Search Results (2,866)

Background and Objectives: Frailty is increasingly recognized as a clinically relevant condition in inflammatory bowel disease (IBD), yet available data remain limited and are often derived from indirect assessment methods. This study aimed to assess frailty using a Fried-derived index and to identify factors associated with frailty in adults with active IBD. Materials and Methods: We analyzed baseline data from a prospective, single-center cohort of adult patients hospitalized with active IBD who required initiation of biologic therapy or small molecules. Frailty was assessed using a modified Fried frailty index comprising shrinking, exhaustion, weakness, slowness, and low physical activity. Patients fulfilling ≥3 criteria were classified as frail, while those meeting 1–2 criteria were classified as pre-frail. Clinical, anthropometric, functional, laboratory, and questionnaire-based patient-reported measures were compared between frail and non-frail patients. Multivariate logistic regression was used to identify factors independently associated with frailty. Results: Seventy-five patients were included, of whom 45 (60%) were male and 44 (58.7%) had ulcerative colitis. The median age was 37 years. Frailty was identified in 17 (22.7%) patients, and 47 (62.7%) were pre-frail. Frail patients were younger (p = 0.001) and had a shorter disease duration (p = 0.036), higher disease activity scores (p = 0.005), higher C-reactive protein levels (p = 0.006), lower hemoglobin levels (p = 0.030) and serum albumin concentrations (p < 0.001), and lower body mass index (p < 0.001). In multivariate analysis, shorter disease duration (OR = 0.83, 95% CI: 0.70–0.97, p = 0.021) and lower serum albumin levels (OR = 0.17, 95% CI: 0.05–0.59, p = 0.005) were independently associated with frailty, whereas severe disease (OR = 2.14, 95% CI: 0.52–8.86, p = 0.294) was not significant after adjustment. Conclusions: Frailty and pre-frailty were highly prevalent in this selected cohort of relatively young adults with active IBD. Shorter disease duration and lower albumin levels were independently associated with frailty. Assessing frailty status may help identify vulnerable patients who could benefit from closer monitoring and multidisciplinary interventions. Full article

Background and Objectives: In recent years, frailty has emerged as a prognostic factor in inflammatory bowel diseases (IBD), particularly among patients with active disease. However, evidence regarding its reversibility after treatment optimization remains limited. This study aimed to assess frailty in active IBD and determine whether frailty status improved after 6 months of clinical management and the achievement of clinical remission. Materials and Methods: This prospective, single-center, observational cohort study included adults with active IBD requiring escalation to advanced therapy who achieved clinical remission at the 6-month follow-up. Patients were evaluated at baseline and after 6 months using a modified Fried frailty phenotype. Quality of life was assessed using the Short Inflammatory Bowel Disease Questionnaire (SIBDQ), and depressive symptoms were assessed using the Center for Epidemiologic Studies Depression (CES-D) scale. Univariate and multivariate logistic regressions were utilized to identify independent factors associated with frailty improvement. Results: The analysis included 54 patients (61.1% male; 42.6% with Crohn’s disease). At baseline, 20.4% were classified as frail, 72.2% as pre-frail, and 7.4% as robust. Following 6 months of clinical management and the achievement of clinical remission, a 100% resolution of frailty was observed, with the robust cohort expanding to 42.6%. Significant improvements occurred across clinical parameters, including handgrip strength, 400 m walk times, and median SIBDQ scores (increasing from 4.4 to 5.9, p < 0.001) alongside a substantial decline in CES-D scores (p = 0.017). Multivariate logistic regression revealed that severe disease at baseline (aOR = 4.51, 95%CI: 1.26–16.18, p = 0.020), anti-TNF therapy initiation (aOR = 3.69, 95%CI: 1.04–13.18, p = 0.044), and higher baseline CES-D scores (aOR = 1.06, 95%CI: 1.00–1.13, p = 0.038) were independently associated with higher odds of frailty improvement. Conclusions: Among patients who achieved clinical remission, frailty and pre-frailty demonstrate substantial short-term improvement following advanced therapy. Functional and psychological recoveries are associated with successful control of baseline disease severity and systemic inflammation. Full article

