The gut microbiota undergoes continuous variations among individuals and across their lifespan, shaped by diverse factors encompassing diet, age, lifestyle choices, medication intake, and disease states. These microbial inhabitants play a pivotal role in orchestrating physiological metabolic pathways through the production of metabolites like bile acids, choline, short-chain fatty acids, and neurotransmitters, thereby establishing a dynamic "gut-organ axis" with the host. The intricate interplay between the gut microbiota and the host is indispensable for gut health, and RNA N6-methyladenosine modification, a pivotal epigenetic mark on RNA, emerges as a key player in this process. M6A modification, the most prevalent internal modification of eukaryotic RNA, has garnered significant attention in the realm of RNA epigenetics. Recent findings underscore its potential to influence gut microbiota diversity and intestinal barrier function by modulating host gene expression patterns. Conversely, the gut microbiota, through its impact on the epigenetic landscape of host cells, may indirectly regulate the recruitment and activity of RNA m6A-modifying enzymes. This review endeavors to delve into the biological functions of m6A modification and its consequences on intestinal injury and disease pathogenesis, elucidating the partial possible mechanisms by which the gut microbiota and its metabolites maintain host intestinal health and homeostasis. Furthermore, it also explores the intricate crosstalk between them in intestinal injury, offering a novel perspective that deepens our understanding of the mechanisms underlying intestinal diseases.

To study the impact of differing specific pathogen-free gut microbiomes (GMs) on a murine model of inflammatory bowel disease, selected GMs were transferred using embryo transfer (ET), cross-fostering (CF), and co-housing (CH). Prior work showed that the GM transfer method and the microbial composition of donor and recipient GMs can influence microbial colonization and disease phenotypes in dextran sodium sulfate-induced colitis. When a low richness GM was transferred to a recipient with a high richness GM via CH, the donor GM failed to successfully colonize, and a more severe disease phenotype resulted when compared to ET or CF, where colonization was successful. By comparing CH and gastric gavage for fecal material transfer, we isolated the microbial component of this effect and determined that differences in disease severity and survival were associated with microbial factors rather than the transfer method itself. Mice receiving a low richness GM via CH and gastric gavage exhibited greater disease severity and higher expression of pro-inflammatory immune mediators compared to those receiving a high richness GM. This study provides valuable insights into the role of GM composition and colonization in disease modulation.

Trimethylamine (TMA) metabolism comprises choline-containing compounds' metabolization, TMA production and trimethylamine N-oxide (TMAO) generation. However, the presence of numerous compounds in the carnitine and phosphatidylcholine (PC) pool compositions complicates profiling work significantly. This study is aimed at developing an efficient method for profiling TMA metabolic pathways, including quantifying known compounds and semi-quantifying the differential metabolites in the carnitine and PC pool compositions. Pseudo-targeted metabolomics is applicable for characterization. Firstly, multivariate statistics were performed to identify valuable metabolites (variable importance in the projection ＞1) from quality control biological samples. Given that TMA metabolism involved in host-gut microbiota interaction, co-metabolites were defined as the intersections of valuable metabolites from different biological samples (serum, liver, and intestinal contents) and further screened. Finally, alterations in TMA metabolism were observed in dextran sulfate sodium-induced colitis, with semi-quantitative analysis for excavated co-metabolites including 11 PCs, 6 lyso-phosphatidylcholines, and 2 acylcarnitines and quantitative analysis for 10 known metabolites. The findings revealed increased TMA production and accumulation of choline-containing compounds in the gut during ulcerative colitis exacerbation. Correspondingly, the circulating level of TMAO was elevated in the colitis group. A comprehensive understanding of TMA metabolism can contribute to disease differential diagnoses and potential mechanism studies.

Emerging science supports the role of lipid metabolism disorders in the occurrence and development of chronic diseases. Dietary intervention has been shown to be an effective strategy for regulating lipid metabolism. Recent studies showed that perilla is rich in various effective ingredients, including fatty acids, flavonoids, and phenolic acids. These ingredients exhibit a myriad of benefits, notably enhancing intestinal health and helping to manage metabolic diseases. Perilla oil stands out as a promising agent for regulating lipid metabolism, underscoring its potential for various health applications. This review introduces the active ingredients in perilla and provides a systematic overview of the mechanism by which perilla oil regulates lipid metabolism to expand its application value. Further research should focus on exploring the dose effect and absorption efficiency of perilla oil in clinical applications.

The ecological conditions of freshwater aquaculture are deteriorating by degrees in recent years. Consequently, the comprehensive utilization of saline-alkaline water has garnered increasing societal attention. Here, crucian carp (Carassius auratus) were exposed to 20, 40 mmol/L NaHCO3 for 30 days (T, F group). Metabolomic analyses were conducted using UPLC-QTOF/MS, complemented by biochemical and microbiology profiling to elucidate the damage of the saline environment to the intestinal microbial structure, which in turn interfered with the energy metabolism. It was observed that carbonate alkalinity (CA) exposure not only caused intestine oxidative stress but also changed the levels of several digestive enzymes, including α-amylase (AMS), chymotrypsin (CHY), lipase (LPS). Metabolomic analysis identified 22 different metabolites (DEMs) in T group and 77 DEMs in F group. MetaboAnalyst analysis indicated that these metabolites are primarily involved in energy-related pathways, including the citric acid cycle, galactose metabolism, and glycine, serine, and threonine metabolism. Intestinal microbial diversity and community composition were altered under carbonate alkalinity exposure, with increase in Proteobacteria abundance and decline in Firmicutes, abundance alongside enrichment of Sphingomonas. Herein, saline-alkaline stress disrupted the physiological homeostasis of the crucian carp intestine, leading to microbial dysbiosis and energy metabolic imbalance. This study provides a theoretical foundation for understanding the stress response of the crucian carp intestine and the role of the intestinal microbiome in host resilience under adverse environmental conditions.

There are significant structural differences between breast milk fat and the fat found in existing infant formulas, and these differences may partly explain the observed variations in growth and development between breastfed and formula-fed infants. This study used mice compared three groups: a control group (mixed vegetable oil), an OPO group (vegetable oil added with OPO), and a human milk fat substitute (HMFS) group formulated to match the fatty acid composition of breast milk. Compared to the control group and OPO group, HMFS-fed mice exhibited reduced body fat content and improved cognitive abilities. Lipidomics studies revealed that these differences in HMFS mice were associated with downregulation of hepatic glycerolipids and upregulation of glycerophospholipids and sphingolipids, facilitating the delivery of long-chain polyunsaturated fatty acids to the brain. Molecular investigations confirmed that HMFS reduces body fat accumulation by inhibiting endogenous fatty acid synthesis and promoting fatty acid β-oxidation, while changes in hepatic lipid profiles result from lipid molecule synthesis and interconversion. Metataxonomic studies demonstrated that HMFS reshaped the gut microbiota, including upregulating Akkermansia and downregulating Desulfovibrio and the Firmicutes/Bacteroidetes ratio, with strong correlations observed between the change of gut microbiota and responded lipids in liver. Overall, the breast milk's unique fatty acid distribution promotes organismal growth by modulating hepatic lipid metabolism, systemic lipid circulation, and gut microbiota. These findings underscore the nutritional benefits of breast milk fat structure and provide insights for the development of next-generation infant formulas.

