Search Results (84)

Background: BDE-47, a pervasive environmental pollutant detected in >90% of human serum samples, is increasingly linked to metabolic disorders. This study investigates the specific impact of BDE-47 exposure on the gut microbiota in prediabetic mice and evaluates the efficacy of therapeutic interventions in mitigating these effects. Objectives: To determine whether BDE-47 exposure induces diabetogenic dysbiosis in prediabetic mice and to assess whether dietary interventions, such as grape exosomes and an antioxidant cocktail, can restore a healthy microbiota composition and mitigate diabetes risk. Methods: In this study, a prediabetic mouse model was established in 54 male SPF-grade C57BL/6J mice through a combination of high-sugar and high-fat diet feeding with streptozotocin injection. Oral glucose tolerance tests (OGTT) were conducted on day 7 and day 21 post-modeling to assess the establishment of the model. The criteria for successful model induction were defined as fasting blood glucose levels below 7.8 mmol/L and 2 h postprandial glucose levels between 7.8 and 11.1 mmol/L. Following confirmation of model success, a 3 × 3 factorial design was applied to allocate the experimental animals into groups based on two independent factors: BDE-47 exposure and exosome intervention. The BDE-47 exposure factor consisted of three dose levels—none, high-dose, and medium-dose—while the exosome intervention factor included three modalities—none, Antioxidant Nutrients Intervention, and Grape Exosomes Intervention. Fresh fecal samples were collected from mice two days prior to sacrifice. Cecal contents and segments of the small intestine were collected and transferred into 1.5 mL cryotubes. All sequences were clustered into operational taxonomic units (OTUs) based on defined similarity thresholds. To compare means across multiple groups, a two-way analysis of variance (ANOVA) was employed. The significance level was predefined at α = 0.05, and p-values < 0.05 were considered statistically significant. Bar charts and line graphs were generated using GraphPad Prism version 9.0 software, while statistical analyses were performed using SPSS version 20.0 software. Results: The results of 16S rDNA sequencing analysis of the microbiome showed that there was no difference in the α diversity of the intestinal microbiota in each group of mice (p > 0.05), but there was a difference in the Beta diversity (p < 0.05). At the gate level, the abundances of Proteobacteria, Campylobacterota, Desulfobacterota, and Fusobacteriota in the medium-dose BDE-7 group were higher than those in the model control group (p < 0.05). The abundance of Patellar bacteria was lower than that of the model control group (p < 0.05). The abundances of Proteobacteria and Campylobacterota in the high-dose BDE-7 group were higher than those in the model control group (p < 0.05). The abundance of Planctomycetota and Patescibacteria was lower than that of the model control group (p < 0.05), while the abundance of Campylobacterota in the grape exosome group was higher than that of the model control group (p < 0.05). The abundance of Patescibacteria was lower than that of the model control group (p < 0.05), while the abundance of Firmicutes and Fusobacteriota in the antioxidant nutrient group was higher than that of the model control group (p < 0.05). However, the abundance of Verrucomicrobiota and Patescibacteria was lower than that of the model control group (p < 0.05). At the genus level, the abundances of Bacteroides and unclassified Lachnospiraceae in the high-dose BDE-7 group were higher than those in the model control group (p < 0.05). The abundance of Lachnospiraceae NK4A136_group and Lactobacillus was lower than that of the model control group (p < 0.05). The abundance of Veillonella and Helicobacter in the medium-dose BDE-7 group was higher than that in the model control group (p < 0.05), while the abundance of Lactobacillus was lower (p < 0.05). The abundance of genera such as Lentilactobacillus and Faecalibacterium in the grape exosome group was higher than that in the model control group (p < 0.05). The abundance of Alloprevotella and Bacteroides was lower than that of the model control group (p < 0.05). In the antioxidant nutrient group, the abundance of Lachnospiraceae and Hydrogenophaga was higher than that in the model control group (p < 0.05). However, the abundance of Akkermansia and Coriobacteriaceae UCG-002 was significantly lower than that of the model control group (p < 0.05). Conclusions: BDE-47 induces diabetogenic dysbiosis in prediabetic mice, which is reversible by dietary interventions. These findings suggest that microbiota-targeted strategies may effectively mitigate the diabetes risk associated with environmental pollutant exposure. Future studies should further explore the mechanisms underlying these microbiota changes and the long-term health benefits of such interventions. Full article