Background: Telemedicine is increasingly used in inflammatory bowel disease (IBD), but its effects on quality of life (QoL) and psychological outcomes remain unclear. Objectives: This study aimed to evaluate the impact of 6-month telemonitoring on QoL, disease activity, treatment adherence, psychological well-being, patient satisfaction, and healthcare utilization. Methods: This randomized, open-label, single-center study conducted in Russia (July 2023–December 2024) included adults with ulcerative colitis or Crohn’s disease, who were assigned 1:1 to telemonitoring or standard care. The intervention involved monthly remote assessments and access to a web-based platform containing educational information, disease activity assessment, and a chat with a gastroenterologist. The primary outcome was health-related QoL (SIBDQ). Exploratory outcomes included general QoL (WHOQOL-26), psychological well-being (HADS), alexithymia (TAS-26), visceral sensitivity (VSI), treatment adherence (GMAS), patient satisfaction (PSQ-18), achievement of clinical remission, and healthcare utilization. Results: Sixty-eight patients completed the study (32 intervention, 36 control). Telemonitoring was associated with lower anxiety levels (β = −1.76, p = 0.021), reduced visceral sensitivity (β = −5.08, p = 0.039), and higher medication adherence (β = 1.75, p = 0.008). No significant associations were observed for SIBDQ, WHOQOL-26 domains, depressive symptoms, alexithymia, achievement of clinical remission, or patient satisfaction with care (p > 0.05). Patients in the telemonitoring group also required fewer outpatient visits (p < 0.001), with no difference in hospitalizations. Within-group analysis demonstrated improvements in QoL, treatment adherence, visceral sensitivity, and disease activity in the telemonitoring group, but not in the controls. Conclusions: Six-month telemonitoring in IBD was associated with lower anxiety, reduced visceral sensitivity, improved treatment adherence, and fewer outpatient visits. The health-related QoL assessed by the SIBDQ did not differ compared to standard care. No clear clinical disadvantage compared with standard care was detected during the study period. Full article

Anemia represents one of the most frequent systemic complications of inflammatory bowel disease (IBD), with a consistently higher prevalence reported in patients with Crohn’s disease (CD) compared with ulcerative colitis (UC). While chronic inflammation, impaired iron absorption, and intestinal blood loss are recognized contributors, microbiome-mediated mechanisms influencing host iron availability remain insufficiently explored. Emerging evidence indicates that CD-associated dysbiosis is characterized by an increased abundance of siderophore-producing bacteria, particularly members of the Enterobacteriaceae family. Because siderophores are high-affinity iron-chelating molecules capable of competing with host iron acquisition systems and partially escaping lipocalin-2-mediated sequestration, their expansion may contribute to reduced luminal iron bioavailability. In this systematic review, we analyzed comparative microbiome studies published between 2016 and 2026 that directly evaluated microbial differences between CD and UC. CD microbiota consistently demonstrated enrichment in siderophore-associated taxa relative to UC. Based on these findings, we propose that microbiome-driven iron competition may represent an additional mechanistic contributor to the increased prevalence and persistence of anemia observed in CD. Although direct in vivo quantification of siderophore activity in IBD remains limited, the convergence of ecological, functional, and strain-level microbiome evidence supports a biologically plausible interaction between microbial iron-scavenging strategies and host iron metabolism. Full article

