Search Results (19,603)

The dextran sodium sulfate (DSS) colitis model is the most widely used experimental model of inflammatory bowel disease (IBD) due to its simplicity and versatility, with over 7000 PubMed entries in the last decade and an exponential rise in recent years. Since its initial description in 1985, DSS colitis has been extensively evaluated across species, most notably in mice and rats, and has yielded substantial insights into IBD pathogenesis. However, the model’s multifactorial nature poses a dual challenge: it offers an opportunity but complicates study design, interpretation, and translational relevance. This complexity is worsened by inconsistent reporting, which hampers reproducibility and comparability across studies. The broad use of the DSS-induced colitis model yields numerous insights about the model, which help better understand its complexity, characteristics and limitations. Although DSS colitis is induced locally, inflammation in the colon and gut barrier destruction may also affect other organs (such as the liver and brain) and their metabolism and molecular responses, which, in turn, may interfere with colitis-underlying mechanisms and drug response, and may influence the interpretation of results. These intrinsic (intra-experimental) characteristics of the DSS model are summarised in the paper (colitis, gut–brain axis, gut–liver axis). In addition, the DSS model is heavily influenced by numerous extrinsic (inter-experimental) factors (environmental, microbiological, genetic), which may further complicate the colitis model, the study outcomes, and data interpretation, and these are also discussed in the paper. As science advances and new data accumulate, understanding the intricate interplay among internal mechanisms, external factors, and technical variables becomes increasingly essential for the accurate interpretation of DSS outcomes. This review synthesises the complexity and interdependence of factors shaping the DSS model, emphasising the need for meticulous reporting and consideration of methodological nuances to enhance reproducibility, interpretation, and translational value in DSS colitis research. In addition, the review provides practical guidance through a “traps and tricks” subsection and checklist table designed to provide a framework and practical recommendations to better understand, apply, and interpret DSS model results in the context of broader systemic and methodological considerations. Full article

Anti-A and anti-B antibodies are essential for monitoring adverse reactions in organ transplants and transfusions. However, their importance is also growing due to their involvement in the pathophysiology of various human diseases, such as infections, although this is currently the subject of heated debate. A characteristic heterogeneity in the titers and classes of anti-A and anti-B antibodies is observed among individuals. Several factors appear to be responsible, such as everyone’s specific immune profile, age, sex, microbiota composition, lifestyle, and health status. The immune profile, the result of a specific genetic predisposition and mediated and controlled by cytokines, shows a bidirectional relationship with ABO antigen expression, the gut microbiota, and the levels and class switching of anti-ABO antibodies. Associations between ABO groups and circulating levels of cytokines and chemokines further highlight this complex interaction. To better understand the role of the immune profile in this context, we evaluated, for the first time, the possible association between polymorphic variants in the regulatory regions of the genes encoding the cytokines IL-8, IL-1, IL-4, IL-6, IFN-γ, and IL-10 and anti-A and anti-B antibody titers and classes by group and in total. We also assessed the levels of these cytokines in each group and their correlations with anti-A and anti-B antibodies, as well as with age and associations with gender. Significant data were obtained that may contribute to a better understanding of the other roles of ABO antibody titers. Full article

Artificial sweeteners have emerged as contaminants of increasing concern due to their widespread consumption, environmental persistence, and resistance to conventional wastewater treatment. This review provides an integrated assessment of global research trends and the environmental behavior of major artificial sweeteners, including sucralose, acesulfame potassium, saccharin, and aspartame. Bibliometric analysis of SCOPUS-indexed publications reveals rapid growth in research since 2010, with key themes focusing on environmental occurrence, treatment technologies, and ecotoxicological effects. These compounds are frequently detected in wastewater effluents, surface waters, groundwater, and even drinking water systems, driven by their high solubility and limited biodegradability. Their persistence raises concerns regarding ecological impacts, including potential alterations to microbial communities and aquatic organisms. In addition, emerging evidence suggests potential human health implications, including gut microbiota disruption, metabolic effects, and risks associated with chronic low-dose exposure, although these remain poorly understood. The performance of existing treatment technologies, including biological processes, adsorption, advanced oxidation, and membrane filtration, is critically evaluated, highlighting limitations in complete removal and in the formation of transformation products. Future research should prioritize sustainable treatment strategies, comprehensive risk assessment, and improved monitoring frameworks to better address both environmental and human health risks associated with artificial sweeteners. Full article