Population studies have revealed associations between host genetic and gut microbiome in humans and mice. However, the molecular bases for how host genetic variation impacts the gut microbial community and bacterial metabolic niches remain largely unknown.

We leveraged 90 inbred hyperlipidemic mouse strains from the hybrid mouse diversity panel (HMDP), previously studied for a variety of cardio-metabolic traits. Metagenomic analysis of cecal DNA followed by genome-wide association analysis identified genomic loci that were associated with microbial enterotypes in the gut. Among these, we detected a genetic locus surrounding multiple amylase genes that were associated with abundances of Firmicutes (Lachnospiraceae family) and Bacteroidetes (Muribaculaceae family) taxa encoding distinct starch and sugar degrading capabilities. The genetic variants at the amylase gene locus were associated with distinct gut microbial communities (enterotypes) with different predicted metabolic capacities for carbohydrate degradation. Mendelian randomization analysis revealed host phenotypes, including liver fibrosis and plasma HDL-cholesterol levels, that were associated with gut microbiome enterotypes.

This work reveals novel relationships among host genetic variation, gut microbial enterotypes, and host metabolic traits and supports the notion that variation of host amylase may represent a key determinant of gut microbiome in mice. Video Abstract.

Nonalcoholic Steatohepatitis (NASH) is a progressive liver disease characterized by inflammation and liver damage. Allicin, a bioactive compound derived from garlic, has demonstrated anti-inflammatory and antioxidant properties. This study explores the effects of allicin on NASH and gut microbiota dysbiosis induced by a high-fat, high-fructose diet (HFFD) in mice. Allicin supplementation significantly alleviated hepatic inflammation, improved glucose metabolism, and modulated the circadian rhythm gene Rev-erbα, which plays a critical role in regulating inflammation. The anti-inflammatory effects of allicin were diminished in Si-Rev-erbα-treated HepG2 cells, highlighting the importance of circadian regulation in mediating these effects. Allicin's anti-inflammatory effects were associated with increased levels of short-chain fatty acids (SCFAs) and the restoration of diurnal oscillations in proinflammatory cytokines and gut microbiota composition, particularly in genera, such as Akkermansia, Bacteroidetes, and Lactobacillus. These findings suggest that allicin could be a promising therapeutic approach for managing NASH, liver dysfunction, and related metabolic disorders through the modulation of circadian rhythms and the gut microbiome.

Feed nutrients are crucial in shaping the gut microbial community, especially for complex interactions. While much research focused on the impacts of dietary protein levels, exploration of protein sources remains insufficient. Accordingly, this study specifically investigated the effects of four protein sources [Clostridium autoethanolicum protein (CAP), cottonseed protein concentrate (CPC), Chlorella vulgaris meal (CVP), and Tenebrio molitor meal (TM)] replacing dietary soybean meal on microbial co-occurrence networks and key metabolic taxa. A 56-day feeding trial involved 1500 grass carp (20.00 g) fed five experimental diets, each incorporating one of the experimental protein sources. Results revealed that CPC and CVP diets improved the weight gain and specific growth rate, with the CPC group demonstrating the highest biomass gain and the CVP group exhibiting the best feed conversion ratio. Findings further indicated that SM-free diets enhanced intestinal immunity and barrier function while negatively impacting microbial diversity. Additional profiling revealed that each treatment exhibited distinct abundance profiles and unique species, with Firmicutes, Bacteroidota, and Proteobacteria as the dominant phyla and key genera such as Bacteroides, Erysipelatoclostridium, and Cetobacterium. Stochastic mechanisms drove the community assembly process, and prolonged SM-free diets led to simplified networks with increased generalists and specialists. Functional gene analysis highlighted roles in amino acid, carbohydrate, and lipid metabolism, underscoring the impact of protein sources on aquatic microbial communities and host-microbiome interactions. Overall, the study suggests the potential suitability of several protein sources as soybean meal substitutes, emphasizing the importance of further investigation into optimal inclusion levels for diverse proteins.

The high prevalence and disability rate of type 2 diabetes (T2D) caused a huge social burden to the world. Currently, new mechanisms and therapeutic approaches that may affect this disease are being sought. With in-depth research on the pathogenesis of T2D and growing advances in microbiome sequencing technology, the association between T2D and gut microbiota has been confirmed. The gut microbiota participates in the regulation of inflammation, intestinal permeability, short-chain fatty acid metabolism, branched-chain amino acid metabolism and bile acid metabolism, thereby affecting host glucose and lipid metabolism. Interventions focusing on the gut microbiota are gaining traction as a promising approach to T2D management. For example, dietary intervention, prebiotics and probiotics, faecal microbiota transplant and phage therapy. Meticulous experimental design and choice of analytical methods are crucial for obtaining accurate and meaningful results from microbiome studies. How to design gut microbiome research in T2D and choose different machine learning methods for data analysis are extremely critical to achieve personalized precision medicine.

Antibiotic resistance genes (ARGs) are a persistent harmful environmental pollutant, epidemic of ARGs thought to be a result of antibiotic misuse. Tannin acid (TA) is a natural plant compounds with bactericidal properties. Nowadays, TA is considered to be a potential replacement of antibiotics. However, the role of TA on ARGs is also not yet clear. To address this knowledge gap, we fed the model plateau animal Qinghai voles (Neodon fuscus) with different concentrations of TA. We used 16S rDNA sequencing for revealing total bacteria, 16S rRNA sequencing for revealing active bacteria, and metatranscriptomics (active function) sequencing for revealing ARGs and other functions. Our results showed that although TA reduced macrolide ARGs, TA group enriched 6-fold for tetracycline ARGs, 3-fold for multidrug ARGs, and 5-fold for aminoglycoside ARGs compared with control group. Moreover, TA reduced animal growth performance, and regulated gut microbiome more stable by improving microbial diversity. And TA promoted the production of short-chain fatty acids by gut microbes, such as lactate and acetate. This study reveals modulation of ARGs and gut microbiome by TA and also provides scientific value for the proper use of TA in feed and medical treatment.

