Frontiers in Microbiology最新文献

Introduction: Crop rotation promotes ecological effects and production by regulating belowground processes, particularly the shaping of the rhizosphere soil microbiome. Rhizosphere metabolites are a key driver of belowground processes and play a crucial role in shaping soil microbial community composition. However, the rhizosphere metabolites of different potato rotations have rarely been reported, and the regulation of key metabolites on the rhizosphere soil microbiome remains unclear.

Methods: This study measured agronomic traits of potatoes, collected potato rhizosphere soils from three crop rotations, including potato monoculture (P-P), maize (Zea mays)-potato rotation (M-P), cowpea (Vigna unguiculata)-potato rotation (V-P), to determine rhizosphere soil metabolites and analyze defense metabolites, and assess the soil bacterial and fungal diversity and community composition.

Results: Compared to monoculture, the potato rotations had positive effects on growth and yield. Potato rotations had more primary metabolites, such as amino acids and carbohydrates and conjugates, but significantly reduced secondary metabolites with defensive functions in rhizosphere soils including phenols and other benzene derivatives, flavonoids, alkaloids and other N-containing compounds, and terpenoids. Potato rotation systems supported higher diversity of bacteria and fungi and enriched beneficial bacteria such as biocontrol, nitrogen fixation, C degradation, denitrification, and pollutant degradation bacteria, while suppressing pathogenic fungi in the rhizosphere soils. Rhizosphere soil metabolites strongly correlated with the microbial community composition. The secondary metabolites, which are predominantly alkaloids, terpenoids, and flavonoids, exerted a dominant regulatory effect on the composition of soil microbial community.

Discussion: These results demonstrate the important regulation of rhizosphere metabolites on soil microbial community composition, deepening our understanding of the benefits of crop rotation via the belowground effect.

Background: The objective of our investigation was to explore the features of gut microbiota dysbiosis and the concentrations of gut metabolites in relation to white matter injury (WMI). Furthermore, we sought to evaluate the influence of gut dysbiosis on neuroinflammation in WMI via intestinal metabolites, and its contribution to pathogenesis.

Methods: A cerebral hypoxia-ischemia-induced WMI model was established in 3-day-old Sprague-Dawley rats. Liquid chromatography-mass spectrometry/gas chromatography-mass spectrometry analyses and 16S rRNA gene sequencing were undertaken to ascertain WMI biomarkers. Mechanistic experiments were used to analyse activation of the H3K9ac/BDNF/TrkB pathway and neuroinflammation.

Results: The analysis of 16S rRNA sequencing disclosed gut microbiota dysbiosis in WMI rats, quantified using linear discriminant analysis effect size. Overall, 341 differentially expressed metabolic markers between the WMI and Sham groups were discovered. The Kyoto Encyclopedia of Genes and Genomes network enhancement evaluation revealed significant downregulation of 20 metabolic processes in the WMI group, which is strongly related to changes in fecal microbial metabolites, and the synthesis process of unsaturated fatty acids was the most significant. Gut microbiota dysbiosis may influence WMI by downregulating metabolites such as eicosapentaenoic acid (EPA). Fecal microbiota transplantation increased EPA concentration in the brain tissue of WMI rats. Gut microbiota-derived EPA promoted H3K9ac and BDNF/TrkB expression and inhibited the transcription of pro-inflammatory TNF-α and IL-1β molecules. These EPA-mediated effects were reversed by TrkB inhibition.

Conclusion: WMI induces gut dysbiosis involving down-regulation of unsaturated fatty acid synthesis. Fecal microbiota transplantation leads to increased levels of EPA. Gut microbiota-derived EPA increases levels of acetylated histone H3K9ac, causes activation of the BDNF/TrkB pathway, reduces neuroinflammation, and improves WMI-associated myelination disorders. It provides a basis for targeted treatment of white matter injury in the future.