Necrotizing enterocolitis (NEC) and sepsis/late-onset sepsis (LOS) are significant contributors to preterm infant morbidity and mortality, with prematurity and low birth weight representing major risk factors for these interconnected conditions. Although the pathogenesis of NEC and LOS is not fully understood, there is a clear association with an immature intestinal mucosal barrier, which may enable bacterial invasion and translocation, resulting in an inflammatory cascade. Increasing recognition of the gut microbiome as a marker for health and disease has driven interest in probiotics, particularly Bifidobacterium spp. and Lactobacillus spp., as potential adjunctive agents for the prevention and management of NEC and LOS in preterm infants, which is the area of focus of this review. The focus of this paper was to analyze clinical studies using different probiotic strains, and compare single-strain versus multi-strain probiotic formulations. Several studies support that probiotic supplementation in preterm infants has the potential to decrease NEC incidence and, to a lesser extent, sepsis/LOS. Nonetheless, inconsistent results due to strain differences and clinical heterogeneity limit the widespread adoption of this mode of therapy, as do safety concerns in this vulnerable population. Further high-quality standardized studies are necessary to establish consistent guidelines for probiotic use in preterm infants. Full article

Atopic dermatitis (AD) is a chronic inflammatory dermatosis driven by skin barrier dysfunction, immune dysregulation, and gut–skin axis imbalance. While probiotics show promise, the therapeutic potential and mechanisms of topical postbiotics in modulating the gut–skin axis remain understudied. Here, we investigated the efficacy of Schleiferilactobacillus harbinensis JNDM-derived cell-free supernatant (CFS) and lysate (ShL) in a DNFB-induced AD mouse model. Topical application of both CFS and ShL significantly attenuated AD-like symptoms, reduced epidermal thickening, and restored the expression of the barrier protein filaggrin. Immunologically, treatment suppressed the Th2-dominant inflammatory cascade (IL-4, IL-5, IL-13, IL-33, TSLP) and reduced serum IgE and IFN-γ levels. Notably, ShL exhibited superior systemic efficacy, significantly inhibiting mast cell infiltration and reducing the spleen index. 16S rRNA sequencing revealed that topical intervention remotely remodeled the gut microbiota, specifically reversing the depletion of the beneficial genus Alistipes and suppressing the compensatory increase in Odoribacter. This microbial restructuring was accompanied by distinct metabolic changes: ShL treatment resulted in an approximately 4-fold elevation in fecal butyrate concentrations compared with the model group. Correlation analysis further validated a strong positive axis linking Alistipes abundance and butyrate levels to skin barrier integrity. Collectively, our findings demonstrate that S. harbinensis postbiotics—particularly the lysate—ameliorate AD through a dual mechanism of local barrier repair and systemic metabolic modulation via the gut–skin axis, presenting a promising non-steroidal therapeutic strategy. Full article

Background: Intestinal barrier problems cause obesity and related health issues. We focus on treatments that fix the gut lining and change gut bacteria. Soy oligosaccharides (SOSs) are prebiotics. They change gut bacteria and help lower fats. The mechanism by which SOS affects high-fat diet (HFD)-induced obesity remains to be fully elucidated. Objectives: We want to see if SOS improves the mucus barrier in the gut by investigating how mucus is produced, modified and released. We hypothesise that SOS can reduce obesity and associated health problems by regulating mucus and gut bacteria. Methods: Accordingly, HFD-fed mice were used in this study. Results: The results showed that SOS alleviated HFD-induced weight gain and glucose disorders. It also enhanced the gut mucus barrier by promoting goblet cell differentiation and regulating mucus-related genes. In addition, SOS intervention was associated with increased abundance of potentially beneficial gut taxa. These bacterial changes were linked to better health measures. In conclusion, our findings demonstrate that SOS confer metabolic protection against HFD-induced obesity, at least partially, by coordinately modulating the mucus–microbiota axis. Conclusions:These data suggest that SOS may alleviate obesity and related disorders by improving the intestinal mucus layer and gut microbiota. 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

