Search Results (1,906)

Background/Objectives: Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide. Emerging evidence highlights the role of the gut microbiota in the development and progression of CRC. Microbial dysbiosis is hypothesized to contribute to chronic inflammation through a variety of mechanisms, such as the production of free radicals, which induce mutagenesis and immune dysregulation in the host, ultimately leading to diseases such as cancer. Methods: Tumor tissue samples or healthy mucosa tissue were collected for bacterial DNA extraction. The V3–V4 region of the 16S rRNA gene was amplified and sequenced using the Illumina MiSeq platform. Bioinformatics analysis was performed with QIIME2, including quality control, DADA2 denoising, alpha and beta diversity calculation, and taxonomic classification using the SILVA database. Results: Differences in microbial composition were observed between groups. The healthy controls exhibited high relative abundances of beneficial genera such as Faecalibacterium, Bacteroides, and Asteroleplasma, whereas the patients with CRC showed enrichment of atypical genera including Novosphingobium, Bradyrhizobium, and Undibacterium. Alpha diversity was lower in the CRC group, and clear clustering by group was observed in the beta diversity analysis. LEfSe analysis identified potential bacterial biomarkers associated with CRC at both the species and genus levels. Conclusions: The findings of this study support the hypothesis that colorectal cancer is associated with distinct alterations in gut microbiota composition, such as an increase in the Novosphingobium genus and a decrease in the Bacteroides genus. An exploratory description of these microbial profiles may aid in the development of microbiome-based diagnostic and therapeutic strategies and contribute to current knowledge of the role of the gut microbiota in CRC in southern Peru. Full article

Opioid-induced constipation (OIC) represents a prevalent adverse effect of opioid analgesics, affecting 60–90% of patients and ssignificantly compromising quality of life. This review delineates the multifactorial pathogenesis of OIC. Peripheral μ-opioid receptor (MOR) activation suppresses enteric neuronal excitability, inhibits intestinal motility and secretion, and impairs rectoanal function. Notably, the colon appears to exhibit a distinctive lack of tolerance to opioids. Enteric glial cell activation has been implicated in neuroinflammation, while interstitial cells of Cajal show impaired pacemaker function. Central mechanisms are increasingly recognized to involve the brain–gut axis. Furthermore, opioid-induced barrier disruption, microbiota dysbiosis, and LPS/TLR4-mediated inflammation are proposed to interact and may contribute to a self-reinforcing cycle. Animal models have been instrumental in dissecting these mechanisms. However, they present limitations in reproducibility, clinical phenotype fidelity, and translational validity, particularly regarding microbiome composition and neuroimmune responses. Future research should prioritize the development of standardized, physiologically relevant animal models incorporating multi-omics approaches, and validate mechanism-based therapeutic strategies, including peripherally acting MOR antagonists and microbiota-targeted interventions, for precision management of OIC. Full article

Ethanol exposure causes microbial imbalance, damages the gut barrier, and increases oxidative stress along the gut–liver axis, leading to the development and progression of alcohol-associated liver disease (ALD). Arginine is a conditionally essential amino acid that may play a key role in maintaining redox homeostasis and mediating host–microbiota crosstalk. We hypothesized that supplemental arginine provided during chronic ethanol exposure in mice would mitigate oxidative damage via the gut–liver axis. Our findings suggest that arginine supplementation mediated hepatic steatosis, preserved body weight and fat, and reduced oxidative stress in the gut–liver axis. These changes were associated with alterations in gut microbiota composition and function. These data support a potential role for arginine supplementation in mitigating ethanol-induced oxidative damage via the gut–liver axis. Full article

Spaceflight exposes astronauts to multiple environmental stressors that promote oxidative stress, including ionizing radiation, microgravity, circadian rhythm disruption, and psychological stress. These factors increase the production of reactive oxygen species (ROS) and disturb redox homeostasis, potentially affecting multiple physiological systems during long-duration missions. In addition to environmental challenges, nutritional factors may further influence oxidative balance in space. Space food systems rely on long-term storage and processing, which can lead to degradation of antioxidant nutrients and alterations in dietary composition. Furthermore, spaceflight conditions may modify eating behaviors and disrupt gut microbiome composition, both of which are closely linked to host redox regulation. This review examines current knowledge on oxidative stress during spaceflight and discusses how space food systems, dietary composition, and microbiome alterations interact with spaceflight stressors to influence redox homeostasis. Potential strategies to mitigate oxidative stress are also discussed, including preservation of antioxidant nutrients, optimization of dietary composition, reduction in pro-oxidant exposures, and microbiome-targeted approaches to support astronaut health during long-duration missions. Full article

