Gut Microbes肠道微生物
Gut Microbes(英文缩写 GUT MICROBES),ISSN 1949-0976,eISSN 1949-0984,中文译名:肠道微生物 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 9.434 | Q1 |
| 2022 | 12.200 | Q1 |
| 2023 | 12.200 | Q1 |
| 2024 | 11.000 | Q1 |
| 2025 | 15.300 | Q1 |
Gut Microbes 最新收录文献
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1. Discovery of dietary polyphenols targeting the autoinducer-2 quorum sensing system of pathogenic bacteria.
1. 靶向病原菌自诱导物-2群体感应系统的膳食多酚的发现PMID:日期:2026-10-03Targeting autoinducer-2 (AI-2) quorum sensing (QS) systems with dietary compounds represents a promising strategy to combat pathogens, yet mechanisms remain elusive. Here, we develop a machine learning-driven framework combining computational screening with multi-level experimental analysis to identify AI-2 quorum sensing interference molecules (QSIMs). A graph neural network (GNN)-based classifier (AI2IMpred) screens over 7000 phytochemicals and identifies dietary polyphenols as potent QSIMs. Using LT2 as a model, we demonstrate that 17 polyphenols, including pterostilbene, 4-methylcatechol, pyrogallol, and 3-methylcatechol, directly target LuxS and LsrB, as confirmed by SPR assays, while molecular docking predicts potential interactions with TqsA and LsrR. Structural analysis revealed that para-substituted hydrocarbyl groups enhance LsrB binding. Furthermore, polyphenol-mediated regulatory effects have been validated via gene expression modulation, bacterial phenotypes, NCM460 cell adhesion/invasion, and cross-pathogen analysis (, , and ). This work provides insights for the potential development of diet-based interventions using polyphenol compounds against drug-resistant pathogenic infections.
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2. Gut bacteria and their metabolites may influence our decisions, intelligence, cognition, and consciousness.
2. 肠道细菌及其代谢产物可能影响我们的决策、智力、认知和意识PMID:日期:2026-10-03The human gut hosts approximately 38 trillion bacteria, representing 400 to 500 species. Gut bacteria are in constant communication with the central nervous system (CNS) via the enteric nervous system (ENS), the peripheral nervous system (PNS), the autonomic nervous system (ANS), the immune system, the enteroendocrine system (EES), and the vagus nerve (VN). Short-chain fatty acids (SCFAs), especially butyrate, strengthen the blood-brain barrier (BBB) and modulate inflammatory signaling, thereby affecting brain function and cognitive performance. Acetate enhances the synthesis of lipid-rich myelin that protects neurons. Signaling molecules that cross the gut wall may optimize synaptic signaling in the frontal cortex. Bacterial metabolites that stimulate inflammatory responses activate the hypothalamic-pituitary-adrenal (HPA) axis, thereby increasing glucocorticoid production. This may reduce activity in the prefrontal cortex and suppress higher-order thinking and decision-making. We discuss how signaling molecules produced by gut bacteria influence the limbic system (thalamus, amygdala, hypothalamus, and hippocampus), primarily involved in emotions, memory, and motivation. The HPA axis and the gut microbiota-oligodendrocyte axis (GMOA) are discussed in more detail. We ask whether interactions between signaling molecules produced by gut bacteria and the limbic system can affect human intelligence, cognition, consciousness, and decision-making, coordinated by the cerebrum (cerebral cortex), prefrontal cortex, and parietal lobe.
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3. Personalized whole-body modeling links gut microbiota to metabolic perturbations in Alzheimer's disease.
