Search Results (1,429)

Objective: To analyze the composition of the oral microbiome in periodontal pocket lesions and on the tongue dorsum of patients with Helicobacter pylori-associated gastric disease. Materials and Methods: Patients diagnosed with gastric disease and H. pylori (HP+) were evaluated in comparison to a control group of H. pylori-negative patients without gastric disease (HP−). Periodontal and oral health clinical parameters (PPD, BoP, PSE, plaque score and modified DMFT) were assessed for each patient. Microbiological samples were collected from the deepest periodontal pockets and tongue dorsum, followed by DNA extraction, 16S rRNA PCR amplification, and Next-Generation-Sequencing (NGS) analyses. Results: Sixty-seven patients (27F; 40M, aged 35–85 years) were enrolled. Of these, 52 were HP+ and 15 were HP−. HP+ patients exhibited a significantly higher presence of decayed teeth (p < 0.05) and slightly fewer missing teeth (p > 0.05). The plaque score was significantly higher in HP+ patients (p < 0.05), while PPD and BoP showed no significant differences (p > 0.05). NGS analysis revealed no presence of H. pylori in any samples of both periodontal and tongue sites. HP+ patients showed a distinct microbial composition, including higher prevalence of Capnocytophaga, Fusobacterium, and Peptostreptococcus genera in both locations (pockets and tongue dorsum). Conclusions: The study demonstrated that HP+ patients exhibit distinct oral microbial profiles compared to HP− patients, especially in areas with deeper periodontal pockets. H. pylori was not detected in the oral microbiomes of either group. Full article

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a major global health challenge characterized by complex adipose–liver interactions mediated by adipokines and hepatokines. Despite rapid field evolution, a comprehensive understanding of research trends and translational advances remains fragmented. This study systematically maps the scientific landscape through bibliometric analysis, identifying emerging domains and future clinical translation directions. Methods: A comprehensive bibliometric analysis of 1002 publications from 2004 to 2025 was performed using thematic mapping, temporal trend evaluation, and network analysis. Analysis included geographical and institutional distributions, thematic cluster identification, and research paradigm evolution assessment, focusing specifically on adipokine–hepatokine signaling mechanisms and clinical implications. Results: The United States and China are at the forefront of research output, whereas European institutions significantly contribute to mechanistic discoveries. The thematic map analysis reveals the motor/basic themes residing at the heart of the field, such as insulin resistance, fatty liver, metabolic syndrome, steatosis, fetuin-A, and other related factors that drive innovation. Basic clusters include metabolic foundations (obesity, adipose tissue, FGF21) and adipokine-centered subjects (adiponectin, leptin, NASH). New themes focus on inflammation, oxidative stress, gut microbiota, lipid metabolism, and hepatic stellate cells. Niche areas show targeted fronts such as exercise therapies, pediatric/novel adipokines (chemerin, vaspin, omentin-1), and advanced molecular processes that focus on AMPK and endoplasmic-reticulum stress. Temporal analysis shows a shift from single liver studies to whole models that include the gut microbiota, mitochondrial dysfunction, and interactions between other metabolic systems. The network analysis identifies nine major clusters: cardiovascular–metabolic links, adipokine–inflammatory pathways, hepatokine control, and new therapeutic domains such as microbiome interventions and cellular stress responses. Conclusions: In summary, this study delineates current trends and emerging areas within the field and elucidates connections between mechanistic research and clinical translation to provide guidance for future research and development in this rapidly evolving area. Full article

Currently, due to the complexity of obtaining samples, specific features of laboratory processing and analysis of the results, there is a lack of data on the microbial signature of the small intestine in healthy and diseased states of the upper gastrointestinal tract. Objective: To investigate the characteristics of the small intestinal microbiome in acute pancreatitis of varying severity and to identify correlations with clinical factors. Methods: This study included 30 patients with acute pancreatitis of varying severity treated between 1 January 2019 and 31 December 2021. The composition of the microbiota was analyzed by metagenomic sequencing of the 16S rRNA gene from jejunal samples. Results: The mortality rate in the study group was 23.3%. The small intestinal microbiome was dominated by Streptococcus (median relative abundance 19.2%, interquartile range 6.4–35.1%), Veillonella (3.4%; 0.6–7%), Granulicatella (2.7%; 0.6–5%), Fusobacterium (2.2%; 0.3–5.9%), Prevotella (1.5%; 0.3–8%), Haemophilus (0.9%; 0.2–10%), Gemella (0.8%; 0.2–4.3%), and Lactobacillus (0.2%; 0.1–0.9%). More severe disease was associated with decreased abundance of Neisseria mucosa, Parvimonas micra, and Megasphaera micronuciformis. In contrast, the relative abundance of the genera Streptococcus (species S. rubneri/parasanguinis/australis), Actinomyces, and several genera within the family Enterobacteriaceae was higher in these patients. Conclusions: The state of the microbiota has important prognostic value and correlates with the duration from the onset of the pain syndrome to the time of receiving qualified care in the hospital. Full article