A total of 180 one-day-old white-feathered broiler chicks were selected and randomly divided into 4 treatments, namely the control group (CON), Escherichia coli groups (E. coli), 2 g/kg polyherbal mixture group (PHM2), and the 4 g/kg polyherbal mixture group (PHM4). The CON and E. coli groups were fed a basal diet, while the PHM2 and PHM4 groups were fed the basal diet supplemented with 2 g/kg and 4 g/kg PHM, respectively. Each group had 3 replicates, with 15 broilers per replicate. On day 17 of the experiment, broilers in the E. coli, PHM2, and PHM4 groups were intraperitoneally injected with 0.8 mL of 1 × 108 CFU/mL of E. coli O78. Broilers in the control group received an equivalent volume of saline. Chicks were euthanized 48 h postinjection for collecting serum, liver, spleen, jejunum, ileum, ileal mucosa, and cecal contents. Our results showed that PHM significantly reversed the weight loss and decreased the diarrhea rate and the mortality of chicks caused by E. coli infection (P < 0.05). In the serum of chicks infected with E. coli, PHM significantly enhanced the antioxidant capacity (P < 0.05), increased the levels of immunoglobulins and anti-inflammatory cytokines (P < 0.05), and decreased the concentrations of proinflammatory cytokines (P < 0.05). Meanwhile, PHM also promoted the mRNA expression of antioxidant-related genes and decreased the expression of proinflammatory cytokines and apoptosis-related genes in the liver, spleen, jejunum, and ileum (P < 0.05). In addition, PHM repaired the intestinal barrier and injury to further reduce the serum concentrations of d-lactate (DAO) and lipopolysaccharide (LPS) (P < 0.05). More importantly, PHM significantly regulated the composition of cecal microbiota, especially by up-regulating the relative abundance of beneficial bacteria, including Faecalibacterium, Bacteroides, Butyricicoccus, and Lactobacillus, and down-regulating the relative abundance of pathogenic bacteria, including Enterococcus, Escherichia, and Shigella (P < 0.05). These beneficial bacteria were significantly positively correlated with antioxidant capacity and intestinal barrier function, while pathogenic bacteria were significantly positively correlated with proinflammatory cytokines (P < 0.05). In conclusion, PHM may be a potential preventive strategy for E. coli-infected poultry, which is closely related to its modulation of gut microbiota.

Ginsenosides, the primary active compounds in Panax ginseng C. A. Mey., are well known for their potent immunomodulatory effects. However, their precise mechanisms, particularly concerning the "intestinal-metabolism-immune axis", have yet to be fully elucidated.

This study aims to investigate how ginsenosides protect immune function through the regulation of the gut-metabolism-immune axis.

A CTX-induced immunodeficient mouse model was established to assess the effects of ginsenosides on immune function, gut microbiota, and metabolic pathways.

The immune organ indices (spleen and thymus), levels of immune cytokines (TNF-α, IFN-γ, IL-6, IL-1β), and immunoglobulins (IgM, IgA) were assessed. Intestinal microbial diversity was analyzed using 16S rRNA sequencing, and metabolomics was employed to identify disruptions in amino acid and lipid metabolic pathways. Spearman correlation analysis and Western blotting were conducted to explore the involvement of the TLR4/MyD88/NF-κB signaling pathway.

Ginsenosides significantly restored immune organ indices and enhanced cytokines and immunoglobulins. 16S rRNA sequencing revealed an increase in probiotic levels and a reduction in potentially harmful bacteria, thereby enhancing intestinal microbiota diversity. Metabolomics analysis showed that ginsenosides ameliorated CTX-induced metabolic disorders and stimulated the production of short-chain fatty acids (SCFAs) and bile acids. Western blot analysis confirmed the upregulation of TLR4, MyD88, and NF-κB p-p65 expression.

This study systematically elucidates the mechanism by which ginsenosides enhance immune function by regulating gut microbiota, restoring metabolic balance, and activating the TLR4/MyD88/NF-κB signaling pathway. These findings provide a molecular foundation for the potential use of ginsenosides in the prevention and treatment of immune-related diseases.

Roux-en-Y gastric bypass (GBP) surgery is an effective treatment for reducing body weight and correcting metabolic dysfunction in individuals with severe obesity. Herein, we characterize the differences between very low energy diet (VLED) and GBP induced weight loss by multi-omic analyses of microbiome and host features in a non-randomized, controlled, single-center study. Eighty-eight participants with severe obesity were recruited into two arms - GBP versus VLED with matching weight loss for 6 weeks and 2-years of follow-up. A dramatic shift in the distribution of gut microbial taxa and their functional capacity was seen in the GBP group at Week 2 after surgery and was sustained through 2 years. Multi-omic analyses were performed after 6 weeks of matching weight loss between the GBP and VLED groups, which pointed to microbiome derived metabolites such as indoxyl sulphate as characterizing the GBP group. We also identified an inverse association between Streptococcus parasanguinis (an oral commensal) and plasma levels of tryptophan and tyrosine. These data have important implications, as they reveal a significant robust restructuring of the microbiome away from a baseline dysbiotic state in the GBP group. Furthermore, multi-omics modelling points to potentially novel mechanistic insights at the intersection of the microbiome and host.

Previous evidence suggests that gut dysbiosis plays an important role in the development and progression of sarcopenia and sarcopenic obesity (SO), but evidence supporting this association is lacking. Thus, this study aimed to investigate the characteristics of gut microbiota in older people with sarcopenia and SO.

A total of 1558 older adults (age ≥65 years) from a community-based cohort in Shanghai, China, underwent sarcopenia screening using the SARC-F questionnaire, with 351 participants completing further assessment. On the basis of the Asian Working Group for Sarcopenia 2019 and the World Health Organization obesity criteria, 60 participants were categorized into three groups: SO (n = 20), sarcopenia without obesity (Sar, n = 18), and controls (Con, n = 22). Gut microbiota composition was analyzed using 16S rRNA sequencing (V3-V4 regions).

Significant differences in the diversity and composition of the gut microbiota were observed in the Sar and SO groups. A reduction in alpha diversity (Chao1 and ACE indices) was found in the SO group. Beta diversity based on unweighted Unifrac PCoA was significantly different among the three groups. LEfSe analysis identified 39 taxa with significant differential abundances across groups. The Sar group exhibited enrichment of Christensenellaceae_R-7_group, Alistipes, Ruminococcus, Odoribacter, Prevotellaceae_UCG-001, Hungatella, Family_XIII_AD3011_group, Anaerotruncus, Ruminiclostridium, and Oxalobacter, along with their high taxonomic classifications. Meanwhile, Enterobacteriaceae, Allisonella, and Peptoclostridium were enriched in the SO group. Feature selection via Boruta algorithm identified five and four discriminatory taxa to construct random forest models, effectively distinguishing individuals with Sar and SO from Con. Key predictors for Sar included reduced Enterococcus, Enterobacter, and Hungatella and increased Odoribacter and Christensenellaceae_R-7_group. Conversely, SO was characterized by decreased Enterobacter, Alloprevotella, and Enterococcus and increased Allisonella. Five-fold cross-validation confirmed robust diagnostic efficacy, achieving AUCs of 0.860 (95 % CI: 0.786-0.996) for Sar and 0.826 (95 % CI: 0.735-0.970) for SO.