3. 个性化全身建模将肠道微生物群与阿尔茨海默病中的代谢紊乱联系起来PMID:日期:2026-09-28The human gut microbiome has been linked to metabolic disturbances in Alzheimer's disease (AD). However, the mechanisms by which gut microbes might influence metabolic dysfunction in AD remain poorly understood. Previously, gut microbiome-personalized whole-body models of human metabolism have been applied to predict how altered gut microbiome compositions may influence metabolites in the blood of healthy aging individuals with increased risk of AD. However, these previous results have not been validated in AD. In this study, we aimed to test these prior predictions in a cohort of AD dementia patients and individuals with mild cognitive impairment (MCI) and a probable AD diagnosis. Therefore, we created gut microbiome-personalized whole-body metabolic models for 34 AD dementia patients, 51 MCI patients, and 298 healthy controls. These models were profiled to predict the metabolic influences of gut microbiomes on blood metabolites with previously reported alterations in AD. We found increased capacities of the host-microbiome co-metabolism to produce S-adenosyl-L-methionine, L-arginine, creatine, taurine, and formate in the blood of AD patients. The metabolic predictions were then linked to key microbial taxa using a novel method that combines modeling-informed prediction sensitivity to alternative microbial abundances with LASSO-based taxonomic stability selection and elastic net regressions. This method found that increased relative abundances of and in AD were major factors driving the predicted metabolic changes. Furthermore, the metabolic predictions were associated with allelic variations in the risk gene in healthy individuals, confirming our previous findings. In conclusion, we identified blood metabolites with known links to AD that were differentially influenced by gut microbiota in AD, and identified possible microbial drivers of these predicted shifts in host-microbiome interactions. These findings may facilitate the development of microbiome-informed treatments of AD.
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4. Plasma indole-3-propionic acid is a gut-derived metabolite and is associated with type 2 diabetes and cardiometabolic outcomes: Evidence from a human antibiotic intervention.
PMID:日期:2026-09-26The gut microbiota influences host metabolism through diverse metabolites, many of which have been linked to glucose homeostasis and type 2 diabetes (T2D). Understanding microbial contributions to metabolite biosynthesis is essential for developing dietary and microbiota-targeted T2D prevention and treatment strategies. We performed targeted plasma metabolomics in individuals with T2D and healthy controls, all receiving histidine supplementation, before and after gut microbiota suppression using 7-day broad-spectrum antibiotic treatment. Associations between pre-antibiotic metabolite levels and fecal metagenomics-derived gut microbiota composition were examined using co-abundance network analysis and Random Forest modeling. Indole-3-propionic acid (IPA) was the only gut-derived metabolite differing between groups before antibiotics, with lower levels in T2D and higher levels associated with reduced T2D odds. Antibiotic treatment reduced IPA to near-undetectable levels in both groups, confirming its predominantly microbial origin. Beyond established inverse associations with BMI and glycemic markers, we found a novel inverse correlation between IPA and glycemic variability, consistent with a protective association with T2D. Plasma IPA was associated with gut microbiota beta diversity. IPA-associated species clustered within a single co-abundance module, but did not include known IPA producers, suggesting plasma IPA is influenced by broader microbial community composition rather than IPA-producing capacity of individual taxa alone. This study provides direct human evidence that plasma IPA is virtually exclusively gut microbiota-derived in individuals with T2D, extending prior findings in healthy populations. It highlights IPA's relevance to metabolic health and T2D, and guides future research on dietary and microbiota-targeted strategies to modulate IPA, advancing T2D prevention and treatment.
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5. Ethanol exposure is associated with spatial and taxon-specific gut microbiota remodeling characterized by ecological adaptation rather than broad activation of microbial ethanol metabolism.
PMID:日期:2026-09-25Alcohol-associated diseases are linked to gut microbiota disruption, but how ethanol intake is associated with microbial functional remodeling remains unclear. Here, using male C57BL/6J mice, we integrated spatiotemporal quantification of ethanol and acetaldehyde across the gastrointestinal tract with 16S rRNA sequencing, metagenomics, metaproteomics, and metabolomics. Our results showed that small-intestinal communities were enriched in taxa and functions related to bile acid tolerance/utilization, whereas cecal communities exhibited pronounced remodeling of multiple core functions associated with ecological adaptation. Although the abundance of several ethanol metabolism-related genes increased, this genetic potential was not broadly translated into detectable protein-level activation. Ethanol metabolism-related proteins were mainly derived from Lachnospiraceae, whose metabolic activity was suppressed. In contrast, Muribaculaceae, Desulfovibrionaceae, and Barnesiellaceae gained functional advantages in substrate acquisition, energy metabolism, oxidative stress defense, and proteostasis. These findings provide a region-resolved functional map indicating that ethanol-associated microbiota remodeling is characterized by ecological adaptation, rather than uniform activation of direct microbial ethanol metabolism.
