搜索结果：Gut microbes

The gut microbiome is increasingly recognized as a central regulator of immune homeostasis, metabolic balance, and therapeutic outcomes. Atopic dermatitis (AD), a chronic inflammatory skin disease, is closely linked to gut microbial dysbiosis. Traditionally regarded as a neurostimulatory therapy, acupuncture (Acu) has demonstrated increasing efficacy in alleviating AD symptoms and improving gastrointestinal function. These observations suggest that the therapeutic effects of Acu in AD may be mediated, in part, by modulation of the gut microbiome. In this study, AD patients were stratified into responder (R) and non-responder (NR) groups based on clinical improvement. Gut microbiome profiling revealed that R patients exhibited greater microbial diversity and compositional stability, indicative of a more balanced gut ecosystem. Specific taxa, including Alistipes ihumii and Odoribacter splanchnicus, were enriched in R individuals and may serve as microbial predictors of treatment responsiveness. Importantly, fecal microbiota transplantation (FMT) from R donors restored Acu efficacy in a mouse model of AD, whereas FMT from NR donors did not. These findings support the gut-skin axis and highlight the integral role of the gut microbiome in mediating the therapeutic effects of Acu for AD, suggesting potential for microbiome-based personalized treatment. Increasing evidence supports the gut microbiome's role in modulating treatment responses in atopic dermatitis (AD), but direct evidence linking acupuncture efficacy with microbiome composition has been lacking. Previous studies did not assess causal relationships via fecal microbiota transplantation (FMT) or functional metagenomics. This study identifies specific gut microbes associated with acupuncture response in AD and confirms their causal role using FMT. It also links functional metabolic pathways to therapeutic efficacy, offering a mechanism-based insight. Our findings support microbiome-informed personalized acupuncture approaches for AD and suggest gut microbiota as a therapeutic modulator in neuroimmune regulation. This study was registered in the Korean Clinical Trial Registry (CRIS, registration number: KCT0005422).

In geriatric syndrome (GS), conditions like cognitive impairment and constipation reduce quality of life. Gut microbiota may influence GS progression via the gut-brain axis. This exploratory study investigated potential causal associations and microbial characteristics between gut microbiota and constipation, including constipation with mild cognitive impairment. Two-sample Mendelian randomization (MR) was performed to explore potential causality between gut microbiota and constipation. Inverse variance weighted (IVW) was the primary method, with sensitivity analyses using MR-Egger, weighted median, and MR-PRESSO. False discovery rate (FDR) correction was applied for multiple testing. Two-sample MR used summary statistics from MiBioGen (n=18,340) and FinnGen (51,956 cases). The observational study included 88 participants. Subsequently, fecal samples from 88 elderly participants (30 constipation+MCI, 28 constipation, 30 controls) were analyzed using 16S rDNA sequencing.Gut microbiota was profiled by 16S rDNA V3-V4 sequencing. Alpha diversity (Chao1, Shannon, Simpson) and beta diversity (Bray - Curtis PCoA with Adonis) were assessed. LEfSe (LDA > 4) identified differentially abundant taxa. Functional potential was predicted by Tax4Fun2. MR analysis indicated that the genus Oscillibacter may exert a protective effect against constipation, whereas the family Rikenellaceae, genus Enterorhabdus, and genus Victivallis were identified as risk factors. 16S sequencing showed significant structural differences among groups, though these findings are observational.LEfSe analysis identified Enterococcus-related taxa as characteristic features of the constipation+MCI group, whereas Bifidobacterium-related taxa were enriched in controls. Relative abundance analysis also suggested group-specific differences in Escherichia-Shigella, Prevotella_9, and Enterobacter. The findings offer preliminary evidence that specific gut microbes may be associated with constipation. Distinct microbial features and functional changes are associated with constipation and constipation+MCI. Gut microbiota dysbiosis might link constipation and cognitive impairment, providing exploratory clues rather than definitive conclusions for future hypothesis-driven and microbiota-targeted studies.

