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Metabolic tug-of-war: Mitochondria starve Toxoplasma of folate 代谢拉锯战:线粒体使弓形虫缺乏叶酸
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2025-10-08 DOI: 10.1016/j.chom.2025.09.002
Evie R. Hodgson, Diana Stojanovski
In a recent Science paper, Medeiros et al. describe how infected cells use mitochondria as metabolic guardians, outcompeting Toxoplasma parasites for folate, an essential vitamin for DNA synthesis. This metabolic immunity strategy transforms the cell’s powerhouse to an active defender, sequestering nutrients away from invaders in a metabolic tug-of-war.
在最近的一篇科学论文中,Medeiros等人描述了受感染的细胞如何利用线粒体作为代谢守护者,与弓形虫寄生虫竞争叶酸(DNA合成所必需的维生素)。这种代谢免疫策略将细胞的动力转化为积极的防御者,在新陈代谢的拔河中将营养物质从入侵者手中隔离开来。
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引用次数: 0
Misfortunes never come singly: Microbial metabolites link heart failure and chronic kidney disease 祸不单行:微生物代谢物与心力衰竭和慢性肾病有关
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2025-10-08 DOI: 10.1016/j.chom.2025.09.001
Jingyuan Fu, Nine V.A.M. Knoers
Heart failure is life threatening and common in chronic kidney disease patients. In this issue,1 Zheng et al. report that toxin-generating E. coli tryptophan metabolism induces myocardial apoptosis, contributing to heart failure risk with kidney dysfunction. The authors show that a probiotic product reduces this risk in preclinical and clinical settings.
心力衰竭是危及生命的,在慢性肾脏疾病患者中很常见。1 Zheng等人在本期报道了产毒大肠杆菌色氨酸代谢诱导心肌凋亡,增加心衰合并肾功能不全的风险。作者表明,益生菌产品在临床前和临床环境中降低了这种风险。
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引用次数: 0
Lost and found: Reconstituting PRR immune function through co-receptor transfer 失而复得:通过共受体转移重建PRR免疫功能
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2025-10-08 DOI: 10.1016/j.chom.2025.09.004
Francisco M. Gordillo-Cantón, Isabel Monte
Plant immune receptors hold great promise for engineering broad-spectrum disease resistance, but their effectiveness is very limited by restricted taxonomic functionality (RTF). In this issue of Cell Host & Microbe, Zhang et al. reveal that cross-species co-receptor transfer can overcome RTF in rice, pointing to new strategies for crop protection.
植物免疫受体在广谱抗病性工程方面具有广阔的应用前景,但其有效性受到限制性分类功能(RTF)的限制。Zhang等人在本期《Cell Host &; Microbe》中揭示了跨物种共受体转移可以克服水稻的RTF,为作物保护提供了新的策略。
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引用次数: 0
Carving out the microbiota of Earth’s largest biomass reservoir 雕刻出地球上最大的生物资源库的微生物群
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2025-10-08 DOI: 10.1016/j.chom.2025.09.008
Moshe Alon, Omri M. Finkel
Despite being an essential part of terrestrial ecosystems for ∼400 million years, the microbiome of wood is surprisingly underexplored. In a recent issue of Nature, Arnold et al. make a long overdue dive into the unique and surprisingly diverse prokaryotic and fungal communities of heartwood and sapwood.
尽管作为陆地生态系统的重要组成部分已有4亿年的历史,但令人惊讶的是,木材的微生物群尚未得到充分的探索。在最近一期的《自然》杂志上,阿诺德等人对心材和边材的独特和令人惊讶的多样化的原核生物和真菌群落进行了长期的深入研究。
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引用次数: 0
Metabolic clash of Cryptosporidium and its host 隐孢子虫及其宿主的代谢冲突
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2025-10-08 DOI: 10.1016/j.chom.2025.09.011
Simona Seizova, Christopher J. Tonkin
In recent papers published in Cell and Cell Host and Microbe, Marzook et al. and Huang et al. investigate how Cryptosporidium, an enteric parasite, can acquire nutrients from its host and deals with potentially toxic products. These studies highlight that transporters are likely key to the success of this parasite.
