Fecal Microbiota Research Articles

From Clinical to Benchside: Lacticaseibacillus and Faecalibacterium Are Positively Associated With Muscle Health and Alleviate Age-Related Muscle Disorder.

Sarcopenia is an age-related muscle disorder that increases risks of adverse clinical outcomes, but its treatments are still limited. Gut microbiota is potentially associated with sarcopenia, and its role is still unclear. To investigate the role of gut microbiota in sarcopenia, we first compared gut microbiota and metabolites composition in old participants with or without sarcopenia. Fecal microbiota transplantation (FMT) from human donors to antibiotic-treated recipient mice was then performed. Specific probiotics and their mechanisms to treat aged mice were identified. Old people with sarcopenia had different microbial composition and metabolites, including Paraprevotella, Lachnospira, short-chain fatty acids, and purine. After FMT, mice receiving microbes from people with sarcopenia displayed lower muscle mass and strength compared with those receiving microbes from non-sarcopenic donors. Lacticaseibacillus rhamnosus (LR) and Faecalibacterium prausnitzii (FP) were positively related to muscle health of old people, and enhanced muscle mass and function of aged mice. Transcriptomics showed that genes related to tricarboxylic acid cycle (TCA) were enriched after treatments. Metabolic analysis showed increased substrates of TCA cycle in both LR and FP supernatants. Muscle mitochondria density, ATP content, NAD+/NADH, mitochondrial dynamics and biogenesis proteins, as well as colon tight junction proteins of aged mice were improved by both probiotics. LR and the combination of two probiotics also benefit intestinal immune health by reducing CD8+ IFNγ+ T cells. Gut microbiota dysbiosis is a pathogenesis of sarcopenia, and muscle-related probiotics could alleviate age-related muscle disorders mainly through mitochondria improvement. Further clinical translation is warranted.

Gut-Derived Ursodeoxycholic Acid from Saponins of Quinoa Regulated Colitis via Inhibiting the TLR4/NF-κB Pathway.

Alteration of the gut microbiota and its metabolites plays a key role in the development of inflammatory bowel disease (IBD). Here, we investigated the mechanism of saponins, a byproduct from quinoa (SQ) processing, in regulating IBD. SQ ameliorated gut microbiota dysbiosis revealed by 16S rRNA sequencing and improved colonic antioxidant activities and barrier integrity in dextran sulfate sodium (DSS)-treated mice. Broad-spectrum antibiotics further proved that the gut-protective effects of SQ were mediated by gut microbiota. Next, fecal microbiota transplantation (FMT) of SQ-induced gut microbiota/metabolites to inoculate DSS-treated mice alleviated colitis significantly. Untargeted metabolomics and lipidomics revealed that ursodeoxycholic acid (UDCA) was enriched as a microbial metabolite after SQ supplementation. UDCA was then found to attenuate DSS-induced colitis in vivo by targeting the TLR4/NF-κB pathway, which was also verified in a Caco-2 cell model treated with a TLR4 agonist/antagonist. Overall, our findings established that gut microbiota-UDCA-TLR4/NF-κB signaling plays a key role in mediating the protective effects of SQ.

Colorectal cancer in Lynch syndrome families: consequences of gene germline mutations and the gut microbiota

BackgroundLynch syndrome (LS)-associated colorectal cancer (CRC) always ascribes to pathogenic germline mutations in mismatch repair (MMR) genes. However, the penetrance of CRC varies among those with the same MMR gene mutation. Thus, we hypothesized that the gut microbiota is also involved in CRC development in LS families.MethodsThis prospective, observational study was performed from December 2020 to March 2023. We enrolled 72 individuals from 9 LS families across six provinces in China and employed 16S rRNA gene amplicon sequencing to analyze the fecal microbiota components among LS-related CRC patients (AS group), their spouses (BS group), mutation carriers without CRC (CS group), and non-mutation carriers (DS group) using alpha and beta diversity indices.ResultsThere were no apparent differences in age or gender among the four groups. Alpha and beta diversity indices exhibited no significant differences between the AS and BS groups, verifying the role of germline mutations in the occurrence of CRC in LS families. Beta diversity analysis exhibited significant differences between the AS and CS groups, revealing the importance of the gut microbiota for the occurrence of CRC in LS families. A greater difference (both alpha and beta diversity indices) was shown between the AS and DS groups, demonstrating the combined impact of the gut microbiota and genetic germline mutations on the occurrence of CRC in LS families. Compared with those in the CS and DS groups, we identified ten microbial genera enriched in the AS group, and one genus (Bacteroides) decreased in the AS group. Among the elevated genera in the AS group, Agathobacter, Coprococcus and Prevotellaceae_NK3B31_group were butyrate-producing genera.ConclusionThis study found the development of CRC in the LS families can be attributed to the combined effects of gene germline mutations as well as the gut microbiota and provided novel insights into the prevention and treatment of CRC in the LS families.