This study demonstrated that the gut microbiota of SO and Sar have distinct diversity and composition profiles. The results provide new insights into the role of gut microbiota in SO, highlighting its potential as a therapeutic target in this condition.

Preventing new cardiovascular events in patients with established cardiovascular disease (CVD) is a daunting task for clinicians. Intestinal microbiota may help identify patients at risk, thus improving the strategies of secondary prevention. The aim of this study was to evaluate the baseline differences between the gut microbiota from coronary heart disease (CHD) patients suffering new major adverse cardiovascular events (MACEs) in the following 7 years, compared with CHD patients who did not undergo new MACE in this period, and to build a score associated with the risk of suffering new MACE.

Within the framework of the CORDIOPREV study, a clinical trial that involved 1002 patients with CHD, intestinal microbiota was examined in patients with available faecal samples (n = 679, 132 MACE), through 16S metagenomics on the Illumina MiSeq and Quiime2 software. Lipopolysaccharide (LPS) was measured using limulus amoebocyte lysate test.

Random survival forest identified 10 bacterial taxa with a higher predictive power for MACE incidence. Receiver operating characteristic curves yielded an area under the curve of 65.2% (59.1%-71.3%) in the training set and 68.6% (59.3%-77.9%) in the validation set. The intestinal microbiota risk score was associated with a MACE incidence hazard ratio of 2.01 (95% confidence interval 1.37-3.22). Lipopolysaccharide analysis showed a greater LPS post-prandial fold change in the MACE group (P = .005).

These results reinforce the relationship between intestinal microbiota and CVD and suggest that a microbiota profile is associated with MACE in CHD patients, in addition to higher endotoxaemia.

Gut microbiota plays a critical role in counteracting enteric viral infection. Our previous study demonstrated that infection of porcine deltacoronavirus (PDCoV) disturbs gut microbiota and causes intestinal damage and inflammation in piglets. However, the influence of gut microbiota on PDCoV infection remains unclear.

Firstly, the relationship between gut microbiota and disease severity of PDCoV infection was evaluated using 8-day-old and 90-day-old pigs. The composition of gut microbiota was significantly altered in 8-day-old piglets after PDCoV infection, leading to severe diarrhea and intestinal damage. In contrast, PDCoV infection barely affected the 90-day-old pigs. Moreover, the diversity (richness and evenness) of microbiota in 90-day-old pigs was much higher compared to the 8-day-old piglets, suggesting the gut microbiota is possibly associated with the severity of PDCoV infection. Subsequently, transplanting the fecal microbiota from the 90-day-old pigs to the 3-day-old piglets alleviated clinical signs of PDCoV infection, modulated the diversity and composition of gut microbiota, and maintained the physical and chemical barrier of intestines. Additionally, metabolomic analysis revealed that the fecal microbiota transplantation (FMT) treatment upregulated the swine intestinal arginine biosynthesis, FMT significantly inhibited the inflammatory response in piglet intestine by modulating the TLR4/MyD88/NF-κB signaling pathway.

PDCoV infection altered the structure and composition of the gut microbiota in neonatal pigs. FMT treatment mitigated the clinical signs of PDCoV infection in the piglets by modulating the gut microbiota composition and intestinal barrier, downregulating the inflammatory response. The preventive effect of FMT provides novel targets for the development of therapeutics against enteropathogenic coronaviruses. Video Abstract.

Hepatocellular carcinoma (HCC) is closely linked to alterations in the gut microbiota. This dysbiosis is characterized by significant changes in the microbial population, which correlate with the progression of HCC. Gut dysbiosis ultimately promotes HCC development in several ways: it damages the integrity of the gut-vascular barrier (GVB), alters the tumor microenvironment (TME), and even affects the intratumoral microbiota. Subsequently, intratumoral microbiota present a characteristic profile and play an essential role in HCC progression mainly by causing DNA damage, mediating tumor-related signaling pathways, altering the TME, promoting HCC metastasis, or through other mechanisms. Both gut microbiota and intratumoral microbiota have dual effects on HCC progression; a comprehensive understanding of their complex biological roles will provide a theoretical foundation for potential clinical applications in HCC treatment.

Increasing evidence links the gut microbiome to carcinogenesis. Disruptions in estrogen regulation by the estrobolome-gut microbiota with estrogen-related functions-may promote breast cancer. However, precise information on estrobolome targets and their underlying mechanisms is limited. This review identifies relevant targets for measuring the estrobolome, focusing on enzymes and microbial taxa involved in processing estrogens, precursors, metabolites, and phytoestrogens, to facilitate the exploration of potential links to breast cancer. Evidence from breast cancer case-control studies is synthesized to assess alignment with these targets, highlight gaps in the evidence, and suggest new paths forward. Findings from case-control studies were heterogeneous and showed limited alignment with estrobolome targets, with only Escherichia coli and Roseburia inulinivorans identified as differentially abundant and functionally relevant between cases and controls. The lack of compelling evidence for estrobolome-specific mechanisms may reflect measurement challenges or may suggest that broader ecological changes in the microbiome, which influence a network of interacting mechanisms, are more influential for carcinogenesis. To clarify the estrobolome's role in breast cancer, future research should use advanced sequencing techniques and methods such as metabolomics and transcriptomics, while considering clinical and behavioral factors that may modify estrobolome mechanisms.

The immune system has long been recognized as a key driver in the progression of heart failure (HF). However, clinical trials targeting immune effectors have consistently failed to improve patient outcome across different HF aetiologies. The activation of the immune system in HF is complex, involving a broad network of pro-inflammatory and immune-modulating components, which complicates the identification of specific immune pathways suitable for therapeutic targeting. Increasing attention has been devoted to identifying gut microbial pathways that affect cardiac remodelling and metabolism and, thereby impacting the development of HF. In particular, gut microbiota-derived metabolites, absorbed by the host and transported to the peripheral circulation, can act as signalling molecules, influencing metabolism and immune homeostasis. Recent reports suggest that the gut microbiota plays a crucial role in modulating immune processes involved in HF. Here, we summarize recent advances in understanding the contributory role of gut microbiota in (auto-)immune pathways that critically determine the progression or alleviation of HF. We also thoroughly discuss potential gut microbiota-based intervention strategies to treat or decelerate HF progression.

