npj Biofilms and Microbiomes最新文献

During the first year after birth, the infant gut microbiome undergoes a rapid and profound compositional and functional transformation, impelled by an intricate network of intrinsic and extrinsic factors. This process results in increased taxonomic and functional diversification, alongside greater interindividual variability. To better understand this early-life ecosystem, this study assessed the interindividual variability of the infant gut microbiome using a comprehensive infant gut microbiome database of 5288 fecal metagenomic data from healthy, full-term infants across various geographical locations. Our study identified six reference microbial communities, termed Early-Life Community State Types (ELi-CSTs), which not only capture specific compositional profiles and heterogeneity of the infant gut microbiome, but also record the extensive transformation experienced by this developing microbial community during the first year of human life. Indicative Species analysis and Random Forest modeling assisted the precise identification of unique, key taxonomic signatures that are critical to the structure of each ELi-CST, highlighting microbial taxa with pivotal roles in shaping the infant gut microbiota. To complement these findings, we established a bacterial biobank through dedicated cultivation efforts of the infant microbiota, comprising 182 genome-sequenced isolates corresponding to key taxa involved in early life gut microbiota assembly. This biobank provided the basis for co-cultivation experiments combined with transcriptome analyses, thereby enabling in vitro investigations into microbial cross-talk among key modulators, and yielding novel insights into the molecular interactions and cooperative dynamics behind early microbiome development.

Bacteria that colonize the human gut must withstand a variety of stressors, including detergent-like compounds known as bile acids. Here, we investigated how bile acids found in the human cecum and colon impact the behavior of the probiotic strain Escherichia coli Nissle 1917 (EcN). We found that lithocholic acid (LCA), which is a microbiota-derived secondary bile acid, promotes the formation of a distinctive surface-coating biofilm by EcN, including on an organoid-derived model of the human colonic epithelium. Mechanistic investigations revealed that LCA upregulates the production of several components of flagella, which are essential for LCA-induced biofilm formation and form part of the biofilm matrix. Furthermore, LCA-induced biofilm formation helps EcN compete against certain pathogenic strains. Taken together, our findings shed light on how an abundant colonic metabolite influences the behavior of a clinically proven probiotic strain, triggering the formation of biofilms that may contribute to pathogen suppression.

This study examines a subterranean estuary seepage face in China's Sanggou Bay by comparing environmental parameters and microbiome data before and after the COVID-19 lockdown, in order to reveal the regulatory mechanisms of coastal resting on microbial community stability and biogeochemical functions. The results revealed that reduced human activities significantly decreased sediment nutrient loading and shifted organic matter sources from terrestrial- to marine-dominated. This environmental restructuring drove profound microbial community reorganization: while α-diversity indices declined, the relative abundance of core species increased, with marked enhancements in community stability and metabolic efficiency, particularly in pathways related to amino acid metabolism, carbohydrate metabolism, and biogeochemical cycling. The study confirms that a coastal rest period can enhance ecosystem resilience by reducing anthropogenic disturbance, optimizing resource allocation, and activating microbial functional plasticity. These findings suggest that rest periods may represent a potential strategy for supporting ecosystem resilience and sustainability.

Plant-parasitic nematodes (PPNs) pose a significant threat to global crop production, yet their associated viral diversity remains poorly characterized, limiting potential virus-mediated biocontrol strategies. In this study, we investigated PPN-associated viruses using both virome data obtained from ten field populations of potato rot nematode (Ditylenchus destructor) collected in Lulong County (Qinhuangdao city, China), a major sweet potato-producing region, along with 536 publicly available transcriptome datasets from the Sequence Read Archive (SRA) database, collectively encompassing twenty-five PPN species. We identified 94 PPN-associated viruses, representing a 7.9-fold increase over prior records. These viruses span eighteen established families and six unclassified viral groups, including the first discovery of orthomyxo-like viruses, Jingmen viruses, and ormycoviruses in PPNs or nematodes, expanding the possible host ranges of these viral groups. Notably, a clade of yue-like viruses harbored up to 10 introns, surpassing 2-3 introns that were only observed in orthomyxoviruses and certain members of the Mononegavirales. Furthermore, we identified two larger nematode-associated bunyaviruses with the L segments exceeding 12,000 bp, which appear to have acquired a putative cysteine proteinase gene potentially originating from their nematode hosts (possibly Pristionchus spp.). Our findings reveal that natural PPN populations could host an unexpectedly high diversity of RNA viruses, higher than previously recognized. Exploring these viruses provides novel insights into viral evolution and establishes a foundation for utilizing viruses as a potential method for controlling PPN diseases.

The human microbiome critically influences metabolism and thereby our health. Constraint-based reconstruction and analysis (COBRA) is a proven framework for generating mechanism-derived hypotheses along the nutrition-host-microbiome-disease axis. However, no large-scale microbiome metabolism visualisation has been available. Therefore, we created the MicroMap, a manually curated network visualisation, which captures the metabolism of over a quarter million microbial genome-scale metabolic reconstructions. The MicroMap contains 5064 unique reactions and 3499 unique metabolites, including for 98 drugs. Users can intuitively explore microbiome metabolism, inspect metabolic capabilities, and visualise computational modelling results. Further, the MicroMap may serve as an educational tool to help diversify the computational modelling community. We generated 257,429 visualisations, covering all our current microbiome reconstructions, to visually compare metabolic capabilities between microbes. The MicroMap integrates with the Virtual Metabolic Human (VMH, www.vmh.life ), the COBRA Toolbox (https://opencobra.github.io ), and is freely accessible at the MicroMap dataverse ( https://dataverse.harvard.edu/dataverse/micromap ), along with all the generated reconstruction visualisations.

