Aim: This study aimed to evaluate the combination of 2′-fucosyllactose (2′-FL) and Bifidobacterium longum subsp. infantis (B. infantis) EFEL8008 as a synbiotic pair for adult gut health, using an in vitro digestion and fecal fermentation model.
Methods: The resistance of 2′-FL to digestion was evaluated through simulated digestion encompassing oral, gastric, intestinal, and brush border membrane phases. Fecal fermentation was conducted using adult microbiota to investigate taxonomic and metabolic alterations following treatment with 2′-FL, EFEL8008, or their combination. Microbial composition was profiled using 16S rRNA gene sequencing and quantitative PCR targeting B. infantis. Short-chain fatty acids (SCFAs) and trimethylamine (TMA) levels were quantified by 1H-NMR.
Results: A total of 86.67% of 2′-FL remained intact after digestion, demonstrating its resistance to digestion throughout the upper gastrointestinal tract. The synbiotic combination significantly increased Bifidobacterium abundance and improved alpha diversity compared to single treatments. Heat tree and correlation analyses indicated selective enrichment of commensal taxa including Bifidobacterium and Lactobacillus, accompanied by a reduction in the abundance of potentially pathogenic genera such as Escherichia-Shigella. In addition, co-treatment markedly elevated the concentrations of acetate, propionate, lactate, and butyrate, and suppressed the microbial conversion of betaine to TMA, suggesting a favorable metabolic outcome.
Conclusion: These results demonstrate that the synbiotic combination of 2′-FL and EFEL8008 promotes beneficial microbial modulation, enhances metabolite production, and supports gut health, highlighting its potential as a next-generation synbiotic strategy.
Aim: Domestic cats, among the most popular pets globally, may harbor antimicrobial resistance genes (ARGs) and zoonotic pathogens that impact human health. This study aims to investigate the resistome and bacteriome composition in the upper respiratory tract of domestic cats with respiratory signs in China.
Methods: We performed metagenomic sequencing on 1,454 oropharyngeal-nasal swabs from cats with respiratory signs across diverse living conditions in 22 Chinese provinces. Resistome and bacteriome profiles were analyzed using these sequencing data.
Results: We characterized the resistome and bacteriome in the upper respiratory tract of cats, identifying a wide range of ARGs - including those conferring resistance to last-resort antibiotics {e.g., carbapenems (blaNDM,
Conclusion: The findings highlight the potential zoonotic risks posed by cats. Including monitoring of this companion species within the One Health approach to address public health concerns is necessary.
The rising prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) poses a significant global public health challenge. Bile acids (BAs), synthesized in the liver and further metabolized in the gut, are essential in maintaining host metabolic homeostasis. Bile salt hydrolase (BSH), an enzyme produced by the gut microbiota, catalyzes the hydrolysis of conjugated BAs, thus regulating the balance between primary and secondary BAs. Growing evidence suggests that BSH activity is intricately linked to the pathogenesis of MASLD. This review comprehensively examines the structural and functional properties of BSH enzymes, their distribution among gut microbial communities, and current methodologies for assessing BSH expression and activity. Furthermore, it highlights the alterations in BSH observed in MASLD and explores the potential mechanistic pathways involved, offering a foundation for the development of novel diagnostic and therapeutic strategies.
This review examines the impacts of F18+ Escherichia coli (E. coli) on the mucosa-associated microbiota, mucosal immune responses, oxidative stress, and intestinal morphology in the jejunum of nursery pigs. F18+ E. coli is a major cause of post-weaning diarrhea (PWD) in nursery pigs, mainly due to the production of enterotoxins that disrupt electrolyte balance in the intestinal lumen, leading to diarrhea, growth retardation, increased mortality, and economic losses. Experimental F18+ E. coli challenge models have shown an increased incidence of diarrhea (28.3%), along with reductions in average daily gain (24.1%), average daily feed intake (12.5%), and gain-to-feed ratio (14.9%). These adverse effects are largely attributed to microbial dysbiosis and heightened mucosal immune responses in the jejunum. The F18+ E. coli challenge also increases the abundance of harmful bacteria while reducing beneficial bacteria in the jejunal mucosa. Research using this challenge model has demonstrated elevated levels of tumor necrosis factor-α (14.9%), interleukin-8 (10.9%), immunoglobulin A (9.2%), immunoglobulin G (19.7%), malondialdehyde (50.7%), and protein carbonyls (32.3%). These immune and oxidative responses are associated with reductions in villus height (VH) (10.2%) and VH-to-crypt depth ratio (10.7%), as well as an increase in Ki-67+ proliferative cells (35.4%) in the jejunum. In conclusion, F18+ E. coli induces PWD and compromises intestinal health in nursery pigs through dysbiosis, inflammation, oxidative stress, and morphological changes, ultimately impairing growth.