This paper presents a comprehensive framework that traces the evolution of consciousness through a continuum of recursive processes spanning reaction, temporogenesis, symbiogenesis, and cognogenesis. By integrating biological cooperation, temporal structuring, and self-referential processing, our model provides a novel perspective on how complexity emerges and scales across evolutionary time. Reaction is established as the foundational mechanism that enables adaptive responses to environmental stimuli, which, through recursive refinement, transitions into temporogenesis-the synchronization of internal processes with external temporal rhythms. Symbiogenesis further enhances this process by fostering cooperative interactions at multiple biological levels, facilitating the emergence of higher-order cognitive functions. Cognogenesis represents the culmination of these recursive processes, where self-awareness and intentionality arise through iterative feedback loops. Our framework offers a biologically grounded pathway to addressing the "hard problem" of consciousness by proposing that subjective experience emerges as a result of progressively complex recursive interactions rather than as a static or isolated phenomenon. In comparing our approach with established theories such as Integrated Information Theory, Global Workspace Theory, and enactive cognition, we highlight its unique contributions in situating consciousness within a broader evolutionary and biological context. This work aims to provide a foundational model that bridges the gap between reaction and reflection, offering empirical avenues for further exploration in neuroscience, evolutionary biology, and artificial intelligence.

Diabetes Mellitus (DM) is a metabolic disease that manifests as a state of "chronic low-grade inflammation". Patients with DM have a disorder of intestinal flora. There is a discernible correlation between this disorder of intestinal flora and the onset and progression of eye diseases, which offers novel insights into treating eye diseases through the modulation of intestinal flora. Here, we demonstrated that a high-fat diet and streptozotocin injection-induced intestinal microbiota dysbiosis can lead to dry eye-like manifestations in T2DM mice. Probiotic and prebiotic treatments not only alleviated intestinal inflammation and barrier disruption, but also mitigated damage to the lacrimal barrier and suppressed immune cell infiltration and inflammatory responses. Additional mechanism investigation found that probiotics and prebiotics inhibited the TLR4/NF-κB signaling pathway and its downstream pro-inflammatory products both in the lacrimal gland and colon. 16S RNA sequencing identified a reduction in the bacterial genera Akkermansia and Lactobacillus in the fecal samples of DM mice. By contrast, treatment with probiotics and prebiotics led to a reshaping of the intestinal microbial community and a reduction in bile acid metabolites, such as taurocholic acid and deoxycholic acid. Our current study demonstrates that probiotic and prebiotic treatments can ameliorate dry eye-like symptoms and associated pathological changes in T2DM mice. Moreover, we proved that a high-fat diet and STZ-induced microbiota dysbiosis were involved in diabetic dry eye through the gut-eye axis.

This study investigated the effects of different non-starch polysaccharide (NSP) sources with NSP degrading enzymes (NSPases) and the influence on the mucosa-associated microbiota and intestinal immunity of nursery pigs, on growth performance and carcass traits at market weight.

One hundred and sixty newly weaned pigs at 7.0 ± 0.3 kg body weight (BW) were allotted in a 2 × 2 factorial with NSP sources and NSPases serving as factors. The 4 dietary treatments were: DDGS, corn distillers' dried grains with solubles as source of NSP; DDGS + NSPases (DDGS +), DDGS with xylanase at 0.01%, 3,000 U/kg of feed and β-mannanase at 0.05%, 400 U/kg of feed; SHWB, soybean hulls and wheat bran replacing corn DDGS as the source of NSP; SHWB with NSPases (SHWB +), SHWB with xylanase at 0.01%, 3,000 U/kg of feed and β-mannanase at 0.05%, 400 U/kg of feed. Pigs were fed for 37 d and housed in groups of 4 pigs per pen. At d 37, the median body weight pig in each pen was euthanized for sampling to analyze intestinal health parameters. Remaining pigs were fed a common diet for subsequent phases to evaluate the carryover effect on growth and carcass traits.

The SHWB decreased (P < 0.05) the relative abundance of Helicobacter, tended to increase (P = 0.074) the relative abundance of Lactobacillus, increased (P < 0.05) immunoglobulin G (IgG) in the jejunal mucosa, tended to increase (P = 0.096) the villus height (VH) in the jejunum, and tended to improve ADG (P = 0.099) and feed efficiency (P = 0.068) during phase 1 compared to DDGS treatment. Supplementation of NSPases increased (P < 0.05) Shannon index of diversity, increased the relative abundance of Streptococcus and Acinetobacter, and tended to increase (P = 0.082) dry matter digestibility. The BW of pigs fed SHWB was more uniform (P < 0.05) at the end of the 120 d study. Additionally, hot carcass weight of pigs fed SHWB tended to be more uniform (P = 0.089) than DDGS treatment.

Soybean hulls and wheat bran replacing DDGS in nursery diets improved uniformity of pigs at market weight, which might be attributed to beneficial modulation of the mucosa-associated microbiota and enhanced intestinal morphology during the nursery phase. Supplementation of NSPases had beneficial effects on the intestinal mucosa-associated microbiota, digestibility, and intestinal immunity in SHWB treatment, whereas no carryover effects were overserved at market weight.

In microbiota research, whole stool sampling is the conventional approach but can be problematic or infeasible for certain patients. This study aims to validate the use of rectal swabbing as an alternative method for microbiota analysis and determine optimal storage conditions suitable for various clinical settings, including intensive care units. We evaluated different sampling techniques and storage temperatures. Our findings indicated that rectal swabs yield microbiota diversity comparable to whole stool samples. Notably, storage conditions significantly impacted microbiota profiles, with increased E. coli and Enterococcus sp. quantifications observed at room temperature (RT). Consequently, we recommend immediate refrigeration of rectal swabs to reliably assess aerobic and total microbiota, particularly for patients requiring urgent care, such as antibiotic treatment.

We developed a pragmatic approach to study total and aerobic gut microbiota, applicable in numerous clinical units, such as intensive care or emergency units, where whole stool sampling is often impractical. This approach employs ESwab devices, which are already commonly used in hospitals.

The USA is home to 83-88 million dogs, with 3-7 million living in shelters. Shelter dogs move through the supply chain from their geographical origin to adoptive homes, with possible exposure to pathogens and shift in their gut microbiota. However, research in this area is limited. This study examined the effects of intestinal colonization by ESBL bacteria on gut taxa abundance, diversity, and functions in 52 shelter dogs of various ages, sexes, and fertility statuses.

We isolated fecal DNA, sequenced their 16S, processed the sequences using DADA2, identified taxa profiles in each dog by Phyloseq, and analyzed Chao1, Shannon, and Simpson alpha diversity by ggplot2 and Wilcoxon test. We analyzed beta diversity using Bray-Curtis dissimilarity matrix from the vegan package. Differential abundance of taxa, gut microbiome functions, and differential abundance of microbiome functions were analyzed using DESeq2, PICRUSt2, and ALDEx2, respectively, with Wilcoxon rank and Kruskal-Wallis tests for comparisons between dog groups.