Eosinophilic esophagitis (EoE) and inflammatory bowel disease (IBD) are immune-mediated disorders of the gastrointestinal (GI) tract that, despite involving different tissues, are increasingly recognized to coexist. Epidemiologic studies demonstrate a bidirectional association, with patients affected by one condition showing a higher-than-expected prevalence of the other, suggesting shared susceptibility rather than incidental overlap. Genetic and epigenetic data support partial convergence in immune regulatory pathways, while epithelial barrier dysfunction and antigen-driven immune activation emerge as common upstream features. Overlapping cytokine networks, including IL-4, IL-13, and IL-23 signaling, contribute to chronic inflammation in both diseases, although differences in tissue environment and immune dominance give rise to distinct inflammatory phenotypes and clinical behavior. Clinical outcomes in patients with dual diagnoses appear heterogeneous, with available data suggesting neither uniformly worsened nor clearly protective disease courses, underscoring the complexity of shared immune mechanisms operating within different anatomic contexts. Beyond inflammatory activity, coexistence of EoE and IBD poses important nutritional and quality-of-life challenges, as overlapping dietary restrictions and chronic symptoms increase the risk of malnutrition, micronutrient deficiencies, and psychosocial burden. Current therapies remain disease-specific, with strong evidence supporting proton pump inhibitors, swallowed topical steroids, dietary therapy, and dupilumab in EoE, and biologics and small molecules targeting TNF-α, IL-12/23, IL-23, integrins, and JAK–STAT signaling in IBD, while evidence guiding treatment in patients with dual diagnosis remains limited. Together, current evidence supports a framework of shared immune machinery with tissue-specific expression that explains coexistence while preserving the distinct identities of EoE and IBD. By integrating emerging genetic, immunologic, and clinical evidence, this review aims to provide a framework for understanding and managing patients with coexisting EoE and IBD. Full article

Spondyloarthritis associated with inflammatory bowel diseases (IBD-SpA), also known as enteropathic arthritis, is an independent entity belonging to the spondyloarthritis (SpA) group. In recent years, a great amount of new data has been published regarding the pathogenesis and treatment of the disease. In this narrative review we present the main pathogenetic pathways along the gut–joint axis, the genetics of IBD and SpA, the role of environmental factors and that of the microbiome, as well as the main immunopathological processes including immune cells and inflammatory mediators. We cover the clinical picture, the specifics of axial and peripheral SpA-IBD, and briefly discuss the diagnostics. There are common options in the pharmacotherapy of SpA and IBD; however, some drugs that control arthritis (e.g., NSAIDs, IL-17 inhibitors) might not be suitable for the treatment of IBD. Based on the pathogenetic role of the microbiome, it is suggested that pharmacotherapy can be supplemented with non-pharmacological remedies, such as diet including the administration of short-chain fatty acids (SCFAs). Finally, we briefly look at the future that might include rational, even personalized treatment. Full article

Differentiating inflammatory bowel disease (IBD) from diarrhea-predominant irritable bowel syndrome (IBS-D) remains a major clinical challenge due to overlapping symptoms and the limited specificity of single biomarkers. A reliable, non-invasive multimarker approach is needed to improve diagnostic accuracy and reduce unnecessary endoscopic procedures. To evaluate the diagnostic performance of serum interleukin-17A (IL-17A), neutrophil-to-albumin ratio (NAR), and fecal calprotectin (FCP), individually and in combination, for discriminating IBD from IBS-D and healthy controls in Egyptian patients. In this case–control study, 300 participants (100 with IBD, 100 with IBS-D, and 100 healthy controls) were enrolled. Serum IL-17A, NAR, and FCP were measured, and subgroup analysis was performed for infected and non-infected IBS-D patients. Diagnostic performance was assessed using receiver operating characteristic (ROC) curve analysis, with optimal cutoffs determined by the Youden index. A combined biomarker model was constructed using logistic regression. All biomarkers demonstrated a significant stepwise increase from healthy controls to IBS-D and IBD (p < 0.001). IL-17A, NAR, and FCP were elevated in IBS-D compared with controls, indicating low-grade inflammation, but were highest in IBD. No significant differences were observed between infected and non-infected IBS-D patients. Among individual markers, NAR showed the highest diagnostic accuracy (AUC = 0.923), followed by FCP (AUC = 0.884) and IL-17A (AUC = 0.859). The combined model significantly improved performance (AUC = 0.973), achieving 89% sensitivity and 96% specificity. IBS-D is associated with measurable systemic and intestinal inflammation independent of infection status. The combined biomarker model integrating IL-17A, neutrophil–albumin ratio, and fecal calprotectin demonstrated promising discriminatory performance for differentiating IBD from IBS-D. These findings suggest the potential applicability of combined non-invasive biomarkers in future diagnostic stratification approaches. However, the model was developed and evaluated within a single cohort, and external validation in independent populations is required before future potential clinical application. A multimarker diagnostic panel integrating IL-17A, neutrophil–albumin ratio, and fecal calprotectin demonstrated promising diagnostic performance for differentiating inflammatory bowel disease from IBS-D. The combined model may contribute to future diagnostic stratification strategies in patients with chronic diarrhea. However, these findings were derived from a single cohort and require validation in independent populations before broader clinical application. Full article

