Search Results (972)

The application of essential oils and plant extracts as natural food preservatives has gained increasing interest; however, their potential impacts on gut health and host physiology remain unknown. This study evaluated the effects of synergistic combinations of peppermint essential oil (EO) + thyme EO and peppermint EO + feijoa peel extract on gut microbiota composition and colonic morphology in a rat model. Sprague–Dawley rats were orally given the synergistic combinations daily for 28 days, and their effects were assessed using 16S rRNA gene sequencing of the caecum microbiota and histological analysis of proximal colon tissues. Alpha diversity metrics showed no significant differences (p > 0.05) between treatment and control groups, and beta diversity indicated no treatment-related shift in the bacterial communities. Taxonomic profiling at the phylum, family, and genus levels showed comparable relative abundances of dominant microbial taxa across all treatments, with no evidence of dysbiosis. Histological examination of proximal colon tissues revealed no significant changes in crypt depth between treated and control groups, confirming the absence of adverse morphological effects on the intestinal epithelium. The results of this study indicate that synergistic combinations of peppermint EO, thyme EO, and feijoa peel extract do not adversely affect the gut microbiota composition and colonic morphology in rats, thereby supporting their application as preservatives in foods. Full article

The gut–heart axis represents a key determinant of cardiovascular (CV) system health. Emerging evidence indicates that intestinal dysbiosis can induce a state of chronic systemic inflammation which, together with mechanisms of endothelial dysfunction, increases the risk of CV diseases. Infective endocarditis (IE) exemplifies this concept, as microbiota alterations may promote bacterial translocation from the gut into the bloodstream, leading to colonization of cardiac valves and subsequent endocardial infection. This narrative review examines current scientific evidence on the relationship between the gut microbiota and CV diseases, with a particular focus on IE. We also summarize the mechanisms underlying impaired intestinal barrier integrity, immune activation, and the production of microbiota-derived metabolites that contribute to CV disease. Special attention is given to potential preventive and therapeutic strategies, including microbiota modulation, targeted antibiotic management, and personalized medicine approaches tailored to individual patient profiles. Full article

Background/Objectives: Hepatocellular carcinoma (HCC) is one of the most common causes of cancer and cancer-related death worldwide. Beyond the well-known factors influencing the risk of HCC, experimental data from animal models and observational human studies support a significant role of the gut microbiota (GM) in HCC initiation and progression. Dysbiosis and increased intestinal permeability synergistically disrupt the ‘gut–liver axis,’ exposing the liver to bacterial metabolites and microbial-associated molecular patterns, thereby contributing to hepatocarcinogenesis. While these findings have expanded our understanding of HCC pathogenesis, a critical translational gap persists as most data derive from preclinical settings, with limited validation in large-scale clinical studies. Methods: This narrative review aimed to contextualise the current evidence on the GM-HCC axis and its clinical translatability. A literature search was conducted in PubMed/MEDLINE, Scopus, and Web of Science up to July 2025 using Medical Subject Headings and related keywords, including HCC, GM, dysbiosis, intestinal permeability, gut–liver axis, microbial metabolites, inflammation/immune modulation, and microbiota-targeted interventions (probiotics, antibiotics, and faecal microbiota transplantation). Reference lists of relevant articles were also screened to identify additional studies. Results: Preclinical models consistently indicate that dysbiosis and impaired gut barrier function can promote hepatic inflammation, immune dysregulation, and pro-tumorigenic signalling through microbe-derived products and metabolite perturbations, supporting a contributory role of the GM in hepatocarcinogenesis. In humans, HCC and advanced chronic liver disease are associated with altered microbial composition and function, increased markers of intestinal permeability, and changes in bile acid and other metabolite profiles; however, reported signatures are heterogeneous across cohorts and analytical platforms. Conclusions: The GM is a biologically plausible and experimentally supported contributor to HCC initiation and progression, with potential for biomarker development and therapeutic targeting. However, clinical translation is limited by predominantly preclinical/associative evidence, interindividual variability, and non-standardised microbiome methods. Large longitudinal studies and adequately powered randomised trials are needed to establish causality, validate biomarkers, and determine whether GM modulation improves HCC prevention, detection, stratification, or outcomes. Full article