Background: Arabinogalactan is a complex plant-derived polysaccharide proposed to function as a selective prebiotic, yet the microbial taxa directly involved in its metabolism and the cooperative dynamics within the gut microbiota remain incompletely defined.
Methods: Here, we combined community-level sequencing with targeted single-cell activity profiling to investigate how arabinogalactan shapes gut microbial composition and function. Fecal samples from ten healthy individuals were incubated ex vivo with arabinogalactan, and microbial responses were assessed using 16S rRNA gene amplicon sequencing alongside Raman-activated cell sorting (RACS) and coculture experiments.
Results: Arabinogalactan consistently enriched Bifidobacterium and Gemmiger across donors, with Bifidobacterium also responding to galactose and Gemmiger and Blautia stimulated by arabinose, the two monosaccharide components of arabinogalactan. RACS enabled the selective isolation of metabolically active arabinogalactan responders, including Bifidobacterium longum (B. longum) and Faecalibacterium prausnitzii, along with other strains from the phyla Actinomycetota, Bacteroidota, and Bacillota. Notably, coculture experiments revealed that B. longum not only degraded arabinogalactan efficiently but also supported the growth of non-degrading species via metabolic cross-feeding. These cooperative interactions highlight B. longum as a keystone species in arabinogalactan utilization and suggest broader community-level benefits from its activity.
Conclusion: Together, our findings demonstrate arabinogalactan’s bifidogenic effect and its potential to promote functionally important microbes within the gut ecosystem. This study also highlights the utility of RACS for linking microbial identity to function, enabling the targeted recovery of active strains from complex communities.
The gut microbiota critically regulates lipid metabolism through microbial metabolites and host signaling pathways. Short-chain fatty acids (SCFAs), derived from dietary fiber fermentation, suppress hepatic lipogenesis via inhibition of SREBP-1c and enhance mitochondrial β-oxidation through GPR41/43 activation. Microbial enzymes convert primary bile acids into secondary bile acids, which activate FXR to inhibit lipogenesis and TGR5 to promote adipose thermogenesis. Lipopolysaccharide (LPS) from dysbiotic microbiota triggers TLR4-NF-κB signaling, exacerbating insulin resistance and adipose inflammation. Branched-chain amino acids (BCAAs), metabolized by gut microbes, drive adipogenesis via mTORC1-PPARγ signaling, with elevated circulating BCAAs linked to obesity. In livestock, microbiota modulation optimizes fat deposition: probiotics in pigs enhance intramuscular fat via Lactobacillus-enriched communities, while dietary succinate or coated sodium propionate reduces abdominal fat in broilers by reshaping cecal microbiota. Fecal microbiota transplantation confirms microbial causality in transferring fat phenotypes. Dysbiosis-associated mechanisms are conserved across species, where SCFAs and bile acids ameliorate metabolic inflammation, whereas LPS and BCAA imbalances worsen lipid dysregulation. Metabolic disorders, including obesity, type 2 diabetes (T2D), and non-alcoholic fatty liver disease (NAFLD), are tightly linked to gut microbiota perturbations. Dysbiosis drives LPS translocation and barrier impairment. These changes, along with altered metabolites, promote inflammation and fat deposition. Future strategies should integrate multi-omics and precision engineering of microbial consortia to advance therapies for both livestock and human metabolic health.
The search for sustainable alternatives to antibiotic growth promoters in poultry production has intensified in recent years, driven by global concerns over antimicrobial resistance and consumer demand for safer food systems. Among the probiotic candidates investigated, Bifidobacterium spp. stand out for their well-documented safety, immunomodulatory properties, and ability to enhance gut health. This review provides a comprehensive analysis of the biological roles, delivery strategies, and microencapsulation techniques for Bifidobacterium spp. as probiotics in poultry. Bifidobacteria contribute to poultry health by modulating the gut microbiota, improving intestinal morphology and digestive enzyme activity, and regulating immune responses through cytokine balance and epithelial barrier reinforcement. However, their strict anaerobic metabolism and sensitivity to gastric acid and processing conditions limit their viability during conventional administration. To address these challenges, we examine various administration routes, including oral, in ovo, spray/litter, and cloacal methods, highlighting their practical advantages and constraints. Special attention is given to microencapsulation technologies, such as spray drying, freeze drying, spray chilling, extrusion, and emulsion, which protect bifidobacteria from environmental stress and enhance their delivery to target intestinal sites. By integrating recent advances in biotechnology and delivery systems, this review underscores the potential of Bifidobacterium spp. as functional feed additives in antibiotic-free poultry production. Tailoring encapsulation materials and administration routes to match specific production goals is key to maximizing probiotic efficacy. Continued research on strain performance under commercial conditions will be essential to facilitate their large-scale application in sustainable poultry farming.
Aim: This study provides a comprehensive genomic characterization of Streptococcus oralis CRC211, a novel bacterial strain isolated from colorectal tumor tissue.
