npj Biofilms and Microbiomes最新文献

Preterm birth is the leading cause of neonatal morbidity and mortality, particularly in low- and middle-income countries. The vaginal microbiome influences pregnancy outcomes by effecting immunity, epithelial integrity and inflammation. Lactobacillus-dominance supports immune tolerance, whereas dysbiosis consisting of anaerobes such as Gardnerella and Prevotella promote inflammation and premature cervical remodelling. This review synthesises evidence linking microbiome composition, ancestry-associated disparities and host responses, and discusses emerging microbiome-based interventions for preterm birth.

Alcoholic Heart Disease (AHD) involves gut microbiota dysbiosis, metabolic disturbances, and circadian disruption, yet their interconnections remain unclear. Using a murine AHD model, we integrated echocardiography, metabolomics, cardiac transcriptomics, and 16S rRNA sequencing to investigate alcohol-induced pathology. It evaluated dietary fiber and acetate interventions for their potential to restore gut microbiota balance, lactate homeostasis, and circadian gene expression. Statistical analyses included correlation networks, receiver operating characteristic (ROC) curves, and pathway enrichment. Chronic alcohol consumption led to gut dysbiosis characterized by an overgrowth of Akkermansia muciniphila and a depletion of Lactobacillus intestinalisand and Bacteroides acidifaciens. This condition was associated with hyperlactatemia fraction, myocardial dysfunction, evidenced by a reduced revealed fraction and cardiac fibrosis. Transcriptomic analysis revealed strong dysregulation of circadian-related genes, including BHLHE41, NFIL3, and PER2. Interventions improved microbial diversity, reduced lactate levels, and successfully regulated cardiac related indicators through the lactate-circadian rhythm pathway. ROC analysis validated BHLHE41, NFIL3, and PER2 as high-accuracy biomarkers (AUC > 0.85). Our study reveals a gut‑heart axis in AHD where microbiota‑derived lactate links to circadian disruption, worsening disease. Dietary fiber and acetate are promising therapies that rebalance metabolites and modulate circadian networks, offering novel biomarkers and strategies for alcohol‑related cardiovascular disease.

Dietary faba bean enhances fish muscle quality but concurrently reduces growth performance. The gut microbiota critically modulates muscle growth and quality. However, the specific microbial taxa, metabolites, and regulatory mechanisms responsible remain to be elucidated. This study established a differential gut microbiota model in faba-bean-fed Yellow River carp (Cyprinus carpio), used whole-intestinal microbiota transplantation (WIMT) to directly test its effect on muscle quality, and supplemented the key bacterium and its metabolite to confirm their contribution. After a 6-week faba bean diet, growth performance declined, whereas muscle texture improved (P < 0.05). This improvement was concomitant with a higher abundance of the genera Aeromonas and Cetobacterium in the gut. Following 8 weeks of daily WIMT from faba-bean-fed donors, Yellow River carp maintained normal growth performance (P > 0.05) and simultaneously showed improved muscle texture, characterized by more small-diameter fibers, lower fat content, and higher collagen levels (P < 0.05), recapitulating the donor's key muscle phenotype. Meanwhile, WIMT reshaped the gut microbiome composition and its metabolic profile, and the marker species Cetobacterium somerae and its metabolite acetic acid showed associations with improvements in muscle quality. Further in vivo validation indicated that C. somerae reduced fat deposition and improved muscle texture, an effect possibly linked to activation of the AMPK-PGC-1α-FoxO pathway, and its metabolite acetic acid mirrored these changes. This study reveals the direct impact of gut microbiota on muscle quality through WIMT in Yellow River carp, provides novel evidence of the fish gut-muscle axis, and offers a scientific basis for improving muscle quality.

