Background and Objectives: Obesity-associated chronic low-grade inflammation supports various systemic alterations. In this descriptive study, 122 apparently healthy adults aged 20 to 35 years were voluntarily included and classified based on body mass index (BMI) as normal-weight (NW), overweight (OW), and obese (OB). This study aims to characterize peripheral blood (PB) lymphocyte (Ly) phenotypes and investigate their correlations with body composition indices (BCIs) in healthy young adults. Materials and Methods: The following BCIs were measured: waist circumference, hip circumference, height, waist-to-hip ratio, waist-to-height ratio, total body fat mass, visceral fat level, weight, and BMI. White blood cell count (WBC), Ly absolute count, serum TNF-α, and IFN-γ were quantified. Ly subpopulations were analyzed as follows: total TLy (TTLy—CD45⁺CD3⁺), early activated TLy (EATLy—CD45⁺3⁺69⁺), total NKLy (TNKLy—CD45⁺CD3⁻CD56⁺CD16⁺), NK^dim (low expression of CD56⁺), NK^bright (high expression of CD56⁺), BLy (CD45⁺CD3⁻CD19⁺), T helper Ly (ThLy—CD45⁺CD3⁺CD4⁺), and T cytotoxic Ly (TcLy—CD45⁺CD3⁺CD8⁺). Results: Higher BMI has significantly higher WBC and BLy (p < 0.0001; p = 0.0085). EATLy significantly decreased from NW to OB (3.10—NW, 1.10—OW, 0.85—OB, p < 0.0001). Only EATLy exhibited significant negative correlations with all the BCIs. A significantly higher TNF-α was observed in the OW and OB groups compared to the NW group. IFN-γ increased linearly but nonsignificantly with BMI. TTLy showed a nonsignificant positive correlation with both IFN-γ and TNF-α, while EATLy showed a negative correlation, significant only for IFN-γ. NKLy subpopulations exhibited a consistent negative correlation with TNF-α, significant only for NK^dim (p = 0.0423), and a nonsignificant consistent positive correlation with IFN-γ. A nonsignificant negative correlation between age and both TNKLy (r = −0.0927) and NK^dim (r = −0.0893) cells was found, while a positive correlation was found with NK^bright (r = 0.0583). Conclusions: In conclusion, the baseline immunological profile of PB is influenced by excessive adipose tissue in healthy young adults.

Background and Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is now widely acknowledged as belonging to the broader category of metabolic disorders, being closely associated with obesity, insulin resistance, and chronic systemic inflammation. Recent evidence indicates that in MASLD, alterations in the gut–liver axis—particularly increased intestinal permeability may serve as a crucial mechanistic link between metabolic dysfunction and hepatic steatosis. Zonulin, a physiological modulator of intestinal tight junctions, has been suggested as an indicator of compromised barrier integrity; however, its specific role in MASLD remains to be fully elucidated. Materials and Methods: We conducted a prospective observational study including 52 adult patients diagnosed with MASLD. Hepatic steatosis was evaluated using the SteatoTest (FibroMax panel), while fecal zonulin levels were measured by ELISA at baseline. Clinical, anthropometric, and metabolic parameters were assessed. We used ROC curve analysis to explore zonulin’s predictive value for moderate-to-severe steatosis (≥S2). Results: Elevated fecal zonulin (>107 ng/mL) occurred in 26.9% of participants. In a binary logistic model with SteatoTest ≥ S2 as outcome, zonulin was independently associated with clinically significant steatosis (OR per 1 ng/mL = 1.017; 95% CI 1.002–1.032; p = 0.029). Discrimination for ≥S2 was AUC = 0.680 (95% CI 0.535–0.825; p = 0.015). The Youden-optimal cut-off was 57.0 ng/mL (sensitivity 68.2%, specificity 63.3%) versus 40.9%/83.3% at the manufacturer’s 107 ng/mL threshold. Conclusions: Fecal zonulin shows modest discriminatory ability for steatosis and is best used as an adjunct to non-invasive assessment; cohort-specific calibration (57.0 ng/mL) outperformed the generic 107 ng/mL threshold.

Gastric cancer (GC) is the fifth most common malignancy worldwide, with 968,784 new cases reported in 2022. Since 1975, when stomach cancer was the most common cancer, its incidence has declined in many regions. This decline can be attributed to improved food preservation and recognition of Helicobacter pylori (H. pylori) as a group 1 carcinogen in intestinal-type GC. The aim of this review was to summarize current strategies for primary and secondary prevention of GC, with an emphasis on H. pylori management, dietary factors, novel biomarkers, and screening approaches relevant in Europe. Papers from large databases, namely Web of Science, Scopus, and PubMed/MEDLINE, were selected (reviews, guidelines, and peer-reviewed studies) from about the last 1–5 years. The research was conducted using the keywords gastric cancer, prevention, primary prevention, secondary prevention, and endoscopy guidelines on prevention of gastric cancer. Primary prevention of GC is directed at screening for H. pylori and dietary changes. Secondary prevention is supported by traditional tumor markers, pepsinogen-based serological biopsy, newer blood-based markers, and major technological progress in endoscopy. High-definition endoscopy, magnification, virtual chromoendoscopy, and artificial intelligence have improved the detection of preneoplastic lesions and early cancer, while advanced therapeutic techniques such as endoscopic mucosal resection and endoscopic submucosal dissection permit organ-sparing treatment. Large projects, including GISTAR, EUROHELICAN, TOGAS, and EUCanScreen, are expected to clarify optimal screening strategies. Although GC incidence has declined, it remains a common and significant malignancy. Understanding the facets of primary and secondary prevention of GC will lead to a reduction in the burden of this disease.