Allergic asthma is a prevalent chronic inflammatory disease of the airways whose pathogenesis has traditionally been attributed to localized immune dysfunction within the lung. However, accumulating evidence from microbiome research supports a broader system-level perspective in which cross-organ interactions contribute to disease susceptibility and progression. In particular, the gut–lung axis has emerged as a key regulatory pathway linking intestinal microbial ecology, immune development, and respiratory health. This review synthesizes current epidemiological, mechanistic, and experimental evidence supporting the role of gut microbiota dysbiosis in allergic asthma. We examine how early-life environmental and nutritional exposures and gut microbiota establishment during critical developmental windows shape long-term immune tolerance and asthma susceptibility. We then summarize characteristic features of asthma-associated gut dysbiosis and discuss how microbial-derived metabolites, including short-chain fatty acids, tryptophan metabolites, pro-allergic lipid mediators such as 12,13-dihydroxy-9Z-octadecenoic acid, and bacterial-derived histamine, modulate distal airway immune responses through epigenetic, receptor-mediated, and immune trafficking mechanisms. Particular emphasis is placed on the role of diet as a key upstream regulator of gut microbiota composition and metabolic function. Finally, we evaluate experimental and translational studies targeting the gut–lung axis, including dietary modulation, microbiome-targeted interventions such as fecal microbiota transplantation, and emerging postbiotic approaches. Collectively, current evidence indicates that gut microbial composition and metabolic function are critical determinants of respiratory immune homeostasis. Targeting the gut–lung axis through nutrition- and microbiome-based strategies offers a promising avenue for the prevention and precision treatment of allergic asthma. Full article

Background: Ulcerative colitis (UC) is a multifactorial disease characterized by aberrant mucosal immune activation in response to intestinal dysbiosis. Contemporary management strategies aim to target inflammation and microbiome alterations while reducing relapse risk. A multidimensional assessment integrating clinical, inflammatory, immune, and microbial endpoints may better capture therapeutic effects beyond symptom control. Aims: To evaluate whether supplementation with Lactobacillus rhamnosus GG co-formulated with vitamin D3 (Dicoflor IBD Immuno) as an adjunct to optimized mesalamine (5-ASA) is associated with coordinated changes across clinical and biological domains in mild-to-moderate UC, using a multidimensional assessment framework. Methods: This single-center, randomized, double-blind, placebo-controlled pilot trial was conducted at Fondazione Ca’ Granda IRCCS Policlinico di Milano between May 2022 and May 2024. Thirty-six patients with mild-to-moderate UC receiving optimized 5-ASA were randomized to LGG+VitD3 (ALD3) or placebo (AP) for 4 weeks. Clinical activity, health-related quality of life (HRQoL), fecal calprotectin, peripheral immune cell subsets, and gut microbiota composition were assessed at baseline and week 4. Results: Both 5-ASA-LGG+VitD3 (ALD3)- and 5-ASA-placebo (AP)-treated patients showed significant improvement in clinical activity and HRQoL, without between-group differences. A higher proportion of clinical responders was observed in the ALD3 group, although this was not statistically significant. LGG+VitD3-supplemented patients showed reduced fecal calprotectin levels and increased frequencies of IL-22-producing CD4⁺ T cells. Microbiome analysis revealed enrichment of short-chain fatty acid-producing taxa, including Coprococcus and Fusicatenibacter, in ALD3-treated patients. Conclusions: In patients with mild UC receiving optimized 5-ASA, LGG+VitD3 supplementation does not improve short-term clinical outcomes beyond placebo but is associated with favorable modulation of inflammatory, immune, and microbial parameters, supporting the relevance of multidimensional biological endpoints in adjunctive UC management. Full article

