Microbiome最新文献

Background: Rodents are primary reservoirs for zoonotic viruses, posing significant public health threats. However, our understanding of how habitat heterogeneity influences viral community composition and the spillover potential remains inadequate.

Results: Here, a comprehensive meta-transcriptomic analysis of rodent-associated viruses was conducted across four distinct ecological habitats in the northern foothills of the Tianshan Mountains, China. Multiple novel viral sequences belonging to families with known zoonotic potential were identified, including Nairo-, Arena-, Flavi-, Picorna-, and Paramyxoviridae. Phylogenetic analyses revealed significant genomic diversity and potential for cross-species transmission, particularly in viruses exhibiting broad tissue tropism. Notably, viruses from the family Nairoviridae were markedly enriched in rodent spleen and kidney tissues from mountain pastures and scenic zones. This enrichment likely reflects the high abundance and diversity of tick vectors in these habitats, which may facilitate viral persistence in rodent reservoirs and increase the risk of zoonotic spillover. In contrast, rodents in farm and community zones exhibited more diverse viral communities across multiple tissues, including the kidneys and intestines, suggesting that these high-density human-animal interfaces provide optimal conditions for multi-host viral circulation. Variations in viral distribution were observed across tissues and geographic locations among rodents from different habitats, indicating that viral patterns are closely influenced by host species, environmental factors, and vector organisms. Habitat differences accounted for 38.8% of the variation in viral community composition, highlighting both ecological diversity and the pivotal role of habitat in viral dynamics.

Conclusions: These findings underscore the complex interplay between habitat type, host ecology, and viral evolution in shaping zoonotic spillover risks. This research offers crucial insights into the emergence of rodent-borne viral diseases and the development of targeted surveillance strategies in high-risk regions. Video Abstract.

Background: Anthropogenic land conversion and population encroachment into wildlife habitats are amplifying zoonotic risks through intensified human-livestock-wildlife contacts. As ecologically resilient rodents exhibiting dynamic population fluxes, long-tailed marmots (Marmota caudata) are crucial viral reservoirs in Central Asian ecosystems. Their sympatric coexistence with domestic herds creates sustained spillover risks, yet comprehensive virome characterization remains limited. This study employs a whole-virome profiling strategy to comprehensively characterize the viral diversity of 101 wild M. caudata across 5 habitats in Xinjiang, aiming to address key knowledge gaps in rodent-borne zoonoses under anthropogenic pressures.

Results: Our study identified 3314 viral contigs spanning 21 families, with intestinal and lung samples exhibiting the highest viral diversity. Organ-specific tropism was characterized by preferential niches, notably adenoviral predominance in intestinal ecosystems and herpesviral selectivity for lymph node microenvironments. Phylogenetic reconstruction suggested potential cross-species transmission of rotavirus and ephemerovirus from bovines to marmots, along with the identification of 72 novel viruses expanding taxonomic diversity across 17 species and 2 genera. Particularly, two novel coronaviruses showing lung tropism are sufficiently divergent to be new subgenus candidates within the genus Betacoronavirus.

Conclusions: This comprehensive virome profiling delineates the ecological niches of marmot-associated viruses and identifies a diversity of uncharacterized mammalian viruses, including taxonomically novel lineages and multiple potential zoonotic pathogens requiring prioritized attention. These findings expand our understanding of the circulation dynamics and diverse background of marmot viruses, providing preliminary data for developing surveillance frameworks and prevention strategies targeting zoonotic risks associated with this ecologically pivotal species. Video Abstract.

Background: The pathogenesis of neonatal calf diarrhoea (NCD), a critical disease that contributes to neonatal mortality in calves, remains nebulous.

Results: Inner Mongolia, a key region for cattle farming in China, was selected as a study area to provide a comprehensive overview of the epidemiology and treatment of calf diarrhoea. No significant correlation was found between the incidence of diarrhoea and sampling points or medications. The severity of diarrhoea cases was stratified into five levels based on faecal characteristics. To elucidate the pathogenesis of NCD, 16S rRNA gene and metagenomic sequencing analyses were performed across severity levels. Microbial diversity analyses revealed distinct variations in microbial communities at different severity levels. Employing binning and LEfSe methodologies, two potential bacterial pathogens were identified: Escherichia coli (bin.216), leveraging non-canonical virulence mechanisms; and Streptococcus ruminantium (bin.338), an uncharacterised diarrhoeagenic bacterium. Furthermore, the viral agent Escherichia phage VpaE1_ev108 was significantly associated with disease progression. Gene function enrichment analysis revealed a broad spectrum of antibiotic resistance genes even in farms without direct antibiotic treatment, underscoring the pervasive prevalence of drug resistance.