Background/Objectives: Endometriosis is a chronic, estrogen-driven gynecological disorder affecting approximately 10% of reproductive-aged women worldwide, with significant physical, psychosocial, and socioeconomic impacts. Recent research suggests a possible involvement of the gut microbiome in endometriosis disease mechanisms through immune manipulation, estrogen metabolism, and inflammatory networks. This narrative review aims to summarize current evidence on gut microbiota changes in endometriosis patients, explore the mechanisms by which gut dysbiosis contributes to disease progression, and examine epidemiological links between gastrointestinal health and endometriosis risk. Methods: A narrative review was conducted to synthesize available literature on the compositional changes in gut microbiota associated with endometriosis. The review also evaluated studies investigating potential mechanisms and epidemiological patterns connecting gut health with endometriosis development and severity. Results: Alterations in gut microbiota composition were observed in endometriosis patients, suggesting roles in immune dysregulation, estrogen metabolism, and inflammation. Potential gut-oriented interventions, including dietary changes, probiotics, and lifestyle modifications, emerged as promising management options. However, methodological variability and research gaps remain barriers to clinical translation. Conclusions: Integrating gut microbiome research into endometriosis management holds potential for improving early diagnosis, patient outcomes, and healthcare system sustainability. The study emphasizes the need for further research to address existing challenges and to develop public health strategies that incorporate microbiome-based interventions in population-level endometriosis care. Full article

Background/Objectives: Chronic inflammation and Western-style diets elevate colorectal cancer (CRC) risk, particularly in individuals with colitis, a feature of inflammatory bowel disease (IBD). Diets rich in polyphenol-containing functional foods, such as cocoa, may reduce gut inflammation and modulate the gut microbiome. This study investigated the impact of cocoa polyphenol (CP) supplementation on inflammation and microbiome composition in mice with colitis, fed either a healthy or Western diet, before, during, and after the onset of disease. We hypothesized that CPs would attenuate inflammation and promote distinct shifts in the microbiome, especially in the context of a Western diet. Methods: A 2 × 2 factorial design tested the effects of the basal diet (AIN93G vs. total Western diet [TWD]) and CP supplementation (2.6% w/w CocoaVia™ Cardio Health Powder). Inflammation was induced using the AOM/DSS model of colitis. Results: CP supplementation did not reduce the severity of colitis, as measured by disease activity index or histopathology. CPs did not alter gene expression in healthy tissue or suppress the colitis-associated pro-inflammatory transcriptional profile in either of the two diet groups. However, fecal microbiome composition shifted significantly with CPs before colitis induction, with persistent effects on several rare taxa during colitis and recovery. Conclusions: CP supplementation did not mitigate inflammation or mucosal injury at the tissue level, nor did it affect the expression of immune-related genes. While CPs altered microbiome composition, most notably in healthy mice before colitis, these shifts did not correspond to changes in inflammatory signaling. Basal diet remained the primary determinant of inflammation, mucosal damage, and colitis severity in this model. Full article

Aging is associated with complex immune dysfunction that contributes to the onset and progression of the “geriatric giants”, including frailty, sarcopenia, cognitive decline, falls, and incontinence. Central to these conditions is immunosenescence, marked by thymic involution, the loss of naïve T cells, T-cell exhaustion, impaired B-cell class switch recombination, and increased autoreactivity. Concurrently, innate immunity deteriorates due to macrophage, neutrophil, and NK cell dysfunction, while chronic low-grade inflammation—or “inflammaging”—amplifies systemic decline. Key molecular pathways such as NF-κB, mTOR, and the NLRP3 inflammasome mediate immune aging, interacting with oxidative stress, mitochondrial dysfunction, and epigenetic modifications. These processes not only impair infection control and vaccine responsiveness but also promote tissue degeneration and multimorbidity. This review explores emerging interventions—ranging from senolytics and immunonutrition to microbiome-targeted therapies and exercise—that may restore immune homeostasis and extend healthspan. Despite advances, challenges remain in translating immunological insights into clinical strategies tailored to older adults. Standardization in microbiome trials and safety optimization in senolytic therapies are critical next steps. Integrating geroscience into clinical care could help to mitigate the burden of aging-related diseases by targeting fundamental drivers of immune dysfunction. Full article