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6. {"_":"A probiotic converts hesperidin to bioactive hesperetin and improves metabolic dysfunction in aging mice.","i":["Bifidobacterium pseudocatenulatum"]}
6. 一种益生菌将橙皮苷转化为具有生物活性的橙皮素并改善衰老小鼠的代谢功能障碍PMID:日期:2026-09-23Dietary flavonoids often require microbial metabolism to generate bioactive metabolites that influence host physiology. Hesperidin, a citrus flavanone glycoside, exhibits limited intestinal absorption and depends on gut microbial biotransformation to yield its active aglycone, hesperetin. Hesperetin activates CDGSH iron-sulfur domain 2 (CISD2), a pro-longevity gene whose expression declines with age, and its pharmacological activation has emerged as a strategy to promote healthy aging. Here, we identified a probiotic strain, CL256B, that efficiently converts hesperidin to hesperetin via coordinated -L-rhamnosidase and -glucosidase activities, achieving ~90% bioconversion efficiency. In naturally aging mice challenged with a Western diet, six-month treatment with probiotic-derived hesperetin significantly improved age-associated metabolic phenotypes, including reduced body weight and adiposity, increased lean mass, enhanced muscle integrity and grip strength, and attenuation of hepatic steatosis. In addition, glucose tolerance, insulin sensitivity, and whole-body energy metabolism were improved. Transcriptomic analyses revealed activation of SIRT1 and HNF4α signaling in the liver and restoration of ribosome homeostasis in skeletal muscle. These findings support a microbiome-enabled strategy in which probiotic-assisted hesperetin bioconversion activates the CISD2 longevity pathway to improve metabolic health during aging.
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7. {"_":"The OMM mice: a decade of dissecting host-microbiome interactions.","sup":["12"]}
PMID:日期:2026-09-22Humans and their associated microbes form a multifaceted ecosystem. Gaining mechanistic insight into this system necessitates reductionist models integrating ecological and immunological dimensions. Over the past decade, the gnotobiotic Oligo-Mouse-Microbiota (OMM) mouse line has exemplified this approach, pairing a standardized consortium of 12 bacterial strains representative of the five major phyla of the mouse microbiota, with the most widely used host background, C57bl/6 mice, in microbiome research. Across numerous studies, this reproducible and experimentally tractable model has enabled the identification of molecular mechanisms underlying colonization resistance, pathogen virulence, microbiota-dependent metabolic and immune pathways, as well as bacterial and bacteriophage dynamics. The modular ability/nature of the OMM model may now be further leveraged and refined in different host and microbial dimensions to address remaining gaps in translational microbiome research, positioning it as a reference framework for mechanistic investigations.
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8. Gut-immune-PVAT axis is involved in ethanol-induced abdominal aortic dysfunction via IL-17RA, TLR4, and FPR1 signaling.