Potentially probiotic NPL 1334 strain of Enterococcus durans benefits rats with diet-induced hypercholesterolemia

PurposeTo study the potential of a candidate probiotic strain belonging to the Enterococcus durans species in alleviating hypercholesterolemia and improving the microbial milieu of rat gut.MethodsA previously isolated and characterized E. durans strain NPL 1334 was further screened in vitro for its bile salt hydrolyzation and cholesterol assimilation ability. An in vivo trial using diet-induced hypercholesterolemic rats was conducted to evaluate the effects of the administered test probiotic strain on the animal’s blood biochemical parameters such as total cholesterol (TC), high-density lipopolysaccharides (HDL), low-density lipopolysaccharides (LDL), triglycerides (TG), on body weight, oxidative stress markers, and its impact on intestinal and fecal microbiota as well as a histopathological examination of the test animal’s livers.ResultsE. durans strain showed good bile salt hydrolyzing ability and ample cholesterol assimilation in vitro. Probiotic-fed hypercholesterolemic rats showed significantly lowered cholesterol, triglyceride and LDL levels. The body weight of probiotic-fed rats was reduced as compared to the control. E. durans also stimulated the growth of beneficial LAB in the intestine of experimental rats and did not harm the liver of the experimental rats.ConclusionE. durans can be a natural therapeutic alternative to manage diet-induced hypercholesterolemia and may eventually enhance anti-cholesterolemic therapies.

Lactobacillus gasseri prevents ibrutinib-associated atrial fibrillation through butyrate.

Ibrutinib, a widely used anti-cancer drug, is known to significantly increase the susceptibility to atrial fibrillation (AF). While it is recognized that drugs can reshape the gut microbiota, influencing both therapeutic effectiveness and adverse events, the role of gut microbiota in ibrutinib-induced AF remains largely unexplored. Utilizing 16S rRNA gene sequencing, fecal microbiota transplantation, metabonomics, electrophysiological examination, and molecular biology methodologies, we sought to validate the hypothesis that gut microbiota dysbiosis promotes ibrutinib-associated AF and to elucidate the underlying mechanisms. We found that ibrutinib administration predisposes rats to AF. Interestingly, ibrutinib-associated microbial transplantation conferred increased susceptibility to AF in rats. Notably, ibrutinib induced a significantly decrease in the abundance of Lactobacillus gasseri (L. gasseri), and oral supplementation of L. gasseri or its metabolite, butyrate, effectively prevented rats from ibrutinib-induced AF. Mechanistically, butyrate inhibits the generation of reactive oxygen species (ROS), thereby ameliorating atrial structural remodeling. Furthermore, we demonstrated that ibrutinib inhibited the growth of L. gasseri by disrupting the intestinal barrier integrity. Collectively, our findings provide compelling experimental evidence supporting the potential efficacy of targeting gut microbes in preventing ibrutinib-associated AF, opening new avenues for therapeutic interventions.

The evolving landscape of live biotherapeutics in the treatment of Clostridioides difficile infection.