Rheumatoid arthritis (RA) is a chronic inflammatory disease of autoimmune background and unknown etiology. The importance of genetic factors in RA development is well-established. Environmental factors have also been extensively researched in relation to risk of RA and managing its symptoms. Smoking, physical activity, diet, and gut microbiota are considered to be the most essential modifiable factors in RA. Among dietary interventions, the most researched is Mediterranean diet, monounsaturated fatty acids, fish consumption, and fish oil (EPA, eicosapentaenoic acid and DHA, that is, docosahexaenoic acid). Others concerned gluten-free and vegan or vegetarian diet, salt intake, supplementation with vitamin D, antioxidants, prebiotics, and probiotics. Diet modifications can alter the gut environment, and the association between RA development or severity and the composition of gut bacteria has already been shown. This review focuses on effectiveness and usefulness of various dietary approaches and supplements in RA prevention and management, including the influence on disease activity and inflammatory status. The composition of gut microbiota and its changes in response to dietary factors are also considered. There is a great need for further research into mutual dependencies of diet, microbiome, and RA activity. The current state of knowledge provides promising evidence for future nutrition and microbial therapies. Full article

Research on the human microbiome, particularly the gut microbiome, has expanded rapidly as its influence on health and behavior becomes increasingly evident. Once understood primarily in terms of digestion and immune function, the microbiome is now recognized as a key contributor to brain function, mood regulation, and social behavior. Emerging evidence links microbial dysbiosis to the onset and persistence of mood disorders, opening new pathways for mental health research and intervention. This paper challenges reductionist biomedical models by advancing a biopsychosocial framework for interpreting health outcomes related to microbiome dynamics. The gut–brain axis illustrates the biological complexity of these interactions, with microbial communities shaping neurodevelopment and neurotransmitter production. Psychologically, alterations in microbial composition have been associated with depression, anxiety, and stress responsivity, while social determinants—including early-life environments, socioeconomic conditions, and relationships—structure microbial variation in ways that may reinforce existing health inequities. Focusing on women’s health, this narrative review examines how microbial states both influence and are shaped by interconnected biological, psychological, and social factors. Interdisciplinary implications of microbiome research for understanding and achieving eubiosis and holistic models care in both research and clinical practice are discussed. Full article

Antibiotic-associated diarrhea (AAD) is primarily driven by disruption of the gut microbiota accompanied by intestinal mucosal injury. Although multiherb formulations are widely used in East Asian medicine, their collective ecological effects and integrated microbiome–host mechanisms have not been systematically synthesized. This systematic review included 17 preclinical studies that investigated multiherbal formulations in AAD models. Given the substantial heterogeneity in the formulation composition, experimental design, and analytical platforms, a descriptive synthesis was performed. The included formulations were categorized into four clusters based on their shared herbal composition: Qiwei Baizhu San (QWBZP), Lizhong Tang (LZT), Gegen Qinlian Tang (GQT), and other supportive multiherbal formulations. The cluster-based synthesis revealed distinct convergent therapeutic strategies. The QWBZP and LZT clusters primarily supported the restoration of host metabolic and digestive functions, whereas the GQT cluster exhibited potent pathogen control effects with the suppression of opportunistic taxa. Across all clusters, a convergent microbiome–host response emerged, characterized by enrichment of commensal bacteria (e.g., Lactobacillus), upregulation of tight junction proteins (e.g., ZO-1, occludin), and attenuation of pro-inflammatory mediators (e.g., TNF-α, myeloperoxidase). Multiherb formulations in AAD models not only act as microbial modulators but also function as host-directed modulators that stabilize the intestinal homeostatic niche. Botanical interventions may facilitate endogenous microbiome recovery by reinforcing mucosal integrity and reducing environmental resistance. This ecological framework provides a rationale for future translational studies evaluating integrated herbal–probiotic strategies and precise microbiome management for patients with AAD, while further clinical validation is warranted. Full article

Atopic dermatitis (AD) is a chronic inflammatory skin disease influenced by several factors, including immune system imbalance, impairment of the epidermal barrier, and alterations in the composition of the gut and skin bacterial and fungal microbiota. This study combines metagenomic sequencing and culture-based methods to explore the impact of probiotic supplementation on the cutaneous microbiota and mycobiota of AD patients. Twenty-five adults diagnosed with AD were enrolled, and skin swabs were analyzed to characterize microbial diversity and load. Culturomic analyses identified 42 bacterial and 6 fungal species, confirming Staphylococcus aureus and Candida parapsilosis as predominant taxa. High-throughput sequencing revealed Staphylococcus spp. and Malassezia spp. as dominant genera, with notable interindividual variability. While probiotic use did not significantly influence bacterial diversity, it was associated with higher richness and evenness in fungal communities, as shown by alpha and beta diversity metrics. Malassezia restricta was more prevalent among probiotic users, whereas Candida parapsilosis and Rhodotorula mucilaginosa were enriched in non-users. These findings indicate an association between probiotic use and differences in the composition and diversity of the skin mycobiota compared with the bacterial microbiota, suggesting that fungal communities may be more responsive to probiotic-associated factors. Integrating metagenomic and culturomic approaches offers valuable insights into the complex interactions among host factors, microbial communities, and probiotic use in AD, paving the way for targeted microbiome-based therapeutic strategies. Full article