Firmicutes (69.3%), Bacteroidota (13.5%), Actinobacteriota (6.77%), Proteobacteria (5.54%), and Fusobacteriota (4.75%) were the major phyla in the gut of shelter dogs. ESBL bacteria colonized dogs had reduced gut microbiota alpha diversity than non-colonized dogs. The abundance levels of the following phyla (Proteobacteria, Deferribacterota, Bacteroidota, Fusobacteriota, and Spirochaetota), class (Gammaproteobacteria, Bacteroidia, Deferribacteres, Brachyspirae, and Fusobacteria), and families (Enterobacteriaceae, Peptostreptococcaceae, Lactobacillaceae, Lachnospiraceae, Prevotellaceae, and Peptostreptococcaceae) were significantly (p < 0.05) varied between the two dog groups. Further stratified analysis by age, sex, and spaying/neutering status influenced the abundance of taxa in ESBL bacteria colonized dogs, indicating these covariates act as effect modifiers. Most gut metabolic and biosynthetic pathways were downregulated in ESBL bacteria colonized dogs compared to non-colonized dogs. However, alpha-linolenic acid metabolism and shigellosis, fluorobenzoate degradation, allantoin degradation, toluene degradation, glycol degradation, fatty acid and beta-oxidation, and glyoxylate metabolism bypass pathways were increased in dogs colonized by ESBL bacteria.

Colonization by ESBL bacteria marks altered gut microbiota. Dog's demography and fertility status modify the alterations, indicating host factors and ESBL bacteria interplay to shape gut microbiota. ESBL bacteria or other factors reprogram gut microbiome functions through down and upregulating multiple metabolic and biosynthesis pathways to promote ESBL bacteria colonization.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a condition wherein excessive fat accumulates in the liver, leading to inflammation and potential liver damage. In this narrative review, we evaluate the tissue microbiota, how they arise and their constituent microbes, and the role of the intestinal and hepatic microbiota in MASLD. The history of bacteriophages (phages) and their occurrence in the microbiota, their part in the potential causation of MASLD, and conversely, "phage therapy" for antibiotic resistance, obesity, and MASLD, are all described. The microbiota metabolism of bile acids and dietary tryptophan and histidine is defined, together with the impacts of their individual metabolites on MASLD pathogenesis. Both periodontitis and intestinal microbiota dysbiosis may cause MASLD, and how individual microorganisms and their metabolites are involved in these processes is discussed. Novel treatment opportunities for MASLD involving the microbiota exist and include fecal microbiota transplantation, probiotics, prebiotics, synbiotics, tryptophan dietary supplements, intermittent fasting, and phages or their holins and endolysins. Although FDA is yet to approve phage therapy in clinical use, there are multiple FDA-approved clinical trials, and this may represent a new horizon for the future treatment of MASLD.

Background: The role of gut dysbiosis in the pathophysiology of atopic dermatitis (AD) through immune system (IS) imbalance is a novel line of investigation currently under discussion. This study aimed to characterize compare the composition and functional profile of the gut microbiota (GM) between adults with AD and healthy individuals. Methods: Observational cross-sectional study, where fecal samples from 70 adults (38 patients and 32 controls) were analyzed using metagenomics and bioinformatics. Results: Differences between the GM of patients with AD and healthy individuals were demonstrated. Reduced microbial diversity was found in subjects with AD. Bacterial species with lower abundance primarily belonged to the families Ruminococcaceae, Akkermansiaceae, and Methanobacteriaceae. Several microbial metabolic pathways were found to be decreased in patients with AD, including amino acid biosynthesis, vitamin biosynthesis, fatty acids and lipids biosynthesis, and energy metabolism. Conclusion: Adults with AD exhibited a distinct GM compared to healthy individuals. Changes were demonstrated both compositionally and functionally. Further investigation is mandatory to elucidate the potential link and causal relationship between gut dysbiosis and AD, which may be crucial for a deeper understanding of the disease's pathophysiology and the development of novel therapeutic approaches.

The gut microbiome functions as a metabolic organ, producing numerous enzymes that influence host health; however, their substrates and metabolites remain largely unknown.

We present MicrobeRX, an enzyme-based metabolite prediction tool that employs 5487 human reactions and 4030 unique microbial reactions from 6286 genome-scale models, as well as 3650 drug metabolic reactions from the DrugBank database (v.5.1.12). MicrobeRX includes additional analysis modules for metabolite visualization and enzymatic and taxonomic analyses. When we applied MicrobeRX to 1083 orally administered drugs that have been approved in at least one jurisdiction at some point in time (DrugBank), it predicted metabolites with physicochemical properties and structures similar to metabolites found in biosamples (from MiMeDB). It also outperformed another existing metabolite prediction tool (BioTransformer 3.0) in terms of predictive potential, molecular diversity, reduction of redundant predictions, and enzyme annotation.

Our analysis revealed both unique and overlapping metabolic capabilities in human and microbial metabolism and chemo- and taxa-specific microbial biotransformations. MicrobeRX bridges the genomic and chemical spaces of the gut microbiome, making it a valuable tool for unlocking the chemical potential of the gut microbiome in human health, the food and pharmaceutical industries, and environmental safety. Video Abstract.

Diarrhea presents a substantial risk of high morbidity and mortality among foals. Although studies have shown connections between gut microbiota and several gastrointestinal diseases, there is still inadequate information on gut microbial alterations in foals during diarrhea. In this study, we conducted 16S rRNA and ITS gene amplicon sequencing to investigate gut bacterial and fungal differences between healthy and diarrheic foals. The results unveiled significant reductions in gut bacterial and fungal diversities among foals experiencing diarrhea, accompanied by notable shifts in the composition of gut microbial communities. A considerable decrease was observed in the relative abundance of 30 bacterial and 34 fungal genera. Moreover, two bacterial and eight fungal genera were utterly undetectable in the gut microbiota of diarrheic foals. Some decreased genera, such as Bifidobacterium and Saccharomyces, were deemed beneficial and recognized as probiotics. The study revealed significant alterations in foals' gut bacterial and fungal communities during diarrhea, which enriched our comprehension of gut microbial dynamics in foals across varying health statuses. These findings offer valuable insights for managing diarrhea through gut microbiota modulation, suggesting that probiotics may be superior to antibiotics in preventing and controlling foal diarrhea.IMPORTANCEThis research advances the understanding of gut bacterial and fungal dynamics in foals, highlighting gut microbiota dysbiosis as a potential contributor to foal diarrhea. Additionally, we observed that many altered bacteria and fungi were downregulated during diarrhea, including some probiotic strains. Consequently, our findings provide evidence that probiotics may offer superior efficacy compared with antibiotics as potential candidates for preventing and treating foal diarrhea.

