Recent advances have highlighted the gut microbiota as a significant contributor to the development and progression of atherosclerosis, which is an inflammatory cardiovascular disease (CVD) characterized by plaque buildup within arterial walls. The gut microbiota, consisting of a diverse collection of microorganisms, impacts the host’s metabolism, immune responses, and lipid processing, all of which contribute to atherosclerosis. This review explores the complex mechanisms through which gut dysbiosis promotes atherogenesis. We emphasize the potential of integrating microbiota modulation with traditional cardiovascular care, offering a holistic approach to managing atherosclerosis. Important pathways involve the translocation of inflammatory microbial components, modulation of lipid metabolism through metabolites such as trimethylamine-N-oxide (TMAO), and the production of short-chain fatty acids (SCFAs) that influence vascular health. Studies reveal distinct microbial profiles in atherosclerosis patients, with increased pathogenic bacteria (Megamonas, Veillonella, Streptococcus) and reduced anti-inflammatory genera (Bifidobacterium, Roseburia), highlighting the potential of these profiles as biomarkers and therapeutic targets. Probiotics are live microorganisms that have health benefits on the host. Prebiotics are non-digestible dietary fibers that stimulate the growth and activity of beneficial gut bacteria. Interventions targeting microbiota, such as probiotics, prebiotics, dietary modifications, and faecal microbiota transplantation (FMT), present effective approaches for restoring microbial equilibrium and justifying cardiovascular risk. Future research should focus on longitudinal, multi-omics studies to clarify causal links and refine therapeutic applications.

Depression is a global health problem that requires an early and accurate diagnosis to ensure quick access to appropriate treatment. Among multiple psychopathological paths, recent attention has focused on analysing the brain–gut–microbiota axis. The intestinal barrier plays a key role, and dysfunctions occurring at this level have implications for mental health. The aim of the present study was to investigate the role of intestinal permeability biomarkers, i.e., calprotectin, zonulin, lipopolysaccharide-binding protein (LBP) and intestinal fatty acid-binding protein (I-FAB), in relation to depression in patients with inflammatory bowel disease (IBD). This is the first study of this kind taking place in Romania, Eastern Europe, with an emphasis on patients with Crohn’s disease and ulcerative colitis. The correlations identified between depression and calprotectin and depression and LBP have the potential to shed light on the process of rapid diagnosis of depression with the help of biomarkers. Since depression is correlated with a decrease in the quality of life in patients with IBD, the need for access to appropriate treatments must be urgent.

Our study highlighted the immune changes by pro-inflammatory biomarkers in the gut–liver-axis-linked ROS-cell death mechanisms in chronic and acute inflammations when gut cells are exposed to endotoxins in patients with hepatic cirrhosis or steatosis. In duodenal tissue samples, gut immune barrier dysfunction was analyzed by pro-inflammatory biomarker expressions, oxidative stress, and cell death by flow cytometry methods. A significant innate and adaptative immune system reaction was observed as result of persistent endotoxin action in gut cells in chronic inflammation tissue samples recovered from hepatic cirrhosis with the A-B child stage. Instead, in patients with C child stage of HC, the endotoxin tolerance was installed in cells, characterized by T lymphocyte silent activation and increased Th1 cytokines expression. Interesting mechanisms of ROS-cell death were observed in chronic and acute inflammation samples when gut cells were exposed to endotoxins and immune changes in the gut–liver axis. Late apoptosis represents the chronic response to injury induction by the gut immune barrier dysfunction, oxidative stress, and liver-dysregulated barrier. Meanwhile, necrosis represents an acute and severe reply to endotoxin action on gut cells when the immune system reacts to pro-inflammatory Th1 and Th2 cytokines releasing, offering protection against PAMPs/DAMPs by monocytes and T lymphocyte activation. Flow cytometric analysis of pro-inflammatory biomarkers linked to oxidative stress-cell death mechanisms shown in our study recommends laboratory techniques in diagnostic fields.

