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Socioeconomic position and the gut microbiota: a narrative synthesis of the association and recommendations. 社会经济地位和肠道微生物群:关联和建议的叙述综合。
IF 12.2 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2026-01-31 DOI: 10.1080/19490976.2026.2623356
Jasmine Samantha Ratcliff,Meena Kumari,Patrick Varga-Weisz,Rick O'Gorman
Evidence suggests that socioeconomic position (SEP) may shape the gut microbiota (GM), representing a mechanism through which social and environmental factors may drive health inequalities, yet no systematic review has examined this association. In this narrative systematic review, we searched PubMed, Web of Science, and Scopus up to 30 November 2024 for observational studies examining associations between measures of SEP and GM diversity, composition, or function in participants of any age, ethnicity, or location. We identified 1,479 unique studies, of which 26 met the inclusion criteria for this review. Associations were observed between SEP indicators and GM features, including alpha (α) and beta (β) diversity, taxonomic composition, and functional pathways. Notably, socioeconomic patterns in α-diversity differed by context, with greater diversity observed in advantaged groups in high-income countries (HICs) but in disadvantaged groups in low- and middle-income countries (LMICs). Differences in β-diversity suggest that advantaged and disadvantaged groups have distinct GM profiles. Furthermore, considerable heterogeneity was evident across studies, particularly in sampling, sequencing, and analytical methods. Overall, socioeconomic-related differences in the GM are evident globally, highlighting the microbiota as a potential target for interventions aimed at reducing health disparities. Further research employing larger and more diverse cohorts, longitudinal designs, metagenomic sequencing approaches, and comprehensive measurement and adjustment of key covariates is needed to deepen understanding of this relationship.
有证据表明,社会经济地位(SEP)可能会影响肠道微生物群(GM),这是社会和环境因素可能导致健康不平等的一种机制,但尚未有系统的综述研究这种关联。在这篇叙叙性系统综述中,我们检索了PubMed、Web of Science和Scopus,检索了截至2024年11月30日的观察性研究,研究了任何年龄、种族或地点的参与者中SEP和转基因多样性、组成或功能之间的关系。我们确定了1479项独特的研究,其中26项符合本综述的纳入标准。SEP指标与转基因特征(α (α)和β (β)多样性、分类组成和功能通路)之间存在相关性。值得注意的是,α-多样性的社会经济模式因环境而异,在高收入国家(HICs)的优势群体中观察到更大的多样性,而在低收入和中等收入国家(LMICs)的弱势群体中观察到更大的多样性。β多样性的差异表明,优势群体和弱势群体具有不同的转基因概况。此外,相当大的异质性在研究中是明显的,特别是在采样,测序和分析方法。总体而言,基因改造中与社会经济相关的差异在全球范围内是明显的,这突出表明微生物群是旨在减少健康差距的干预措施的潜在目标。进一步的研究需要采用更大、更多样化的队列、纵向设计、宏基因组测序方法以及对关键协变量的综合测量和调整来加深对这种关系的理解。
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引用次数: 0
Precise probiotic therapy: Advances, bottlenecks, and the road to microbiome-informed nutrition. 精确的益生菌治疗:进展,瓶颈,以及通往微生物营养的道路。
IF 12.2 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2026-01-30 DOI: 10.1080/19490976.2026.2623359
Yuesong Jiang,Shuaiming Jiang,Zhengting Wang,Pengfei Zhu,Jiachao Zhang,Fei Teng,Shi Huang
The human gut microbiome is a cornerstone of health, yet conventional probiotic therapies often exhibit limited efficacy owing to heterogeneity in host-microbe-environment dynamics. This review dissects the biological and environmental drivers of such variability and highlights emerging frameworks that integrate cross-sectional and longitudinal multi-omics data to predict probiotic treatment outcomes and host metabolic responses. We further spotlight breakthroughs in methodological development in efficient mining and engineering of probiotic strains, which enable the rational design of functionally enhanced, personalized probiotics. By synthesizing these advances, the review underscores the transformative potential of combining data-driven models with precision-engineered microbial therapeutics to address current limitations and usher in a new era of future microbiome-informed nutrition and personalized interventions.