Conclusions: The findings of this study revealed significant gut microbial dysbiosis in calves with severe diarrhoea, through which two putative NCD-associated pathogens were identified: E. coli (bin.216) and S. ruminantium (bin.338). Marked enrichment of Bacteroides spp. and Methanobrevibacter_A sp. 900313645 was observed in healthy cohorts, suggesting their potential protective roles. Therapeutic strategies employing phage-mediated pathogen targeting combined with probiotic transplantation have demonstrated dual benefits, potentially reducing antimicrobial dependency and preserving microbial homeostasis through ecological network reconstruction. Video Abstract.

Background: Accurately forecasting the dynamic behavior of microbial communities from sparse longitudinal data remains a critical challenge for microbiome-based precision medicine and ecological monitoring. Most existing models depend on data interpolation and assume population-level dynamics, which limits their ability to capture personalized microbial changes in real-world scenarios.

Results: We propose MicroProphet, a personalized temporal-aware framework capable of accurately forecasting microbial abundance trajectories from incomplete longitudinal observations without requiring data imputation. Powered by a time-aware Transformer architecture, MicroProphet reconstructs subject-specific microbial trajectories using only the initial 30% of observed time points, capturing critical transitional states through an attention mechanism. We demonstrated its robust cross-ecosystem generalizability across synthetic communities, human gut microbiomes, infant gut development, and corpse decomposition. The framework consistently achieves high predictive accuracy and biological interpretability. In clinical contexts, the framework enables early detection of disease-associated microbial shifts and supports timing optimization for microbiome-targeted interventions. In forensic settings, it accurately infers decomposition timelines from early microbial signals.

Conclusions: By transforming incomplete, noisy microbiome data into actionable, individualized forecasts, MicroProphet lays the foundation for a new class of temporal-aware systems in microbial ecology and precision health.

Background: The gut microbiota in patients with Graves' orbitopathy (GO) may influence the disease's progression, but its specific role and function in the progression of GO treatment are not well understood.

Methods: We performed fecal microbiota sequencing using the 16S rRNA-gene sequencing on patients with GO (n = 48), Graves' disease (GD, n = 40), and healthy controls (HC, n = 36). Subsequently, fecal samples from patients with GO, GD, and healthy donors were transplanted into antibiotic-treated pseudo-germ-free mice. Finally, the 48 patients with GO were randomly divided into two groups: one group received intravenous glucocorticoids (ivGC) and atorvastatin (n = 24), while the other group received ivGC only (n = 24), to observe the effects of atorvastatin on GO progression and its impact on gut microbiota.

Results: Patients with GO exhibit a distinct gut microbiota composition, particularly marked by increased levels of Prevotella and Bacteroides, compared to patients with GD and HC. Correlation analysis revealed a direct positive association between Prevotella and thyrotropin receptor antibody levels. Antibiotic-treated pseudo-germ-free mice that received fecal transplants from patients with GO exhibited a slower rate of weight gain, significant impairment of intestinal barrier integrity, and markedly increased levels of serum LBP and inflammatory factors. A combined treatment regimen of ivGCs and atorvastatin significantly reduced ocular clinical symptoms in patients with GO, including clinical activity score, exophthalmos, and intraocular pressure, while also promoting a healthier gut microbiota composition and a reduction in Prevotella levels.

Conclusions: Gut microbiota imbalance, particularly involving Prevotella, contributes to GO's development and progression. Atorvastatin may slow GO progression by correcting dysregulated gut microbiota, especially reducing Prevotella. Video Abstract.

Background: Gut-educated IgA-secreting plasma cells that disseminate beyond the mucosa and into systemic tissues can help prevent disease in several contexts. Many species of bacteria have been described as efficient inducers of mucosal IgA, including the commensal bacteria Bacteroides fragilis (Bf); however, less is known about inducers of systemic IgA responses.

