcdtB)或纯化的cdtB蛋白表明基因毒素对空肠梭菌的促转移特性至关重要。在c -jejuni定植的小鼠中,产生cdt的c -jejuni向肠外植入肿瘤的易位增加可能导致这些肿瘤的加速转移。总之,这些发现表明,肿瘤内细菌来源的基因毒素加速肿瘤转移,可能为癌症管理开辟新的诊断和治疗途径。
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引用次数: 0
Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19 颅-脑膜-脑轴刺突蛋白的持续存在可能导致COVID-19的神经系统后遗症
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2024-11-29 DOI: 10.1016/j.chom.2024.11.007
Zhouyi Rong, Hongcheng Mai, Gregor Ebert, Saketh Kapoor, Victor G. Puelles, Jan Czogalla, Senbin Hu, Jinpeng Su, Danilo Prtvar, Inderjeet Singh, Julia Schädler, Claire Delbridge, Hanno Steinke, Hannah Frenzel, Katja Schmidt, Christian Braun, Gina Bruch, Viktoria Ruf, Mayar Ali, Kurt-Wolfram Sühs, Ali Ertürk
SARS-CoV-2 infection is associated with long-lasting neurological symptoms, although the underlying mechanisms remain unclear. Using optical clearing and imaging, we observed the accumulation of SARS-CoV-2 spike protein in the skull-meninges-brain axis of human COVID-19 patients, persisting long after viral clearance. Further, biomarkers of neurodegeneration were elevated in the cerebrospinal fluid from long COVID patients, and proteomic analysis of human skull, meninges, and brain samples revealed dysregulated inflammatory pathways and neurodegeneration-associated changes. Similar distribution patterns of the spike protein were observed in SARS-CoV-2-infected mice. Injection of spike protein alone was sufficient to induce neuroinflammation, proteome changes in the skull-meninges-brain axis, anxiety-like behavior, and exacerbated outcomes in mouse models of stroke and traumatic brain injury. Vaccination reduced but did not eliminate spike protein accumulation after infection in mice. Our findings suggest persistent spike protein at the brain borders may contribute to lasting neurological sequelae of COVID-19.
SARS-CoV-2感染与长期的神经系统症状有关,尽管其潜在机制尚不清楚。利用光学清除和成像技术,我们观察到SARS-CoV-2刺突蛋白在人类COVID-19患者的头骨-脑膜-脑轴中积累,并在病毒清除后持续很长时间。此外,长期COVID患者脑脊液中神经退行性变的生物标志物升高,人类头骨、脑膜和脑样本的蛋白质组学分析显示炎症通路失调和神经退行性变相关变化。在sars - cov -2感染小鼠中观察到类似的刺突蛋白分布模式。在脑卒中和创伤性脑损伤小鼠模型中,单独注射刺突蛋白足以诱导神经炎症、颅-脑膜-脑轴蛋白质组改变、焦虑样行为和加重预后。在小鼠感染后,接种疫苗减少但没有消除刺突蛋白的积累。我们的研究结果表明,大脑边界持续的刺突蛋白可能导致COVID-19持续的神经系统后遗症。
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