人类肠道微生物群是健康的基石,但由于宿主-微生物-环境动力学的异质性,传统的益生菌疗法往往表现出有限的疗效。这篇综述剖析了这种变异的生物学和环境驱动因素,并强调了整合横向和纵向多组学数据来预测益生菌治疗结果和宿主代谢反应的新兴框架。我们进一步关注益生菌菌株高效开采和工程方法发展的突破,这使得合理设计功能增强的个性化益生菌成为可能。通过综合这些进展,该综述强调了将数据驱动模型与精确工程微生物疗法相结合的变革潜力,以解决当前的局限性,并开创未来微生物组信息营养和个性化干预的新时代。
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引用次数: 0
Muribaculum intestinale negatively impacts glioma growth in mice through the toll-like receptor 2. 肠道Muribaculum通过toll样受体2对小鼠神经胶质瘤生长产生负面影响。
IF 12.2 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2026-01-30 DOI: 10.1080/19490976.2026.2623349
Francesco Marrocco,Germana Cocozza,Fabrizio Antonangeli,Rizwan Khan,Giuseppe Pietropaolo,Abdechakour Elkihel,Gabriele Favaretto,Xingzi Lin,Romina Mancinelli,Ludovica Maria Busdraghi,Alice Reccagni,Gianluca Scarno,Giuseppe Sciumè,Mattia Laffranchi,Ling Peng,Valerio Iebba,Silvano Sozzani,Giuseppina D'Alessandro,Cristina Limatola
Glioblastoma (GBM) is the most common and malignant brain tumor in adult humans. Recent studies have demonstrated a link between the composition of the gut microbiota and glioma progression. Here, we describe that the growth of glioma in mice is inversely correlated with the relative abundance of the anaerobic bacterium Muribaculum intestinale in the feces. We found that M. intestinale administration: 1) induced an inflammatory environment in the gut; 2) reduced glioma growth; 3) increased the pro-inflammatory profile of tumor-associated microglial cells and the frequency of CD8+ T cells; and 4) increased the peripheral TNF-α levels. The effects induced by M. intestinale administration were significantly attenuated upon toll-like receptor 2 (TLR2) silencing using TLR2-targeting siRNA. As a pattern-recognition receptor, TLR2 detects microbial-associated molecular patterns and orchestrates host immune responses to infection. Collectively, these data demonstrate that M. intestinale induces a pro-inflammatory response in glioma bearing mice, inhibiting tumor growth via TLR2-dependent signaling.
胶质母细胞瘤(GBM)是成人最常见的恶性脑肿瘤。最近的研究表明,肠道微生物群的组成与胶质瘤的进展之间存在联系。在这里,我们描述了胶质瘤在小鼠体内的生长与粪便中厌氧细菌Muribaculum ininale的相对丰度呈负相关。我们发现:1)在肠道中诱导炎症环境;2)神经胶质瘤生长减少;3)增加肿瘤相关小胶质细胞的促炎谱和CD8+ T细胞的频率;4)外周血TNF-α水平升高。使用靶向TLR2的siRNA对toll样受体2 (toll-like receptor 2, TLR2)进行沉默处理后,大肠杆菌对TLR2的影响明显减弱。作为一种模式识别受体,TLR2检测微生物相关的分子模式并协调宿主对感染的免疫反应。总的来说,这些数据表明,m.n testinale在胶质瘤小鼠中诱导促炎反应,通过tlr2依赖性信号抑制肿瘤生长。
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引用次数: 0
Akkermansia muciniphila's nifJ gene enhances colostrum sIgA synthesis by branched-chain amino acid degradation to branched short-chain fatty acids. 嗜muciniphila的nifJ基因通过支链氨基酸降解成支链短链脂肪酸促进初乳sIgA合成。
IF 12.2 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2026-01-29 DOI: 10.1080/19490976.2026.2620128
Deyuan Wu,Fuyong Li,Wenyu Xiong,Zihao Huang,Kaidi Ma,Jun Huang,Sensen Cai,Jinping Deng,Jie Peng,Xiong Xia,Chengquan Tan
Colostrum secretory immunoglobulin A (sIgA) confers the first immune defense line for neonates to adapt to the external environment, while gut microbes have received attention for their high reactivity with sIgA. Here, we report that high levels of sIgA in sow colostrum are associated with the enrichment of Akkermansia muciniphila and branched-chain amino acid (BCAA) metabolism in the intestine. Mechanistically, we demonstrate through mice models that A. muciniphila-derived nifJ mediates BCAA degradation to branched short-chain fatty acids, which further enhance transforming growth factor-β (TGF-β) and C-C motif chemokine ligand 28 (CCL28) expression in mammary tissues through the G protein-coupled receptor pathway, ultimately increasing sIgA content in colostrum. These findings establish a mechanistic link between the maternal gut microbiota and offspring immune development, highlighting the specific functional localization of the nifJ gene of A. muciniphila.