Characterizing human microbiota in host-dominated samples is crucial for understanding host-microbe interactions, yet is challenged by the high host DNA context (HoC). Current depletion strategies are limited by DNA loss and require immediate processing. In this paper, we introduce 2bRAD-M, a reduced metagenomic sequencing method that enables efficient host-microbe analysis without prior host depletion. Validated on mock samples with >90% human DNA, 2bRAD-M achieved over 93% in AUPR and L2 similarity. In both saliva and oral cancer samples, 2bRAD-M closely matched WMS profiles; in the former, it captured diurnal and host-specific patterns with only 5-10% of the sequencing effort. In an early childhood caries (ECC) study, 2bRAD-M identified key bacterial indicators and distinguished ECC from healthy subjects (AUC = 0.92). By providing high-resolution microbial profiles without host depletion, 2bRAD-M offers a practical and efficient solution for HoC-challenged microbiome research.

H. pylori induces gastritis and promotes gastric carcinogenesis. Antimicrobial therapy against H. pylori often causes gastrointestinal dysbiosis, with side effects like vomiting, diarrhea, and antibiotic resistance, hindering effective eradication. This study investigated the effects and mechanisms of probiotics in balancing microbiota to alleviate H. pylori-related gastritis. Using in vivo and in vitro gastritis models with various H. pylori virulence strains, the study employed 16S rRNA amplicon sequencing and qPCR to link gastric microbiota with inflammation. Genomic mining and microbiota reconstruction identified Lactococcus garvieae LG3092 and GarQ as key microecological-targeting regulators. Results showed that different H. pylori induce varying levels of gastritis in vivo, with elevated IL-1β, IL-6, and TNF-α levels linked to pro-inflammatory bacteria. LG3092 secretes GarQ, specifically targeting Man-PTS receptors on pro-inflammatory bacteria, disrupting their membranes and modulating the gastric microbiota, highlighting the potential of probiotics in combination with other therapies to managing H. pylori infection and related gastritis.

Amyotrophic lateral sclerosis (ALS) remains a devastating neurodegenerative disorder with poorly understood pathogenesis. We conducted Mendelian randomization (MR) analyses integrating cardiovascular factors, gut microbiota (GM) composition, and immune cell phenotypes with transcriptomic profiling to establish causal relationships with ALS susceptibility. MR revealed causal associations between elevated low-density lipoprotein cholesterol, apolipoprotein B, systolic blood pressure, and increased ALS risk. GM analysis identified protective Alistipes species effects and detrimental Bacteroides associations. Multiple immune cell subsets demonstrated significant disease associations, particularly CD3 + T cell populations and CD62L+ monocytes. Colocalization studies identified 53 genes with shared genetic architecture, enabling differential expression analysis across datasets. Predictive modeling developed a five-gene biomarker panel achieving 96% training accuracy and 93% external validation. Quantitative PCR confirmed differential expression patterns for biomarkers in patient cohorts. This multi-omics investigation establishes ALS as a complex disorder with actionable cardiovascular and microbiome therapeutic targets, providing applications for risk stratification and prevention.

Anorexia nervosa (AN) is associated with profound alterations in gut microbiota and host metabolic profiles. While previous studies have primarily focused on the acute phase of AN, the chronic form, severe and enduring anorexia nervosa (SEAN), remains underexplored in terms of microbiome dynamics. In this study, we characterized gut microbiota composition (via 16S rRNA gene amplicon sequencing), serum and fecal metabolites (via mass spectrometry), and an extensive range of clinical, anthropometric, biochemical, and psychiatric parameters in females with acute AN, SEAN, and in healthy controls. SEAN patients exhibited higher antidepressant usage and greater lifetime stress exposure. Acute AN patients presented with more pronounced eating disorder severity and depressive symptoms. Elevated levels of intestinal fatty acid-binding protein in SEAN patients suggest mucosal damage. Microbiota analysis revealed reduced alpha diversity and distinct community composition in both AN groups, with SEAN showing the greatest interindividual variability. Both AN cohorts exhibited significantly lower serum and fecal γ-aminobutyric acid (GABA) levels, which were negatively correlated with taxa such as Christensenellaceae, Ruminococcaceae, and Escherichia-Shigella, i.e., microorganisms potentially associated with GABA degradation or impaired synthesis. Additionally, reductions in short-chain fatty acids suggest impaired microbial fermentation and dysregulation of the gut-brain axis. Collectively, these findings reveal progressive, functionally relevant changes in microbiota-host interactions in SEAN. These alterations likely reflect the persistent disease state and may contribute to its continuation.

Inflammatory bowel disease (IBD) is closely related to changes in the gut microbiota, with proton pump inhibitors (PPIs) possibly playing a role. PPIs use is associated with altering gut microbiota and potentially influencing IBD onset and progression. This review explores the mechanisms by which PPIs affect gut microbiota and IBD, suggests strategies to mitigate dysbiosis, outlook on the causal relationship validation between PPIs use and IBD risk, emphasizing the broader impact of acid suppressants on gut health.