Methods: Whole-genome sequencing and comparative genomic analyses were performed.
Results: The high-quality assembled genome (15.03 Mb, 40.94% guanine-cytosine content) contains 2 prophage regions spanning 160.5 kb, which may facilitate the horizontal transfer of virulence genes. Functional annotation identified 3,674 genes, with significant enrichment in metabolic pathways (amino acid and carbohydrate metabolism) and virulence factors (116 genes in Virulence Factors Batabase), including adhesins and biofilm-associated proteins that likely promote tumor colonization. Comparative genomic analysis revealed that CRC211 shares 92.29% average nucleotide identity with reference Streptococcus oralis strains, while pan-genome analysis demonstrated an open genome structure with 1,222 conserved core genes. In addition, the strain also carries 75 antimicrobial resistance genes, underscoring its potential clinical relevance. Notably, the genomic profile indicates adaptations for nutrient acquisition and immune evasion in the tumor microenvironment.
Conclusion: These findings establish CRC211 as a colorectal cancer (CRC)-associated strain with distinct genomic features that may contribute to tumor progression. The study provides critical insights into its possible oncogenic mechanisms and highlights potential applications in mic ases,indels - changerobiota-based diagnostics or therapeutics for colorectal cancer.
Aim: This study aimed to screen Lactococcus lactis strains with varying gamma-aminobutyric acid (GABA) production and evaluate their effects on intestinal dysfunction and neurobehavioral abnormalities in an irritable bowel syndrome (IBS) mouse model, with a focus on GABAergic signaling and dose-dependent mechanisms.
Methods: Three Lactococcus lactis strains were selected based on GABA yield and genetic analysis. IBS was induced in mice via Citrobacter rodentium infection and water avoidance stress. Intestinal integrity, inflammation, histopathology, and behavior were assessed. GABA levels in the colon and serum were measured by liquid chromatography-mass spectrometry (LC-MS). GABA receptor subunit expression in the colon, hippocampus, and amygdala was analyzed via quantitative real-time polymerase chain reaction and Western blotting.
Results: GABA-producing strains alleviated intestinal dysfunction in IBS mice by reducing IL-6 gene expression and iNOS activity, upregulating CLDN2, and improving tissue integrity. Anxiety-like behaviors and cognitive deficits were also attenuated. Colonic GABA levels, GABRA13 mRNA, and GABRA3 protein expression increased in a dose-dependent manner, whereas TRPV1 mRNA and TRPV1 protein levels were downregulated. Serum GABA remained unchanged. In the central nervous system, the expression of hippocampal GABAA and GABAB receptors was elevated, with both GABRA13 mRNA and GABRA3 protein levels positively correlating with colonic GABA concentrations. GABRA15 expression was upregulated in the amygdala.
Conclusion: GABA-producing Lactococcus lactis effectively alleviates IBS-related intestinal dysfunction and neurobehavioral abnormalities by coordinately modulating GABAergic signaling in both the gut and the central nervous system, exhibiting a clear dose-dependent effect across multiple key phenotypes.
The rising prevalence of multidrug-resistant (MDR) bacterial infections, coupled with the diminishing efficacy of antibiotics, has reinvigorated interest in bacteriophage (phage) therapy as a promising alternative, leveraging its unique bactericidal mechanisms and precise targeting capabilities. Concurrently, phage display technology has advanced tumor diagnostics and targeted drug delivery through high-throughput peptide screening. This review systematically evaluates the mechanisms, strategies, and clinical progress of phage-based applications in anti-infective and oncological therapies. Clinical evidence highlights its efficacy against respiratory, oral, wound, bloodstream, and urinary tract infections, alongside solid tumors. However, challenges persist, including limited host range, bacterial resistance, immunogenicity, inefficient delivery systems, and regulatory uncertainties. Future efforts should prioritize AI-driven phage optimization, standardized pharmacokinetic assessment, and interdisciplinary collaboration to accelerate clinical translation. Despite current limitations, phage therapy represents a transformative and scalable approach for combating antimicrobial resistance and advancing precision oncology, positioning it as a pivotal tool in addressing global health crises.
Postoperative insulin resistance (PIR) is a common metabolic complication that significantly affects patient recovery and long-term outcomes. Recent studies have revealed a robust association between the gut microbiota and PIR, underscoring the potential role of microbial communities in modulating insulin sensitivity. In this comprehensive review, we synthesize current literature on the interplay between PIR and the gut microbiota, delve into the underlying mechanisms linking the two, and provide an overview of recent research progress in this field. Evidence suggests that the gut microbiota may influence PIR through mechanisms involving metabolic endotoxins, short-chain fatty acids, branched-chain amino acids, and other metabolites. Overall, the gut microbiota plays a crucial role in the onset and progression of PIR. This review aims to provide a theoretical basis for developing PIR intervention strategies based on microbiome regulation.