Clostridioides difficile (C. difficile) infection (CDI) is common after antibiotic exposure and presents significant morbidity, mortality and healthcare costs worldwide. The rising incidence of recurrent CDI, driven by hypervirulent strains, widespread antibiotic use and increased community transmission, has led to an urgent need for novel therapeutic strategies. Conventional antibiotic treatments, although effective, face limitations due to rising antibiotic resistance and high recurrence rates, which can reach up to 60% after multiple infections. This has prompted exploration of alternative therapies such as fecal microbiota-based therapies, including fecal microbiota transplantation (FMT) and live biotherapeutics (LBPs), which demonstrate superior efficacy in preventing recurrence. They are aimed at restoring the gut microbiota. Fecal microbiota, live-jslm and fecal microbiota spores, live-brpk have been approved by the U.S. Food and Drug Administration in individuals aged 18 years or older for recurrent CDI after standard antimicrobial treatment. They have demonstrated high efficacy and a favorable safety profile in clinical trials. Another LBP under study includes VE-303, which is not derived from human donor stool. This review provides a comprehensive overview of the current therapeutic landscape for CDI, including its epidemiology, pathophysiology, risk factors, diagnostic modalities and treatment strategies. The review delves into the emerging role of live biotherapeutics, with a particular focus on fecal microbiota-based therapies. We explore their development, mechanisms of action, clinical applications and potential to revolutionize CDI management.

Fecal microbiota transplantation combined with inulin promotes the development and function of early immune organs in chicks.

Modern management of chicks hinders the vertical transmission of intestinal microbiota, which is closely related to immunity. Inulin is a substrate that can be utilized by the microbiota. This study aimed to determine whether fecal microbiota transplantation (FMT) combined with inulin played a "1 + 1 > 2" role in enhancing the development and function of immune organs. Chicks were treated with 1 % inulin and/or fecal microbiota suspension on days 1-6. The growth performance, immune organ development, and immune indicators were evaluated on days 7, 14, and 21. Results showed that the combination of FMT and inulin significantly increased the immune organ index on day 7 and promoted the morphological structure and the expression of proliferating cell nuclear antigen (PCNA) in immune organs on days 7, 14, and 21. Each treatment increased the gene expression of interferon-gamma (IFN-γ), interleukin-4 (IL-4), interleukin-2 (IL-2), B cell-activating factor receptor (BAFFR), B cell linker (BLNK), C-X-C Motif Chemokine Ligand 12 (CXCL12), C-X-C Motif Chemokine Receptor 4 (CXCR4), and Biotin (Bu-1) to varying degrees. FMT combined with inulin significantly increased the expression of IgA-positive cells on days 7 and 14. In conclusion, the synergistic effect of FMT and inulin had beneficial impacts on the development and function of immune organs.

Increased Crystallite Stability Enhances Gut Microbial Fermentability of Type 5 Resistant Starch.

The amylolytic susceptibility of starch-lipid complexes with different forms of crystallites has been studied extensively, but the fermentation properties of these complexes remain little understood. Hence, the in vitro fecal fermentation properties of starch-lipid complexes with VI-type and VII-type crystallites were investigated in the present study. Compared to VI-type complexes, fermentation of VII-type complexes caused more severe disruption to the crystallites and resulted in greater acid, reducing sugar, and short-chain fatty acids (SCFAs) production. Moreover, fermentation of VII-type complexes promoted a greater relative abundance of SCFAs-producing bacteria in the fecal microbiota than did VI-type complexes. Our results show that the more stable VII-type complexes are utilized more effectively than VI-type complexes, which can be attributed to the bacteria binding more readily to VII-type than to VI-type complexes. Therefore, VII-type complexes were considered to deliver better health benefits than VI-type complexes due to their greater potential for producing SCFAs and stimulating beneficial gut microbial activity in the colon.

Fecal Microbiota Strongly Correlates with Tissue Microbiota Composition in Colorectal Cancer but Not in Non-Small Cell Lung Cancer.