Grazing is a free-range farming model commonly practiced in low-external-input agricultural systems. The widespread use of veterinary antibiotics in livestock farming has led to significant environmental accumulation of antibiotic residues and antibiotic resistance genes (ARGs), posing global health risks. This study investigated the antibiotic residues, bacterial community, ARG profiles, and mobile genetic elements (MGEs) in cattle feces from three provinces in western China (Ningxia, Xinjiang, and Inner Mongolia) under grazing modes. The HPLC-MS detection showed that the concentration of tetracycline antibiotics was the highest in all three provinces. Correlation analysis revealed a significant negative correlation between antibiotic residues and the diversity and population abundance of intestinal microbiota. However, the abundance of ARGs was directly proportional to antibiotic residues. Then, the Sankey analysis revealed that the ARGs in the cattle fecal samples were concentrated in 15 human pathogenic bacteria (HPB) species, with 9 of these species harboring multiple drug resistance genes. Metagenomic sequencing revealed that carbapenemase-resistant genes (bla_KPC and bla_VIM) were also present in considerable abundance, accounting for about 10% of the total ARGs detected in three provinces. Notably, Klebsiella pneumoniae strains carrying bla_CTX-M-55 were detected, which had a possibility of IncFII plasmids harboring transposons and IS19, indicating the risk of horizontal transfer of ARGs. This study significantly advances the understanding of the impact of antibiotic residues on the fecal microbiota composition and ARG profiles in grazing cattle from northwestern China. Furthermore, it provides critical insights for the development of rational antibiotic usage strategies and comprehensive public health risk assessments. Full article

This study compared the metabolic consequences of fecal microbiota transplantation (FMT) from donor mice that had been either administered pulsed electromagnetic field (PEMF) therapy or exercised to recipient mice fed a high-fat diet (HFD). Eight weeks of PEMF treatment (10 min/week) enhanced PGC-1α-associated mitochondrial and metabolic gene expression in white and brown adipose to a greater degree than eight weeks of exercise (30–40 min/week). FMT from PEMF-treated donor mice recapitulated these adipogenic adaptations in HFD-fed recipient mice more faithfully than FMT from exercised donors. Direct PEMF treatment altered hepatic phospholipid composition, reducing long-chain ceramides (C16:0) and increasing very long-chain ceramides (C24:0), which could be transferred to PEMF-FMT recipient mice. FMT from PEMF-treated mice was also more effective at recovering glucose tolerance than FMT from exercised mice. PEMF treatment also enhanced bone density in both donor and HFD recipient mice. The gut Firmicutes/Bacteroidetes (F/B) ratio was lowest in both the directly PEMF-exposed and PEMF-FMT recipient mouse groups, consistent with a leaner phenotype. PEMF treatment, either directly applied or via FMT, enhanced adipose thermogenesis, ceramide levels, bone density, hepatic lipids, F/B ratio, and inflammatory blood biomarkers more than exercise. PEMF therapy may represent a non-invasive and non-strenuous method to ameliorate metabolic disorders. Full article