Results: Here, we show that the generation of bone marrow IgA plasma cells and high levels of serum IgA specific to Bf requires robust intestinal colonization. Bf-specific IgA responses were severely diminished in mice lacking Peyer's patches, but not mice lacking a cecal patch. Colonization resulted in few changes in the host transcriptional profile in the gut, suggesting a commensal relationship and minimal extrafollicular stimulation. The high levels of Bf-specific serum IgA induced by colonization provided protection from peritoneal abscess formation in a bowel perforation model of Bf dissemination.

Conclusion: These findings demonstrate a critical role for bacterial colonization and interaction with Peyer's patches for the induction of a robust systemic IgA response. The presence of high levels of serum IgA specific to Bf confers protection from bacterial dissemination and abscess formation in a model of bowel perforation. Video Abstract.

Background: Continuous cropping obstacles (CCO) pose a persistent threat to global soybean sustainability, yet paradoxically attenuate under prolonged monoculture. To explore this, we investigated the soil-plant-microbiome dynamics across 1-year, short-term continuous cropping (STCC, 7-13 years), and long-term continuous cropping (LTCC, 19-25 years) systems.

Results: Our results reveal that LTCC reduces the accumulation of allelopathic autotoxin by 49.06% (P < 0.05) and enriches beneficial rhizosphere metabolites (e.g., antibiotics, monoterpenes, and glycoside compounds), driving a shift in the microbial community towards taxa with pathogen-suppressive and nutrient-cycling functions. LTCC cultivated a microbiome with enhanced genes for stress resistance and nutrient uptake. Conversely, STCC exacerbates CCO stress, with microbial dysbiosis peaking at 13 years (Simpson index down 15.4%). Notably, 25-year LTCC restores ecosystem stability and enzyme activity, restructuring microbial communities with pathogen-suppressive and nutrient-cycling functions. By reintroducing depleted taxa including Pseudomonas, Burkholderia, and Enterobacter spp., we constructed a synthetic community, SC7. SC7 boosted soil enzymes and root nodules to shield plants from stress, increasing yield by 4.83% and mimicking long-term system advantages.

Conclusions: This study demonstrates the self-repair capacity of soybean monoculture. It bridges the gap between mechanistic insights, specifically the microbiome-metabolite feedback, and actionable solutions, such as SC7 inoculation. As a result, it advances sustainable intensification strategies for global soybean production. Video Abstract.

Background: The maternal gut microbiota can modulate host physiological homeostasis through metabolites. Maternal reproductive potential hinges on placental angiogenesis and nutrient transport efficiency, directly determining fetal developmental outcomes. However, the specific molecular mechanisms by which microbial metabolites influence reproductive potential remain to be elucidated. This study aimed to clarify the mechanisms by which maternal gut microbiota affects reproductive potential.

Results: We initially analyzed the metabolic profiles by untargeted metabolomics and the fecal microbiota by 16S rRNA sequencing in sows with different reproductive potential. Sows with high reproductive potential exhibited elevated plasma arginine and fecal thiamine levels. Meanwhile, Lactococcus was enriched in the feces of sows with high reproductive potential. Subsequently, we evaluated the effects of thiamine (a signature metabolite identified) on maternal reproductive potential, gut microbiota, placental angiogenesis, and nutrient transport capacity using a rat model. The results showed that thiamine supplementation in pregnant rats effectively promoted offspring growth and enhanced transplacental thiamine metabolism. Moreover, thiamine modulated maternal gut microbiota composition, increased the abundance of Prevotellaceae Ga6A1 group and Bacteroidale RF16 group unclassified, and promoted butyrate production. We found that thiamine improved placental function by enhancing thiamine-related metabolic enzymes and acetyl-CoA content. It also promoted the migratory capacity of pTr cells. Importantly, thiamine facilitated placental angiogenesis by activating Notch signal transduction, which in turn initiated the PI3K/AKT signaling cascade. Ultimately, this cascade regulated the efficiency of placental nutrient metabolism and the expression of nutrient transporters.