Host-associated microbiomes are increasingly recognized as key determinants of plant health, disease development, and ecosystem functioning. Plant pathogens, especially fungal pathogens, have been reported to secrete antimicrobial effectors to modulate the host microbiota and promote colonization. Plant-parasitic nematodes (PPNs) could also modulate host microbial communities, but the processes involved remain to be clarified. Here, we identify a secreted antifungal effector, BxylTLP6, from Bursaphelenchus xylophilus, the causal agent of pine wilt disease. BxylTLP6 degrades fungal cell walls and inhibits multiple plant-associated fungi, while the released oligoglucans serve as food-derived cues that guide nematode foraging toward fungal resources. In planta, silencing Bxyltlp6 significantly delayed disease progression. ITS-based mycobiome profiling revealed that BxylTLP6 modulates the pine endophytic fungal community by promoting Ascomycota, suppressing Basidiomycota, inhibiting wood-decaying fungi, and enriching pathogenic or parasitic taxa. These shifts are associated with enhanced nematode survival and pathogenicity. Our findings support the view that a TLP effector can modulate behavior and influence the host fungal microbiome, shedding light on how PPN may manipulate microbial environments to enhance their fitness.

Chronic liver disease (CLD) causes 2 million annual deaths (4% of all global deaths). While gut bacteria are widely studied, intestinal fungi remain largely overlooked despite their critical roles in maintaining microecological homeostasis. This review summarizes fungal characteristics in alcohol-related liver disease, metabolic dysfunction-associated steatotic liver disease, primary sclerosing cholangitis, and cirrhosis, analyzing roles of fungi and their metabolites. Targeting the gut fungal community may offer therapeutic strategies for CLD.

Associations between the gut microbiota and cardiometabolic health are well established, but evidence from longitudinal studies remains limited. In the prospective multi-ethnic HELIUS cohort, we investigated whether baseline gut microbiota composition was associated with long-term cardiometabolic outcomes. Fecal samples from 4792 participants were collected at baseline and analyzed using 16S rRNA sequencing. At follow-up, new diagnoses of hypertension, dyslipidemia, and diabetes were assessed, and major adverse cardiovascular events (MACE and MACE + , including angina pectoris) were obtained from hospital and mortality registries. Logistic regression was used to study associations with incident cardiometabolic disease, while Cox regression evaluated associations with MACE among participants without cardiovascular disease at baseline. During follow-up, 129 participants experienced MACE (2.7%) and 180 MACE+ (3.8%). Higher abundance of Eubacterium xylanophilum group spp. and Akkermansia muciniphila was associated with lower MACE+ risk, whereas Ruminococcus gnavus group spp. was associated with higher MACE risk, although only Eubacterium xylanophilum group spp. remained significant after full adjustment. Several taxa were associated with incident cardiometabolic disease, and exploratory metabolomics linked Ruminococcus gnavus group spp. to bile acid and acylcarnitine metabolites. These findings suggest that gut microbiota composition is longitudinally associated with cardiometabolic disease.

Soil acidification disrupts the structure and function of soil microbiomes, resulting in increased vulnerability to soil-borne pathogens. While the link between soil acidification and disease susceptibility is well-established, the mechanisms underlying the suppression of plant defense remain poorly understood. In this study, we found that soil acidification perturbed the co-evolved assembly process of endophytic microbiomes in watermelon roots, leading to the collapse of a critical microbe-metabolite-host defense axis essential for resistance against Fusarium oxysporum f. sp. niveum (FON). Integrated field surveys and multi-omics analyses revealed that acidification-induced dysbiosis in the root endophytic microbiomes, characterized by the depletion of keystone Pseudomonas species (Pseudomonadaceae), strongly correlated with increased Fusarium wilt incidence. Central to this interaction was citrulline, a metabolite produced by root Pseudomonas endophytes that functioned as a symbiotic effector promoting bacterial colonization and a defense modulator inhibiting FON-induced oxidative burst. Disruption of citrulline biosynthesis abolished these protective effects, whereas exogenous citrulline application restored disease resistance. These findings underscored the role of root endophyte-derived citrulline in sustaining microbial fitness and plant defense, revealing a tripartite interaction impacted by soil acidification. Collectively, this study provides insights for developing microbiome-based strategies to enhance sustainable crop protection in degraded agroecosystems.