Microbiota could be of interest in the diagnosis of colorectal and non-small cell lung cancer (CRC and NSCLC). However, how the microbial components of tissues and feces reflect each other remains unknown. In this work, our main objective is to discover the degree of correlation between the composition of the tissue microbiota and that of the feces of patients affected by CRC and NSCLC. Specifically, we investigated tumor and non-tumor tissues from 38 recruited patients with CRC and 19 with NSCLC. DNA from samples was submitted for 16S rDNA metagenomic sequencing, followed by data analysis through the QIIME2 pipeline and further statistical processing with STATA IC16. Tumor and non-tumor tissue selected genera were highly correlated in both CRC and NSCLC (100% and 81.25%). Following this, we established tissue-feces correlations, using selected genera from a LEfSe analysis previously published. In CRC, we found a strong correlation between the taxa detected in feces and those from colorectal tissues. However, our data do not demonstrate this correlation in NSCLC. In conclusion, our findings strongly reinforce the utility of fecal microbiota as a non-invasive biomarker for CRC diagnosis, while highlighting critical distinctions for NSCLC. Furthermore, our data demonstrate that the microbiota components of tumor and non-tumor tissues are similar, with only minor differences being detected.

Gut microbial dysbiosis, IgA, and Enterococcus in common variable immunodeficiency with immune dysregulation

BackgroundCommon variable immunodeficiency (CVID) is characterized by hypogammaglobulinemia and recurrent infections. Significant morbidity and mortality are caused by immune dysregulation complications (CVIDid), which affect around one-third of CVID patients and have a poorly understood etiology. Here, we investigate the hypothesis that gut microbial dysbiosis contributes to the inflammation underlying CVIDid.ResultsBacterial invasion of colonic crypts was observed in CVID (3/15) and X-linked agammaglobulinemia (XLA, 1/3), but not in healthy control (HC, 0/9) biopsies. Fecal gut microbiota was characterized using 16S rRNA-targeted amplicon sequencing. Increased bacterial load, decreased alpha diversity and distinct beta diversity were observed in CVIDid (n = 42) compared to HC (n = 48), and similar results were seen in CVID with IgA deficiency (n = 40) compared to HC. CVIDid and CVID-IgA showed enrichment of the genus Enterococcus, and in vitro studies confirmed the inflammatory potential of Enterococcus gallinarum and Enterococcus hirae in patient monocytes. ConclusionsThis study further supports the hypothesis that a dysregulated gut microbiota, with IgA deficiency as an important driving factor, contributes to systemic inflammation in primary antibody deficiency, and introduces enterococci as potential pathobionts in CVIDid.EQUitBFVXYmTZpXE6XWtg9Video

16S rRNA and metabolomics reveal the key microbes and key metabolites that regulate diarrhea in Holstein male calves.

Diarrhea is a prevalent disease among calves, which significantly hinders their growth and development, thereby impacting farm productivity and revenue. This study aimed to investigate the impact of diarrhea on calf growth. Holstein male calves with similar birth weight (39.5 ± 4.2 kg) were included in this study, and key parameters such as fecal score, diarrhea incidence, and growth performance from birth to weaning were measured. Rectal fecal samples from both diarrheic (n = 24) and healthy calves (n = 24) aged 1-4 weeks were analyzed using 16S rRNA gene sequencing and untargeted metabolomics. Our findings indicated a high prevalence of diarrhea among calves between 1-4 weeks of age on pasture, which led to a marked decrease in growth performance, including average daily gain. At the genus level, the relative abundance of GCA-900066575 in one-week-old diarrheic calves was significantly higher; Escherichia-Shigella and Pseudoflavonifractor were more abundant in two-week-old calves; while Tyzzerella and Lachnospiraceae_UCG-004 increased significantly in four-week-old calves, and correlated negatively with average daily gain, suggesting that these bacteria may promote the occurrence of diarrhea. Correlation analysis revealed that fecal metabolites such as arachidonic acid, cis-vaccenic acid, oleic acid, choline, creatinine, and others were significantly negatively correlated with calf growth performance and were significantly increased in diarrheic calves. WGNCA identified that dark magenta module metabolites were significantly associated with diarrhea traits from 1-4 weeks. Thirteen metabolites, including glycerophospholipids (such as 1-stearoyl-2-hydroxy-sn-glycero-3-phosphoethanolamine), fatty acids (such as dodecanoic acid), and arachidonic acid, were positively correlated with GCA-900066575, Escherichia-shigella, Tyzzerella, and Clostridium_butyricum, but negatively correlated with UBA1819, Lachnoclostridium_sp_YL32, and Clostridium_scindens. Therefore, GCA-900066575, Escherichia-shigella, Lachnospiraceae_UCG-004, and Tyzzerella are likely key bacterial genera causing diarrhea in calves, while arachidonic acid, glycerol phospholipids, and fatty acids are critical metabolites associated with this condition. These alterations in the fecal microbiota and metabolite composition were found to be the principal contributors to growth retardation in diarrheic calves.