Obesity is a major global concern and is generally attributed to a combination of genetic and environmental factors. Several hypotheses have been proposed to explain the evolutionary origins of obesity epidemic, including thrifty and drifty genotypes, and changes in thermogenesis. Here, we put forward the hypothesis of metaflammation, which proposes that due to intense selection pressures exerted by environmental pathogens, specific genes that help develop a robust defense mechanism against infectious diseases have had evolutionary advantages and that this may contribute to obesity in modern times due to connections between the immune and energy storage systems. Indeed, incorporating the genetic variations of gut microbiota into the complex genetic framework of obesity makes it more polygenic than previously believed. Thus, uncovering the evolutionary origins of obesity requires a multifaceted approach that considers the complexity of human history, the unique genetic makeup of different populations, and the influence of gut microbiome on host genetics.

The aim of this study was to investigate the effects on the tibia, liver, and gut, and on performance, when supplementing nursery pigs with different levels of rare earth-chitosan chelate (RECC). A total of 80 piglets, weaned at 7.67 ± 0.09 kg, were randomly assigned to groups RECC0 (RECC, 0 mg/kg diet), RECC200 (RECC, 200 mg/kg diet), RECC400 (RECC, 400 mg/kg diet), and RECC600 (RECC, 600 mg/kg diet), with four replicates in each group and five pigs per replicate during a 28 d experiment. Samples of the left hind tibia, serum, and feces were collected for analysis. The results indicated that, compared to pigs from group RECC0, pigs from group RECC200 presented with the following: a longer trabecular perimeter (p < 0.05), a larger trabecular area (p < 0.01), a higher trabecular number (p < 0.05), a smaller degree of trabecular separation (p < 0.01), and a lower number of osteoclasts (p < 0.01) in the tibia; higher abundances of beneficial fecal bacteria such as g_Prevotellaceae_NK3B31_group, g_UCG_005, g_Rikenellaceae_RC9_gut_group, g_Acetitomaculum, g_Glutamicibacter, g_Frisingicoccus, and g_Alistipes; higher (p < 0.01) serum levels of IgM, IgA, IgG, and IL-10; a lower (p < 0.01) serum concentration of TNF-α; a higher (p < 0.05) average daily gain and feed conversion ratio; and a lower (p < 0.01) incidence of diarrhea. The dietary addition of RECC contributes to improvements in tibia quality, gut health, and performance in nursery pigs.

Due to the continued aging of the global population, cardiovascular diseases (CVDs) remain the main cause of death worldwide, with millions of fatalities from diseases, including stroke and coronary artery disease, reported annually. Thus, novel therapeutic approaches and targets are urgently required for diagnosing and treating CVDs. Recent studies emphasize the vital part of gut microbiota in both CVD prevention and management. Among these, Faecalibacterium prausnitzii (F. prausnitzii) has emerged as a promising probiotic capable of improving intestinal health. Although preliminary investigations demonstrate that F. prausnitzii positively enhances cardiovascular health, research specifically connecting this strain to CVD outcomes remains limited. Based on current research and assessment of possible clinical applications, this paper aimed to investigate the positive effects on cardiovascular health using F. prausnitzii and its metabolites. Targeting gut flora is expected to become a mainstay in CVD treatment as research develops.

The complex interactions between host genetics and the gut microbiome are well documented. However, the specific impacts of gene expression patterns and microbial composition on each other remain to be further explored.

Here, we investigated this complex interplay in a sizable population of 705 hens, employing integrative analyses to examine the relationships among the host genome, mucosal gene expression, and gut microbiota. Specific microbial taxa, such as the cecal family Christensenellaceae, which showed a heritability of 0.365, were strongly correlated with host genomic variants. We proposed a novel concept of regulatability ( r b 2 ), which was derived from h2, to quantify the cumulative effects of gene expression on the given phenotypes. The duodenal mucosal transcriptome emerged as a potent influencer of duodenal microbial taxa, with much higher r b 2 values (0.17 ± 0.01, mean ± SE) than h2 values (0.02 ± 0.00). A comparative analysis of chickens and humans revealed similar average microbiability values of genes (0.18 vs. 0.20) and significant differences in average r b 2 values of microbes (0.17 vs. 0.04). Besides, cis ( h cis 2 ) and trans heritability ( h trans 2 ) were estimated to assess the effects of genetic variations inside and outside the cis window of the gene on its expression. Higher h trans 2 values than h cis 2 values and a greater prevalence of trans-regulated genes than cis-regulated genes underscored the significant role of loci outside the cis window in shaping gene expression levels. Furthermore, our exploration of the regulatory effects of duodenal mucosal genes and the microbiota on 18 complex traits enhanced our understanding of the regulatory mechanisms, in which the CHST14 gene and its regulatory relationships with Lactobacillus salivarius jointly facilitated the deposition of abdominal fat by modulating the concentration of bile salt hydrolase, and further triglycerides, total cholesterol, and free fatty acids absorption and metabolism.

Our findings highlighted a novel concept of r b 2 to quantify the phenotypic variance attributed to gene expression and emphasize the superior role of intestinal mucosal gene expressions over host genomic variations in elucidating host‒microbe interactions for complex traits. This understanding could assist in devising strategies to modulate host-microbe interactions, ultimately improving economic traits in chickens.

Introduction. The study of gut microbiota is now an essential dimension in many clinical studies. For instance, microbiota diversity investigation can help us to better manage cirrhotic patients by the identification of markers of severity and the identification of possible sources of pathogens.Hypothesis/Gap Statement. Conducting clinical research on gut microbiota for fragile patients in intensive care units, such as cirrhotic patients, poses significant challenges.Aim. In this study, we developed a comprehensive toolkit for investigating gut microbiota in fragile patients using rectal swabbing combined with straightforward lifestyle and clinical questionnaires.Methodology . We applied this prospective approach to 49 well-phenotyped cirrhotic patients as a function of their compensation status (compensated patients with outpatients' recruitment vs decompensated patients in intensive care units).Results . Our results, consistent with the literature, showed that liver function impairment is associated with lower microbiota diversity. Additionally, we monitored aerobic microbiota in decompensated cirrhotic patients, observing the invasion of extended spectrum beta-lactamase (ESBL)-producing Escherichia coli in the gut's aerobic microbiota prior to severe infection caused by these pathogens.Conclusion. We propose this pragmatic methodology for larger cohort studies, aiming to enhance the monitoring of immunocompromised patients by using microbiota analysis as a predictive tool for the severity of associated pathologies and the identification of agents responsible for severe infections.