Background/Objectives: Inflammatory bowel disease (IBD) represents a growing therapeutic challenge, and the identification of novel treatment strategies remains an unmet clinical need. Drug repurposing offers a pragmatic and cost-effective alternative to de novo drug development. This study aimed to identify candidate drugs for repurposing in IBD through inverse signal detection within a large spontaneous pharmacovigilance database. Methods: In this observational, retrospective pharmacovigilance study, data from the FDA Adverse Event Reporting System (FAERS) were analyzed using OpenVigil 2.1. Drugs inversely associated with IBD were identified based on a ROR < 1 and an adjusted p-value < 0.05. Candidates were subsequently filtered to exclude agents with implausible indications, unfavorable pharmacokinetic profiles, or recognized contraindications to use in IBD. Although this screening process yielded a broader set of repurposing candidates across multiple drug classes, the present study focused specifically on antidiabetic medications, which were subjected to a targeted literature review evaluating their immunomodulatory properties, anti-inflammatory mechanisms, and existing preclinical and clinical evidence in the context of IBD. Results: Of 3585 initial drug–event combinations evaluated, 73 candidates met predefined criteria for statistical significance, pharmacokinetic feasibility, and clinical relevance. Within this broader pool, ten antidiabetic agents which demonstrated meaningful inverse signal strength were selected for in-depth analysis: dulaglutide (ROR 0.181, 95% CI 0.136–0.242), insulin lispro (ROR 0.206, 95% CI 0.161–0.263), insulin glargine (ROR 0.246, 95% CI 0.205–0.295), insulin (ROR 0.340, 95% CI 0.295–0.390), insulin aspart (ROR 0.349, 95% CI 0.267–0.455), empagliflozin (ROR 0.400, 95% CI 0.311–0.514), liraglutide (ROR 0.419, 95% CI 0.319–0.552), metformin (ROR 0.446, 95% CI 0.407–0.489), sitagliptin (ROR 0.460, 95% CI 0.376–0.563), and semaglutide (ROR 0.622, 95% CI 0.507–0.764). The subsequent literature review discussed relevant immunomodulatory and anti-inflammatory properties for each of these agents, providing a mechanistic rationale for their potential therapeutic role in IBD. Conclusion: This study identifies antidiabetic drugs as plausible repurposing candidates for IBD, supported by both pharmacovigilance-derived inverse signals and a body of mechanistic and clinical literature suggesting shared pathophysiological pathways between the two conditions. However, it should be acknowledged that the clinical evidence supporting the therapeutic efficacy of several candidates remains variable or incomplete, and robust interventional data are largely lacking. Ultimately, the findings of this study generate testable hypotheses and highlight a set of candidate therapies that warrant dedicated experimental and clinical investigation, including well-designed prospective trials, to determine their true therapeutic potential in IBD management. Full article