Antibiotic resistance has arisen as a formidable challenge to global health governance. Antimicrobial peptides (AMPs) have garnered considerable attention as highly potent alternative to antibiotic for preventing resistant pathogens. In this study, the AMP Hidefensin5 (Hi5), derived from Hermetia illucens, was designed and exhibited antibacterial activity against gram-negative pathogenic bacteria at a concentration of 100 μg/mL. Furthermore, the ecological effects of applying crude Hi5 fermentation and purified Hi5 as feed additives on the structure of the gut microbiota and the antibiotic resistance gene (ARG) profile of zebrafish were assessed. The findings indicated that compared with unpurified Hi5, purified Hi5 markedly enhanced the microbial α-diversity and simultaneously reduced the accumulation of pathogenic bacteria (PBs) and the prevalence of drug resistance-related metabolic pathways, as well as the energy metabolic burden within the gut microbiota. With respect to the ARG resistome, purified Hi5 application reduced the absolute ARG abundances across risk ranks I to IV and the co-association patterns of ARGs-mobile genetic elements-PBs, whereas unpurified Hi5 increased the risk of pathogens developing drug resistance. This study confirmed that purified AMP application contributed to hindering the development of drug-resistant PBs, providing a valuable reference for antimicrobial resistance risk management in antibiotic-free aquaculture.

The gut microbial community plays a key role in maintaining the host immune homeostasis. However, current analytical approaches analyze individual taxa rather than gut communities, thereby missing community-level functions performed by units, such as ecological guilds. Delineating ecological units is a promising approach for summarizing the functional output of microbes and their impact on the host. In this study, we investigated gut bacteria in 33 tuberculosis patients and 47 healthy controls using enterosignatures (ESs), ecological units of co-occurring bacteria related by function. We focused on detecting enterosignatures enriched in the gut communities of tuberculosis (TB) patients. For each patient-enriched enterosignature, we counted the metabolic pathways encoded by its member species. In this manner, we characterized the functional potential of ecological guilds enriched in TB patients. Finally, we tested whether ecological guilds correlate more closely with disease and host biomarkers. We show that inferred ESs represent reproducible units that facilitate proper comparison of identified ecological guilds to those observed in worldwide donor populations. Namely, dominant enterosignatures in the analyzed healthy donors reproduced the same ecological guilds observed among healthy individuals worldwide. In contrast, most TB patients carried two enterosignatures (ES-Bifi and ES-Esch) that were hallmarks of disturbed gut communities and atypical for healthy adults. We estimated the abundance of metabolic pathways encoded by member species of these patient-enriched ESs. We found that an increase in bacterial species comprising ES-Bifi and ES-Esch harbor an increased number of pathways for fermenting simple sugars, with end products such as acetate and lactate. A greater number of ecological guilds that ferment glucose to lactate might indicate an altered gut environment in patients, including increased acidity and disturbed carbohydrate flux. Taken together, our analyses suggest that ESs represent a biologically meaningful unit for reducing the complexity of the human gut microbiome and a tool for recognizing sharper patterns behind noisy taxonomic and functional diversity.

Gut microbiota dysbiosis is a crucial driver of the initiation and progression of colorectal cancer (CRC), where functional gut microbes and their metabolites play key roles in the microecological regulation of CRC. Currently, the association between Lachnospiraceae and CRC progression, as well as the underlying mechanisms, remains incompletely understood and warrants further investigation. Bioinformatics analysis was performed to explore the co-pathway association between gut microbiota and metabolites in CRC patient samples. In vivo animal models were established to assess the regulatory effects of Lachnospiraceae on CRC tumorigenesis and gut microbiota homeostasis. The anti-CRC activities of Lachnospiraceae and its metabolite malate were investigated using in vitro experiments that measured cell viability, proliferation, apoptosis, and colony formation. Western blotting was performed to detect the expression levels of key proteins in the Wingless/Integrated (Wnt)/β-catenin signaling pathway. Bioinformatics analysis revealed that malate was significantly downregulated in CRC patients, accompanied by gut microbiota dysbiosis driven predominantly by short-chain fatty acid (SCFA)-related Firmicutes such as Lachnospiraceae and Ruminococcaceae. In vivo, Lachnospiraceae restored gut microbiota homeostasis, reduced tumor number, and decreased tumor load. In vitro, Lachnospiraceae suppressed colorectal tumorigenesis and increased colonic D-malate levels. Lachnospiraceae bacterium biologics abstracts accession-2278 (BAA-2278) is associated with anti-CRC effects in preclinical models, potentially mediated through regulation of gut microbiota homeostasis and inhibition of Wnt/β-catenin signaling via its metabolite malate.