This study investigates the role of trehalose in modulating gut microbiota metabolism and alleviating symptoms of severe acute pancreatitis (SAP). Here, we found that gut microbial metabolism was imbalanced in SAP. In particular, we observed increased lipid metabolism and decreased carbohydrate and amino acid metabolism, which were reversed by gut microbiota depletion. Moreover, the production of trehalose was significantly increased after gut microbiota depletion. Interestingly, trehalose treatment effectively reduced pancreatic injury and ameliorated the SAP-induced microbial metabolism imbalance by promoting carbohydrate metabolism and suppressing lipid metabolism. The effect of trehalose was depend on the gut microbiota, especially the expansion of Muribaculaceae. Mechanistically, trehalose-remodelled gut microbiota suppressed SAP-induced increases in serum TG, IL-6, IL-17A, and TNF-α levels, inhibited caspase-3-mediated apoptosis, and reduced macrophage infiltration into the pancreas. Overall, our study revealed that trehalose ameliorates SAP by modulating gut microbial metabolism homeostasis, providing new insights into the "microbial metabolism‒gut‒pancreatic axis".

Copper-induced transmission of antimicrobial resistance has been well documented in livestock farming environments, but the in vivo mechanisms driving fecal resistome development remain unclear. Here, 120 mg/kg CuSO₄ and copper-peptide were supplemented to piglets, and the fecal resistome development was first analyzed by metagenomic sequencing. In this study, dietary CuSO₄ drove abundant and diverse ARGs and MRGs. Following CuSO₄ deprivation, ARGs and copper resistance exhibited a persistent promotion, whereas most MRGs rapidly declined. The resistance development was characterized by abundant MGEs. This phenomenon expanded the multiple-antibiotic resistance reservoir in fecal community, which was preferentially harbored by pathogens. Furthermore, dietary CuSO₄ disturbed colonic homeostasis, characterized by impaired epithelial integrity and reduced butyrate-producing bacteria abundance, which coincided with an oxidative stress environment and increased prevalence of multiple-resistant pathogens, such as Escherichia coli and Enterococcus spp. In vitro validation further supported these associations, showing that butyrate supplementation and hypoxic conditions alleviated Cu²⁺-induced ROS generation and reduced the frequency of ARGs conjugative transfer. Overall, this study suggests that dietary inorganic copper may contribute to microbial disturbances linked to oxidative stress and potentially facilitate antimicrobial resistance transmission among pathogens, highlighting organic copper as a sustainable alternative for mitigating resistance risks in farmed animals.

Disruption of the gut mucus barrier is critical in the development of infectious or chronic inflammatory diseases. The suckling-to-weaning transition is pivotal to the barrier maturation and is associated with a high incidence of gastrointestinal infections. Using a novel microfluidic device, we investigated the penetration and organizational properties of motile Escherichia coli bacteria at the interface of purified intestinal mucus from piglets before and after weaning. In weaned piglets, bacteria penetrated more than 100 μm into the mucus. Meanwhile, significant bacterial aggregation was observed in the mucus of suckling piglets, hindering penetration. Although we observed, on average, higher immunoglobulin A (IgA) concentrations in suckling piglet mucus, the high variability across samples suggested that concentration alone is insufficient to account for the aggregation behavior. Supernatant from purified suckling piglet mucus restored bacterial aggregation and limited penetration in weaned piglet mucus, similar to the effect observed with human breast milk IgA. Our results emphasize the importance of mucosal IgA specificity in relation to the mother's immunological history, primarily transmitted through breast milk and lost during weaning. This microfluidic ex-vivo approach provides an original platform to interrogate bacterial behavior in complex mucosal environments, opening new avenues for predictive and translational research.