初乳分泌免疫球蛋白A (sIgA)是新生儿适应外界环境的第一道免疫防线,肠道微生物因其对sIgA的高反应性而备受关注。在这里,我们报道母猪初乳中高水平的sIgA与嗜粘阿克曼氏菌的富集和肠内支链氨基酸(BCAA)代谢有关。在机制上,我们通过小鼠模型证明了A. muciniphila衍生的nifJ介导BCAA降解为支链短链脂肪酸,通过G蛋白偶联受体途径进一步增强乳腺组织中转化生长因子-β (TGF-β)和C-C基序列趋化因子配体28 (CCL28)的表达,最终增加初乳中sIgA的含量。这些发现建立了母体肠道微生物群与后代免疫发育之间的机制联系,突出了嗜粘杆菌nifJ基因的特定功能定位。
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引用次数: 0
Fusobacterium nucleatum plays a pathogenic role in a murine model of irritable bowel syndrome by modulating intestinal purine metabolism and promoting mast cell activation. 核梭杆菌通过调节肠嘌呤代谢和促进肥大细胞活化,在肠易激综合征小鼠模型中起致病作用。
IF 12.2 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2026-01-28 DOI: 10.1080/19490976.2026.2620124
Songyuan Hou,Tingting Ning,Si Liu,Xinyi Yang,Haozhen Ye,Yesheng Zhou,Chenxu Wang,Jiaqi Zhu,Shaochong Lu,Nan Zhang,Shengtao Zhu
Gut microbiota dysbiosis has been implicated in the pathogenesis of irritable bowel syndrome (IBS), a globally prevalent functional gastrointestinal disorder; however, mechanistic insights remain limited. We determined that the bacterium Fusobacterium nucleatum (F. nucleatum) played a pathogenic role in a murine model of IBS. Monocolonization of antibiotic-treated or germ-free mice with F. nucleatum induced IBS-like symptoms, including visceral hypersensitivity, increased fecal water content, and accelerated gastrointestinal transit, accompanied by mast cell activation. These effects were effectively prevented by treatment with the antibiotic metronidazole, as well as by the mast cell depleting agent imatinib or the mast cell stabilizer sodium cromoglicate. Mechanistically, F. nucleatum upregulated the expression of purine nucleoside phosphorylase (PNP) in intestinal epithelial cells (IECs), a key enzyme in the purine degradation pathway. The elevated PNP activity promoted purine degradation and uric acid production in IECs, which in turn directly activated mast cells. This F. nucleatum-driven mast cell activation mediated IBS-like symptoms in ABX treated mice but was abrogated by blocking uric acid synthesis. In summary, our findings highlight the crucial role of purine metabolism reprogramming and low-grade mucosal immune responses in F. nucleatum-mediated IBS-like symptoms in mice, providing promising therapeutic perspectives for targeting F. nucleatum-positive IBS patients.