Background: Myeloproliferative neoplasms (MPN), a group of chronic hematologic neoplasms, are driven by inflammatory mechanisms that influence disease initiation and progression. Emerging evidence highlights the gut microbiome and plasma metabolome as pivotal immunomodulators, yet their causal roles in MPN pathogenesis remain uncharacterized. Methods: We conducted a two-sample Mendelian randomization (MR) analysis to systematically evaluate causal relationships between 196 gut microbial taxa, 526 plasma metabolites, and MPN risk. Instrumental variables were derived from genome-wide association studies (GWASs) of microbial/metabolite traits. Validation utilized 16S rRNA sequencing data from NCBI Bioproject PRJNA376506. Mediation and multivariable MR analyses elucidated metabolite-mediated pathways linking microbial taxa to MPN. Results: Our MR analysis revealed that 7 intestinal taxa and 17 plasma metabolites are causally linked to MPN. External validation confirmed the three taxa’s differential abundance in MPN cohorts. Mediation analysis revealed two mediated relationships, of which succinylcarnitine mediated 14.5% of the effect, and lysine 27.9%, linking the Eubacterium xylanophilum group to MPN. Multivariate MR analysis showed that both succinylcarnitine (p = 0.004) and lysine (p = 0.040) had a significant causal effect on MPN. Conclusions: This study identifies novel gut microbiota–metabolite axes driving MPN pathogenesis through immunometabolic mechanisms. The validated biomarkers provide potential therapeutic targets for modulating inflammation in myeloproliferative disorders. Full article

Short-chain fatty acids (SCFAs) are metabolites derived from the fermentation of dietary fibre by gut bacteria. SCFAs function as essential regulators of host-microbiome interactions by participating in numerous physiological and pathological processes within the gastrointestinal (GI) tract. In recent years, the depletion of SCFAs has been increasingly linked to the pathogenesis of GI diseases. In this review, we summarize the current understanding of the therapeutic mechanisms of SCFAs in GI diseases, including inflammatory bowel disease, irritable bowel syndrome, metabolic dysfunction-associated steatotic liver disease, and acute pancreatitis. We next highlight potential therapeutic approaches that increase the endogenous production of SCFAs, including prebiotics, probiotics, and fecal microbiota transplantation. We conclude that, although SCFAs are promising therapeutic agents, further research is necessary due to variability in treatment efficacy, inconsistent clinical outcomes, and a limited understanding of SCFAs’ mechanisms of action. Full article

Background/Objectives: Gut dysbiosis has been implicated in multiple sclerosis (MS), but microbial signatures remain inconsistent across studies. Machine learning (ML) algorithms based on global microbiome data integration can reveal key disease-associated microbial biomarkers and new insights into MS pathogenesis. This study aimed to investigate gut microbial signatures associated with MS and to evaluate the potential of ML for diagnostic applications. Methods: Fecal samples from 29 relapsing–remitting MS patients during exacerbation and 27 healthy controls were analyzed using 16S rRNA gene sequencing. Differential abundance analysis was performed, and data were integrated with 29 published studies. Four ML models were developed to distinguish MS-associated microbiome profiles. Results: MS patients exhibited reduced levels of Eubacteriales (p = 0.037), Lachnospirales (p = 0.021), Oscillospiraceae (p = 0.013), Lachnospiraceae (p = 0.012), Parasutterella (p = 0.018), Faecalibacterium (p = 0.004), and higher abundance of Lachnospiraceae UCG-008 (p = 0.045) compared to healthy controls. The Light Gradient Boosting Machine classifier demonstrated the highest performance (accuracy: 0.88, AUC-ROC: 0.95) in distinguishing MS microbiome profiles from healthy controls. Conclusions: This study highlights specific microbiome dysbiosis in MS patients and supports the potential of ML for diagnostic applications. Further research is needed to elucidate the mechanistic role of these microbial alterations in MS progression and their therapeutic utility. Full article