Careful dissection of insect gut tissues is essential for microbiome studies to ensure accurate characterization of internal microbial communities and preservation of DNA integrity. Because insect-associated microbiomes are highly sensitive to contamination, effective removal of external microbes prior to dissection is critical to minimize bias in downstream analyses. While ethanol- and bleach-based surface sterilization methods are commonly used, standardized workflows integrating field collection, sterilization, and dissection remain limited. Here, we present a step-by-step protocol for the field collection, surface sterilization, and dissection of gut tissues from the agricultural pest Diaprepes abbreviatus (Coleoptera: Curculionidae), optimized for genomic DNA extraction and microbiome analyses. Using wild-caught specimens, this workflow incorporates a rigorous surface sterilization and dissection strategy that minimizes external contamination while preserving biologically relevant microbial signatures and DNA integrity for downstream microbiome analyses. The protocol provides a standardized framework for insect gut microbiome studies and can be broadly adapted to other wild-caught insect species requiring careful collection, disinfection, and sterile dissection prior to molecular analysis. The protocol integrates field collection and laboratory processing steps into a streamlined workflow that minimizes contamination while preserving tissue integrity for downstream applications. Key features • Designed for wild-caught Diaprepes abbreviatus collected directly from agricultural host trees, this protocol can also be adapted for other insect species. • Integrates field collection, surface sterilization, and sterile gut dissection into a single workflow to minimize contamination. • Sequential ethanol and diluted bleach treatment effectively removes external microbes prior to dissection. • Enables isolation of intact gut tissues suitable for high-quality DNA extraction and downstream microbiome sequencing.

Radiotherapy is an essential component of multimodal treatment for solid tumors, and more than half of patients with cancer receive radiation during their disease course. Because of the unique anatomical and physiological features of the intestine, radiation enteritis (RE) remains a common and clinically challenging complication of abdominal and pelvic irradiation, with limited effective treatment options. In this review, we re-examine RE from a host-microbiome perspective. We summarize classical pathophysiological mechanisms and discuss how radiotherapy reshapes gut microbial composition and metabolism. We also highlight the roles of microbial metabolites, including short-chain fatty acids, bile acids and tryptophan derivatives, in barrier repair, immune homeostasis and stem-cell regeneration. Finally, we discuss microbiome heterogeneity across disease phases, tumor types and host factors, as well as microbiota-mediated gut-brain, gut-cardiopulmonary, gut-skin and gut-bone-marrow axes involved in systemic radiation injury. We further outline microbiome-based strategies for individualized risk stratification and early prediction, and recent advances and limitations of probiotics and synbiotics, fecal microbiota transplantation, dietary and lifestyle interventions, drugs and natural products, engineered microbes and novel delivery systems, highlighting the gut microbiome as a promising entry point to improve prevention and treatment of RE and systemic radiation toxicity.

