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Background The evidence on the role of gut microbiota in post-infectious irritable bowel syndrome (PI-IBS) is convincing. Lactobacillus spp. positively affect IBS symptoms, although the mechanisms through which probiotics exert their beneficial effects are largely unknown. The aim of the study is to evaluate the role of Lactobacillus casei DG (LC-DG) and its postbiotic (PB) in modulating the inflammatory/immune-response in PI-IBS in an ex-vivo organ culture model. Methods Ex vivo cultures of ileal and colonic mucosa from 10 PI-IBS, diarrhea predominant subtype (D) patients, and 10 healthy controls (HC) were treated with LPS, LC-DG and PB. Interleukin (IL)-1α, IL-6, IL-8 and IL-10 mRNA levels were assessed by real-time PCR and Toll like receptor 4 (TLR-4) protein expression by Western blotting. Results At baseline, IL-1α, IL-6 and IL-8 mRNA levels as well as TLR-4 protein expression were significantly higher while IL-10 mRNA levels were lower in PI-IBS D than in HC in both ileum and colon. LC-DG and PB significantly reduced the mRNA levels of pro-inflammatory cytokines and TLR-4 while increased that of IL-10 after LPS stimulation. The protective effect was more pronounced for PB than LC-DG treatment. Conclusion LC-DG and its PB attenuate the inflammatory mucosal response in an ex-vivo organ culture model of PI-IBS D.

The prevalence of metabolic disorders, such as type 2 diabetes (T2D), obesity, and non-alcoholic fatty liver disease (NAFLD), which are common risk factors for cardiovascular disease (CVD), has dramatically increased worldwide over the last decades. Although dietary habit is the main etiologic factor, there is an imperfect correlation between dietary habits and the development of metabolic disease. Recently, research has focused on the role of the microbiome in the development of these disorders. Indeed, gut microbiota is implicated in many metabolic functions and an altered gut microbiota is reported in metabolic disorders. Here we provide evidence linking gut microbiota and metabolic diseases, focusing on the pathogenetic mechanisms underlying this association.

Gastric cancer (GC) still represents one of the leading causes of cancer-related mortality and is a major public health issue worldwide. Understanding the etiopathogenetic mechanisms behind GC development holds immense potential to revolutionize patients’ treatment and prognosis. Within the complex web of genetic predispositions and environmental factors, the connection between Helicobacter pylori (H. pylori) and gastric microbiota emerges as a focus of intense research investigation. According to the most recent hypotheses, H. pylori triggers inflammatory responses and molecular alterations in gastric mucosa, while non-Helicobacter microbiota modulates disease progression. In this review, we analyze the current state of the literature on the relationship between H. pylori and non-Helicobacter gastric microbiota in gastric carcinogenesis, highlighting the mechanisms by which microecological dysbiosis can contribute to the malignant transformation of the mucosa.

Hepatic encephalopathy (HE) is a severe complication of advanced liver disease and acute liver failure. The clinical spectrum ranges from minor cognitive dysfunctions to lethargy, depressed consciousness, and coma and significantly impact the quality of life, morbidity, and mortality of the patients. It is commonly accepted that the gut milieu is essential for the development of HE; however, despite intensive research efforts, the pathogenesis of HE is still not fully elucidated. As our knowledge of gut microbiota moves from the pioneering era of culture-dependent studies, the connection between microbes, inflammation, and metabolic pathways in the pathogenesis of HE is becoming increasingly clear, providing exciting therapeutic perspectives. This review will critically examine the latest research findings on the role of gut microbes in the pathophysiological pathways underlying HE. Moreover, currently available therapeutic options and novel treatment strategies are discussed.