Autoimmune flares are often accompanied by abrupt surges of circulating plasmablasts—short-lived, high-output antibody-secreting cells generated through extrafollicular B-cell activation in response to microbial cues. Three categories of microbial input appear to repeatedly trigger these “plasmablast storms”: latent herpesvirus reactivations (Epstein–Barr virus, cytomegalovirus, human herpesvirus-6, varicella–zoster virus), acute respiratory or gastrointestinal infections including SARS-CoV-2, and chronic oral or gut dysbiosis. Although biologically distinct, these stimuli converge on innate sensing pathways driven by pathogen-associated molecular patterns such as unmethylated CpG DNA, single-stranded RNA, lipopolysaccharide, and bacterial lipoglycans. Through Toll-like receptors and type I interferon signalling, microbial signatures accelerate class switching, amplify inflammatory cytokine milieus, and lower B-cell activation thresholds, enabling rapid plasmablast mobilisation. Dysbiosis further maintains B cells in a hyper-responsive state by disrupting mucosal homeostasis and altering microbial metabolite profiles, thereby reducing the stimulus required to trigger plasmablast bursts. Once generated, these waves of oligoclonal plasmablasts home to inflamed tissues, where chemokine and adhesion landscapes shape their retention during flares. Emerging evidence suggests that such episodic plasmablast expansions promote autoantibody diversification, somatic hypermutation, and epitope spreading, progressively eroding tolerance. This review synthesizes these insights into a unified model in which infections and dysbiosis promote microbe-licensed plasmablast storms that influence the tempo and severity of autoimmune disease. Full article

Adiposity-Based Chronic Disease (ABCD) is known to increase the risk of aggressive prostate cancer (PCa), recurrent disease after treatment for localized PCa, and PCa mortality. A key mechanistic link contributing to this enhanced risk is chronic inflammation originating from excess white visceral adipose tissue (WAT; VAT) and periprostatic adipose tissue (ppWAT). Contributing to systemic inflammation is gut dysbiosis, which itself may be caused by ABCD as well as background local inflammation (prostatitis), which is common in aging men and may be exacerbated by the urinary microbiome. Investigating the molecular biology driving inflammation and its association with increased PCa risk, a recent paper applied a network and gene set enrichment to adipokine drivers in the ABCD-PCa network. It found prominent roles for MCP-1, IL-1β, and CXCL-1 in addition to confirming the importance of exposure to lipopolysaccharides and bacterial components, corroborating the role of gut dysbiosis. To further unravel the mechanistic links between ABCD and PCa risk, this critical review will discuss the current literature on prominent inflammatory signaling pathways activated in ABCD; the influence of gut dysbiosis, the urinary microbiome, and chronic prostatitis; and current hypotheses on how these domains may result in the development of aggressive PCa over a man’s life. Moreover, we performed a novel pathway enrichment analysis to further evaluate the associations between ABCD, PCa risk, gut dysbiosis, and the prostate microbiome, the results of which were partitioned into extracellular and intracellular signaling pathways. In the extracellular space, novel mechanistic links between gut dysbiosis and MCP-1, IL-1β, CXCL1, and leptin via bacterial pathogen signaling and the intestinal immune network (for IgA production), crucial for gut immune homeostasis, were found. Within the intracellular space, there were downstream signals activating chemokine and type 2 interferon pathways, focal adhesion PI3K/Akt/mTOR pathways, as well as the JAK/STAT, NF-κB, and PI3K/Akt pathways. Overall, these findings point to an emerging molecular pathway for PCa oncogenesis influenced by ABCD, gut dysbiosis, and inflammation, and further research, possibly with lifestyle program-based clinical trials, may discover novel biomarker panels and molecular targeted therapies for the prevention and treatment of PCa. Full article

Background: Growing evidence indicates that oral microbiome dysbiosis contributes to systemic inflammation, immune activation, and neural dysfunction. These processes may influence the onset and progression of major neuropsychiatric and neurodegenerative disorders. This review integrates clinical, epidemiological, and mechanistic findings linking periodontal pathogens and oral microbial imbalance to Alzheimer’s disease (AD), Parkinson’s disease (PD), depression, and anxiety. Methods: A narrative review was conducted using PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar to identify recent studies examining alterations in the oral microbiota, microbial translocation, systemic inflammatory responses, blood–brain barrier disruption, cytokine signaling, and neural pathways implicated in brain disorders. Results: Evidence from human and experimental models demonstrates that oral pathogens, particularly Porphyromonas gingivalis, Fusobacterium nucleatum, and Treponema denticola, can disseminate systemically, alter immune tone, and affect neural tissues. Their virulence factors promote microglial activation, cytokine release (IL-1β, IL-6, TNF-α), amyloid-β aggregation, and α-synuclein misfolding. Epidemiological studies show associations between oral dysbiosis and cognitive impairment, motor symptoms in PD, and alterations in mood-related taxa linked to stress hormone profiles. Immunometabolic pathways, HPA-axis activation, and the oral–gut–brain axis further integrate these findings into a shared neuroinflammatory framework. Conclusions: Oral dysbiosis emerges as a modifiable contributor to neuroinflammation and brain health. Periodontal therapy, probiotics, prebiotics, synbiotics, and targeted inhibitors of bacterial virulence factors represent promising strategies to reduce systemic and neural inflammation. Longitudinal human studies and standardized microbiome methodologies are still needed to clarify causality and evaluate whether restoring oral microbial balance can modify the course of neuropsychiatric and neurodegenerative disorders. Full article