Parkinson's disease (PD) is a neurodegenerative disorder increasingly associated with gut microbiota alterations, yet the mechanisms by which microbial metabolites influence PD remain unclear. Here, we applied an integrative computational and experimental strategy to identify key gut microbial metabolites and host genes potentially involved in PD. Differentially abundant gut microbes were obtained from the gutMDisorder database and their corresponding metabolites from gutMGene, with predicted protein targets generated using the Similarity Ensemble Approach. Transcriptomic data from PD brain tissues were analyzed to identify differentially expressed genes, which were intersected with metabolite targets, followed by enrichment and protein-protein interaction analyses. Three machine learning algorithms were applied for gene prioritization, while molecular docking evaluated metabolite-gene binding affinities and ProTox3.0 predicted toxicity and blood-brain barrier permeability. In vitro assays further assessed the functional effects of 3-indolepropionic acid in a rotenone-induced SH-SY5Y cell model. Our analyses identified 44 PD-associated microbial taxa linked to 77 metabolites and 905 predicted target genes, with 29 overlapping differentially expressed genes enriched in synaptic signaling and dopaminergic pathways. Dopamine receptor D2 (DRD2) emerged as a central hub gene, with strong docking interactions predicted for two indole metabolites, 3-(1H-indol-3-yl)propanoate and 3-indolepropionic acid. Functional validation showed that 3-indolepropionic acid improved cell viability, reduced apoptosis, and preserved DRD2 expression under neurotoxic stress. Together, these findings suggest that specific gut microbial metabolites may modulate host dopaminergic signaling via DRD2, offering new insights into the microbiota-brain axis and potential targets for further PD research.

In recent years, gut microbiota has emerged as a central modulator of cardiovascular health and disease. This has led to a transition from the old understanding of cardiovascular pathology as a largely cardiac-centric problem to a systemic, multi-organ process. A growing body of evidence demonstrates that changes in the makeup of gut microbes, generally called dysbiosis, are significant in the development and progression of cardiovascular illnesses, including heart failure. Moreover, there are bidirectional interactions between the failing heart and the gut. In heart failure, impaired hemodynamics and venous congestion further worsen intestinal hypoperfusion and barrier dysfunction in a self-perpetuating cycle that exacerbates dysbiosis and systemic inflammation. The gut-heart axis offers a fresh paradigm for illness progression beyond classical neurohormonal and hemodynamic processes. The gut microbiota acts as an endocrine organ by producing bioactive metabolites such as TMAO (trimethylamine N-oxide), SCFA (short-chain fatty acids) and bile acids, which, via several routes, have a serious impact on host health and disease. This narrative review aims to summarize the current evidence for the gut microbiota as a new cardiovascular risk factor, focusing on biological mechanisms and clinical and epidemiological evidence.

Roux-en-Y gastric bypass (RYGB) induces durable weight loss and metabolic improvement, but the role of oral microbiota in shaping postsurgical gut ecology and metabolic outcomes is unclear. We examined whether RYGB promotes transfer and expansion of oral strains in the distal gut and how these relate to hepatic and glycemic health. In 25 patients from a longitudinal RYGB cohort, paired oral and fecal samples were collected before and 12 months after surgery. We examined the presence, abundance, and structure of cohort-specific canonical oral strains in the gut, and assessed α/β-diversity, cross-site correlations, and clinical associations using univariate tests and linear models. Machine-learning models evaluated the prognostic value of oral canonical strains for hepatic and glycemic outcomes. Oral taxon richness increased after RYGB, while Shannon diversity and individual signatures remained stable. In the gut, canonical oral strains expanded: shared oral-gut strains and their summed abundance rose significantly, converging into a reproducible post-RYGB niche. Abundance and fold change of oral-canonical strains associated with FIB-4, ASAT and fasting glucose, and predictive models suggested a prognostic signal for fasting glucose, TBF% and HbA1c. RYGB is associated with reproducible, strain-level enrichment of oral microbiota in the gut, with links to hepatic and glycemic outcomes.