在最近发表在Cell and Cell Host and Microbe杂志上的论文中,Marzook等人和Huang等人研究了肠道寄生虫隐孢子虫(Cryptosporidium)如何从宿主那里获取营养并处理潜在的有毒产物。这些研究强调,转运蛋白可能是这种寄生虫成功的关键。
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引用次数: 0
The HY5-NPR1 module governs light-dependent virulence of a plant bacterial pathogen HY5-NPR1模块控制植物细菌病原体的光依赖性毒力
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2025-10-07 DOI: 10.1016/j.chom.2025.09.016
Pengtao Liu, Zhao Zhao, Yaqi Tang, Yangyang Zhou, Jie Liu, Kaiqi Xu, Yaxin Chen, Xiaoting Li, Yaru Tang, Li Yang
(Cell Host & Microbe 33, 1606–1622.e1–e10; September 10, 2025)
(细胞宿主与微生物33,1606-1622.e1-e10; 2025年9月10日)
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引用次数: 0
Immunometabolic reprogramming of macrophages by gut microbiota-derived cadaverine controls colon inflammation 肠道微生物源性尸胺对巨噬细胞的免疫代谢重编程控制结肠炎症
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2025-09-30 DOI: 10.1016/j.chom.2025.09.009
Rodrigo de Oliveira Formiga, Qing Li, Yining Zhao, Márcio Augusto Campos Ribeiro, Perle Guarino-Vignon, Rand Fatouh, Leonard Dubois, Laura Creusot, Virginie Puchois, Salomé Amouyal, Iria Alonso Salgueiro, Marius Bredon, Loïc Chollet, Tatiana Ledent, Cyril Scandola, Jean-Philippe Auger, Camille Danne, Gerhard Krönke, Emma Tkacz, Patrick Emond, Harry Sokol
Cadaverine is a polyamine produced by the gut microbiota with links to health and disease, notably inflammatory bowel disease (IBD). Here, we show that cadaverine shapes monocyte-macrophage immunometabolism in a context- and concentration-dependent fashion to impact macrophage functionality. At baseline, cadaverine is taken up via L-lysine transporters and activates the thioredoxin system, while during inflammation, cadaverine signals through aconitate decarboxylase 1 (Acod1)-itaconate. Both pathways induce activation of transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2), which supports mitochondrial respiration and promotes immunoregulatory macrophage polarization. Conversely, under higher concentrations, cadaverine acts via histamine 4 receptor, leading to glycolysis-driven inflammation and pro-inflammatory functions in macrophages. Likewise, cadaverine exhibits paradoxical effects in experimental colitis, either protective or detrimental, evoking opposite fates on macrophages depending on levels dictated by Enterobacteriaceae. In IBD patients, elevated cadaverine correlated with higher flare risk. Our findings implicate cadaverine as a microbiota-derived metabolite manipulating macrophage energy metabolism with consequences in intestinal inflammation and implications for IBD pathogenesis.