肠道菌群失调与肠易激综合征(IBS)的发病机制有关,IBS是一种全球普遍存在的功能性胃肠道疾病;然而,机械的见解仍然有限。我们确定了核梭杆菌(F. nucleatum)在小鼠肠易激综合征模型中起致病作用。经抗生素处理或无菌的核仁梭菌小鼠单菌落诱导ibs样症状,包括内脏过敏、粪便含水量增加、胃肠道转运加速,并伴有肥大细胞活化。抗生素甲硝唑以及肥大细胞消耗剂伊马替尼或肥大细胞稳定剂克罗莫格利酸钠可有效预防这些影响。在机制上,核梭菌上调肠上皮细胞(IECs)嘌呤核苷磷酸化酶(PNP)的表达,PNP是嘌呤降解途径的关键酶。PNP活性的升高促进了iec中嘌呤降解和尿酸的产生,进而直接激活肥大细胞。这种核胞梭菌驱动的肥大细胞激活在ABX治疗小鼠中介导ibs样症状,但通过阻断尿酸合成而消除。总之,我们的研究结果强调了嘌呤代谢重编程和低级别粘膜免疫反应在F. nucleatum介导的小鼠IBS样症状中的关键作用,为针对F. nucleatum阳性IBS患者提供了有希望的治疗前景。
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引用次数: 0
Self-aggregating Lactiplantibacillus plantarum enhances type-I interferon responses via the cytosolic sensors NOD2 and cGAS. 自聚集植物乳杆菌通过细胞质传感器NOD2和cGAS增强i型干扰素应答。
IF 12.2 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2026-01-28 DOI: 10.1080/19490976.2026.2615490
Selvin Solis,Elaina M Maldonado,Subhankar Mukhopadhyay,Gwénaël Jan,José María Landete,Carlos Maluquer de Motes,Jorge Gutierrez-Merino
The gut microbiome plays a critical role in health, disease and immunity. To date, we have access to large datasets describing how the microbial diversity present in the gut correlates with many clinical conditions. However, the microbiome composition is taxonomically complex; influenced by many environmental factors; and variable between individuals and communities, thereby limiting functional and mechanistic insights into the microbiota‒host interactions. We are still unsure of the molecular mechanisms by which gut commensal microbes intrinsically possess to interact with the immune system and induce beneficial responses. This study has addressed this important question by revealing that only certain members of Lactobacillaceae, a bacterial family very well known for its probiotic properties, interact very intimately with macrophages because of their ability to simultaneously overexpress adhesive cell wall proteins and to self-aggregate, leading to significant production of type I interferon (IFN-I) cytokines. IFN-I cytokines are essential to confer protection against viral infections and auto-immune disorders. Specifically, we have proved that this enhanced IFN-I feature is strain-dependent and predominantly driven by cGAS, a molecule that activates the cytosolic sensor STING upon the recognition of bacterial DNA. Furthermore, another cytosolic sensor, NOD2, seems to be an additional stimulus to amplify IFN-I production, suggesting the involvement of successive molecular events for a prominent probiotic response. Our findings provide insight into how specific molecules of probiotic bacteria modulate or stimulate host responses, providing a better understanding of the molecular crosstalk between the microbiome and immune cells.
肠道微生物群在健康、疾病和免疫中起着至关重要的作用。迄今为止,我们已经获得了描述肠道微生物多样性如何与许多临床条件相关的大型数据集。然而,微生物组的组成在分类上是复杂的;受多种环境因素影响的;并且在个体和群落之间是可变的,从而限制了对微生物-宿主相互作用的功能和机制的了解。我们仍然不确定肠道共生微生物内在地与免疫系统相互作用并诱导有益反应的分子机制。这项研究通过揭示乳酸菌科(一个以益生菌特性而闻名的细菌家族)的某些成员与巨噬细胞非常密切地相互作用来解决这个重要问题,因为它们能够同时过度表达粘附细胞壁蛋白和自聚集,从而导致I型干扰素(IFN-I)细胞因子的显著产生。IFN-I细胞因子对病毒感染和自身免疫疾病的保护至关重要。具体来说,我们已经证明了这种增强的IFN-I特征是菌株依赖的,主要由cGAS驱动,cGAS是一种分子,在识别细菌DNA时激活细胞质传感器STING。此外,另一种细胞质传感器NOD2似乎是放大IFN-I产生的额外刺激,表明一系列分子事件参与了显著的益生菌反应。我们的研究结果为益生菌的特定分子如何调节或刺激宿主反应提供了见解,为微生物组和免疫细胞之间的分子串扰提供了更好的理解。
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引用次数: 0
The enteric DNA virome differs in infants at risk for atopic disease. 肠道DNA病毒组在婴儿特应性疾病的风险中是不同的。
IF 12.2 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2026-01-27 DOI: 10.1080/19490976.2026.2616066
Tyrus J Perdue,Cassandra E Newkirk,Robert Beblavy,Antti E Seppo,Erin C Davis,Michael B Sohn,Kirsi M Järvinen,Cynthia L Monaco
