Search Results (1,520)

Early weaning in intensive lamb production improves reproductive efficiency but predisposes lambs to diarrhea, oxidative stress, and intestinal barrier dysfunction, highlighting the need for non-antibiotic strategies to protect gut health. This study evaluated whether a sheep-derived mixed probiotic could alleviate early weaning–induced intestinal injury and clarified its potential molecular mechanisms. Early weaning reduced body weight, average daily gain and feed efficiency, increased diarrhea, decreased plasma and colonic catalase (CAT), glutathione peroxidase (GSH-PX), and superoxide dismutase (SOD) activities, increased malondialdehyde (MDA), elevated interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), reduced interleukin-10 (IL-10) and transforming growth factor-β (TGF-β), increased plasma and mucosal immunoglobulin A, M, and G (IgA, IgM, IgG), and increased colonic lipopolysaccharide (LPS) with reduced diamine oxidase (DAO). Intestinally, EW induced villus atrophy, deeper crypts, lower villus height-to-crypt depth ratios, goblet cell loss, higher histopathological scores, and decreased colonic mucin 2, zonula occludens-1, claudin-1, and occludin. Probiotic supplementation partially reversed these alterations, restoring antioxidant enzyme activities, improving villus architecture and barrier protein expression, and rebalancing cytokine and immunoglobulin profiles. Transcriptomic and network analyses showed that early weaning activated Cytokine–cytokine receptor, NF-κB, TNF and Th17 pathways, whereas probiotics suppressed a weaning-responsive inflammatory gene module, downregulated key hub genes, and enhanced peroxisome proliferator-activated receptor (PPAR) signaling. These results show that supplementing early-weaned lambs with a mixed probiotic generated from sheep is an efficient nutritional strategy to reduce intestinal oxidative and inflammatory damage associated with weaning and to enhance their health and performance. Full article

The global shift toward antibiotic-free poultry production has created an urgent need for sustainable feed additives that promote gut health and productivity. This study aimed to develop and evaluate a novel double-layered microencapsulated phytosynbiotic (DMP) comprising Tiliacora triandra extract, probiotics, and cereal by-products using lyophilization. In Experiment 1, we investigated the effects of cell wall materials (corn, defatted rice bran, and wheat bran) and different particle sizes (0.6 and 1.0 mm) on the physicochemical characteristics and probiotic encapsulation efficiency. Results revealed that wheat bran, particularly at the smaller particle size of 0.6 mm, enhanced probiotic viability, probiotic stability under simulated gastrointestinal and thermal conditions, and nutrient retention. Compared with other materials, wheat bran also provided superior powder flowability, lower density, and favorable color attributes. In Experiment 2, we assessed the influence of probiotic strains (P. acidilactici, Lactiplantibacillus plantarum TISTR 926, and Streptococcus thermophilus TISTR 894) on functional properties of the DMP. All strains exhibited high encapsulation efficiency and stability during gastrointestinal simulation, thermal exposure, and storage. However, P. acidilactici had superior fermentation kinetics and produced greater levels of beneficial short-chain fatty acids, especially acetic and butyric acids. Antibacterial activity was strain-dependent, with notable inhibitory effects against Gram-positive pathogens, primarily through bacteriostatic mechanisms. Overall, these findings confirm that the developed DMP formulations effectively stabilize probiotics and bioactive phytochemicals, offering a promising strategy for enhancing gut health and performance in antibiotic-free broiler production systems. Full article