尸胺是一种由肠道菌群产生的多胺,与健康和疾病有关,尤其是炎症性肠病(IBD)。在这里,我们表明尸胺以环境和浓度依赖的方式影响单核细胞-巨噬细胞的免疫代谢,从而影响巨噬细胞的功能。在基线时,尸胺通过l -赖氨酸转运体被吸收并激活硫氧还蛋白系统,而在炎症期间,尸胺通过aconitate decarboxylase 1 (Acod1)- itacon酸发出信号。这两种途径都诱导转录因子、核因子红细胞2相关因子2 (Nrf2)的激活,支持线粒体呼吸,促进免疫调节性巨噬细胞极化。相反,在较高浓度下,尸胺通过组胺4受体起作用,导致巨噬细胞糖酵解驱动的炎症和促炎功能。同样,尸胺在实验性结肠炎中表现出矛盾的作用,要么是保护性的,要么是有害的,根据肠杆菌科决定的水平,对巨噬细胞产生相反的命运。在IBD患者中,尸胺升高与更高的发作风险相关。我们的研究结果表明尸胺作为一种微生物衍生的代谢物,操纵巨噬细胞的能量代谢,影响肠道炎症和IBD的发病机制。
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引用次数: 0
A bacterial signal coordinates plant-microbe fitness trade-off to enhance sulfur deficiency tolerance in plants 细菌信号协调植物与微生物的适应度权衡,以增强植物的硫缺乏耐受性
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2025-09-26 DOI: 10.1016/j.chom.2025.09.007
Arijit Mukherjee, Mrinmoy Mazumder, Arun Verma, Hitesh Tikariha, Raktim Bhattacharya, Qi En Ooi, Sanjay Swarup
Plant-associated microorganisms interact with each other and with host plants via intricate chemical signals, offering multiple benefits, including enhanced nutrition. We report a mechanism through which the rhizosphere microbiome improves plant growth under sulfur (S) deficiency. Disruption of plant S homeostasis caused a coordinated shift in the composition and S-metabolism of the rhizosphere microbiome. Leveraging this, we developed an 18-membered synthetic rhizosphere bacterial community (SynCom) that rescued the growth of Arabidopsis and a leafy Brassicaceae vegetable under S-deficiency. This beneficial trait is taxonomically widespread among SynCom members, with bacterial pairs providing both synergistic and neutral effects on host growth. Notably, stronger competitive interactions among SynCom members conferred greater fitness benefits to the host, suggesting a trans-kingdom (plant-microbe) fitness trade-off. Finally, guided chemical screening, deletion knockout mutants, and targeted metabolomics identified and validated microbially released glutathione (GSH) as the necessary bioactive signal that coordinates the trans-kingdom fitness trade-off and improves plant growth under sulfur limitation.
植物相关微生物通过复杂的化学信号相互作用,并与寄主植物相互作用,提供多种益处,包括增强营养。我们报告了一个机制,通过根际微生物组促进植物生长的硫(S)缺乏。植物S稳态的破坏引起根际微生物组组成和S代谢的协调变化。利用这一点,我们开发了一个由18个成员组成的合成根际细菌群落(SynCom),该群落在缺s条件下挽救了拟南芥和芸苔科绿叶蔬菜的生长。这种有益的性状在SynCom成员中广泛存在,细菌对对宿主生长既有协同作用,也有中性作用。值得注意的是,SynCom成员之间更强的竞争相互作用给宿主带来了更大的适应性利益,这表明存在跨界(植物-微生物)适应性权衡。最后,通过指导化学筛选、缺失敲除突变体和靶向代谢组学,鉴定并验证了微生物释放的谷胱甘肽(GSH)是协调跨界适应性权衡和改善硫限制下植物生长的必要生物活性信号。
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引用次数: 0
A Bacteroides fragilis protease activates host PAR2 to induce intestinal pain and inflammation 脆弱拟杆菌蛋白酶激活宿主PAR2诱导肠道疼痛和炎症
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2025-09-26 DOI: 10.1016/j.chom.2025.09.010
Markus Lakemeyer, Rocco Latorre, Kristyna Blazkova, Hannah M. Wood, Dane D. Jensen, Nayab Shakil, Scott C. Thomas, Deepak Saxena, Yatendra Mulpuri, David Poolman, Paz Duran, Laura J. Keller, David E. Reed, Brian L. Schmidt, Néstor N. Jiménez-Vargas, Fangxi Xu, Alan E. Lomax, Nigel W. Bunnett, Matthew Bogyo
Protease-activated receptor 2 (PAR2) is a central regulator of intestinal barrier function, inflammation, and pain. Upregulated intestinal proteolysis and PAR2 signaling are implicated in inflammatory bowel diseases (IBDs) and irritable bowel syndrome (IBS), conditions often associated with gut microbiome alterations. To identify potential bacterial regulators of PAR2 activity, we developed a functional assay for PAR2 processing to screen a library of diverse gut microbes. We identify multiple bacteria that secrete proteases capable of cleaving host PAR2. Using chemoproteomic profiling with a covalent irreversible inhibitor, we uncovered a previously uncharacterized Bacteroides fragilis serine protease 1 (Bfp1) and show that it cleaves and activates PAR2 in multicellular and murine models. PAR2 cleavage by Bfp1 disrupts the intestinal barrier, sensitizes nociceptors, and triggers colonic inflammation and abdominal pain. Collectively, our findings uncover Bfp1-mediated PAR2 processing as an axis of host-commensal interaction in the gut that has the potential to be targeted for therapeutic intervention in IBD or IBS.