A Menu for Microbes: Unraveling Appetite Regulation and Weight Dynamics Through the Microbiota-Brain Connection Across the Lifespan.

Appetite, as the internal drive for food intake, is often dysregulated in a broad spectrum of conditions associated with over- and under-nutrition across the lifespan. Appetite regulation is a complex, integrative process comprising psychological and behavioral events, peripheral and metabolic inputs, and central neurotransmitter and metabolic interactions. The microbiota-gut-brain axis has emerged as a critical mediator of multiple physiological processes, including energy metabolism, brain function, and behavior. Therefore, the role of the microbiota-gut-brain axis in appetite and obesity is receiving increased attention. Omics approaches such as genomics, epigenomics, transcriptomics, proteomics, and metabolomics in appetite and weight regulation offer new opportunities for featuring obesity phenotypes. Furthermore, gut microbiota-targeted approaches such as pre- pro- post- and synbiotic, personalized nutrition, and fecal microbiota transplantation are novel avenues for precision treatments. The aim of this narrative review is (1) to provide an overview of the role of the microbiota-gut-brain-axis in appetite regulation across the lifespan and (2) to discuss the potential of omics and gut microbiota-targeted approaches to deepen understanding of appetite regulation and obesity.

Microbiome-Driven Therapeutics: From Gut Health to Precision Medicine

The human microbiome, a complex ecosystem of microorganisms residing in and on the body, plays a pivotal role in the regulation of a wide range of physiological processes, including digestion, immune responses, and metabolic functions. In recent years, the rapidly growing field of microbiome-driven therapeutics has garnered significant attention owing to its potential to revolutionize healthcare. This review explores the evolving landscape of microbiome-based therapies, with a particular focus on the gut microbiome and its implications for both gut health and precision medicine. We highlight recent advances in understanding how microbial communities influence disease pathogenesis and treatment outcomes, spanning conditions such as inflammatory bowel disease (IBD), metabolic disorders, neurological diseases, and even cancer. This article also discusses emerging therapeutic strategies, including probiotics, prebiotics, fecal microbiota transplantation (FMT), and microbial-based drugs, as well as the challenges associated with their clinical implementation. Additionally, we examined how the integration of microbiome profiling and metagenomic data is advancing the field of precision medicine, paving the way for personalized and effective treatments. This review serves as a comprehensive resource that synthesizes current knowledge, identifies key gaps in microbiome research, and offers insights into the future direction of microbiome-driven therapeutics, thus providing a valuable framework for clinicians, researchers, and policymakers seeking to harness the potential of microbiomes to advance personalized healthcare solutions.

Altered microbiome and metabolome profiling in fearful companion dogs: An exploratory study.

Behavioral dysfunctions in dogs represent one of the main social concerns, since they can endanger animals and human-dog relationship. Together with the trigger stimulus (human, animal, place, scent, auditory stimuli, objects), dogs can experience stressful conditions, either in multiple settings or unique situations, more often turning into generalized fear. Such a dysfunctional behavior can be associated with genetic susceptibility, environmental factors, traumatic experiences, and medical conditions. The available therapy, based on behavior approaches, environmental management, and neurochemical manipulation, through nutrition, supplements, medicines, and pheromones, represent the mainstays of the treatments currently accessible. Growing evidence in humans and animals highlight the importance of the gut-brain axis in the modulation of the brain physiology and behavior as well. Here, taking advantage of the next generation sequencing approach, we sought to investigate the potential connection between gut microbiota and microbiome in dogs suffering from generalized fear (n = 8), when compared to healthy subjects (n = 8), who all lived in different families. Faecal microbiota evaluation showed a differential abundance of taxa related to Proteobacteria and Firmicutes Phyla, between case and control dogs. Moreover, serum metabolomics documented significant alterations of molecules associated to GABA and glutamate neurotransmission in the patients, as well as bile acids metabolism. Overall, our preliminary and integrated investigations highlighted an intriguing role for the microbiome-metabolome network, allowing to further unveil the potential pathophysiology of relational issues in companion animals and paving the way for more effective therapeutical approaches.