The presence of significant fibrosis is an indicator for liver disease staging and prognosis. The aim of the study was to determine reproducibility of real-time shear wave elastography using a hepatic biopsy as the reference standard to identify patients with chronic liver disease. Forty patients with chronic liver disease and 12 normal subjects received shear wave elastography performed by skilled operators. Interoperator reproducibility was studied in 29 patients. Fibrosis was evaluated using the Metavir score. The median and range shear wave elastography values in chronic liver disease subjects were 6.15 kPa and 3.14-16.7 kPa and were 4.49 kPa and 2.92-7.32 kPa in normal subjects, respectively. With respect to fibrosis detected by liver biopsy, shear wave elastography did not change significantly between F0 and F1 (p = 0.334), F1 and F2 (p = 0.611), or F3 and F4 (0.327); a significant difference was observed between the F0-F2 and F3-F4 groups (p = 0.002). SWE also correlated with inflammatory activity (Rs = 0.443, p = 0.0023) and ALT levels (Rs = 0.287, p = 0.0804). Age, sex and body mass index did not affect shear wave elastography measurements. Using receiver operator characteristic curves, two threshold values for shear wave elastography were identified: 5.62 kPa for patients with fibrosis (≥F2; sensitivity 80%, specificity 69.4%, and accuracy 77%) and 7.04 kPa for patients with severe fibrosis (≥F3; sensitivity 88.9%, specificity 81%, and accuracy 89%). Overall interobserver agreement was excellent and was analysed using an interclass correlation coefficient (0.94; CI 0.87-0.97).This study shows that shear wave elastography executed by skilled operators can be performed on almost all chronic liver disease patients with high reproducibility. It is not influenced by age, sex or body mass index, identifies severely fibrotic patients and is also related to inflammatory activity.

The gut microbiota may have an impact on obesity. To date, the majority of studies in obese patients reported microbiota composition in stool samples. The aim of this study was to investigate the duodenal mucosa dysbiosis in adult obese individuals from Campania, a region in Italy with a very high percentage of obese people, to highlight microbial taxa likely associated with obesity. Duodenum biopsies were taken during upper gastrointestinal endoscopy in 19 obese (OB) and 16 lean control subjects (CO) and microbiome studied by 16S rRNA gene sequencing. Duodenal microbiome in our groups consisted of six phyla: Proteobacteria, Firmicutes, Actinobacteria, Fusobacteria, Bacteroidetes and Acidobacteria. Proteobacteria (51.1% vs. 40.1%) and Firmicutes (33.6% vs. 44.9%) were significantly (p < 0.05) more and less abundant in OB compared with CO, respectively. Oribacterium asaccharolyticum, Atopobium parvulum and Fusobacterium nucleatum were reduced (p < 0.01) and Pseudomonadales were increased (p < 0.05) in OB compared with CO. Receiver operating characteristic curve analysis showed Atopobium and Oribacterium genera able to discriminate with accuracy (power = 75% and 78%, respectively) OB from CO. In conclusion, increased Proteobacteria and decreased Firmicutes (Lachnospiraceae) characterized the duodenal microbiome of obese subjects. These data direct to further studies to evaluate the functional role of the dysbiotic-obese-associated signature.

Background The gut microbiota plays a key role in the progression of chronic liver disease and the development of hepatocellular carcinoma (HCC). However, findings on microbiota composition in such patients remain inconsistent, likely due to differences in disease aetiology and sample type. The mucosa-associated microbiota (MAM), residing in the intestinal mucin layer, more accurately reflects mucosal health than faecal microbiota, being more stable and less influenced by diet. This study aimed to characterise the ileal and sigmoid MAM in patients with chronic hepatitis C (CHC), liver cirrhosis (LC), and HCC. Methods We performed DNA metabarcoding sequencing of mucosa samples collected from the ileum and sigmoid colon of patients at different stages of liver disease and healthy controls (HC). The predicted functions were analysed via phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt2) to infer metabolic pathways that can be expressed in the microbiome. Results Among 33 participants (20 HCV-related liver disease and 13 healthy controls), MAM α-diversity decreased significantly in advanced disease stages, particularly in LC and HCC, regardless of the metric applied ( p  ≤ 0.05). β-diversity analyses showed distinct microbial community structures across groups. Both ileal and sigmoid MAM were dominated by Bacteroidetes, Firmicutes, and Proteobacteria, with enrichment of Firmicutes_D, Proteobacteria, and Fusobacteria in LC and HCC. Several genera, including Bulleidia , Pantoea , Clostridium_Q , Rothia , and Streptococcus , were significantly increased in HCC, whereas beneficial taxa such as Akkermansia and Butyricimonas were depleted. Functional predictions indicated enrichment of degradative pathways (e.g., taurine, chitin derivatives, and carbohydrate metabolism) in LC and HCC. Conclusion Our pilot study suggests that MAM alterations do not directly mirror liver disease progression but show distinct patterns associated with different stages. These associations, more evident in advanced disease, involve bacterial taxa linked to gut integrity, inflammation, and carcinogenesis. This exploratory work lays the groundwork for future studies to validate these findings and investigate their relevance to microbiome-based diagnostics and therapies in HCC.