Dietary bioactive compounds derived from plant-based and fermented foods act as plei-otropic modulators of human health, exerting antioxidant, anti-inflammatory, cardiopro-tective, neuroprotective, and metabolic effects beyond basic nutrition. Whole foods (fruits, vegetables, grains, nuts) provide synergistic mixtures of bioactives, whereas fermented foods generate a wide range of microbial-derived metabolites (peptides, organic acids) as well as probiotics that enhance nutrient bioavailability and support gut health. The gut microbiota plays a central mediating role in the biological effects of dietary bioactives through a dynamic, bidirectional interaction: dietary compounds shape microbial composition by promoting beneficial taxa and suppressing pathogens, while microbial metabolism converts these compounds into bioactive metabolites, including short-chain fatty acids, that profoundly influence host health. Despite their demonstrated health potential, the clinical translation of many dietary bioactives is limited by low bioavailability, which is influenced by digestion processes, food matrix and processing conditions, host genetics, and individual microbiota profile. Overcoming these limitations requires a deeper understanding of the synergistic interactions among dietary bioactives, probiotics, microbial metabolites, and host signaling pathways. This review provides an integrated perspective of the sources, mechanisms of action, and health effects of food-derived bioactive compounds and probiotic mediated effects, while highlighting current translational challenges and future directions for the development of effective functional foods and personalized nutrition strategies. Full article

Gut microbial metabolites play a crucial role in modulating cognitive function. In a previous animal study, oral administration of Lactiplantibacillus plantarum MWFLp-182 (L. plantarum MWFLp-182) significantly increased inosine levels in both the serum and feces of D-galactose (D-gal)-induced mice, which was accompanied by improved cognitive performance. Building on this finding, we further investigated the neuroprotective mechanisms of inosine derived from L. plantarum MWFLp-182 in alleviating D-gal-induced neuronal damage in HT-22 cells. Reverse transcription-quantitative PCR (RT-qPCR) was used to analyze the addition of inosine (250 μg/mL, 500 μg/mL), which considerably reduces oxidative stress induced by D-gal (20 mg/mL), on the regulation of mRNA expression of the nuclear factor erythroid 2-related factor (Nrf2)/hemeoxygenase 1 (HO-1) signaling pathway factors. Compared to the D-gal group, the inosine-treated group exhibited a 4.3-fold and 8.7-fold increase in HO-1 and Nrf2 levels, respectively. Furthermore, inosine alleviates neuroinflammation by modulating the mRNA expression of the Toll-like receptor 4 (TLR4)/myeloid differentiation primary response protein 88 (MyD88)/nuclear factor kappa B (NF-κB) signaling pathway. Compared to the D-gal group, the inosine-treated group showed reductions of 41.75%, 28.29%, and 32.17% in TLR4, MyD88, and NF-κB levels, respectively. Moreover, immunofluorescence staining revealed that inosine exhibits anti-apoptotic properties by enhancing the levels of neurotrophic factors, including nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), while simultaneously lowering the expression of the pro-apoptotic protein bcl-2-associated X (Bax). These findings suggest that inosine, a differentially expressed metabolite identified in a probiotic-intervention mouse model, alleviates D-gal-induced neuronal damage in HT-22 cells by modulating oxidative, inflammatory, and apoptotic pathways, providing mechanistic insights into the neuroprotective effects of this metabolite. Full article

Background/Objectives: Rotavirus remains a major cause of severe acute gastroenteritis
in infants worldwide. The suboptimal efficacy of current vaccines underscores the need
for alternative microbiome-based interventions, including postbiotics. Extracellular
vesicles (EVs) from probiotic and commensal E. coli strains have been shown to mitigate
diarrhea and enhance immune responses in a suckling-rat model of rotavirus infection.
Here, we investigate the regulatory mechanisms activated by EVs in rotavirus-infected
enterocytes. Methods: Polarized Caco-2 monolayers were used as a model of mature
enterocytes. Cells were pre-incubated with EVs from the probiotic E. coli Nissle 1917 (EcN)
or the commensal EcoR12 strain before rotavirus infection. Intracellular Ca²⁺
concentration, ROS levels, and the expression of immune- and barrier-related genes and
proteins were assessed at multiple time points post-infection. Results: EVs from both
strains exerted broad protective effects against rotavirus-induced cellular dysregulation,
with several responses being strain-specific. EVs interfered with viral replication by
counteracting host cellular processes essential for rotavirus propagation. Specifically, EV
treatment significantly reduced rotavirus-induced intracellular Ca²⁺ mobilization, ROS
production, and COX-2 expression. In addition, both EV types reduced virus-induced
mucin secretion and preserved tight junction organization, thereby limiting viral access
to basolateral coreceptors. Additionally, EVs enhanced innate antiviral defenses via
distinct, strain-dependent pathways: EcN EVs amplified IL-8-mediated responses,
whereas EcoR12 EVs preserved the expression of interferon-related signaling genes.
Conclusions: EVs from EcN and EcoR12 act through multiple complementary
mechanisms to restrict rotavirus replication, spread, and immune evasion. These findings
support their potential as effective postbiotic candidates for preventing or treating
rotavirus infection. Full article