This article describes the microbiome of the outer ear and the earwax in the ear canal, which performs various protective functions against bacterial infections. This article is based on an analysis of literature gathered from databases including PubMed, Google Scholar, Web of Science, and Scopus, primarily from the last 15 years. The search strategy included MeSH terms: ear canal, microbiome, earwax, cerumen, antibacterial peptides, ear infections, biofilm. Only peer-reviewed articles were included. The natural ear canal microbiota provides so-called colonization resistance, which protects against invasion by pathogenic microorganisms. Earwax is composed primarily of keratin secreted by epithelial cells and substances secreted by sweat and apocrine glands. It plays a key role in the physiology of the ear canal, maintaining a low pH, limiting moisture, and exhibiting antimicrobial properties. Both an excess and a deficiency of earwax can lead to dysbiosis of the outer ear, and consequently to the development of various infections. In an era of increasing antibiotic resistance and the search for new solutions in the fight against pathogenic microorganisms, understanding the natural properties of earwax is becoming increasingly important. Full article

The intestinal barrier is essential for gastrointestinal and systemic homeostasis by enabling nutrient absorption while limiting the translocation of pathogens and toxins. When barrier function is impaired, bacterial components such as lipopolysaccharides (LPSs) may cross the epithelium and promote inflammatory signaling. In dogs, chronic inflammatory enteropathies are frequent disorders associated with barrier dysfunction, dysbiosis, and immune dysregulation, and may progress to protein-losing enteropathy or systemic inflammation. Humic substances, particularly humic acid (HA), are natural organic compounds with reported antioxidative, immunomodulatory, and barrier-supporting effects; however, the cellular mechanisms underlying these effects in intestinal and immune models remain insufficiently characterized. This study evaluated the effects of a commercially available HA-based supplement on epithelial barrier integrity and inflammatory responses using an in vitro system combining IPEC-J2 intestinal epithelial cells and primary canine peripheral blood mononuclear cells (PBMCs). Epithelial barrier integrity (FD4 paracellular flux), reactive oxygen species, and cytokine production (TNF-α, IL-6) were assessed under basal and LPS-stimulated conditions. HA treatment preserved epithelial barrier function and reduced LPS-induced pro-inflammatory cytokine production, supporting further investigation of HA as a nutraceutical adjunct for gut health support in dogs with chronic enteropathies. Full article

Background/Objectives: Gut dysbiosis in Chronic Fatigue Syndrome (CFS) drives low-grade inflammation and shifts tryptophan metabolism toward neurotoxic pathways. The causal link between bacterial translocation, kynurenine pathway dysregulation, and symptom severity remains under-defined. We evaluated the impact of a high-concentration multi-strain probiotic on the “gut-kynurenine axis” and clinical status in CFS patients with co-morbid IBS-U and confirmed dysbiosis. Methods: Forty female patients with confirmed dysbiosis (GA-map™ Dysbiosis Index > 2) received the CDS22 formula (450 billion CFU/day) for 12 weeks. We compared urinary tryptophan metabolite profiles (LC-MS/MS), gut dysbiosis markers (3-indoxyl sulfate), and fatigue severity (FSS) against 40 age-matched healthy controls. Results: Baseline analysis revealed profound metabolic perturbations: elevated bacterial proteolytic markers (3-IS), substrate depletion (low tryptophan), and a neurotoxic signature (high quinolinic acid [QA], low kynurenic acid [KYNA]). Following the intervention, fatigue scores declined by 40.3%, with 97.5% of patients reaching the remission threshold (FSS < 36). Biochemically, 3-IS levels decreased to the range observed in healthy controls and attenuated xanthurenic acid levels. Although absolute QA concentrations remained elevated compared to controls, the neuroprotective KYNA/QA ratio increased significantly (+45%). Increased systemic tryptophan availability correlated directly with clinical symptom reduction (Spearman’s rho = −0.36, p = 0.024). Conclusions: The CDS22 formulation was associated with a restoration of intestinal eubiosis and functional tryptophan partitioning. Clinical remission coincides with a metabolic shift favoring neuroprotection (increased KYNA/QA ratio), validating the gut–kynurenine axis as a modifiable therapeutic target. Peripheral metabolic improvement relative to the healthy baseline appeared sufficient for symptom relief in this specific phenotype, despite incomplete clearance of neurotoxic metabolites. Full article