Candida albicans is a ubiquitous commensal fungus that may be lethal once it gains access to the bloodstream, following a breach in protective barriers such as skin or gut lining. Intravenous injection of C. albicans (4.5 × 10⁴ yeasts/gm of mouse) leads reproducibly to systemic infection with a median survival of about 75 h. We studied the effects of two human innate immune effectors on the course of systemic infections. The soluble human pentraxin serum amyloid P component (hSAP) retards death in murine disseminated candidiasis. In contrast, another soluble pentraxin, human C-reactive protein (hCRP), hastens death. To examine the pathological basis for these differences, necropsies were performed, and the right kidney was removed for study. Candidiasis caused abundant collagen deposition (the precursor to fibrosis) and loss of contrast between the kidney medulla and cortex. Daily administration of subcutaneous hSAP following the intravenous injection of C. albicans preserved the discrete histological difference between cortex and medulla and lessened host collagen deposition. Yeasts and hyphae within abscesses were decorated with hSAP. Contrastingly, kidneys from animals administered C. albicans and hCRP showed extensive collagen deposition and loss of the boundary between the cortex and the medulla of the kidney. hCRP did not bind to fungi but bound to damaged tissue surrounding abscesses, leading to a more destructive infection with loss of tissue. Staining cells with antibodies to CD45 (to detect T-lymphocytes, myelocytes, monocytes, and macrophages) and antibodies to Ly-6G (neutrophils, and granulocytes) showed that hSAP retarded infiltration of inflammatory cells into diseased areas. The results are consistent with the hypothesis that early administration of hSAP represses the migration of inflammatory cells, dampens the production of collagen by fibroblasts, and dampens the overall immune response of the host to infection. In doing so, hSAP prolonged life, whereas hCRP facilitated the infectious process and hastened death. Full article

Short-chain fatty acids (SCFAs) are key biomarkers of gut microbiota activity; however, routine quantification in fecal samples relies largely on chromatography, which is instrument-intensive and throughput-limited chromatography techniques. Herein, we present a rapid machine-learning-assisted electroanalysis platform for SCFAs profiling that integrates a disposable three-electrode planar gold chip with voltammetric fingerprinting and artificial neural network (ANN)-based signal decoupling. To generate orthogonal chemical information and improve the discrimination of structurally similar species, a dual pretreatment strategy combining acid-catalyzed esterification and alkaline dissociation was employed prior to electrochemical analyses. Differential pulse voltammetry (DPV) and cyclic voltammetry (CV) were employed to acquire high-dimensional fingerprints, from which current-, potential-, and area-based descriptors were extracted using a cross-information feature strategy. A hierarchical modeling framework improved total SCFAs prediction by incorporating ANN-predicted propionate and butyrate concentrations as auxiliary inputs. While linear calibration was achievable in standard mixtures, direct linear models performed poorly in real fecal matrices due to strong sample-dependent matrix interference. In contrast, the ANN captured nonlinear relationships among multifeature inputs and suppressed matrix effects. Validation against gas chromatography–mass spectrometry in an independent fecal test cohort (n = 30) demonstrated excellent agreement and low prediction errors, with mean absolute error/root mean square error values of 0.063/0.072 mM (propionic acid), 0.029/0.034 mM (butyric acid), and 0.135/0.202 mM (total SCFAs). The DPV/CV acquisition requires only minutes per sample, whereas pretreatment takes 1~3 h depending on the target route but can be performed in parallel for batch processing; thus, overall throughput is determined mainly by batch pretreatment rather than per-sample instrument time. This electrochemical–ANN workflow provides a portable, high-throughput alternative to chromatography for fecal SCFAs profiling in clinical screening and microbiome research. Full article