Background: The association between liver disease and gut microbiota is being widely investigated. Probiotics, such as Bacillus amyloliquefaciens, are among the most notable microbiomes examined in this study. Bacillus amyloliquefaciens shows potential for promoting growth and effectively regulating gut microbiota, though its mechanism of action remains unclear. Methods: The early gavage administration of Bacillus amyloliquefaciens BA5 conferred protection against liver injury in carbon tetrachloride (CCl₄)-induced mice. Growth parameters (body weight and organ index), serum biochemical markers (ALT, AST, T-SOD, MDA, GSH-Px, and T-AOC), liver and jejunum histopathology, and gut microbiota composition were comprehensively evaluated. Results: BA5 supplementation restored serum T-AOC, T-SOD, and GSH-Px levels and attenuated CCl₄-induced increases in ALT, AST, and MDA, suggesting potent anti-oxidant properties. Furthermore, histopathologic assessment showed that CCl₄-induced mice developed acute liver injury and intestinal villi were destroyed, while the BA5 group restored the pathological changes in the tissues to the normal group level. In addition, immunohistochemical staining revealed that BA5 increased the expression level of Claudin-1 which was a key biomarker for assessing the integrity of epithelial/endothelial barriers. Regarding gut microbiota, BA5 significantly enhanced the abundance of beneficial bacteria (Lactobacillus) and decreased the abundance of hazardous bacteria (Fusobacterium, Lachnoclostridium, Phascolarctobacterium, and Escherichia–shigella) caused by CCl₄. Notably, BA5 alone remarkably increased gut microbial diversity compared with that of the Control group. Conclusions: Overall, these findings suggest that BA5 holds promise as a potential therapeutic agent for alleviating CCl₄-induced acute liver injury in mice by mitigating oxidative stress and modulating gut microbiota. Full article

Lactobacilli strains are one of the major groups belonging to probiotics. Lactobacilli strains are known to be beneficial microbes widely studied and utilized for their health benefits and applications in various fields. Recently, Lactobacilli strains have emerged as promising agents in cancer management due to their ability to influence various physiological processes. Lactobacilli strains have shown potential in producing tumor-suppressive compounds, enhancing immune responses, and reshaping gut microbiota balance for the management of various cancer types. Lactobacilli strains demonstrated tumor-suppressive activity through mechanisms including induction of apoptosis, inhibition of migration, and regulation of key oncogenic signaling pathways. However, the effects of Lactobacilli strains appear to be strain- and cancer-type-dependent, necessitating further research to identify the most effective strains for the proper cancer type with the optimal treatment regimens. In this review article, we focus on Lactobacilli strains studied between 2021 and 2025 that have demonstrated tumor-suppressive properties in various experimental models. In addition, this article explores the current limitations in research methodologies and proposes potential avenues for future investigations in this area of study. Full article