Plasmid-mediated dissemination of antibiotic resistance genes (ARGs) poses a major public health threat. In contrast to the well-studied resistance plasmids within pathogens, those from non-pathogenic environmental reservoirs remain underexplored. Here, we characterized transferable multidrug-resistant plasmids captured from community air and wastewater via conjugation assays. Transconjugants obtained from these environmental samples were profiled phenotypically against 17 antibiotics and genetically via short- and long-read sequencing. Conjugative plasmid transfer was successfully captured from 33 (20.6%) of 160 environmental samples, yielding 78 transconjugant isolates and 40 plasmid types. The captured plasmids conferred resistance to 4-18 antibiotics, with near-universal resistance to ampicillin (98.7%) and retained susceptibility to polymyxin B (84.6%). Among 150 ARG instances identified across 19 classes, aac(3)-IId was the most prevalent. The dominant plasmids ps15D023_8 (wastewater) and peccDNA113 (airborne) were particularly notable; peccDNA113 carried 4 ARGs, 9 virulence factors (including fimH and AcrB), and confers resistance to at least 7 antibiotics. Critically, the carbapenemase gene blaNDM-5 was detected, and peccDNA113 shows homology to clinical plasmids, indicating a high risk of clinical-environmental exchange. These findings highlight community environments as crucial reservoirs for mobile, high-risk resistance plasmids and underscore the urgent need for expanded surveillance beyond clinical settings.

We have used nucleotide skews as the proxy to understand the evolution of archaeal genomes. Our genome-wide studies using substantial datasets suggest that translational selection and the nature of the genetic code are universally conserved determinants of asymmetric guanine and cytosine distributions. We propose that in the case of the majority of bacterial chromosomes, mutational processes and/or DNA repair also result in the strand-specific nucleotide skews. This is in stark contrast to what we observe for archaeal chromosomes and plasmids, and reveals that archaea have a greatly reduced ability to create mutations and/or repair DNA damage in a strand-specific manner. We suggest that in the future, the described computational and statistical approach will help to understand the evolutionary dynamics of the archaeal chromosomes through the tree of life.

[This corrects the article DOI: 10.3389/fmicb.2026.1636784.].

Microbial communities play essential roles in mediating plant defenses against insect pests. However, how host-associated microbiota and metabolites jointly respond to bark beetle infestation remains largely unexplored. Here, we integrated microbiome and metabolome profiling to elucidate how Pinus tabuliformis regulates its phloem and rhizosphere responses under varying levels of Dendroctonus valens infestation. Both bacterial and fungal diversity, as well as the relative abundance of dominant taxa such as Erwinia and Pseudoxanthomonas, shifted significantly with infestation intensity. Concurrently, key plant defense metabolites-including terpenoids, jasmonates, and polyphenols-were markedly elevated. Pathway enrichment analysis indicated that the phloem was characterized by enhanced phenylpropanoid and flavonoid biosynthesis, whereas the rhizosphere soil accumulated terpenoids and polyketides, implicating both compartments in resistance modulation. In the phloem, differential bacterial and fungal taxa displayed distinct positive and negative correlations with phenylpropanoid intermediates and downstream derivatives, while in the rhizosphere, bacteria from Bacillota and fungi such as Candida and Ogataea were strongly linked to diterpenoids, sesquiterpenoids, flavonoids, and indole derivatives. These findings demonstrate that P. tabuliformis mounts a compartment-specific, microbiome-associated metabolic response to D. valens infestation, providing new insights into the ecological roles of symbiotic microbiota in plant defense and offering a mechanistic foundation for microbe-based pest management strategies.

Introduction: Comorbid obesity and depression (COMBD) represents a complex metabolic-neuropsychiatric challenge with limited therapeutic options. While Electroacupuncture (EA) is effective for both metabolic and mood disorders, the systemic mechanisms-particularly the interplay between the gut microbiome and hippocampal plasticity-remain elusive.