Schizopygopsis younghusbandi is an endemic and economically important fish in the Qinghai-Xizang Plateau, but its aquaculture is limited by harsh environmental conditions and incomplete understanding of host–microbiome–environment interactions. This study applied metagenomic sequencing to examine how different culture environments affect growth, water microbial communities, and gut microbiome network stability. Three-year-old juveniles (initial body weight 50.57 ± 1.88 g) were reared for 90 days in five systems: conventional pond (P), wetland (WL), concrete tank (G), river (R), and recirculating aquaculture system (RC). No significant differences in initial body weight or length were observed among groups (p > 0.05). Fish in the RC system achieved the highest final body weight, weight gain rate, and specific growth rate (p < 0.05), while survival rates were highest in the river and RC groups and lowest in ponds (p < 0.05). Microbial diversity and community composition differed significantly among culture modes, with bacterial and protozoan communities showing the strongest environmental responsiveness. Co-occurrence network analyses revealed that RC and G systems exhibited higher network complexity, density, and proportion of positive correlations, reflecting enhanced microbial interaction and ecological stability, whereas the WL system showed reduced network connectivity. Correlation analysis indicated that bacterial abundance was positively associated with total nitrogen, total phosphorus, and dissolved oxygen (p < 0.05), highlighting environmental regulation of microbial assemblages. Overall, the aquaculture environment shapes gut microbial networks, which closely relate to growth performance. Recirculating aquaculture systems can mitigate growth limitations in plateau fish by stabilizing the environment and reinforcing gut microbial communities, providing a sustainable strategy for high-altitude aquaculture development. Full article

Lung cancer remains the leading cause of cancer-related mortality worldwide, and although immunotherapy has transformed the treatment landscape of advanced non-small cell lung cancer (NSCLC), durable benefit is limited to a subset of patients. PD-L1 immunohistochemistry and tumor mutational burden, while clinically utilized, demonstrate imperfect predictive capacity, underscoring the need for more robust biomarkers. This review highlights emerging multimodal biomarkers—including circulating tumor DNA (ctDNA), the gut microbiome, and artificial intelligence (AI)-driven radiomics—as promising tools to enhance the prediction of immunotherapy response. Longitudinal ctDNA monitoring offers a minimally invasive method to assess tumor burden dynamics, detect early molecular response, distinguish pseudo-progression from true progression, and stratify risk, with ctDNA clearance correlating with improved survival outcomes. The gut microbiome has also been associated with ICI efficacy, as specific bacterial taxa and composite scoring systems correlate with treatment response, though methodological heterogeneity limits clinical translation. Radiomic analyses leveraging CT and PET imaging extract quantitative tumor features that, when integrated with clinical and molecular data, demonstrate improved predictive performance compared to single-modality approaches. Despite promising advances, challenges including assay standardization, external validation, data harmonization, interpretability of AI models, and infrastructure requirements remain barriers to widespread adoption. Multimodal integration of genomic, microbiome, and imaging biomarkers represents a critical step toward precision immuno-oncology, with prospective validation needed to translate these approaches into improved outcomes for patients with advanced NSCLC. Full article