Background/Objectives. Lactiplantibacillus plantarum CRL681 has previously demonstrated a strong antagonistic effect against Escherichia coli O157:H7 in food matrices; however, the molecular mechanisms underlying this activity remain poorly understood. Since initial interactions between beneficial bacteria and pathogens occur mainly at the cell surface and in the extracellular environment, the characterization of the bacterial secretome is essential for elucidating these mechanisms. In this study, the secretome of L. plantarum CRL681 was comprehensively characterized using an integrated in silico and in vitro approach. Methods. The exoproteome and surfaceome were analyzed by LC-MS/MS under pure culture conditions and during co-culture with E. coli O157:H7. Identified proteins were functionally annotated, classified according to subcellular localization and secretion pathways, and evaluated through protein–protein interaction network analysis. Results. A total of 275 proteins were proposed as components of the CRL681 secretome, including proteins involved in cell surface remodeling, metabolism and nutrient transport, stress response, adhesion, and genetic information processing. Co-culture with EHEC induced significant changes in the expression of proteins associated with energy metabolism, transport systems, and redox homeostasis, indicating a metabolic and physiological adaptation of L. plantarum CRL681 under competitive conditions. Notably, several peptidoglycan hydrolases, ribosomal proteins with reported antimicrobial activity, and moonlighting proteins related to adhesion were identified. Conclusions. Overall, these findings suggest that the antagonistic activity of L. plantarum CRL681 against E. coli O157:H7 would be mediated by synergistic mechanisms involving metabolic adaptation, stress resistance, surface adhesion, and the production of non-bacteriocin antimicrobial proteins, supporting its potential application as a bioprotective and functional probiotic strain. Full article

Obesity is closely linked to dyslipidemia, hepatic injury, and chronic inflammation through disturbances in the gut–liver axis. Here, we evaluated the anti-obesity effects of L. rhamnosus (Lacticaseibacillus rhamnosus) CU262 in a high-fat diet (HFD) mouse model and elucidated mechanisms using an integrated multi-omics strategy. Male C57BL/6 mice received CU262 during 12 weeks of HFD feeding. Phenotypes, serum/liver biochemistry, gut microbiota (16S rRNA sequencing), fecal short-chain fatty acids (SCFAs), and hepatic transcriptomes (RNA-seq) were assessed. CU262 significantly attenuated weight gain and adiposity; improved serum TC, TG, LDL-C and HDL-C; lowered ALT/AST and FFA; and mitigated oxidative stress and inflammatory imbalance (↓ IL-6/TNF-α, ↑ IL-10). CU262 restored alpha diversity, reduced the Firmicutes/Bacteroidetes ratio, enriched beneficial taxa (e.g., Akkermansia), and increased acetate and butyrate. Liver transcriptomics showed CU262 reversed HFD-induced activation of cholesterol/steroid biosynthesis and endoplasmic reticulum stress, with downregulation of key genes (Mvk, Mvd, Fdps, Nsdhl, and Dhcr7) and Pcsk9, yielding negative enrichment of steroid and terpenoid backbone pathways and enhancement of oxidative phosphorylation and glutathione metabolism. Correlation analyses linked Akkermansia and SCFAs with improved lipid/inflammatory indices and repression of cholesterol-synthetic and stress-response genes. These findings demonstrate that CU262 alleviates HFD-induced metabolic derangements via microbiota-SCFA-hepatic gene network reprogramming along the gut–liver axis, supporting its potential as a functional probiotic for obesity management. Full article

Parkinson’s disease (PD), the second most common neurodegenerative disorder globally, relies primarily on dopamine replacement therapy for conventional treatment. This approach fails to reverse core pathological processes and is associated with long-term side effects. Recent research on the microbiota-gut-brain axis (MGBA) has revealed that PD pathology may originate in the gut, forming a vicious cycle from the gut to brain through α-synuclein propagation, gut dysbiosis, intestinal barrier disruption, and neuroinflammation. This offers a novel perspective for managing PD through dietary interventions that modulate the gut microbiome. However, single probiotic or prebiotic interventions show limited efficacy. This review systematically introduces the novel concept of “synbiotics combining medicinal plant polysaccharides with probiotics,” aiming to integrate traditional “medicinal food” wisdom with modern microbiome science. The article systematically elucidates the pathological mechanisms of MGBA dysfunction in PD and the intervention mechanisms of probiotics and emphasizes the structural and functional advantages of medicinal plant polysaccharide as superior prebiotics. The core section delves into the multifaceted synergistic mechanisms between these two components: enhancing probiotic colonization and vitality, optimizing microbial metabolic output, synergistically reinforcing the intestinal and blood-brain barriers, and jointly regulating immune and neuroinflammation. This approach targets the MGBA to achieve multi-level intervention for PD. Full article