The gut microbiota is increasingly examined as a therapeutic target because it contributes to epithelial barrier integrity, microbial metabolite production, bile acid transformation, immune regulation, and communication between the gut and distant organs. This structured narrative review synthesizes evidence on microbiota involvement in metabolic, gastrointestinal, hepatic, cancer, and neuroimmune conditions, including MASLD/MASH, inflammatory bowel disease, irritable bowel syndrome, obesity, type 2 diabetes, hypertension, colorectal cancer, Parkinson’s disease, and autism spectrum disorder. Across these conditions, microbiome findings are biologically plausible but heterogeneous. Many associations are shaped by diet, geography, medication exposure, host genetics, disease stage, sampling methods, and analytical pipelines. Microbial alterations should therefore be interpreted as context-dependent signals and candidate modifiers rather than universal causal markers. Conventional microbiota targeted strategies include diet, physical activity, prebiotics, probiotics, synbiotics, postbiotics, and fecal microbiota transplantation. These approaches are clinically familiar, but their effects are often broad, host specific, strain dependent, and difficult to assign to one mechanism. Fecal microbiota transplantation has the clearest clinical role in recurrent Clostridioides difficile infection, while evidence for most other indications remains inconsistent. Engineered microbial therapeutics offer greater experimental precision through signal sensing, payload delivery, metabolic modulation, and genetic circuit design. However, most evidence remains preclinical or early translational. Progress requires stronger human trials, standardized methods, mechanistic validation, safety monitoring, ecological containment, transparent reporting, and proportionate regulation.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as part of the broader spectrum of metabolic disorders, with links to obesity, insulin resistance, and systemic inflammation. Emerging evidence points to a role of the gut–liver axis, particularly intestinal permeability, in its pathogenesis. Zonulin—a regulator of tight junctions—has been proposed as a marker of impaired barrier function, but its relevance in MASLD remains unclear. Methods: We conducted a prospective observational study including 52 adult patients diagnosed with MASLD. Hepatic steatosis was evaluated using the SteatoTest (FibroMax panel), while fecal zonulin levels were measured by ELISA at baseline. Clinical, anthropometric, and metabolic parameters were assessed. We used ROC curve analysis to explore zonulin’s predictive value for moderate-to-severe steatosis (≥S2). Results: Fecal zonulin levels above 107 ng/mL were found in 26.9% of participants. This group showed a higher frequency of moderate-to-severe steatosis (78.6%) compared to those with lower zonulin levels (55.3%), although the correlation with SteatoTest was weak (r = 0.19, p > 0.05). No significant associations were found between zonulin and liver fibrosis, insulin resistance (HOMA-IR), or the BARD score. The AUC for detecting steatosis ≥ S2 was 0.68. Conclusions: Although limited as a standalone diagnostic tool, fecal zonulin may reflect underlying gut barrier dysfunction in MASLD and show moderate association with hepatic steatosis. Its role as a complementary biomarker in non-invasive stratification frameworks warrants further study, especially in larger cohorts with control groups.

Background: Short-chain fatty acids (SCFAs) support mucosal integrity and reduce inflammation, while nesfatin-1 is a neuropeptide with antiapoptotic, anti-inflammatory, antioxidant, and anorexigenic actions. Their roles in inflammatory bowel disease (IBD) and links to quality of life (QoL) are unclear. Methods: We conducted a cross-sectional study including adults with Crohn’s disease (CD), ulcerative colitis (UC), and healthy controls (HC). Serum total short-chain fatty acids and nesfatin-1 were measured using enzyme-linked immunosorbent assays (ELISA). Quality of life was assessed using the Inflammatory Bowel Disease Questionnaire (IBDQ). Group comparisons and correlation analyses were performed using non-parametric statistical methods. Results: Serum total SCFA concentrations did not differ significantly between patients with CD, UC, and HC (p = 0.29). Nesfatin-1 levels showed between-group variability, with lower values in CD compared with healthy controls, while patients with UC showed intermediate and variable levels (p = 0.064). An inverse correlation between SCFAs and nesfatin-1 was observed in UC and in the combined IBD cohort, but not in CD. Quality of life was comparably impaired in CD and UC. No statistically significant associations were observed between serum SCFAs or nesfatin-1 and IBDQ scores. Conclusions: In this pilot exploratory study, circulating SCFAs and nesfatin-1 showed distinct patterns across IBD subtypes, with evidence of subtype-specific associations between these biomarkers. However, no relationship with quality of life was demonstrated. Larger longitudinal studies are required to confirm these findings and clarify their clinical relevance.