Obesity is a multifactorial disorder, and the gut microbiome has been suggested to contribute to its onset. In order to better clarify the role of the microbiome in obesity, we evaluated the metatranscriptome in duodenal biopsies from a cohort of 23 adult severely obese and lean control subjects using next generation sequencing. Our aim was to provide a general picture of the duodenal metatranscriptome associated with severe obesity. We found altered expressions of human and microbial genes in the obese compared to lean subjects, with most of the gene alterations being present in the carbohydrate, protein, and lipid metabolic pathways. Defects were also present in several human genes involved in epithelial intestinal cells differentiation and function, as well as in the immunity/inflammation pathways. Moreover, the microbial taxa abundance inferred by our transcriptomic data differed in part from the data that we previously evaluated by 16S rRNA in 13/23 individuals of our cohort, particularly concerning the Firmicutes and Proteobacteria phyla abundances. In conclusion, our pilot study provides the first taxonomic and functional characterization of duodenal microbiota in severely obese subjects and lean controls. Our findings suggest that duodenal microbiome and human genes both play a role in deregulating metabolic pathways, likely affecting energy metabolism and thus contributing to the obese phenotype.

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

AimCancer, particularly gastric cancer (GC), is prevalently an epigenetic phenomenon that is dependent on an altered DNA methylation pattern. In gastric carcinogenesis, many genes show aberrant methylation; however, none of them may be used as a biomarker of cancer risk and progression. The authors aimed to evaluate the global DNA methylation of gastric mucosa in Helicobacter pylori (Hp)-related chronic gastritis, in GC and in 10 patients with preneoplastic lesions (ie, atrophy and intestinal metaplasia) followed up for 10 years.MethodsThe authors analysed 93 dyspeptic patients who underwent upper endoscopy, 41 surgical GC samples and 10 patients with preneoplastic gastric lesions followed up for 10 years after successful Hp eradication therapy. Global DNA methylation status and surrogate markers of cell proliferation and apoptosis were evaluated by immunohistochemistry using the anti-5-methylcytosine (5-MC), anti-Ki-67 and anti-p53 (anti-apoptotic marker)-specific antibodies, respectively.ResultsGlobal DNA methylation of gastric mucosa gradually decreased from normal mucosa to Hp-positive gastritis, Hp-positive chronic atrophic gastritis, independent of Cag-A status and GC; however, the variation was significant (p<0.05) only between Hp-negative subjects and Hp-positive chronic gastritis. Interestingly, the 5-MC immunostaining was absent in areas of intestinal metaplasia. In the 10 patients with preneoplastic lesions, global DNA methylation decreased over time despite the eradication of Hp infection, but reached significance only at 10 years versus baseline. The 5-MC immunostaining negatively correlated with Ki-67 and p53 expression in all groups.ConclusionGlobal DNA hypomethylation is an early molecular event in Hp-related gastric carcinogenesis. Further studies with more cases and a longer follow-up are needed to establish the potential GC predictive role of DNA hypomethylation.