Conclusions: Cumulatively, the gut microbiota regulates early offspring development through metabolite-mediated host interactions. This study provides new evidence that maternal gut microbiota-derived thiamine activates placental Notch signaling to coordinate angiogenesis and nutrient transport, thereby improving pregnancy outcomes. These findings provide novel perspectives and potential actionable strategies for maternal microbial regulation of maternal-fetal health during gestation.

Background: The emerging concept of the pathobiome has revolutionized our understanding of disease etiology by emphasizing the complex interactions between multiple pathogens and their hosts during disease progression. Although significant advancements have been made in characterizing the pathobiome in human, animal, and plant diseases, the pathobiome associated with seaweed diseases remains unexplored. Saccharina japonica, a commercially important farmed seaweed, has increasingly suffered from bleaching disease during its nursery stage, severely compromising the supply of healthy sporelings and sea field cultivation. Despite its significant economic consequences, the pathobiome associated with this bleaching disease and its interactions with the host remain unclear, posing a major challenge for disease control.

Results: Through multi-omics and meta-omics analyses, we identified the pathobiome associated with bleaching disease in S. japonica and elucidated its interactions with the host. The pathobiome is dominated by the core taxa Bin_7 (Glaciecola sp.), Bin_12 (Arenicella sp. 017854775), and Bin_22 (Arenicella sp.), which employ virulence mechanisms such as chemotaxis, motility, and toxin secretion to initiate infection. In response, the host S. japonica activates a multifaceted defense, including mechanisms like cell wall strengthening, reactive oxygen species bursts, and antibiotic production to combat the invading pathobiome. To counteract these host defenses, the core pathobiome taxa upregulate genes associated with antioxidant enzymes and antibiotic resistance, enabling their establishment and persistence within the host.

Conclusions: This study provides the first analysis of the pathobiome in seaweed diseases. By identifying the core taxa of the pathobiome, their virulence mechanisms, and the host defense responses, we elucidate the pathobiome-host interactions underlying S. japonica bleaching disease. These findings significantly advance our understanding of the pathobiome in seaweed diseases and lay the groundwork for developing targeted strategies to control the bleaching disease in seaweed aquaculture. Video Abstract.

Background: Many coastal ecosystems worldwide are impacted by wastewater discharges, which introduce nutrients, pollutants, and allochthonous microbes that can alter microbiome composition and function. Although the severity and distribution of these impacts vary across regions, their potential consequences for key ecological processes remain a concern. The resilience and functional adaptability of native coastal microbiomes are still poorly understood. To study the immediate ecological impact of wastewater discharge on a coastal seawater microbiome, we conducted short-term microcosm experiments, exposing a coastal microbiome to two types of treated wastewater: (i) unfiltered wastewater containing nutrients, pollutants, and allochthonous microbes; and (ii) filtered wastewater containing only nutrients and pollutants.

Results: By integrating multi-omics and metabolic assays, we show that wastewater-derived organic matter and nutrients (mostly ammonia and phosphate) did not alter the taxonomic composition of the coastal microbiota, but triggered reorganization of metabolic pathways in them. We observed enhanced metabolism of proteins, amino acids, lipids, and carbohydrates, particularly of the lineages Alteromonadales, Rhodobacterales, and Flavobacteriales. Glaciecola (Alteromonadales), a copiotroph with antagonistic traits, significantly contributed to these shifts. Conversely, allochthonous taxa like Legionellales and Pseudomonadales had minimal impact. Elevated phosphorus concentrations resulting from wastewater input reduced the synthesis of proteins linked to scavenging phosphorus from organic phosphorus compounds, including alkaline phosphatase activity in native Rhodobacterales and Flavobacteriales, with important ecological implications for phosphorus-depleted coastal ecosystems. Furthermore, the presence of wastewater caused a decline in relative abundance and metabolic activity of Synechococcus, potentially affecting carbon cycling. Yet, the coastal microbiome rapidly respired wastewater-derived dissolved organic carbon, resulting in bacterial growth efficiencies consistent with global coastal averages.

Conclusions: Our findings highlight the capacity of coastal microbiomes to withstand wastewater discharge, with critical implications for assessment of anthropogenic perturbations in coastal ecosystems. However, wastewater-driven changes in metabolic functions and niche utilization within the autochthonous microbial community, impacting phosphorus cycling and potentially affecting carbon cycling, may have long-term consequences for ecosystem functioning. Video Abstract.