Methods: We established a COMBD rat model using a high-fat diet combined with chronic unpredictable mild stress (CUMS). An integrated multi-omics approach comprising 16S rDNA sequencing, LC-MS/MS serum metabolomics, and hippocampal transcriptomics was utilized to decipher the therapeutic mechanisms of EA.

Results: EA treatment significantly attenuated body weight gain and reversed depressive-like behaviors. Crucially, EA restructured the dysbiotic gut microbiota, specifically increasing the abundance of short-chain fatty acid (SCFA)-producing bacteria. This microbial restoration was strongly correlated with a reprogrammed serum metabolic profile. In the hippocampus, transcriptomic analysis identified Cd74 as a pivotal upstream regulator modulated by EA. Furthermore, EA mitigated hippocampal oxidative stress and restored synaptic plasticity, evidenced by increased dendritic spine density and upregulated synaptic protein expression.

Conclusion: Our findings suggest that EA ameliorates COMBD via a coordinated "Microbiota-Metabolism-Brain" axis. Specifically, EA creates a neuroprotective milieu by promoting beneficial SCFA-producing bacteria and regulating metabolic signals, which subsequently targets hippocampal Cd74 to restore synaptic plasticity. This study provides a novel mechanistic basis for the clinical application of EA in treating complex metabolic-mood comorbidities.

The unique environmental conditions at high altitudes drive the gut microbiota of resident animals to develop distinct structural and functional traits, thereby offering an ideal natural model for investigating the synergistic adaptation of hosts and microorganisms to extreme environmental stressors. This review systematically expounds the mechanism of metabolic adaptation of gut microbiota to high-altitude through the phenotypic characteristics of "high productivity and low inflammation," and understands the mediating effect of short-chain fatty acids and secondary bile acids, which are derived metabolites of flora. SCFAs can enhance the intestinal barrier, regulate the function of immune cells, act on the gut-brain axis, and then affect the feeding behavior. SBAs, as signal molecules, regulate the lipid and energy metabolism of the host through the gut-liver axis. This division of labor and coordination, driven by different metabolites and achieved through specific gut-X axis pathways, constitutes a microecological regulatory network that enables the host to maintain metabolic homeostasis in high-altitude areas. Understanding this natural model can reveal the role of "flora metabolite organ axis" in maintaining health. It can also provide reference direction for obesity intervention caused by high-fat diet (HFD) and other factors, such as regulating the function of gut microbiota through strategies such as dietary regulation, probiotics and prebiotics supplementation, and fecal microbiota transplantation (FMT), and regulating the specific gut-X axis pathway, so as to restore metabolic balance.

Introduction: Listeria monocytogenes (Lm) poses a significant risk to food safety due to its adaptability and pathogenicity. In contrast, Listeria phages show great promise as biocontrol agents.

Method: This study comprehensively analyzed 97 complete Listeria phage genomes from 14 countries across four continents, including 16 newly isolated phages exhibiting specific phenotypic characteristics.

Results: The phages were grouped into nine genomic clusters that clearly distinguished between virulent and temperate lifestyles. Temperate phages demonstrated greater genomic diversity than virulent ones. Cluster 1 phages were assigned to the genus Pecentumvirus, exhibiting a broad geographical distribution with diverse sources, and appear to have an ecological advantage based on their genomic characteristics. Evolutionary analyses classified the major capsid protein (MCP), receptor-binding protein (RBP), and endolysin of Listeria phages into nine, seven, and eight distinct types, respectively. These three proteins exhibited high levels of conservation within the virulent clusters, but significant diversity within the temperate clusters. Notably, the RBPs of types R1, R2, R4, and R6 are associated with broad host ranges and distributed across Clusters 1, 2, 7, and 8 phages. Cluster 3 phages lacked identifiable RBP sequences, suggesting an absence of canonical domains that can be detected using standard prediction tools.

Discussion: These findings refine the classification of Listeria phages, significantly advancing our understanding of their taxonomy, genomic diversity, and global distribution.