As a representative form of extreme weather, typhoons inflict widespread and systemic damage, posing a severe threat to the livestock industry. The stress they induce, typhoon stress (TS), is an unavoidable and complex environmental challenge that severely disrupts the ovarian function of Wenchang chickens. In this preliminary study, we employed a two-group comparison design (n = 6 per group) integrating behavioral observations, serum biochemical assays, histopathological examinations, and molecular analyses (qPCR, 16S rDNA sequencing, and transcriptome sequencing) to explore the role of the microbiota–gut–brain–ovarian axis (MGBOA) in this process. The findings revealed that TS markedly reduced water intake and locomotor activity, while it elevated serum corticosterone (CORT) and oxidative stress markers. It also induced shifts in gut microbiota composition, including a decrease in Bacteroides and an increase in Escherichia–Shigella. Furthermore, TS compromises duodenal intestinal barrier integrity, as evidenced by downregulation of the tight junction proteins TJP1 and CLDN1, structural damage to intestinal villi, and a reduced villus-to-crypt ratio. In the hypothalamus, VIP mRNA expression was upregulated, while GHSR expression was downregulated; the expression of the tight junction protein CLDN5 was also reduced. In the ovary, reproductive potential was suppressed, manifested by a reduction in follicle number and downregulation of STAR expression. Ovarian transcriptome analysis highlighted enrichments in pathways associated with inflammation (e.g., Toll-like receptor signaling) and lipid metabolism (e.g., PPAR signaling). These results support the hypothesis that TS impairs egg production via the MGBOA, providing preliminary mechanistic insights into how environmental stressors might disrupt animal productivity through MGBOA-mediated pathways. 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

To evaluate the potential biological effects of electromagnetic fields from offshore wind farms on Sebastes schlegelii, a laboratory-controlled chronic exposure experiment was conducted using a magnet-based static magnetic field system. Each group contained 60 fish distributed across four replicate tanks, with 15 fish per tank, and the fish were continuously exposed for 20 d under controlled water-quality conditions. Daily video monitoring of collective shoaling behavior was combined with multi-tissue physiological and biochemical analyses. Electromagnetic field exposure increased the swimming speed, burst frequency, activity ratio, spatial coverage, occupancy entropy, and polarization, while reducing the nearest neighbor distance, group radius, and group area. At the physiological level, cortisol increased mainly in the liver and brain, ACTH showed tissue-dependent modulation, SOD remained relatively stable, and glutathione increased in multiple tissues, especially in the liver, gut, and brain. Correlation analysis indicated a close coupling between behavioral reorganization and endocrine–redox regulation, suggesting that chronic EMF exposure shifted Sebastes schlegelii into a stress-associated but functionally coordinated collective state. Full article

Isoxanthohumol (IX) is a prenylated flavonoid derived from hop cones (Humulus lupulus) that is gaining increasing recognition for its potential biological effects. Despite numerous studies on its precursor, xanthohumol, studies on IX remain limited. Of particular interest is its metabolism, particularly its biotransformation by gut microbiota to 8-prenylnaringenin (8-PN), a potent phytoestrogen, which indicates the complex nature of its biological activity and potential health implications. This review summarizes the current state of knowledge on IX and its derivatives, covering their microbial metabolism, their impact on the gut microbiome, and the metabolic consequences of this conversion. Furthermore, it examines the relationship between the molecular structure of IX and its derivatives and their biological activity, highlighting existing research gaps and the need for further research on the safety and therapeutic potential of these compounds Full article

The microbiota–gut–brain axis (MGBA) is a complex bidirectional communication network integrating neural, endocrine, immune, and metabolic pathways linking intestinal microbiota to central nervous system function. Increasing evidence indicates that microbiota-derived signals are critical regulators of neurodevelopment and may contribute to vulnerability to neurodegenerative disorders across the lifespan. In this narrative review, we synthesize experimental and clinical evidence to define the key biological mechanisms underlying microbiota–brain interactions. Converging data indicate that immune activation, barrier dysfunction, and microbial metabolites, particularly short-chain fatty acids and tryptophan-derived compounds, represent central mediators linking gut dysbiosis to neuroinflammatory and neurodegenerative processes. Early-life microbial perturbations, driven by factors such as antibiotic exposure, diet, and psychosocial stress, appear to induce long-term immunometabolic programming that may increase susceptibility to neurological disorders later in life. Clinical studies consistently associate dysbiosis with neurodevelopmental conditions and major neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease; however, causal relationships remain incompletely defined due to heterogeneity and the predominance of observational data. Overall, the available evidence supports a lifespan model in which microbiota-driven immune and metabolic dysregulation contributes to both early neurodevelopmental trajectories and late-life neurodegeneration. While microbiome-based biomarkers and therapeutic strategies show promise, their clinical translation requires validation in longitudinal and interventional studies. Full article