Background: Low-dose antibiotic contamination in animal feed is a persistent global food safety challenge. Transient early-life exposure to low-dose penicillin (LDP) is known to induce metabolic syndrome (MetS) in adult mice, but the underlying mechanisms are unclear. Introduction: This study investigated the role of gut microbiota (GM) and intestinal immunity in mediating the long-term metabolic effects of early-life LDP exposure. Methods: Mice were exposed to LDP transiently during early life. GM composition was analyzed. Intestinal IgA responses were quantified. Bacterial encroachment, systemic and adipose tissue inflammation, and diet-induced MetS were assessed. Germ-free (GF) mice received GM transplants from LDP-exposed or control mice to test causality and persistence. Results: Early-life LDP exposure significantly disrupted GM composition, particularly in the ileum, in 30-day-old mice. These GM alterations caused persistent suppression of intestinal IgA responses, evidenced by reduced IgA-producing cells and sIgA levels. This suppression was constrained to early-life exposure: transferring LDP-modified GM to GF mice produced only a transient reduction in fecal sIgA. The LDP-induced sIgA reduction decreased IgA binding of bacteria, leading to increased bacterial encroachment and systemic and adipose tissue inflammation. These pathological changes exacerbated diet-induced MetS. Discussion: Our findings demonstrate that early-life LDP exposure induces persistent intestinal IgA deficiency through lasting GM alterations initiated in early development. This deficiency drives bacterial encroachment, inflammation, and ultimately exacerbates MetS. Conclusions: The exacerbation of diet-induced metabolic syndrome by early-life LDP exposure occurs through an intestinal sIgA-dependent pathway triggered by persistent GM disruption. This highlights a critical mechanism linking early-life antibiotic exposure, gut immune dysfunction, and long-term metabolic health, with significant implications for food safety. Full article

The human gut microbiome is intricately linked to systemic and organ-specific immune responses and is highly responsive to dietary modulation. As metagenomic techniques enable in-depth study of an ever-growing number of gut microbial species, it has become increasingly feasible to decipher the specific functions of the gut microbiome and how they may be modulated by diet. Diet exerts both supportive and selective pressures on the gut microbiome by regulating a multitude of factors, including energy density, macronutrient and micronutrient content, and circadian rhythm. The microbiome, in turn, contributes to local and systemic immune responses by providing colonization resistance against pathogens, shaping immune cell activity and differentiation, and facilitating the production of bioactive metabolites. Emerging research has strengthened the connections between the gut microbiome and cardiometabolic disorders (e.g., cardiovascular disease, obesity, type-2 diabetes), autoimmune conditions (e.g., type-1 diabetes, rheumatoid arthritis, celiac disease), respiratory disease, chronic kidney and liver disease, inflammatory bowel disease, and neurological disorders (e.g., Alzheimer’s, Parkinson’s disease, depressive disorders). Here, we outline ways in which dietary factors impact host response in diseases through alterations of gut microbiome functionality and composition. Consideration of diet-mediated microbial effects within the context of the diseases discussed highlights the potential of microbiome-targeted treatment strategies as alternative or adjunct therapies to improve patient outcomes. Full article

Systemic lupus erythematosus (SLE) is more prevalent in female mice and humans and is associated with microbiota dysbiosis. We analyzed the fecal microbiota composition in female and male NZBxNZWF1 (BWF1) mice, a model of SLE, using 16S RNA gene sequencing. Composition of gut microbiota differed between adult disease-prone female (pre-disease) and disease-resistant male mice. Transfer of male cecal contents by gavage into female mice suppressed kidney disease (decreased proteinuria) and improved survival. After our mouse colony was moved to a new barrier facility with similar housing, male cecal transplants failed to suppress disease in female recipients. After two years, the protective phenotype reemerged: male cecal transplants once again suppressed disease in female mice. We compared the gut microbiota composition in female and male BWF1 mice for the three different periods, during which the male microbiota either protected or failed to protect female recipients. In female vs. male mice and in female mice receiving male cecal transplants, we found Bacteroides was high, Clostridium was low (high Bacteroides/Clostridium ratio), and Alistipes was present during periods when male cecal transplants suppressed disease. These data suggest that specific bacterial populations may have opposing effects on disease suppression in a model of microbiota transplantation. Full article