The gut microbiome of termites plays a crucial role in lignocellulose degradation and nutrient recycling. This study presents the first metagenomic characterization of the gut microbiota in two lower termite species, Anacanthotermes ahngerianus and Anacanthotermes turkestanicus, collected from distinct ecological habitats. In Uzbekistan, the first lives in building a mound in nature in the West part while the second mainly lives in contact with human constructions in the East part without building a proper mound. Both species showed similar bacterial dominance (~53%) in their guts but A. ahngerianus exhibited higher overall microbial diversity (Shannon index: 4.046 vs. 3.363; Simpson's index: 0.927 vs. 0.776). Moreover, both termite species showed differences in microbial profiles, including bacterial taxa and eukaryotic groups relevant to lower-termite gut symbiosis. Protist-associated eukaryotic reads were retained because flagellated protists are essential symbionts of lower termites, whereas unexpected non-protist eukaryotic assignments were interpreted cautiously and were not used as evidence of functional gut symbionts or host adaptation. Functional profiling revealed enrichment of pathways related to carbohydrate metabolism, amino acid transport, and energy production in both species. However, A. turkestanicus exhibited stronger bacterial dominance associated with lignocellulose degradation and nitrogen cycling, while A. ahngerianus maintained a more balanced representation of bacteria, fungi, and viruses. These findings suggest that species identity and ecological habits may be associated with differences in gut microbiome structure and predicted functional potential.

Diarrhea-predominant irritable bowel syndrome (IBS-D) is characterized by diarrhea and is often accompanied by depression, abdominal symptoms, and emotional comorbidities. Preclinical and clinical studies have shown that dysfunction of the brain-gut axis is a key pathogenic factor in IBS-D, yet the specific mechanisms remain unclear. Saikosaponin D (SSD), a major bioactive component of Bupleurum chinense DC., exhibits anti-inflammatory, antidepressant, and antitumor activities, with multi-target and multi-pathway interactions. Acetic acid and restraint stress induced an IBS-D mouse model. SSD (purity ≥ 98%, Macklin Inc.) was administered orally at low, medium, and high doses (5, 10, 20 mg/kg). Visceral sensitivity, inflammatory status, intestinal barrier function, HPA axis activity, and gut microbiota composition were systematically evaluated using behavioral tests, Western blot, qRT-PCR, and 16S rRNA sequencing. SSD significantly alleviated visceral hypersensitivity and depression-like behavior, inhibited the peripheral HMGB1-TLR4/NF-κB inflammatory pathway, and restored intestinal barrier integrity. SSD also downregulated hypothalamic Nesfatin-1/CRH/p-CREB expression, suppressed hyperactivation of the stress-related HPA neuroendocrine axis, and reshaped the gut microbial community structure (β-diversity). Network pharmacology analysis suggested that SSD targets were significantly enriched in brain-gut axis-related pathways. The present results indicate that SSD could ameliorate IBS-D by synergistically regulating peripheral inflammation, central stress, and intestinal microbes via the brain-gut-microbiota axis, providing experimental evidence for its potential application in TCM-based treatment.