Coffee is globally popular beverage, renowned for its taste and stimulating properties. This study aims to explore the impact of two different types of coffee, depending on extraction methods, on the gut microbiota. Fecal samples from healthy donors (n = 20) were cultured with or without coffee using in vitro fecal incubation. Both coffee-treated groups exhibited lower microbial diversity and greater structural differences in their communities compared to the control. Notably, the Bifidobacterium genus was overrepresented in the instant coffee (IC)-treated groups, whereas the Blautia genus was underrepresented in both coffee-treated groups. Additionally, genes for TCA cycle and vitamin B6 metabolism were more prevalent in coffee-treated groups than in the control. However, the precursor pathways leading to the TCA cycle differed between the DC- and IC-treated groups, reflecting the distinct chemical compositions of each coffee type. These findings demonstrate that extraction method of coffee significantly affects its impacts on gut microbial structure.

The online version contains supplementary material available at 10.1007/s10068-024-01717-7.

Humans consume large amounts of non-starch polysaccharides(NPs) daily. Some NPs, not absorbed by the body, proceed to the intestines. An increasing number of studies reveal a close relationship between NPs and gut microbiota(GM) that impact the human body. This review not only describes in detail the structures of several common NPs and their effects on GM, but also elucidates the degradation mechanisms of NPs in the intestine. The purpose of this review is to elucidate how NPs interact with GM in the intestine, which can provide valuable information for further studies of NPs.

Alzheimer's Disease (AD) is a debilitating neurocognitive disorder with an unclear underlying mechanism. Recent studies have implicated gut microbiota dysbiosis with the onset and progression of AD. The connection between gut microbiota and AD can significantly affect the prevention and treatment of AD patients. This systematic review summarizes primary outcomes of human and mouse AD models concerning gut microbiota alterations. A systematic literature search in February through March 2023 was conducted on PubMed, Embase, and Web of Science. We identified 711 as potential manuscripts of which 672 were excluded because of irrelevance to the identified search criteria. Primary outcomes include microbiota compositions of control and AD models in humans and mice. In total, 39 studies were included (19 mouse and 20 human studies), published between 2017 and 2023. We included studies involving well-established mice models of AD (5xFAD, 3xTg-AD, APP/PS1, Tg2576, and APPPS2) which harbor mutations and genes that drive the formation of Aß plaques. All human studies were included on those with AD or mild cognitive impairment. Among alterations in gut microbiota, most studies found a decreased abundance of the phyla Firmicutes and Bifidobacteria, a genus of the phylum Actinomycetota. An increased abundance of the phyla Bacteroidetes and Proteobacteria were identified in animal and human studies. Studies indicated that gut microbiota alter the pathogenesis of AD through its impact on neuroinflammation and permeability of the gastrointestinal tract. The ensuing increase in blood-brain barrier permeability may accelerate Aβ penetrance and formation of neuritic plaques that align with the amyloid hypothesis of AD pathogenesis. Further studies should assess the relationship between gut microbiota and AD progression and therapy preserving beneficial gut microbiota.

Recurrent pregnancy loss (RPL) involves multiple consecutive miscarriages in early pregnancy, affecting a significant number of Indian women and placing substantial physical and emotional stress on expecting couples. This expert consensus aims to highlight probiotics as a promising option for enhancing fertility and supporting successful pregnancy outcomes, offering hope to individuals and couples affected by RPL. A group of fourteen experts with diverse expertise in gynecology, obstetrics, and fertility from across India gathered between June 29 and June 30, 2024. According to the experts, advanced maternal age emerges as an independent risk factor for miscarriage, with increased risks among older Indian women. The major contributors to RPL include thyroid disease and polycystic ovarian disease. Experts emphasize that the vaginal microbiome dysbiosis, characterized by the reduced dominance of Lactobacilli, is associated with adverse pregnancy outcome, such as preterm birth, early pregnancy loss, and increased events of RPL. Oral probiotic supplementation, particularly strains like L. acidophilus and L. rhamnosus, may improve embryo implantation, reduce miscarriage risk, and support pregnancy maintenance. A healthy lifestyle choice and minimal use of antibiotics are important in creating a positive reproductive outcome. The present expert opinion supports the potential benefits of probiotics, particularly Lactobacillus species, in managing RPL and improving reproductive outcomes. By promoting a balanced microbiota, reducing inflammation, and modulating immune responses, probiotics may play a critical role in enhancing reproductive success.

Although natural polysaccharides often have growth-promoting effects on animals, little is known about how polysaccharides act when they are administered as feed additives. This work shows that Amomum longiligulare polysaccharide 1 (ALP1) improves the growth performance of piglets by promoting the proliferation of jejunal epithelial cells. ALP1 improves the growth performance of piglets, increasing the average daily gain by 32.71 % and reducing the feed-to-gain (F/G) ratio by 21.93 %. The gut microbiota is an important regulatory target of polysaccharides. The results of jejunal microbiota transplantation trials indicate that the jejunal microbiota from ALP1-fed piglets exhibits better growth performance and that the F/G ratio is reduced by 12.72 %. Furthermore, 16S rDNA sequencing and nontargeted metabolomic analyses reveal that ALP1 supplementation can increase the abundance of Lactobacillus in the jejuna of piglets, resulting in a high abundance of 11Z-eicosenoic acid (EA). In addition, EA increases the villus height-to-crypt depth (VH/CD) ratio in the jejunum by 27.41 %, potentially increasing epithelial cell proliferation. These results suggest that oral ALP1 supplementation promotes growth by modulating the composition of the jejunal microbiota and its associated metabolites.

The gut microbiota has been strongly linked to gastrointestinal cancer, but the relationship between gut microbiota and esophageal cancer (EC) is still not fully understood. We conducted a 2-sample Mendelian randomization (MR) study to unveil the potential impact of intestinal microorganisms on EC in East Asian populations. In order to delve deeper into the potential causal relationship between gut microbiota and EC, we conducted a 2-sample MR analysis, utilizing 211 single nucleotide polymorphisms associated with gut microbiota, sourced from the largest genome-wide association study on gut microbiota, for our analysis. To estimate the causal relationship, we employed the inverse variance weighting method. In addition, to assess the potential influence of pleiotropy, we used MR-Egger regression in our analysis. Among the 10 specific bacterial taxa identified using the inverse variance weighting as being associated with the risk of EC, we observed a positive association between family Bacteroidaceae (P = .04), genus Bacteroides (P = .04), genus Bilophila (P = .02), genus Candidatus Soleaferrea (P = .02) and the EC, while family Victivallaceae (P = .03), genus Eubacterium coprostanoligenes (P = .01), genus Catenibacterium (P = .01), genus Coprococcus2 (P = .01), unknowngenus.id.959 (P = .02) and unknowngenus.id.1868 (P = .01) may be associated with a reduced risk of EC. Our MR analysis indicate a probable association between gut microbiota and the development and advancement of EC. These findings offer novel perspectives on the possible application of targeted gut bacteria for the prevention and management of EC.