Over time, extensive research has underscored the pivotal role of gut microbiota in the onset and progression of various diseases, with a particular focus on fecal microbiota transplantation (FMT) as a potential therapeutic approach. The practice of transferring fecal matter from a healthy donor to a patient provides valuable insights into how alterations in gut microbiota can impact disease development and how rectifying dysbiosis may offer therapeutic benefits. Re-establishing a balanced symbiotic relationship in the gastrointestinal tract has shown positive results in managing both intestinal and systemic conditions. Currently, one of the most pressing global health issues is metabolic syndrome—a cluster of conditions that includes insulin resistance, lipid imbalances, central obesity and hypertension. In this context, FMT has emerged as a promising strategy for addressing key components of metabolic syndrome, such as improving insulin sensitivity, body weight and lipid profiles. However, further well-structured studies are needed to refine treatment protocols and establish the long-term safety and efficacy of this intervention. Full article

The human gut microbiota—an intricate and dynamic ecosystem—plays a pivotal role in metabolic regulation, immune modulation, and the maintenance of intestinal barrier integrity. Although antibiotic therapy is indispensable for managing bacterial infections, it profoundly disrupts gut microbial communities. Such dysbiosis is typified by diminished diversity and shifts in community structure, especially among beneficial bacterial genera (e.g., Bifidobacterium and Eubacterium), and fosters antibiotic-resistant strains and the horizontal transfer of resistance genes. These alterations compromise colonization resistance, increase intestinal permeability, and amplify susceptibility to opportunistic pathogens like Clostridioides difficile. Beyond gastrointestinal disorders, emerging evidence associates dysbiosis with systemic conditions, including chronic inflammation, metabolic syndrome, and neurodegenerative diseases, underscoring the relevance of the microbiota–gut–brain axis. The recovery of pre-existing gut communities post-antibiotic therapy is highly variable, influenced by drug spectrum, dosage, and treatment duration. Innovative interventions—such as fecal microbiota transplantation (FMT), probiotics, synbiotics, and precision microbiome therapeutics—have shown promise in counteracting dysbiosis and mitigating its adverse effects. These therapies align closely with antibiotic stewardship programs aimed at minimizing unnecessary antibiotic use to preserve microbial diversity and curtail the spread of multidrug-resistant organisms. This review emphasizes the pressing need for microbiota-centered strategies to optimize antibiotic administration, promote long-term health resilience, and alleviate the disease burden associated with antibiotic-induced dysbiosis. Full article

Background/Objectives: Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by difficulties in social interaction, communication, and repetitive behaviors. Recent evidence indicates a significant relationship between ASD and imbalances in microbiota, particularly in the oral and gastrointestinal areas. This review examines the impact of oral microbiota, self-injurious behaviors (SIB), sensory sensitivity, and dietary choices on the comorbidities associated with ASD. Methods: An extensive literature review was conducted using PubMed and Scopus. The focus was on human studies with full-text availability, utilizing search terms related to ASD, oral health, oral microbiota, and neurodevelopmental disorders. The research was evaluated for methodological quality and its relevance to the connections between microbiota, oral health, and ASD. Results: Individuals with ASD face unique oral health challenges, including injuries from self-injurious behaviors and increased sensory sensitivity, which complicate oral hygiene and care. Selective eating can lead to nutritional deficiencies and worsen oral health issues. Dysbiosis in oral and gut microbiota, marked by altered levels of acetate, propionate, and butyrate, interferes with gut-brain and oral-brain connections, contributing to behavioral and neurological symptoms. Treatment options such as probiotics, fecal microbiota transfer, and sensory integration therapies can potentially alleviate symptoms and improve quality of life. Conclusions: The relationship between ASD, oral health, and microbiota suggests a bidirectional influence through neuroinflammatory mechanisms and metabolic disturbances. Proactive strategies focusing on microbiota and dental health may help reduce comorbidities and enhance the overall management of ASD, underscoring the need for further research into microbiota–host interactions and their therapeutic potential. Full article