Background/Objectives: IL23R encodes a pivotal component of the IL-23/Th17 signaling axis and represents a validated genetic susceptibility locus for inflammatory bowel disease (IBD), psoriasis, and ankylosing spondylitis. Despite extensive GWAS data, the functional consequences of the full spectrum of IL23R missense single-nucleotide variants (SNVs) have not been systematically characterized. This study aimed to identify high-risk missense SNVs through a multi-tool in silico pipeline. Methods: A total of 723 missense SNVs from NCBI dbSNP were verified against transcript NM_144701.3/Q5VWK5-1 (629 aa) using Ensembl VEP (GRCh38). Sequential filtering was performed using applied SIFT, PolyPhen-2, PROVEAN, E-SNPs&GO, MutPred2, and ConSurf (grade ≥ 7); AlphaMissense and FATHMM-MKL were used as independent annotation layers. Protein stability was assessed with MuPro and DynaMut2 (AlphaFold2 AF-Q5VWK5-F1-v6; pLDDT = 68.19); structural characterization was performed with Project HOPE, and interaction networks were constructed using STRING and GeneMANIA. Results: Sequential filtering identified 37 high-risk missense variants. MuPro predicted destabilizing effects for 36/37 variants, with concordant DynaMut2 results for 35/37. Project HOPE identified disulfide bond disruption in 11 variants, charge-altering substitutions in 8, and glycine/proline backbone conformational changes in 11. STRING analysis identified IL12RB1 (0.999), IL23A (0.999), JAK2 (0.995), IL12B (0.986), and STAT3 (0.980) as the leading IL23R interactors. The protective variant R381Q was appropriately characterized as neutral by PROVEAN (−1.16) and AlphaMissense (likely_benign), supporting the specificity of the pipeline. Conclusions: Comprehensive in silico analysis identified 37 high-risk IL23R missense candidates with convergent computational evidence of predicted deleteriousness, predominantly involving cysteine bridge disruption, charge alteration, and glycine/proline backbone conformational changes. These variants are presented as prioritized candidates for future functional validation and may inform subsequent investigations of IBD susceptibility and IL-23 pathway pharmacogenomics. Full article

Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), is a chronic relapsing inflammatory disorder characterized by epithelial barrier dysfunction, immune dysregulation, microbiota imbalance, and progressive tissue remodeling. Because the pathogenesis of IBD involves complex interactions among genetic, immunological, microbial, and environmental factors, experimental animal models have become indispensable tools for investigating disease mechanisms and evaluating therapeutic strategies. Various experimental colitis models have been developed to reproduce distinct pathological features of human IBD, including chemically induced models, genetically engineered systems, adoptive immune-transfer models, and infectious or microbiota-associated models. Rodent models remain the most widely used experimental platforms because of their accessibility, reproducibility, and well-established genetic manipulation technologies. These systems have significantly contributed to understanding inflammatory signaling pathways, epithelial barrier injury, immune cell dysregulation, and gut microbial crosstalk. However, important species-specific differences in intestinal anatomy, immune responses, microbiota composition, and pharmacokinetics limit direct translation of rodent findings into clinical applications. To overcome these limitations, increasing attention has been directed toward large-animal models, particularly pig and minipig systems, which more closely resemble human gastrointestinal anatomy, digestive physiology, immune regulation, and microbiome-related characteristics. Porcine models additionally support clinically relevant procedures, including repeated colonoscopy, serial biopsy sampling, pharmacokinetic evaluation, and longitudinal therapeutic monitoring. Recent advances in genome-editing technologies and multi-omics approaches have further enhanced the translational utility of porcine IBD models. This review summarizes major experimental colitis animal models, discusses their pathological and translational characteristics, and highlights the growing importance of pig and minipig systems as human-applicable platforms for preclinical therapeutic evaluation and translational IBD research. Full article