Background: Bloating, gas, and abdominal discomfort are common in healthy individuals but lack effective interventions. Probiotics can alleviate some gastrointestinal (GI) symptoms; however, evidence for their impact on bloating, gas and abdominal discomfort in otherwise healthy populations remains limited. Mechanistic studies suggest that synbiotics may influence the underlying mechanisms of bloating, including increased gas production, impaired gut motility, and visceral hypersensitivity, but there is a paucity of data from large trials evaluating clinical outcomes. Accordingly, we evaluated the effects of a multi-species synbiotic on GI symptoms. Methods: In a randomized, double-blind, placebo-controlled, decentralized trial, participants (n = 350) with self-reported bloating/indigestion received either a multi-species synbiotic (53.6 billion AFU multi-species probiotic and 400 mg pomegranate extract; DS-01) or placebo daily for 6 weeks. Outcomes included GI quality-of-life (DQLQ), bloating and gas (PROMIS-GI 13a), abdominal discomfort (PROMIS-GI 5a), constipation, regularity, mood-related symptoms, and safety. Results: The multi-species synbiotic improved GI quality-of-life compared to placebo (0.80 vs. 1.20; p < 0.05) at Week 6. Bloating and gas were reduced in the synbiotic arm compared to placebo (16.0 vs. 21.0; p < 0.01), with more participants reporting never/rarely bloating (72.3% vs. 55.9%; p < 0.001). Abdominal discomfort also decreased (8.0 vs. 10.0; p < 0.01). Additionally, there was a statistically significant improvement in constipation symptoms and regularity in the synbiotic arm relative to placebo. Conclusions: Daily supplementation with this multi-species synbiotic significantly improved GI quality-of-life, bloating, gas, abdominal discomfort, and bowel habits. This is the first synbiotic to demonstrate meaningful improvements in bloating and gas in a generally healthy, diverse, real-world population. Full article

Pseudomonas aeruginosa is a resilient Gram-negative pathogen frequently implicated in healthcare associated infections, particularly among immunocompromised individuals and those with chronic conditions such as cystic fibrosis (CF), chronic obstructive pulmonary disease (COPD), or cancer. It is well known for its high resistance to antibiotic treatment. This review briefly mentions P. aeruginosa’s resistance mechanisms, biofilm formation, and virulence factors, while primarily focusing on treatment challenges and recent advancements in therapeutic strategies aimed at overcoming resistance. Covered are novel non-antibiotic interventions such as quorum sensing inhibitors, quorum quenching agents, iron chelators, lectin and efflux pump inhibitors, as well as antimicrobial peptides and nanoparticles. Traditional medicine, phytochemicals, and probiotics are also evaluated. Additionally, this review explores the development of a viable vaccine, bacteriophage therapy, lactoferrin-hypothiocyanite combination, and topical use of electrochemical scaffolds. This review emphasizes the need for extensive safety studies and in vivo validation of these emerging non-antibiotic therapeutic strategies to determine their efficacy, pharmacological behavior, and clinical feasibility before they can be translated into practice. Many of these emerging treatments could play a vital role in future combination therapies by enhancing the efficacy of existing antibiotics and countering resistance and virulence mechanisms. Advancing these approaches from laboratory to clinical application remains a major challenge, making the development of approved therapies or vaccines a critical scientific and public health priority. Full article