The gut microbiota plays a vital role in the physiological functions and health of animals. Domestic pigs (Sus scrofa domesticus) and wild boars (Sus scrofa scrofa), which share a common ancestor, present a unique model for exploring the evolutionary changes in gut microbiota due to domestication. Comparing the gut microbiota of these two groups provides a unique opportunity to identify microorganisms that may have been lost or altered during domestication. This study employed 16S rRNA sequencing to compare the gut microbiota compositions of domestic pigs and wild boars, analyzing 69 fecal samples from both groups. Our results indicate significant differences in the taxonomic profiles of the gut microbiota between the two groups. Specifically, the genera Bifidobacterium and Lactobacillus, were found in higher abundance in wild boars. In contrast, domestic pigs exhibited a decreased variety of these potentially health-enhancing bacteria, likely due to factors such as simplified diets and antibiotic use. Functional gene analysis revealed that pathways related to carbohydrate metabolism, lipid metabolism, immune response, and environmental adaptability were more enriched in wild boars. These findings demonstrate significant differences in the gut microbiota composition between domestic pigs and wild boars, underscoring the impact of domestication on microbial diversity. Further research is necessary to explore the potential of transferring beneficial microbes from wild to domestic populations. Full article

Background: Emerging infectious diseases threaten human and animal health, with most pathogens originating from wildlife. Bats are natural hosts for many infectious agents. Previous studies have demonstrated that changes in some specific genes in bats may contribute to resistance to viral infections, but they have mostly overlooked the immune function of the bat gut microbiota. Aims: In this study, we used fecal transplants to transfer the gut microbiota from the Greater Horseshoe Bat (Rhinolophus ferrumequinum) into mice treated with antibiotics. The gut microbiota changes in mice were detected using 16S rRNA high-throughput sequencing technology. Flow cytometry was used to detect changes in associated immune cells in the spleen and mesenteric lymph nodes of the mice. Results: The results showed that the gut microbiota of mice showed characteristics of some bat gut microbiota. The Greater Horseshoe Bat’s gut microbiota changed some immune cells’ composition in the spleen and mesenteric lymph nodes of mice and also conferred a faster and higher proportion of natural killer cell activation. Conclusion: This result provides new evidence for the regulatory immune function of bat gut microbiota and contributes to a deeper insight into the unique immune system of bats. Full article

Background. Antibiotic-resistant (AR) bacteria pose an increasing threat to public health, but the dynamics of antibiotic resistance gene (ARG) spread in complex microbial communities are poorly understood. Conjugation is a predominant direct cell-to-cell mechanism for the horizontal gene transfer (HGT) of ARGs. We hypothesized that commensal Escherichia coli donor strains would mediate the conjugative transfer of ARGs to phylogenetically distinct bacteria without antibiotic selection pressure in gastrointestinal tracts of mice carrying a human-derived microbiota with undetectable levels of E. coli. Our objective was to identify a mouse model to study the factors regulating AR transfer by conjugation in the gut. Methods. Two donor E. coli strains were engineered to carry chromosomally encoded red fluorescent protein, and an ARG- and green fluorescent protein (GFP)-encoding broad host range RP4 conjugative plasmid. Mice were orally gavaged with two donor strains (1) E. coli MG1655 or (2) human-derived mouse-adapted E. coli LM715-1 and their colonization assessed by culture over time. Fluorescence-activated cell sorting (FACS) and 16S rDNA sequencing were performed to trace plasmid spread to the microbiota. Results. E. coli LM715-1 colonized mice for ten days, while E. coli MG1655 was not recovered after 72 h. Bacterial cells from fecal samples on days 1 and 3 post inoculation were sorted by FACS. Samples from mice given donor E. coli LM715-1 showed an increase in cells expressing green but not red fluorescence compared to pre-inoculation samples. 16S rRNA gene sequencing analysis of FACS GFP positive cells showed that bacterial families Lachnospiraceae, Clostridiaceae, Pseudomonadaceae, Rhodanobacteraceae, Erysipelotrichaceae, Oscillospiraceae, and Butyricicoccaceae were the primary recipients of the RP4 plasmid. Conclusions. Results show this ARG-bearing conjugative RP4 plasmid spread to diverse human gut bacterial taxa within a live animal where they persisted. These fluorescent marker strategies and human-derived microbiota transplanted mice provided a tractable model for investigating the dynamic spread of ARGs within gut microbiota and could be applied rigorously to varied microbiotas to understand conditions facilitating their spread. Full article