The interaction between epigenetic mechanisms and the gut microbiome is potentially crucial for the development and maintenance of intestinal health. Lysine acetylation, an important post-translational modification, plays a complex and critical role in the epigenetic regulation of the host by the gut microbiota. However, there are currently no reports on how gut microbiota dysbiosis affects host physiology in early life through global lysine acetylation. In this study, we constructed a mouse model of gut microbiota dysbiosis using antibiotic cocktail therapy (ABX). Using liquid chromatography-tandem mass spectrometry (LC-MS/MS) in the cecum, we analyzed the cecal lysine acetylome and proteome. As a result, we profiled the lysine acetylation landscape of the cecum and identified a total of 16,579 acetylation sites from 5218 proteins. Differentially acetylated proteins (DAPs) are involved in various metabolic pathways, including the citrate cycle (TCA cycle), butanoate metabolism, pyruvate metabolism, glycolysis/gluconeogenesis, and fatty acid biosynthesis. Moreover, both glycolysis and gluconeogenesis are significantly enriched in acetylation and protein modifications. This study aimed to provide valuable insights into the epigenetic molecular mechanisms associated with host protein acetylation as influenced by early-life gut microbiota disturbances. It reveals potential therapeutic targets for metabolic disorders linked to gut microbiota dysbiosis, thereby establishing a theoretical foundation for the clinical prevention and treatment of diseases arising from such dysbiosis. Full article

Colorectal cancer (CRC) is associated with factors such as an unhealthy diet, physical inactivity, obesity, diabetes, and chronic inflammatory conditions like inflammatory bowel disease (IBD), as well as TP53 mutations, which are observed in a broad spectrum of CRC. Additionally, alteration in the composition of the gut microbiome community and metabolism plays a significant role in the development of colorectal cancer and its therapeutic effects. It is well known that treatment with sodium butyrate (NaB), an intestinal microbial metabolite, can induce apoptosis by activating histone deacetylase (HDAC) in cancer cells. Therefore, this study examined the relationship between NaB-induced apoptosis and p53 protein level in colorectal cancer cells. Treatment with NaB triggered cell death in the HCT116 cell line. Furthermore, a notable elevation in p53 protein level was detected following treatment with a high concentration of NaB, compared to both the control group and the low concentration NaB. Furthermore, apoptotic cell death was diminished in a p53-deficient cell line (HCT 116 p53^−/−) and p53 protein expression was more stabilized. Although p53 mRNA expression was not affected, acetylation of p53 protein was clearly observed by high concentration NaB treatment. To demonstrate the relationship between p53 acetylation and cell death, HT29 cells were treated with a high concentration of NaB. In HT29 cells with a mutation in the p53 gene, increased cell viability, overproduction p53 protein, and hyperacetylation of p53 were observed compared to the control. The results of this study suggest that p53 protein expression plays an important role in the effectiveness of therapy utilizing gut microbiota metabolites. Full article

Background: Depression is a mental disorder characterized by a combination of somatic and cognitive disturbances, in which a predominantly sad or irritable mood significantly interferes with the patient’s functioning. This condition can affect individuals of all ages and socioeconomic backgrounds. Currently, various studies are exploring a possible association between oral dysbiosis and depression—an increasingly relevant topic, as confirmation of such a relationship could position the oral microbiota as a potential etiological or diagnostic factor for depression, given its accessibility and ease of analysis. Aim: To present a qualitative synthesis of studies addressing how oral dysbiosis influences the onset of depression, as well as the importance of controlling this alteration of the oral microbiota to aid in the prevention of the disease. Materials and Methods: The PRISMA guidelines (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) outline the procedures to be followed for conducting this systematic review. The article search was carried out on 22 May 2025, across the PubMed, Scopus, Scielo, and The Cochrane Library databases, using terms related to “depression” and “oral dysbiosis”. Studies published within the last 10 years that addressed the potential association between oral dysbiosis, and depression were included. Furthermore, the quality of the studies was assessed using various tools depending on their design: the Newcastle–Ottawa Scale (NOS) was applied to case-control and cohort studies; the Joanna Briggs Institute (JBI) critical appraisal checklist was used for cross-sectional studies; and experimental studies were evaluated using SYRCLE’s Risk of Bias Tool. Results: A total of eleven studies were included in this systematic review. The findings suggest the presence of alterations in the oral microbiota of patients with depression, particularly in terms of composition, structure, and diversity. A reduction in alpha diversity—an indicator of local microbial balance—was observed, along with an increase in beta diversity, indicating greater inter-individual variability, which may be associated with inflammatory processes or immunological dysfunctions. Some studies reported differing results, which may be attributable to methodological variability regarding study design, or the populations sampled. Conclusions: This systematic review suggests that the oral microbiome could be considered a diagnostic biomarker and therapeutic target for depression, as the analyzed studies demonstrate a significant association between oral microbiome dysbiosis and this mental disorder. However, the methodological heterogeneity among the studies highlights the need for further research to confirm this potential relationship. Full article