Background/Objectives: Metabolism is fundamental to all living organisms. It comprises a highly complex network of fine-tuned chemical reactions that sustain life but also generate by-products that damage cellular biomolecules, including DNA, thereby contributing to aging and disease. As metabolism can be largely modified by dietary alterations, it has the potential to positively or negatively affect health and disease. Interestingly, many aging-associated illnesses known to be influenced by diet also show a causal relation with DNA damage. As DNA keeps all instructions for life, and DNA lesions, if unrepaired, interfere with vital processes such as DNA replication and transcription, DNA damage may be an important mediator of the impact of nutrition on health and aging. Methods: Here, we discuss the genome-protective effects of various oral interventions in mice, aiming to elucidate which nutritional alterations lower DNA damage and promote overall health. Results: Our analysis covers a wide range of interventions with reported positive impacts on genomic stability, including modified diets (e.g., dietary restriction, probiotics, micronutrients, fatty acids, and hormones), NAD+ precursors (e.g., nicotinamide riboside), plant derivatives, and synthetic drugs. Among these, caloric and dietary restriction emerge as the most potent, generic modulators of DNA damage and repair processes, enhancing aspects of repair efficiency through metabolic recalibration and improved cellular resilience. Other interventions, like NAD+ precursors, activate partly similar pathways without necessitating reduced food intake. Conclusions: While many interventions show promise, their effects are often less pronounced or are process-specific compared to caloric or dietary restriction. Additionally, many substances lack comprehensive exploration of their genome-protective effects in mice, with often only a small number of studies examining their impact on genome stability. Moreover, the heterogeneity between studies limits direct comparison. However, the observed overlap in mechanistic effects between treatments lends credibility to their potential efficacy. Ultimately, a deeper understanding of these mechanisms could pave the way for translating these findings into, e.g., combination treatments to promote healthy aging in humans. Full article

Multidrug resistance (MDR) in Gram-negative bacteria is a global issue and needs to be addressed urgently. MDR can emerge through genetic mutations and horizontal gene transfer and deteriorate under antibiotic selective pressure. The emergence of resistance to last-resort antibiotics, which are used to treat MDR bacteria, is of particular concern. Colistin has been recognized as a last-line antibiotic for the treatment of MDR Gram-negative bacterial infections caused by Escherichia coli, Acinetobacter baumannii, Klebsiella pneumoniae, and Pseudomonas aeruginosa. Recently, the increasing reports of colistin resistance pose a significant threat to public health, caused by both acquired and intrinsic mechanisms. The review aimed to elucidate the trends in colistin resistance, the use of colistin in human and veterinary medicine, underlying resistance mechanisms and transmission pathways, and potential mitigation of this emerging threat through novel intervention strategies. Colistin resistance is mediated by plasmid-encoded phosphoethanolamine transferases (mcr-1 to mcr-10) and chromosomal lipid A remodeling pathways. In Escherichia coli, resistance involves mcr-1–10, acrB efflux mutations, pmrA/pmrB, arnBCADTEF, and mgrB inactivation. Klebsiella pneumoniae exhibits mcr-1, mcr-8, mcr-9, mgrB disruption and phoP/phoQ–pmrAB activation. Acinetobacter baumannii harbors mcr-1–4, while Salmonella enterica and Enterobacter spp. carry mcr variants with arnBCADTEF induction. Therapeutic options include adjunct strategies such as antimicrobial peptides, nanomaterials, therapeutic adjuvants, CRISPR-Cas9-based gene editing, probiotics, vaccines, and immune modulators to restore susceptibility. This review identified that specific and wide actions are required to handle the growing colistin resistance, including genomic surveillance, tracing novel resistance mechanisms, and the application of alternative management strategies. The One Health approach is considered a key strategy to address this growing issue. Full article

The human gut microbiota plays a key role in health and disease across the lifespan and is shaped by complex intrinsic and extrinsic factors. Dysbiosis is increasingly recognized as a contributor to a wide range of clinical conditions, with diarrhoea—particularly antibiotic-associated diarrhoea—representing an early clinical marker of microbiota disruption. This narrative review summarizes current evidence on the probiotic yeast Saccharomyces boulardii CNCM I-745 and its clinical applications in both paediatric and adult populations. Available clinical data support its safety and efficacy in the prevention and management of gastrointestinal disorders, particularly diarrhoeal conditions, and suggest a potential role in promoting microbiota resilience. Key mechanisms of action, safety considerations, and findings from randomized controlled trials and meta-analyses are discussed. However, current data remains limited by heterogeneity among studies and a lack of long-term, mechanistic data, highlighting the need for further well-designed studies to clarify its role across different clinical settings. Full article