Background and Objectives: Intestinal barrier dysfunction is increasingly recognized as a contributor to inflammatory bowel disease (IBD) pathophysiology. Zonulin, a regulator of epithelial tight-junction permeability, has emerged as a potential non-invasive biomarker; however, its clinical relevance remains uncertain. This study evaluated whether fecal zonulin levels reflect clinical disease activity in inflammatory bowel disease and explored their association with ileal involvement in Crohn’s disease (CD). Materials and Methods: Forty-six consecutive IBD patients (26 CD, 20 UC) were prospectively included. Fecal zonulin was measured using a commercially available ELISA. In this study, the term “fecal zonulin” refers to ELISA-detected zonulin-related proteins. Clinical disease activity was assessed using CDAI for CD and the Mayo score for UC. Standard blood and fecal inflammatory markers were obtained, and subgroup analyses were performed according to disease type and location. Results: Fecal zonulin levels were significantly higher in active IBD compared with remission (106.37 vs. 53.80 ng/mL, p = 0.002). Patients with CD had higher zonulin concentrations than those with UC (91.4 vs. 51.0 ng/mL, p = 0.001). Zonulin showed a moderate positive correlation with fecal calprotectin (r = 0.338; p = 0.021). In multivariable analysis, clinical disease activity remained independently associated with zonulin levels, whereas ileal involvement was no longer statistically significant. Conclusions: Fecal zonulin is associated with disease activity in IBD, suggesting that fecal zonulin-related proteins may represent a potential adjunctive marker of epithelial barrier dysfunction and clinical disease activity in IBD. However, these findings should be considered exploratory and require validation in larger, longitudinal multicenter studies using standardized assays and endoscopic correlation. Full article

The global prevalence of autoimmune diseases ranges from 3% to 8%, with women at a significantly higher risk than men. The core mechanisms underlying these diseases include impaired T-cell and B-cell immune tolerance, abnormal cytokine production, and aberrant activation of related signaling pathways. Conventional treatments primarily focus on suppressing immune responses, but their efficacy remains limited and they are often associated with substantial side effects. Nanomedicine leverages nanoscale materials to enable precise diagnosis and targeted therapy. Nanocarriers can penetrate biological barriers, enhance cellular uptake, and prolong circulation time in vivo, demonstrating considerable potential for drug delivery. Common nanoscale drug delivery platforms include nanoparticles, polymeric micelles, liposomes, dendrimers, mesoporous materials, hydrogels, and exosomes. Each carrier type possesses distinct characteristics in terms of drug-loading capacity, stability, responsiveness, and biocompatibility, thereby enabling targeted delivery and controlled release. This review summarizes recent advances in nano-delivery technologies for three representative chronic autoimmune diseases: diabetes mellitus (DM), inflammatory bowel disease (IBD), and rheumatoid arthritis (RA). Nano-delivery systems can improve therapeutic outcomes by optimizing drug delivery, targeting complications, and modulating the pathological microenvironment. They enhance drug bioavailability, reduce off-target and systemic adverse effects, and provide novel strategies for the precise and efficient treatment of chronic autoimmune diseases. Full article

