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This study evaluated the supplementation of a precision biotic (PB) on the enterohepatic health markers and growth performance of broiler chickens undergoing an enteric challenge. In the first study, three treatments were used: Unchallenged Control (UC); Challenged Control (CC; dietary challenge and 10× dose of coccidia vaccine); and a challenged group supplemented with PB (1.3 kg/ton). In the second study, three treatments were used: control diet, diet supplemented with Avilamycin (10 ppm), and a diet supplemented with PB (0.9 kg/ton). All the birds were exposed to natural challenge composed by dietary formulation and reused litter from a coccidiosis positive flock. In Trial 1, PB decreased ileal histological damage, increased villi length, and the expression of SLC5A8 in ileal tissue versus CC; it reduced ileal expression of IL-1β compared to both UC and CC treatments. PB increased the expression of cell cycling gene markers CCNA2 and CDK2 in the ileum compared to CC. In Trial 2, PB improved the growth performance, intestinal lesion scores and intestinal morphology of broiler chickens. These results indicate that birds supplemented with PB are more resilient to enteric challenges, probably by its action in modulating microbiome metabolic pathways related to nitrogen metabolism and protein utilization.

A dietary glycan-based precision biotic (Glycan PB) was evaluated on the performance, welfare indicators, and litter characteristics of broiler chickens. In Trial 1, the main effects of Glycan PB dose (0, 250 and 500 g/metric ton (MT)) and xylanase supplementation (0 or 100 g/MT) were tested, as was their interaction. In Trial 2, pens located inside a commercial house were used to test the effect of Glycan PB supplementation (500 g/MT) versus a control diet. In Trial 1, Glycan PB supplementation at 250 and 500 g/MT improved feed conversion ratio (FCR) by 7 and 11 points when compared to diets without Glycan PB (p < 0.001). At 35 d, Glycan PB reduced the pH and ammonia concentration in diets with xylanase. In Trial 1, the supplementation with 500 g of Glycan PB/MT of feed reduced litter scores (p < 0.05). In both trials, 500 g of Glycan PB/MT of feed increased the proportions of birds without footpad lesions (Trial 1: 72.2% vs. 82.7%; p < 0.001; Trial 2: 14 to 27.3% (p = 0.05) or gait defects (Trial 1: 96.1% vs. 98.4%; p < 0.001) and decreased the proportion of birds with footpad lesions (Trial 2: 86% vs. 72.7%; p = 0.05).

Antibiotic-induced gut dysbiosis (AID) is a frequent and serious side effect of antibiotic use and mitigating this dysbiosis is a critical therapeutic target. We propose that the host diet can modulate the chemical environment of the gut resulting in changes to the structure and function of the microbiome during antibiotic treatment. Gut dysbiosis is typically characterized by increases in aerobic respiratory bacterial metabolism, redox potential, and abundance of Proteobacteria. In this study, we explore dietary fiber supplements as potential modulators of the chemical environment in the gut to reduce this pattern of dysbiosis. Using defined-diets and whole-genome sequencing of female murine microbiomes during diet modulation and antibiotic treatment, we find that fiber prebiotics significantly reduced the impact of antibiotic treatment on microbiome composition and function. We observe reduced abundance of aerobic bacteria as well as metabolic pathways associated with oxidative metabolism. These metatranscriptomic results are corroborated by chemical measurements of eH and pH suggesting that fiber dampens the dysbiotic effects of antibiotics. This work indicates that fiber may act as a potential therapeutic for AID by modulating bacterial metabolism in the gut to prevent an increase in redox potential and protect commensal microbes during antibiotic treatment. Here, the authors show that fiber supplementation protects from antibiotic-induced gut microbiome damage by reducing the abundance of aerobic bacteria as well as metabolic pathways associated with oxidative metabolism.

The majority of the epithelial surfaces of our body, and the digestive tract, respiratory and urogenital systems, are colonized by a vast number of bacteria, archaea, fungi, protozoans, and viruses. These microbiota, particularly those of the intestines, play an important, beneficial role in digestion, metabolism, and the synthesis of vitamins. Their metabolites stimulate cytokine production by the human host, which are used against potential pathogens. The composition of the microbiota is influenced by several internal and external factors, including diet, age, disease, and lifestyle. Such changes, called dysbiosis, may be involved in the development of various conditions, such as metabolic diseases, including metabolic syndrome, type 2 diabetes mellitus, Hashimoto’s thyroidis and Graves’ disease; they can also play a role in nervous system disturbances, such as multiple sclerosis, Alzheimer’s disease, Parkinson’s disease, and depression. An association has also been found between gut microbiota dysbiosis and cancer. Our health is closely associated with the state of our microbiota, and their homeostasis. The aim of this review is to describe the associations between human gut microbiota and cancer, and examine the potential role of gut microbiota in anticancer therapy.

Human cytomegalovirus (CMV) is a highly prevalent herpesvirus that is often transmitted to the neonate via breast milk. Postnatal CMV transmission can have negative health consequences for preterm and immunocompromised infants, but any effects on healthy term infants are thought to be benign. Furthermore, the impact of CMV on the composition of the hundreds of bioactive factors in human milk has not been tested. Here, we utilize a cohort of exclusively breastfeeding full-term mother-infant pairs to test for differences in the milk transcriptome and metabolome associated with CMV, and the impact of CMV in breast milk on the infant gut microbiome and infant growth. We find upregulation of the indoleamine 2,3-dioxygenase (IDO) tryptophan-to-kynurenine metabolic pathway in CMV+ milk samples, and that CMV+ milk is associated with decreased Bifidobacterium in the infant gut. Our data indicate two opposing CMV-associated effects on infant growth; with kynurenine positively correlated, and CMV viral load negatively correlated, with infant weight-for-length at 1 month of age. These results suggest CMV transmission, CMV-related changes in milk composition, or both may be modulators of full-term infant development. Cytomegalovirus (CMV) is often transmitted to infants through breast milk. Here, in a cohort of exclusively breastfeeding full-term mother-infant pairs, the authors identify changes in milk composition, infant growth, and the infant gut microbiome associated with the presence of CMV in milk.