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the selective loss of dopaminergic neurons in the substantia nigra, resulting in motor symptoms such as bradykinesia, tremor, rigidity, and postural instability, as well as a wide variety of non-motor manifestations. Branched-chain amino acids (BCAAs)—leucine, isoleucine, and valine—are essential nutrients involved in neurotransmitter synthesis, energy metabolism, and cellular signaling. Emerging evidence suggests that BCAA metabolism is intricately linked to the pathophysiology of PD. Dysregulation of BCAA levels has been associated with energy metabolism, mitochondrial dysfunction, oxidative stress, neuroinflammation, and altered neurotransmission. Furthermore, the branched-chain ketoacid dehydrogenase kinase (BCKDK), a key regulator of BCAA catabolism, has been implicated in PD through its role in modulating neuronal energetics and redox homeostasis. In this review, we synthesize current molecular, genetic, microbiome, and clinical evidence on BCAA dysregulation in PD to provide an integrative perspective on the BCAA–PD axis and highlight directions for future translational research. We explored the dualistic role of BCAAs as both potential neuroprotective agents and metabolic stressors, and critically examined the therapeutic prospects and limitations of BCAA supplementation and BCKDK targeting. Full article

Increasing evidence demonstrates the mutualistic connection between the microbiome and acute myeloid leukemia (AML) treatment. Drugs disrupt the microbial balance and, conversely, changes in the microbiome influence therapy. A new field, pharmacomicrobiomics, examines the role of the microbiome in pharmacokinetics, pharmacodynamics, and drug toxicity. The multimodal therapeutic management of AML, along with disease-related immunosuppression, infection, and malnutrition, creates the unique microbial profile of AML patients, in which every delicate modification plays a crucial role in pharmacotherapy. While both preclinical and real-world data have confirmed a bilateral connection between standard chemotherapy and the microbiome, the impact of novel targeted therapies and immunotherapy remains unknown. Multi-omics technologies have provided qualitative and mechanistic insights into specific compositional and functional microbial signatures associated with the outcomes of AML therapy, but require a large-scale investigation to draw reliable conclusions. In this review, we outline the role of the microbiome within the therapeutic landscape of AML, focusing on the determinants of post-treatment dysbiosis and its effects on the therapeutic response and toxicity. We explore emerging strategies for microbiota modulation, highlighting their safety and efficacy. Advances in microbiome-based approaches are an inevitable step toward precision medicine in AML. However, clinical research in a well-defined group of immunocompromised patients is needed to study their variable effects on human health and determine safety issues. Full article

Psoriasis is a chronic inflammatory autoimmune disease that causes significant deterioration of the quality of life, and due to its multifactorial causes, it is often difficult to manage. Apart from genetic and environmental components, an important part of its pathophysiology comprises an oxidative stress induction that the standard antioxidative mechanisms of the human body cannot compensate for. Moreover, in many psoriatic patients, there is a documented imbalance between antioxidant and pro-oxidative factors. Usually, psoriasis is evaluated using the Psoriasis Area and Severity Index (PASI) score. It has been demonstrated that dietary choices can lead to significant modification of PASI scores. Hypocaloric diets that are rich in antioxidants are highly effective in this regard, especially when focusing on vegetables and restricting consumption of animal-derived protein. Specific dietary regimens, namely the Mediterranean diet and potentially the ketogenic diet, are very beneficial, in the former case owing in large part to the omega-three fatty acids it provides and its ability to alter gut microbiome, a factor which seems to play a notable role in the pathogenesis of the disease. Another option is the topical application of vitamin D and its analogues, combined with corticosteroids, which can ameliorate the manifestations of psoriasis at the level of the skin. Finally, oral vitamin D supplementation has a positive impact on psoriatic arthritis and can mitigate the risk of associated comorbidities. Full article