蛋白酶激活受体2 (PAR2)是肠屏障功能、炎症和疼痛的中枢调节因子。肠道蛋白水解和PAR2信号的上调与炎症性肠病(IBDs)和肠易激综合征(IBS)有关,这些疾病通常与肠道微生物组改变有关。为了确定PAR2活性的潜在细菌调节因子,我们开发了一种PAR2加工的功能测定方法来筛选不同的肠道微生物库。我们鉴定出多种细菌分泌能够切割宿主PAR2的蛋白酶。利用一种共价不可逆抑制剂的化学蛋白质组学分析,我们发现了一种以前未被表征的脆弱拟杆菌丝氨酸蛋白酶1 (Bfp1),并表明它在多细胞和小鼠模型中切割和激活PAR2。Bfp1裂解PAR2破坏肠道屏障,使痛觉感受器敏感,引发结肠炎症和腹痛。总的来说,我们的研究结果揭示了bfp1介导的PAR2加工作为肠道宿主-共生相互作用的一个轴,有可能成为IBD或IBS治疗干预的靶点。
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引用次数: 0
The microbiota extends the reproductive lifespan of mice by safeguarding the ovarian reserve 微生物群通过保护卵巢储备来延长小鼠的生殖寿命
IF 30.3 1区 医学 Q1 MICROBIOLOGY Pub Date : 2025-09-25 DOI: 10.1016/j.chom.2025.09.006
Sarah K. Munyoki, Julie P. Goff, Amanda Reshke, Erin Wilderoter, Nyasha Mafarachisi, Antonija Kolobaric, Yi Sheng, Steven J. Mullett, Gabrielle E. King, Jacob D. DeSchepper, Richard J. Bookser, Carlos A. Castro, Stacy L. Gelhaus, Mayara Grizotte-Lake, Kathleen E. Morrison, Anthony J. Zeleznik, Timothy W. Hand, Miguel A. Brieño-Enriquez, Eldin Jašarević
Infertility affects one in six people, but the underlying mechanisms remain unclear. We show that the microbiota governs female reproductive longevity in mice. Germ-free mice have fewer primordial follicles, increased atresia, and ovarian fibrosis, leading to smaller litters, fewer offspring, and a shorter reproductive lifespan. Germ-free mice are born with a similar ovarian reserve but display excessive activation, impaired progression, and increased atresia during post-natal development. Microbiome colonization during a critical post-natal window rescues premature ovarian reserve loss by normalizing follicle kinetics and gene expression patterns. These changes parallel increased short-chain fatty acids (SCFAs), and SCFA administration mitigates ovarian dysfunction in germ-free mice. Similar oocyte dysfunction occurred in conventionally raised mice fed a high-fat diet, but additional dietary fiber helped preserve oocyte quality and embryo competence. Thus, host-microbe interactions shape female fertility, and microbiota-targeted interventions may offer strategies to address reproductive disorders.
六分之一的人患有不孕症,但其潜在机制尚不清楚。我们表明,微生物群控制着雌性小鼠的生殖寿命。无菌小鼠的原始卵泡减少,闭锁增加,卵巢纤维化,导致产仔少,后代少,生殖寿命短。无菌小鼠出生时具有类似的卵巢储备,但在出生后发育过程中表现出过度激活、进展受损和闭锁增加。微生物定植在一个关键的产后窗口挽救卵巢储备的损失通过正常化卵泡动力学和基因表达模式。这些变化与短链脂肪酸(SCFA)增加平行,SCFA管理减轻无菌小鼠卵巢功能障碍。类似的卵母细胞功能障碍发生在喂食高脂肪饮食的常规饲养小鼠中,但额外的膳食纤维有助于保持卵母细胞质量和胚胎能力。因此,宿主-微生物的相互作用塑造了女性的生育能力,微生物群靶向干预可能为解决生殖障碍提供策略。
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引用次数: 0
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Cell host & microbe
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