Atopic disease prevalence, including atopic dermatitis, food allergy, asthma, and allergic rhinitis, has risen dramatically in industrialized countries. Traditional, single family farming lifestyles protect against atopic disease, but the mechanisms are incompletely understood. While there are established epidemiologic connections between childhood respiratory viral infections and the infant gut bacterial microbiome with allergic disease development, the influence of the early enteric virome on atopic disease development is unknown. We analyzed the enteric virome in 131 infants from high-atopy-risk urban/suburban environments and low-atopic-risk single-family farming communities. While similar at 12 months, enteric bacteriophage communities significantly differed by farm-life versus urban lifestyle at six weeks and six months of age. A lifestyle protective from atopic disease demonstrated higher colonization rates of Bifidobacterium longum subsp. infantis (B. infantis), an important beneficial commensal, with phageome communities differing in infants colonized by B. infantis at all time points. Simultaneously, Mastadenovirus and Bocaparvovirus were more prevalent in urban infant stools at six months of age. Sparser phage-phage networks were found at all timepoints in infants who later developed atopic disease. These data suggest that the early infant enteric DNA virome develops differently in farming and urban lifestyles and may factor into risk of atopic disease development.
包括特应性皮炎、食物过敏、哮喘和过敏性鼻炎在内的特应性疾病患病率在工业化国家急剧上升。传统的单一家庭农业生活方式可以预防特应性疾病,但其机制尚不完全清楚。虽然儿童呼吸道病毒感染与婴儿肠道细菌微生物组与过敏性疾病发展之间存在既定的流行病学联系,但早期肠道病毒对特应性疾病发展的影响尚不清楚。我们分析了来自高特应性风险城市/郊区环境和低特应性风险单一家庭农业社区的131名婴儿的肠道病毒。虽然在12个月大时相似,但在6周和6个月大时,肠道噬菌体群落因农场生活方式和城市生活方式而显著不同。预防特应性疾病的生活方式表明长双歧杆菌亚种的定植率较高。婴儿(B. infantis)是一种重要的有益共生菌,在所有时间点被婴儿B. infantis定植的婴儿中,噬菌体群落不同。同时,乳房腺病毒和Bocaparvovirus在6个月大的城市婴儿粪便中更为普遍。在后来发展为特应性疾病的婴儿中,在所有时间点都发现了稀疏的噬菌体网络。这些数据表明,早期婴儿肠道DNA病毒组在农业和城市生活方式中发育不同,并可能影响特应性疾病发展的风险。
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引用次数: 0
Gut bacteria presence in the brain is increased after ischemic stroke in mice. 小鼠缺血性中风后,大脑中存在的肠道细菌增加。
IF 12.2 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2026-01-26 DOI: 10.1080/19490976.2026.2617694
Alex Peh,Evany Dinakis,Michael Nakai,Rikeish R Muralitharan,Samoda Rupasinghe,Jenny L Wilson,Connie H Y Wong,Hamdi A Jama,Charlotte M O Barker,Mahnaz Modarresi,Barbara K Kemp-Harper,Tenghao Zheng,Francine Z Marques,Brad R S Broughton
Systemic infections are a common cause of complications and death after stroke. These infections can occur due to the breakdown of the gut epithelial barrier and the translocation of bacteria from the gut to peripheral systemic tissues. However, it remains unclear whether gut bacteria also translocate to the brain and contribute to stroke-induced neuronal damage. In this study, we observed a significant number of peptidoglycan- and lipopolysaccharide-positive bacteria in the ischemic hemisphere of mice subjected to either photothrombotic (PT) stroke or middle cerebral artery occlusion (MCAO). In contrast, no bacteria were observed in the ischemic brains of germ-free mice following MCAO. Absolute quantification via PCR also revealed increased bacteria in the ischemic hemisphere and blood of PT mice. Bacterial translocation to the brain is associated with the breakdown of the gut-epithelial and blood-brain barriers. Although inhibition of sympathetic tone reduces gut-epithelial barrier permeability, the bacterial load in the brain and functional deficits poststroke, it does not affect cerebral apoptosis, neuroinflammation or infarct volume. Collectively, these findings indicate that activation of the sympathetic nervous system after stroke promotes the migration of gut-derived bacteria into the ischemic brain, and this process worsens motor function in mice.