8. 肠-免疫-血管周围脂肪组织轴通过IL-17RA、TLR4和FPR1信号通路参与乙醇诱导的腹主动脉功能障碍PMID:日期:2026-09-21Alcohol consumption and gut dysbiosis are risk factors for cardiovascular diseases (CVD), yet their mechanistic interplay remains unclear. We investigated whether gut microbiota-associated signaling modulates ethanol-induced abdominal aorta and perivascular adipose tissue (PVAT) dysfunction. Male C57BL/6J mice subjected to a chronic plus binge ethanol protocol exhibited leaky gut, systemic inflammation, and vascular dysfunction, along with greater systemic exposure to microbiota-derived products (fMLP and LPS) and immune response activation, including M1 macrophage polarization and Th17 expansion. Ethanol-induced vascular hyporesponsiveness was linked to FPR1 upregulation, while smooth muscle FPR1 conditional deletion prevented this effect. PVAT-intact aorta from ethanol-treated mice exhibited increased contractile responses compared with PVAT-devoid vessels, indicating PVAT dysfunction. This phenotype was attenuated by pharmacological inhibition or genetic deletion of FPR1. Notably, these PVAT-dependent alterations were absent in germ-free, Rag1, IL-17RA, or TLR4 mice, supporting a role for gut microbiota-driven immune response signaling. Redox imbalance also contributed to vascular and PVAT dysfunction. Our findings demonstrate that ethanol exposure triggers a gut-redox cascade which elicits the Th17/TLR4 axis and targets the PVAT to drive vascular injury. In conclusion, positioning PVAT as a central integrator of gut microbiota-derived signals identifies the gut-vascular interface as a promising therapeutic target for alcohol-related CVD.
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9. The cervicovaginal gut microbiota axis as a key determinant of systemic physiology.
PMID:日期:2026-09-21The gut and vaginal microbiomes are both essential to human health, yet they have largely been studied in isolation. Gut microbiota are central to host metabolism, immunity, and the gut-brain axis, while the vaginal microbiome, typically dominated by species, protects against infection and shapes reproductive outcomes. Although dysbiosis at either site has been linked to systemic disease, the possibility that these communities are interrelated and that the vaginal microbiome could serve as a clinically accessible proxy for systemic microbial states remains underexplored. This represents a clear gap in the literature. In this review, we examine physiological connections between digestive and genitourinary systems, explore how endocrine and immune networks exert dual control across compartments, and analyze correlations between dysbiosis and disease states. We then consider emerging technologies for microbiome analysis and their clinical and translational implications, including the potential for vaginal microbiome profiling to function as a diagnostic surrogate for the gut and as a complementary biomarker platform for prediction of neurologic disease risk. By building a systems-level understanding of the joint immuno-microbial interactome, evaluating advances in computational and omics-based technologies, and situating these tools within emerging healthcare frameworks, we argue that the cervicovaginal-gut microbiota axis is a unique and understudied source for medical discovery.
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10. CRISPR-Cas immune repertoires as an ecological record of bacterial interactions with mobile genetic elements in the human gut.
10. CRISPR-Cas免疫库作为人类肠道中细菌与可移动遗传元件相互作用的生态记录PMID:日期:2026-09-21Bacteria in the human gut influence host physiology and disease risk, but their ecology is strongly shaped by mobile genetic elements (MGEs) such as phages and plasmids. Past interactions between bacteria and MGEs can be inferred from CRISPR-Cas cassettes, which contain short DNA fragments derived from invading elements. To lay the groundwork for research on the impact of such interactions on the human host, we constructed an extended microbiome resource comprising 1.7 K prokaryotic mOTUs, 19.5 K viral vOTUs, and 24.2 K plasmid PTUs, using fecal shotgun metagenomes from 1034 adults over 55 y of age residing in South-East Norway. We also recovered 74.2 K unique CRISPR-Cas cassettes to map past bacteria-MGE interactions and assessed their associations with the human diet and lifestyle factors. CRISPR-Cas spacers, and which viruses and plasmids they targeted, varied substantially within bacterial species, but were predominantly directed towards cohort-specific MGEs. Moreover, bacteria were more likely to target MGEs present in the same sample, consistent with local exposure. Plasmid MGEs were more often targeted by Type II CRISPR-Cas cassettes, whereas viruses were more likely to be targeted by Type I CRISPR-Cas cassettes. Bacteria also shared more targets within taxonomic families than across families, where mobilizable plasmids were more frequent among the targets. CRISPR-Cas cassettes mirrored microbiome associations to human demographic and lifestyle factors and enabled the recovery of dairy-associated . Together, this research provides a large-scale resource and a structured analysis of bacteria-MGE interactions in the gut microbiome and their contribution to microbial ecosystem dynamics.