Dairy products—encompassing yogurt, kefir, cheese, and cultured milk beverages—are emerging as versatile, food-based modulators of gut microbiota and host physiology. This review synthesizes mechanistic insights demonstrating how live starter cultures and their fermentation-derived metabolites (short-chain fatty acids, bioactive peptides, and exopolysaccharides) act synergistically to enhance microbial diversity, reinforce epithelial barrier integrity via upregulation of tight-junction proteins, and modulate immune signaling. Clinical evidence supports significant improvements in metabolic parameters (fasting glucose, lipid profiles, blood pressure) and reductions in systemic inflammation across metabolic syndrome, hypertension, and IBS cohorts. We highlight critical modulatory factors—including strain specificity, host enterotypes and FUT2 genotype, fermentation parameters, and matrix composition—that govern probiotic engraftment, postbiotic yield, and therapeutic efficacy. Despite promising short-term outcomes, current studies are limited by heterogeneous designs and brief intervention periods, underscoring the need for long-term, adaptive trials and integrative multi-omics to establish durability and causality. Looking forward, precision nutrition frameworks that harness baseline microbiota profiling, host genetics, and data-driven fermentation design will enable bespoke fermented dairy formulations, transforming these traditional foods into next-generation functional matrices for targeted prevention and management of metabolic, inflammatory, and neuroimmune disorders.

The prevalence of obesity is rising every year and associated comorbidities such as cardiovascular diseases are among the leading causes of death worldwide. The gut microbiota has recently emerged as a potential target for therapeutic applications to prevent and treat those comorbidities. In this review, we focus on three conditions related to obesity in which the use of gut microbiota modulators could have benefits; mood disorders, eating behaviors, and body detoxification of persistent organic pollutants (POPs). On one hand, modulation of gut-derived signals to the brain in a context of obesity is involved in the development of neuroinflammation and can subsequently alter behaviors. An altered gut microbiome could change these signals and alleviate their consequences. On the other hand, obesity is associated with an increased accumulation of lipophilic contaminants, such as POPs. Targeting the microbiota could help body detoxication by reducing bioavailability, enhancing degradation by bioremediation or their excretion through the enterohepatic circulation. Thus, a supplementation of prebiotics, probiotics, or synbiotics could represent a complementary strategy to current ones, such as medication and lifestyle modifications, to decrease depression, alter eating behaviors, and lower body burden of pollutants considering the actual obesity epidemic our society is facing.

Cardiovascular diseases are associated with gut dysbiosis, but the role of microbe-derived metabolites as biomarkers or modulators of cardiovascular disease are not well understood. This is a targeted metabolomics study to investigate the association of nine microbe-derived metabolites with lower extremity peripheral artery disease (PAD), a form of atherosclerosis, and major adverse cardiac events (MACE). The study cohort consists of individuals with intermittent claudication and ankle-brachial index (ABI) < 0.9 (N = 119) and controls without clinically-apparent atherosclerosis (N = 37). The primary endpoint was MACE, a composite endpoint of myocardial infarction, coronary revascularization, stroke, transient ischemic attack, or cardiac-related death. Plasma metabolite concentrations differed significantly between the PAD and control groups. After adjustment for traditional atherosclerosis risk factors, kynurenine, hippuric acid, indole-3-propionic acid (IPA), and indole-3-aldehyde (I3A) concentrations were negatively associated with PAD, whereas indoxyl sulfate and 3-hydroxyanthranilic acid were positively associated. Hippuric acid, IPA, and I3A correlated with ABI, a surrogate for atherosclerotic disease burden. Those in the highest I3A concentration quartile had significantly improved freedom from MACE during follow-up compared to those in the lowest quartile. This study identifies specific indole- and phenyl-derived species impacted by gut microbial metabolic pathways that could represent novel microbiome-related biomarkers of PAD.

Inulin-type fructans (ITF) are known for their capacity to modulate gut microbiota, energy metabolism and to improve glycemia in several animal models of obesity, and in humans. The potential contribution of ITF as modulators of sugar digestion by host enzymes has not been evaluated yet. A sucrose challenge has been performed on naive mice fed a standard diet supplemented with or without native chicory inulin (Fibruline 5%) for 3 weeks. The area under the curve of glycemia as well as sucrase activity in the small intestine were lowered after inulin treatment. Pyrosequencing of the 16S rRNA gene confirmed important changes in gut microbiota (mostly in favor of Blautia genus) due to inulin extract supplementation. Interestingly, the suppressive effect of inulin extract on postprandial glycemia also occurred when inulin was directly added to the sucrose solution, suggesting that the effect on sucrose digestion did not require chronic inulin administration. In vitro tests confirmed a direct inhibition of sucrase enzyme by the inulin extract, thereby suggesting that native chicory inulin, in addition to its well-known prebiotic effect, is also able to decrease the digestibility of carbohydrates, a phenomenon that can contribute in the control of post prandial glycemia. We may not exclude that the sucrose escaping the digestion could also contribute to the changes in the gut microbiota after a chronic treatment with inulin.