全身感染是中风后并发症和死亡的常见原因。这些感染可能是由于肠道上皮屏障的破坏和细菌从肠道转移到周围系统组织而发生的。然而,目前尚不清楚肠道细菌是否也会转移到大脑并导致中风引起的神经元损伤。在这项研究中,我们观察到在遭受光血栓性中风(PT)或大脑中动脉闭塞(MCAO)的小鼠的缺血半球中有大量肽聚糖和脂多糖阳性细菌。相比之下,MCAO后无菌小鼠缺血脑内未观察到细菌。PCR的绝对定量也显示了PT小鼠缺血半球和血液中细菌的增加。细菌向大脑的移位与肠上皮和血脑屏障的破坏有关。虽然抑制交感神经张力降低了肠上皮屏障的通透性、脑内细菌负荷和脑卒中后的功能缺陷,但它不影响脑凋亡、神经炎症或梗死体积。总的来说,这些发现表明,中风后交感神经系统的激活促进了肠道来源的细菌迁移到缺血的大脑,这一过程恶化了小鼠的运动功能。
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引用次数: 0
Distinct T and innate-like lymphocyte reprogramming following lyophilized fecal microbiota transplantation in recurrent C. difficile infection. 复发性难辨梭菌感染的冻干粪便微生物群移植后不同的T细胞和先天样淋巴细胞重编程。
IF 12.2 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2026-01-23 DOI: 10.1080/19490976.2026.2620127
Yunfeng Gao,Shima Shahbaz,Shokrollah Elahi,Tanya M Monaghan, ,Dina Kao
Fecal microbiota transplantation (FMT) is highly effective in preventing recurrent Clostridioides difficile infection (rCDI), yet its immunological mechanisms remain poorly defined. While bacterial engraftment and recovery of microbial diversity are central to FMT efficacy, accumulating evidence suggests that host immune reprogramming is involved. In murine models, regulatory CD4⁺ T cells are indispensable for clearing C. difficile. To address this mechanistic gap, we examined systemic immune reprogramming following FMT by performing flow cytometry and single-cell RNA sequencing (scRNA-seq) on a subset of successfully treated participants from a clinical trial comparing lyophilized FMT (LFMT) with lyophilized sterile fecal filtrate (LSFF, no live bacteria) for preventing rCDI. Flow cytometry was performed on peripheral mononuclear cells from 19 LFMT recipients and 18 LSFF recipients, and scRNA-seq analysis was performed on two LFMT recipients. Although flow cytometry results did not show significant changes in the assessed markers after rCDI resolution in either treatment group, exploratory scRNA-seq in the two LFMT recipients revealed distinct LFMT-associated transcriptional signatures across adaptive and innate-like lymphocyte populations. LFMT was associated with upregulated activation and regulatory genes (CD69, STAT1, TOX, RORA, FOXP3) in CD4⁺ and CD8⁺ T cells, suggesting enhanced immune regulation with reduced cytotoxic gene expression (GZMB, PRF1, GNLY). Innate-like lymphocytes displayed broad activation, with natural killer cells showing increased KLRD1, PRF1, and IL2RB and mucosal-associated invariant T cells (MAIT cells) upregulating STAT1, JUN, and RORA while downregulating KLRB1 and STAT3. These transcriptional programs are consistent with recalibration of T cell homeostasis and innate-like lymphocyte activation, potentially driven by microbial restoration. Collectively, this exploratory study provides the first single-cell immune atlas of LFMT in rCDI, identifying coordinated activation of regulatory, effector, and innate immune pathways. Given the small sample size, these findings should be considered hypothesis-generating, requiring validation in larger cohorts.