Sucralose is one of the most widely used non-nutritive sweeteners and has long been considered metabolically inert and safe within established acceptable daily intake levels. However, emerging evidence suggests that chronic exposure to sucralose may alter gut microbial composition, epithelial barrier function, mucosal inflammation, and immune responses. This review examines current experimental and clinical evidence on the effects of sucralose on the gut–immune axis, with particular attention to its potential implications for colitis and colorectal cancer (CRC). Preclinical studies indicate that sucralose may reduce beneficial short-chain fatty acid-producing taxa, alter microbial metabolic pathways, disrupt epithelial barrier-related molecules, and promote inflammatory and immune changes associated with colitis severity and inflammation-driven tumorigenesis. Experimental evidence also suggests that sucralose may impair CD8⁺ T-cell fitness and reduce responsiveness to immune checkpoint inhibitors through microbiome-dependent mechanisms involving altered arginine and citrulline metabolism. Human studies further indicate that sucralose can modify gut and oral microbiome composition and influence metabolic responses, although these effects appear heterogeneous and context-dependent. Overall, the current literature suggests that sucralose may act as a modifier of microbiome–immune interactions in susceptible settings, but most mechanistic evidence remains preclinical, and human data are still insufficient to establish causality. These findings highlight the need for prospective studies to determine whether sucralose-associated microbial and immune alterations translate into clinically meaningful effects in colitis, CRC, and immunotherapy response. Full article

This study investigated phase-dependent changes in gut microbiome composition, predicted functional potential, and lipid metabolism in intensively reared broiler chickens and ducks across the starter, grower, and finisher phases (from day-old to 42 days of age), over six production cycles (four chicken and two duck cycles), using 16S rRNA sequencing and blood lipids profiling. A total of 70 pooled manure samples were collected (46 from chickens and 24 from ducks), along with 34 blood samples (22 from chickens and 12 from ducks), all obtained under standard production conditions. Microbial diversity remained stable across growth phases within each species, whereas clear interspecies differences were observed (p < 0.01). Microbiome maturation involved a shift from early facultative and environmentally associated taxa during the starter phase (day-old to 14 days of age), including Acinetobacter (p < 0.01) and Enterococcus (p < 0.001), toward a more stable, host-adapted community. At the level of predicted functional pathways, shifts between growth phases were more pronounced in ducks. Predicted gene-level profiles showed phase-specific differentiation in chickens, with starter-associated genes linked to core carbon and nitrogen metabolism and finisher-associated genes related to structural and transport functions, whereas ducks exhibited a more balanced reorganization involving carbohydrate, energy, and nitrogen metabolism. Host lipid profiles between adjacent growth phases showed dynamic shifts in ducks (p < 0.05). These species-specific lipid patterns were mirrored by microbiome–lipid associations, as demonstrated by correlation analyses between dominant bacterial genera and blood lipid parameters, revealing more coordinated relationships in chickens and more heterogeneous patterns in ducks. Overall, these findings demonstrate species-specific organization of gut microbiome changes and their integration with blood lipid profiles under intensive production conditions. Full article

Background: Patients with kidney failure requiring dialysis experience a high burden of vaccine-preventable diseases, and vaccine hypo-responsiveness is a key contributor. Uraemic toxins and gut dysbiosis are potential causes of hypo-responsiveness. Aim: This study aimed to determine whether uraemic toxin concentrations or gut dysbiosis are associated with vaccine response in haemodialysis patients. Methods: This was a single centre, observational cohort study of maintenance dialysis patients receiving a conventional 2-dose primary COVID-19 vaccination course. Demographic, clinical and vaccination data were collected from the eMR. Vaccine response (Elecsys Anti-SARS-CoV-2 immunoassay), serum uraemic toxin concentrations (indoxyl sulphate, p-cresyl sulphate, and trimethylamine N-oxide by liquid chromatography), and stool microbiome (16S rRNA gene sequencing) were measured 8 weeks after the second dose of vaccine. Results: Forty participants (43% female, mean age 66 years; 59% Caucasian) were included, 70% of whom were classified as a vaccine responder. Antibiotic exposure, prednisolone use and lymphopenia were significantly associated with hypo-responsiveness. Microbiome profiling identified differences in beta diversity between responders and non-responders, positively correlated with short-chain fatty acid producers (Parabacteriodes) and negatively with pathobionts (Escherichia/Shigella). Differential abundance analysis identified lower levels of Tyzzerella, Gemmiger, and Hungatella and higher levels of Turicibacter in vaccine responders. Total uraemic toxin burden and individual toxin concentrations did not differ between responders and hypo-responders (all p > 0.05). Stratification by low versus high/very high toxin burden groupings was not associated with response (p > 0.99). Conclusions: Differences in gut microbial composition were observed between vaccine responder groups, while uraemic toxin concentrations were not associated with vaccine responsiveness. These findings suggest gut microbiota composition may contribute to vaccine hypo-responsiveness in individuals receiving dialysis and warrant further investigation in larger mechanistic studies. Full article