Recent research indicates that the microbiome has a significant impact on the progression of inflammatory bowel disease (IBD) and that creating therapies that change its composition could positively impact the outcomes of IBD treatment. This review summarizes the results of extensive studies that examined IBD patients undergoing several therapies, including anti-TNF medication, vedolizumab, ustekinumab, probiotics, and fecal microbiota transplantation (FMT), and the alterations in their gut microbiota’s composition and function. The objective was to investigate the variety and effectiveness of microbial species in order to discover new biomarkers or therapeutic targets that could improve the outcome of treatment for these patients. This research aimed to offer useful insights into personalized medicine techniques for managing IBD. Beneficial bacteria such as Faecalibacterium prausnitzii and Roseburia have been consistently linked to favorable clinical outcomes, whereas pathogenic bacteria such as Escherichia coli and Clostridioides difficile are associated with worsening disease conditions. Although many studies have examined the role of gut microbiota in IBD, there is still a need for more targeted research on the connection between specific microbial communities and treatment outcomes. This study sought to address this gap by exploring the intricate relationship between the gut microbiota composition and the effectiveness of IBD medications.

Background: Recent studies have shown that gut microbiota have important roles in different human diseases. There has been an ever-increasing application of high-throughput technologies for the characterization of microbial ecosystems. This led to an explosion of various molecular profiling data, and the analysis of such data has shown that machine-learning algorithms have been useful in identifying key molecular signatures. Results: In this review, we first analyze how dysbiosis of the intestinal microbiota relates to human disease and how possible modulation of the gut microbial ecosystem may be used for disease intervention. Further, we introduce categories and the workflows of different machine-learning approaches and how they perform integrative analysis of multi-omics data. Last, we review advances of machine learning in gut microbiome applications and discuss challenges it faces. Conclusions: We conclude that machine learning is indeed well suited for analyzing gut microbiome and that these approaches are beneficial for developing gut microbe-targeted therapies, helping in achieving personalized and precision medicine.

Recent research highlights a potential link between metabolic dysfunction–associated steatotic liver disease (MASLD) and intestinal barrier dysfunction. Increased intestinal permeability (IP) may facilitate the translocation of bacteria, endotoxins (e.g., lipopolysaccharides [LPS]), and pathogen-associated molecular patterns into the portal venous system, fostering a pro-inflammatory environment and contributing to liver inflammation. This study aimed to identify correlations between intestinal barrier biomarkers (occludin, LPS, and intestinal-type fatty-acid-binding proteins [I-FABP]) and MASLD. A single-center prospective cross-sectional study was conducted, including 72 MASLD patients and 68 healthy controls. Fibroscan-controlled attenuation parameter (CAP) was performed in all subjects. Blood samples were analyzed for biochemical parameters, and serum levels of occludin, LPS, and I-FABP were measured using the ELISA method with the Human occludin, LPS, and I-FABP ELISA Kit test systems (FineTest, Wuhan, China). LPS and I-FABP levels were significantly higher in MASLD patients compared to controls, with the highest LPS levels observed in the diabetic MASLD subgroup. Occludin levels showed no statistically significant differences between groups. All 3 biomarkers were positively correlated with BMI, with the highest levels in obese subjects. LPS was positively correlated with CRP levels. Using Fibroscan-CAP, we found a positive correlation between LPS and both liver stiffness and CAP score, as well as between I-FABP and liver stiffness. MASLD patients exhibit increased IP, with enterocyte injury present irrespective of diabetes status, though more pronounced in diabetic MASLD. Occludin does not appear to be a reliable biomarker for evaluating intestinal barrier function in MASLD. Obesity is linked to elevated biomarkers, suggesting an association between increased IP and obesity. I-FABP and LPS may serve as noninvasive biomarkers for assessing hepatic fibrosis and steatosis in MASLD patients. Notably, LPS, given its correlation with elevated CRP levels, could be utilized as a marker of disease progression and severity.