粪便微生物群移植(FMT)在预防复发性艰难梭菌感染(rCDI)方面非常有效,但其免疫学机制仍不明确。虽然细菌植入和微生物多样性的恢复是FMT疗效的核心,但越来越多的证据表明,宿主免疫重编程也参与其中。在小鼠模型中,调节性CD4 + T细胞对于清除艰难梭菌是必不可少的。为了解决这一机制上的差距,我们通过流式细胞术和单细胞RNA测序(scRNA-seq)对一组成功治疗的参与者进行了FMT后的系统性免疫重编程,这些参与者来自一项比较冻干FMT (LFMT)和冻干无菌粪便滤液(LSFF,无活细菌)预防rCDI的临床试验。对19例LFMT受体和18例LSFF受体的外周单核细胞进行流式细胞术检测,对2例LFMT受体进行scRNA-seq分析。尽管流式细胞术结果没有显示两组治疗组在rCDI溶解后评估的标记物发生显著变化,但在两个LFMT受体中探索性scRNA-seq显示了适应性和先天样淋巴细胞群中不同的LFMT相关转录特征。LFMT与CD4 +和CD8 + T细胞中活化和调控基因(CD69、STAT1、TOX、RORA、FOXP3)上调相关,提示通过降低细胞毒性基因(GZMB、PRF1、GNLY)表达增强免疫调节。先天样淋巴细胞表现出广泛的激活,自然杀伤细胞显示KLRD1、PRF1和IL2RB增加,粘膜相关不变T细胞(MAIT细胞)上调STAT1、JUN和RORA,下调KLRB1和STAT3。这些转录程序与T细胞稳态的重新校准和先天样淋巴细胞激活一致,可能是由微生物恢复驱动的。总的来说,这项探索性研究提供了rCDI中LFMT的第一个单细胞免疫图谱,确定了调节、效应和先天免疫途径的协调激活。考虑到样本量小,这些发现应该被认为是假设生成,需要在更大的队列中验证。
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引用次数: 0
Mucin-degrading gut bacteria: context-dependent roles in intestinal homeostasis and disease. 黏液降解肠道细菌:肠道内稳态和疾病的环境依赖作用。
IF 12.2 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2026-01-23 DOI: 10.1080/19490976.2026.2614054
Eunike Tiffany,Kyoung Su Kim,Panida Sittipo,Dong-Woo Lee,Yun Kyung Lee
Akkermansia muciniphila, Bacteroides thetaiotaomicron, Mediterraneibacter (formerly Ruminococcus) gnavus, and other mucin-degrading (MD) bacteria play pivotal roles in shaping gut microbial ecosystems, maintaining gut barrier function, and mediating host-microbiota crosstalk. These bacteria influence intestinal homeostasis by modulating epithelial cell differentiation, immune responses, and gut microbiota composition through mucin degradation and the production of bioactive metabolites. Their abundance and functional activities fluctuate dynamically in response to dietary components, host immunity, and environmental factors, resulting in context-dependent effects on gastrointestinal and systemic health. This review summarizes current insights into the ecology and metabolic capabilities of MD bacteria, highlighting their dual roles in metabolic disorders, inflammatory diseases, infection susceptibility, and neuroimmune conditions. Understanding the ecological niches and molecular interactions of MD bacteria offers promising approaches for microbiota-targeted therapies aimed at restoring gut and systemic homeostasis.
嗜粘杆菌、拟杆菌(Bacteroides thetaiotaomicron)、地中海杆菌(mediterranean bacter,原Ruminococcus)和其他黏液降解(MD)细菌在塑造肠道微生物生态系统、维持肠道屏障功能和介导宿主-微生物群串音方面发挥着关键作用。这些细菌通过调节上皮细胞分化、免疫反应和肠道微生物群组成,通过粘蛋白降解和产生生物活性代谢物来影响肠道内稳态。它们的丰度和功能活性随着饮食成分、宿主免疫和环境因素的变化而动态波动,从而对胃肠道和全身健康产生依赖于环境的影响。本文综述了目前对MD细菌的生态学和代谢能力的研究,强调了它们在代谢紊乱、炎症性疾病、感染易感性和神经免疫疾病中的双重作用。了解MD细菌的生态位和分子相互作用为旨在恢复肠道和系统稳态的微生物群靶向治疗提供了有希望的方法。
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Gut Microbes
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