The Effects of Microbes on Human Personality: Anxiety and Depression

The crucial involvement of the gut microbiota in sustaining human health and immune functionality is underscored by numerous studies, highlighting its pivotal role in mediating the intricate gut-brain axis. This underscores the capability of gut microbial inhabitants to modulate neurotransmission, dictate behavioral patterns, and exert further influences. Substantial evidence has converged on the association between gastrointestinal microbial compositions and conditions such as anxiety and depression, implying a regulatory interplay. This discussion examines data from preclinical in vivo studies and clinical literature, including investigations using germ-free animal models, as well as evaluations of therapeutic interventions involving prebiotics, probiotics, synbiotics, and postbiotics. Additionally, it explores the implications of fecal microbiota transplantation (FMT). By employing such diverse methodological approaches, a comprehensive understanding of the gut microbiome's contribution to neuropsychiatric well-being is emerging, underscoring the importance of gut-microbial balance for overall health.

Exploring the role of the gut microbiome in modulating response to anti-PD-1 immunotherapy in melanoma patients

The gut microbiome plays a crucial role in modulating the immune response to cancer immunotherapies, particularly anti-PD-1 inhibitors, which have revolutionized the treatment of melanoma. Despite the success of these therapies in some patients, the response remains highly variable. Recent studies suggest that the composition and diversity of the gut microbiome can influence the efficacy of anti-PD-1 therapy by shaping systemic immunity, particularly through its effects on T-cell activation and tumor microenvironment dynamics. Specific microbial species, such as Akkermansia muciniphila and Bifidobacterium, as well as microbial metabolites like short-chain fatty acids (SCFAs), have been associated with enhanced immune responses and improved treatment outcomes. Conversely, dysbiosis, or microbial imbalance, has been linked to resistance to immunotherapy. This review explores the mechanisms by which the microbiome influences immune responses and discusses strategies such as fecal microbiota transplantation (FMT), dietary interventions, and probiotics to modulate the microbiome and enhance melanoma treatment outcomes. Understanding the microbiome's role in immunotherapy could lead to more personalized, effective treatment strategies for melanoma and other cancers.

Gut Microbiota-Based Interventions for Parkinson's Disease: Neuroprotective Mechanisms and Current Perspective.

Recent evidence links gut microbiota alterations to neurodegenerative disorders, including Parkinson's disease (PD). Replenishing the abnormal composition of gut microbiota through gut microbiota-based interventions "prebiotics, probiotics, synbiotics, postbiotics, and fecal microbiota transplantation (FMT)" has shown beneficial effects in PD. These interventions increase gut metabolites like short-chain fatty acids (SCFAs) and glucagon-like peptide-1 (GLP-1), which may protect dopaminergic neurons via the gut-brain axis. Neuroprotective effects of these interventions are mediated by several mechanisms, including the enhancement of neurotrophin and activation of the PI3K/AKT/mTOR signaling pathway, GLP-1-mediated gut-brain axis signaling, Nrf2/ARE pathway, and autophagy. Other pathways, such as free fatty acid receptor activation, synaptic plasticity improvement, and blood-brain and gut barrier integrity maintenance, also contribute to neuroprotection. Furthermore, the inhibition of the TLR4/NF-кB pathway, MAPK pathway, GSK-3β signaling pathway, miR-155-5p-mediated neuroinflammation, and ferroptosis could account for their protective effects. Clinical studies involving gut microbiota-based interventions have shown therapeutic benefits in PD patients, particularly in improving gastrointestinal dysfunction and some neurological symptoms. However, the effectiveness in alleviating motor symptoms remains mild. Large-scale clinical trials are still needed to confirm these findings. This review emphasizes the neuroprotective mechanisms of gut microbiota-based interventions in PD as supported by both preclinical and clinical studies.