Fibromyalgia (FM) has been increasingly studied in the context of gut-brain-immune interactions, and several reports have suggested an association between FM and alterations in gut or oral microbial communities. However, prior studies have often suffered from heterogeneous comorbidities, inconsistent sampling procedures, and limited control for environmental factors, making it unclear whether FM is associated with a reproducible, site-independent microbial signature. To determine whether women with FM exhibit consistent alterations in gut or oral microbiota when evaluated under strictly standardized physiological, clinical, and environmental conditions. A prospective, observational, case-control study. The Department of Pain Medicine and Department of Medical Microbiology at Gazi University, Türkiye. The patient selection comprised 31 women (16 with FM; 15 healthy controls) who met rigorous inclusion and exclusion criteria, minimizing confounding from diet, metabolic disease, medications, hormonal status, and recent infections. No therapeutic intervention was performed; all patients provided paired oral mucosal and fecal samples during the follicular phase of the menstrual cycle. Sequencing of 16S rRNA V3-V4was performed on DNA extracted from all samples. Alpha and beta diversity metrics, taxonomic profiles, and differential abundance analyses (including LEfSe with FDR correction) were compared between groups. The clinical severity of FM was assessed using scores on the visual analog scale (VAS), Widespread Pain Index (WPI), and Symptom Severity Scale (SSS). No statistically significant differences were observed between FM patients and controls in fecal or oral alpha diversity (Shannon, Simpson, Chao1, Observed OTU indices, all P > 0.05). Beta diversity analyses (Bray-Curtis PERMANOVA) revealed no between-group separation in either compartment (fecal R² = 0.032, P = 0.529; oral R² = 0.032, P = 0.464). Both groups displayed preserved core microbial communities in the gut, dominated by Firmicutes and Bacteroidota and, in the oral cavity, Streptococcus-enriched profiles. Minor genus-level variations were detected, but none remained significant after FDR correction. Cross-site analyses confirmed the expected ecological divergence between oral and fecal habitats but identified no FM-specific microbial pattern. Post hoc sensitivity analysis indicated that the study was powered to detect only moderate effect sizes (R² ≥ 0.11), suggesting that subtle differences might have remained undetected. A modest sample size, a lack of quantitative dietary assessment, and reliance on 16S rRNA sequencing limited the detection of subtle or functional microbial alterations. Additionally, the cross-sectional design precludes causal inference. Under highly controlled sampling and exclusion conditions, FM was not associated with detectable alterations in the diversity or composition of gut or oral microbes. These findings suggest that previously reported dysbiosis may reflect comorbidity-driven or phenotype-specific variation rather than a universal microbial hallmark. Larger, multi-omic and phenotype-stratified studies are needed to clarify functional host-microbiome interactions in FM.

The growing food allergy epidemic is thought to be related to changing environmental factors, particularly changes in the gut microbiome. While prior work has demonstrated that food allergy can be modulated by gut microbes, little is known about how food allergen-specific CD4+ T cells are affected by gut microbial composition. Here, we report that food allergy severity differs between mice obtained from 2 different specific pathogen-free mouse vendors (Jackson Labs [Jax] and Taconic Biosciences [Tac]). Mice from Tac develop diarrhea and anaphylaxis after fewer allergen exposures than mice from Jax. Using food allergen peptide: MHCII tetramers, we also find that Tac mice have fewer allergen-specific regulatory T cells in the small intestine compared to mice from Jax with concomitant increase in allergen-specific Th2 cells. In addition, Tac mice have increased intestinal permeability. Increased food allergy severity, phenotype of allergen-specific T cells, and increased gut permeability were transferable to Jax animals via co-housing, which corresponded to a shift in Jax microbial communities towards those found in Tac mice. Our findings demonstrate that food allergen-specific Treg cells can be modulated by gut microbial community composition, which in turn is correlated to food allergy severity.

The gut microbiota influences host metabolism, but the mechanisms of lipid uptake from food remain mysterious. Here we used stable isotope-labelled tracers in gnotobiotic mouse models, which revealed that host uptake of dietary lipids depends on microbial colonization. Systemic lipid metabolism modelling predicted that the gut microbiota restricts intestinal lipid absorption, and labelled lipid administration verified that the gut contents of microbiota-colonized mice contained up to 12-fold more lipids than those of germ-free animals. A combination of lipidomics and proteomics showed that gut microbes trigger Myd88 signalling, leading to a downregulation of hepatic Cyp7b1 activity and increased taurocholate production. Taurocholate stimulates phospholipase A1 activity in bile, causing the degradation of phosphatidylcholine that is essential for luminal micelle formation and lipid uptake. A diverse microbiome was associated with lower phosphatidylcholine content. This previously unrecognized host-gut microbiota interplay via enzymes in bile could provide future targets to modulate dietary lipid absorption.