Background: The incidence of inflammatory bowel disease (IBD) is growing in the population. At present, the etiology of inflammatory bowel disease remains unclear, and there is no effective and low-toxic therapeutic drug. This study aimed to investigate the role of Lobenzarit (Lbz) in the treatment of colitis in mice as well as the underlying mechanism. Methods: In this experiment, colitis was induced in mice with dextran sulphate sodium (Dss). Subsequently, the role of Lbz in colitis and its underlying mechanisms were examined using H&E staining, TEM, ELISA, PCR, and other assays. Results: Lbz significantly attenuated the related symptoms of Dss-induced colitis in mice. In addition, Lbz suppressed neutrophil infiltration and restored macrophage polarization towards an anti-inflammatory state. Lbz also inhibited (p < 0.05) the activation of signaling pathways TLR4 and MAPK (51.61% decrease for TLR4 and 56.94% decrease for MAPK), reduced the release of inflammatory factors as it significantly decreased (p < 0.05) colonic IL-1β, TNF-α, IFN-γ, COX2, and VEGF (47.63, 42.49, 53.42, 58.74, and 61.28% decreases respectively) thereby attenuating the inflammatory response in mice. Lbz administration also restored the permeability of the intestinal barrier by increasing (p < 0.05) tight junction-associated proteins (claudin-1, occludin, and ZO-1 with a 5.36- and 2.26-fold increase for claudin-1 and ZO-1, respectively) and decreasing (p < 0.05) MALK levels by 53.51%. In addition, Lbz upregulated colonic Cytochrome C oxidase II, PDH, and ATP synthase levels and upregulated CD163, CD206, c-Maf, and PPAR-γ levels as compared to the DSS-treated group. Conclusions: Lbz has a repairing effect on Dss-induced colitis and may alleviate Dss-induced colitis by targeting the TLR4 pathway and promoting intestinal stem cell proliferation. Full article

Background/Objectives: Inflammatory bowel diseases (IBD) are conditions of the gastrointestinal tract with treatments linked to side effects and relapses. Spondias mombin L. is a species with anti-inflammatory action, but there is little information in the literature about its application in the treatment of IBD. The aim of this study was to evaluate the intestinal anti-inflammatory activity of hydroalcoholic extract of Spondias mombin L. (HESm) in a rat model of ulcerative colitis (UC). Methods: Hydroalcoholic extract was obtained using the turboextraction technique, followed by identification of its major components using ultra-high performance liquid chromatography (UFLC). Intestinal anti-inflammatory activity was evaluated in an acute model of UC induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS). Groups received a vehicle, prednisolone (2 mg/kg), or HESm (125, 250 or 500 mg/kg) before and after UC induction. Ulcerated area, score, and intestinal weight/length ratio were analyzed. Histopathological analysis and the extract’s effect on the contractility of the intestinal segment were carried out. Results: UFLC identified the presence of quercetin, a flavonoid widely cited for the species. At doses of 125, 250, and 500 mg/kg, the extract reduced areas of injury by 86.82, 92.67, and 85.06%, respectively, compared to the control, in addition to reducing scores and weight/length ratio of the colons. Histopathological analysis confirmed the results. In contractility, the extract at the highest concentration tested reduced the response of the muscarinic agonist carbamylcholine to 53.7 ± 4.2% of control contraction. Conclusions: Results demonstrate the species’ ability to reduce injuries caused by colitis, suggesting its potential to contribute to the clinical management of IBD in the future. Full article

Micro- and nanoplastics (MNPs) are pervasive in food-contact environments and the human diet, positioning the gastrointestinal (GI) tract as the primary portal of entry and a plausible site of early biological effects. Human exposure is supported by detection of microplastics in stool and colon tissue, and emerging clinical studies report associations between fecal microplastic burden and GI disease states, including inflammatory bowel disease (IBD) and colorectal cancer (CRC). Preclinical studies provide mechanistic plausibility, reporting that ingested MNPs can modulate microbial ecology, alter mucus membrane integrity, increase intestinal permeability through changes in cellular tight junction biology, and induce inflammatory gene expression. These effects can vary by MNP polymer type, particle size/shape, aging state, and exposure dose. Human-relevant experimental platforms increasingly demonstrate size- and concentration-dependent uptake and host responses while revealing substantial inter-individual variability. We synthesize current evidence on dietary sources and key physiochemical properties as they relate to mechanistic pathways connecting MNP exposure to dysbiosis–immune activation–neoplasia axes, in addition to methodological limitations that constrain current clinical utility. Further research including standardized biomonitoring and exposure protocols, environmentally realistic chronic low-dose mixtures, longitudinal human cohorts, and interventional designs that test whether exposure reduction modifies GI inflammation biomarkers and cancer-relevant pathways are critical to clarifying causality. Full article