Therapeutic Potential of Vanillic Acid in Ulcerative Colitis Through Microbiota and Macrophage Modulation.

This study investigated the protective effects of the dietary polyphenol vanillic acid (VA) on dextran sulfate sodium-induced acute ulcerative colitis (UC) in mice, focusing on its impact on the gut microbiota and inflammatory responses. VA was supplemented following dextran sulfate sodium administration, and key indicators, including body weight, disease activity index, colon length, spleen index, and inflammatory markers, were assessed. VA supplementation significantly alleviated UC symptoms, preserved intestinal barrier integrity, and reduced pro-inflammatory cytokine levels. Additionally, VA positively altered the gut microbiota composition, promoting beneficial bacteria such as Akkermansia muciniphila while suppressing the arachidonic acid metabolism pathway. Fecal microbiota transplantation confirmed that the VA-modified gut microbiota contributed to these protective effects. VA also facilitated macrophage polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype, further mitigating inflammation. These findings highlight the potential of VA as a natural dietary intervention for UC, emphasizing its role in regulating the gut microbiota and inflammatory pathways, which may have significant nutritional relevance in managing inflammatory bowel diseases.

Fecal Microbiome and Metabolomic Profiles of Mixed-Fed Infants Are More Similar to Formula-Fed than Breastfed Infants.

Many infants consume both human milk and infant formula (mixed-fed); however, few studies have investigated how mixed feeding affects the gut microbiome composition and metabolic profiles compared to exclusive breastfeeding or formula feeding. Herein, how delivery mode and early nutrition affect the microbiome and metabolome of 6-week-old infants in the STRONG Kids2 cohort was investigated. Fecal samples were collected from exclusively breastfed (BF; n = 25), formula-fed (FF; n = 25) or mixed-fed (MF; n = 25) participants. Within each feeding group, infants were either delivered vaginally (VD; n = 13) or by Cesarean section (CS; n = 12). Feeding mode affects the fecal microbiome diversity, composition, and functional potential, as well as metabolomic profiles regardless of delivery mode. Alpha and beta diversity of MF differed from that of BF (p < 0.05) but were comparable to FF infants. Functional analyses have shown 117 potential metabolic pathways differed between BF and FF, 112 between BF and MF, and 8 between MF and FF infants (p < 0.05, q < 0.10). Fecal metabolomic profiles of MF and FF clustered together and separated from BF infants. In total, 543 metabolites differed between BF and FF, 517 between BF and MF, and 3 between MF and FF (p < 0.05, q < 0.10). Delivery mode affected overall microbial composition (p = 0.022) at the genus level and 24 potential functional pathways, with 16 pathways being higher in VD than CS infants (p < 0.05, q < 0.10). Metabolomic analysis identified 47 differential metabolites between CS and VD, with 39 being lower in CS than VD (p < 0.05, q < 0.10). In summary, fecal microbiota composition and function and metabolite profiles of 6-week-old MF infants are closer to FF than BF infants.

Precision microbial regulation: Strategies for modulating GIT microbiota for host health

AbstractRecent advancements in analytical techniques have unveiled the spatiotemporal diversity of the gastrointestinal tract (GIT) microbiota and their associations with host well‐being. Despite these insights, the precise regulation of GIT microbiota remains a significant challenge. Currently, microbial regulatory strategies, including fecal microbiota transplantation (FMT), synthetic microbial communities (SynComs), genetically engineered microorganisms (GEMs), phages, and nanomaterials, are increasingly utilized for their precise influence on GIT microbiota. This review emphasizes the necessity for developing targeted regulatory strategies in GIT and provides a comprehensive summary and comparison of these approaches to explore their regulatory potential. We discuss recent advancements in these strategies, focusing on their mechanisms, efficacy, safety considerations, clinical trials, and optimization at the application level. Finally, we highlight support methods for optimizing modulation strategies, including the timing of microbial regulation, the selection of microbial targets, and the importance of monitoring the gastrointestinal environment to guide effective microbial interventions.