Background: Early gut microbiota (GM) dysbiosis can affect a child’s health and has been linked to the onset of pathologies later in life. Breast milk is recognized as a major driver of the structure and dynamics of an infant’s GM. In addition to nutritious and prebiotic compounds, milk contains a microbiota that is shaped by several maternal factors, including gut microorganisms and medications. However, the impact of the latter on the milk microbiota is still largely unknown. Here, we investigated the effects of amoxicillin on the milk microbiota and GM of lactating Göttingen Minipigs sows, a promising model for studying medication transfer during lactation. Methods: Three sows were given amoxicillin (7 mg/kg/day) for three weeks starting from the second week after farrowing. Fecal and milk samples were collected before and after treatment and profiled by 16S rRNA amplicon sequencing. Results: Göttingen Minipigs’ milk microbiota showed similarities to that of humans and conventional sows, with minor compositional shifts after treatment. At the genus level, we observed a decrease in Staphylococcus and o_Bacteroidales;Other;Other, and an increasing trend in the abundance of Streptococcus, Stenotrophomonas, f_Rhodobacteraceae;Other, Proteiniclasticum, f_Propionibacteriaceae;Other and Gemella. In contrast, as expected, the GM was strongly affected by amoxicillin, even at the phylum level. Conclusions: In addition to demonstrating the relevance of Göttingen Minipigs as a valid model for studying the impact of medications on maternal milk and GM, our findings suggest that the milk microbiota may be more stable during antibiotic treatment than the GM. Full article

Gut microbiota dysbiosis has a critical role in the pathogenesis of inflammatory bowel diseases, prompting the exploration of novel therapeutic approaches like fecal microbiota transplantation, which involves the transfer of fecal microbiota from a healthy donor to a recipient with the aim of restoring a balanced microbial community and attenuating inflammation. Fecal microbiota transplantation may exert beneficial effects in inflammatory bowel disease through modulation of immune responses, restoration of mucosal barrier integrity, and alteration of microbial metabolites. It could alter disease course and prevent flares, although long-term durability and safety data are lacking. This review provides a summary of current evidence on fecal microbiota transplantation in inflammatory bowel disease management, focusing on its challenges, such as variability in donor selection criteria, standardization of transplant protocols, and long-term outcomes post-transplantation. Full article

Gut dysbiosis, resulting from an imbalance in the gut microbiome, can induce excessive production of reactive oxygen species (ROS), leading to inflammation, DNA damage, activation of the immune system, and epigenetic alterations of critical genes involved in the metabolic pathways. Gut dysbiosis-induced inflammation can also disrupt the gut barrier integrity and increase intestinal permeability, which allows gut-derived toxic products to enter the liver and systemic circulation, further triggering oxidative stress, inflammation, and epigenetic alterations associated with metabolic diseases. However, specific gut-derived metabolites, such as short-chain fatty acids (SCFAs), lactate, and vitamins, can modulate oxidative stress and the immune system through epigenetic mechanisms, thereby improving metabolic function. Gut microbiota and diet-induced metabolic diseases, such as obesity, insulin resistance, dyslipidemia, and hypertension, can transfer to the next generation, involving epigenetic mechanisms. In this review, we will introduce the key epigenetic alterations that, along with gut dysbiosis and ROS, are engaged in developing metabolic diseases. Finally, we will discuss potential therapeutic interventions such as dietary modifications, prebiotics, probiotics, postbiotics, and fecal microbiota transplantation, which may reduce oxidative stress and inflammation associated with metabolic syndrome by altering gut microbiota and epigenetic alterations. In summary, this review highlights the crucial role of gut microbiota dysbiosis, oxidative stress, and inflammation in the pathogenesis of metabolic diseases, with a particular focus on epigenetic alterations (including histone modifications, DNA methylomics, and RNA interference) and potential interventions that may prevent or improve metabolic diseases. Full article