Faecalibacterium prausnitzii is a dominant and health-associated member of the human gastrointestinal tract that is consistently depleted in individuals with metabolic, cardiovascular, and psychiatric disorders. Despite its importance in gut health, little is known about the bacteriophages (or phages) that infect this species. Phages are increasingly recognized as key regulators of bacterial population dynamics in the gut microbiota; however, while prophages of F. prausnitzii have been described, no lytic phages targeting this bacterium have been reported. Here, we describe the isolation and characterization of the first lytic F. prausnitzii bacteriophage, vB_Fpr_FP01. Whole-genome sequencing and comparative genomics analysis demonstrate that FP01 represents a novel species, clustering within a genus that includes an uncharacterized phage within the class Caudovirales. Comparative analysis also identified closely related viral sequences in the human gut virome dataset, suggesting that related phages occur in gut-associated environments. These findings expand the current knowledge of F. prausnitzii-associated phages and provide a framework for future studies investigating phage‒host interactions and their role in shaping gut microbial communities.

The intestinal flora forms a complex ecosystem that interacts with the host, influencing health and fitness through mechanisms that connect with distant organs like the brain, liver, muscles, and testes. The gut microbiota plays a vital role in regulating androgen production and metabolism, and can cross the blood-testis barrier to influence spermatogenesis. This review highlights the significance of the gut-testis axis in male reproductive and sexual health, based on extensive studies exploring how gut microbes impact testicular function. Gaining this understanding deepens our knowledge of the gut-testis axis and its role in male reproductive health.

Pollen limitation compromises honey bee health and pollination services, and existing pollen substitutes are typically formulated around crude protein content while lacking the long-chain omega-3 fatty acids naturally present in pollen and bee-collected re-sources. To address both protein and fatty acid gaps in current substitutes, this study evaluated marine-protein and insect-larvae-based diets. We assessed how formulations using Asian seabass (Lates calcarifer) and insect larvae affect the nutrition, physiology, longevity, and gut microbiota of Apis mellifera L. Newly emerged bees were fed for 35 days on: sugar syrup (negative control), sugar syrup and natural pollen (positive control), or four experimental diets: seabass-based (SB), or SB supplemented with meal-worm (SBM), or wax moth (SBW), or black soldier fly (SBB). Experimental diets (12.48-15.59% crude protein, vs. 17.24% in natural pollen) while SB supplied eicosapentaenoic acid (39.3-53.3 mg/100 g) and docosahexaenoic acid (37.2-52.3 mg/100 g), and SBB was additionally rich in lauric acid (604.3 mg/100 g). SBB- and SBM-fed bees exhibited the greatest hypopharyngeal gland development (0.123 mm and 0.115 mm, respectively, vs. 0.060 mm in sugar-only controls), with no significant difference from SB alone. All SB-based diets supported significantly greater survival than the sugar-only control (log-rank p < 0.0001) and did not differ significantly from the natural pollen treatment with SBB showing the highest and most consistent day-35 survival (81.1%). All sea-bass-based diets significantly altered the gut microbial community structure, promoting short-chain fatty acid (SCFA)-associated bacteria such as Faecalibacterium prausnitzii and Blautia wexlerae. This enrichment may reflect not only the omega-3 and lauric acid content of the diets but also the presence of substrates that can be utilized by gut microbes, which may exert prebiotic-like effects by favoring SCFA-producing bacteria. These results demonstrate that marine and insect-derived nutrients can supply protein while also providing beneficial lipids and microbially utilizable substrates that promote the enrichment of beneficial SCFA-associated bacteria not typically dominant in the honey bee gut. These enriched diets, particularly SBB, are promising candidates war-ranting further evaluation at the colony and field levels.

Despite the importance of the gut microbiota in human health, isolation and studies of phages infecting abundant gut bacteria have increased only in the past few years. The majority of phages isolated and characterized thus far infect facultative or strict aerobic bacteria. The aim of this study is to isolate and sequence new phages that infect Bacteroides species, which are abundant and prevalent members of the human gut microbiota across populations. Here, we report the isolation and genomes of seven phages infecting three human gut Bacteroides species from the United States. These phages are within the Caudoviricetes class and have siphovirus structural morphology. We observe a variable host range among five B. fragilis-infecting phages. This work provides resources to support further characterizations of gut-resident phages and their biology.