Probiotics, prebiotics, and postbiotics are of interest for their potential gastrointestinal and immunological benefits in pet health. This study aimed to assess whether a unique blend of Bacillus subtilis, Bacillus clausii, Bacillus coagulans (Weizmannia coagulans), FOS, GOS, and a postbiotic yeast extract could provide beneficial gut and immunological effects when fed to healthy, adult dogs. Twenty-four healthy adult beagle dogs (mean age 5.17 yrs) were fed the probiotic, prebiotic, and yeast chew (PPYC) or control chew (CC) supplement for 31 days, accompanied by fecal and blood sampling. Following 31 days, PPYC fed dogs had decreased (p < 0.05) fecal calprotectin concentration, a biomarker indicative of reduced intestinal inflammation, compared with dogs receiving the CC. In the PPYC group, blood C-reactive protein levels, an indicator of tissue inflammation, tended (p = 0.11) to be reduced. In addition, dogs receiving the PPYC supplement showed an increase in the IL-17a cytokine (p < 0.05). Despite dogs being in a clinically healthy state, changes in some dysbiosis-related bacterial strains were observed. There was an increase (p < 0.05) in the % of total bacteria of Blautia in the PPYC group by the end of the study, as well as an increase in the percent change from Day 0 of C. hiranosis (p < 0.05). Increased alpha diversity, a measure related to the resilience to environmental change, was observed in the PPYC group (p < 0.05). These results suggest that after consuming a supplement containing probiotics, prebiotics and a postbiotic yeast extract, markers of gut and systemic health were improved in otherwise healthy dogs. Full article

During the last ten years, the scientific community has increasingly acquired greater knowledge of the importance of oral microbiota, in general, for the physical condition of humans. Not only oral diseases, related to oral dysbiosis, are examined, but also several systemic inflammatory degenerative diseases induced by this condition. This narrative review aims to shed light on the communication mechanisms between the oral cavity and different mucosal compartments, and to explain how the changes in microorganisms may alter their balance, leading to disease. Many potential pathogenic bacteria can induce oral dysbiosis, among them Porphyromonas gingivalis and Fusobacterium nucleatum are the most explored; however, other bacterial species such as Tannerella forsythia, Treponema denticola, Aggregatibacter actinomycetemcomitans and Filifactor alocis are able to give rise to local and systemic diseases through the release of toxins. The two-way communication system between the gastrointestinal tract and the central nervous system, known as the gut–brain axis, is strongly influenced by the gut microbiota and can ultimately be studied even more broadly and in depth if we consider the influence of the oral microbiota on this axis. Taste receptors’ activity also has a significant role, being able to affect a subject’s food choice by interacting with the microbiota. Qualitative and quantitative alterations in microorganisms existing in the main mucosal compartments may easily lead the host to develop systemic degenerative inflammatory diseases. Full article

Kuwait faces a significant public health challenge from obesity and Type 2 Diabetes Mellitus (T2DM), conditions known to disrupt the natural balance of oral bacteria. This imbalance, or dysbiosis, can promote gum disease and may worsen metabolic health. While the intragastric balloon (IGB) is a common, less invasive weight-loss procedure, its specific effect on the community of bacteria in saliva remains unclear, especially for high-risk groups. The objective of this study was to investigate changes in the salivary microbiota of obese prediabetic patients following IGB placement. We recruited 20 obese patients (11 female, 9 male; average age 31.5) from a clinic in Kuwait. Saliva samples were collected just before IGB (Allurion™) insertion and again 6 weeks after that. Using 16S rRNA gene sequencing, we identified the bacterial species present and used bioinformatic tools to analyze diversity and abundance. Our analysis revealed that the overall diversity and structure of the salivary microbial community remained stable after the procedure. However, we detected notable changes in specific types of bacteria. The relative abundance of several genera, including Veillonella, Porphyromonas, and Fusobacterium, shifted significantly. At the species level, Porphyromonas pasteri and Haemophilus parainfluenzae became less abundant, while certain Veillonella and Streptococcus species increased in number after the IGB was placed. In conclusion, for obese prediabetic patients in Kuwait, the salivary microbiome demonstrates remarkable stability in the weeks following IGB surgery. The procedure did not drastically alter the overall ecosystem, but it did trigger specific, subtle changes in certain bacterial populations. This suggests the oral microbiota is resilient, adapting to the new physiological conditions without a major upheaval. Full article

The gut microbiome has emerged as a key regulator of human health, influencing not only metabolism and immunity but also the development and treatment of cancer. Mounting evidence suggests that microbial dysbiosis contributes to oncogenesis by driving chronic inflammation, producing genotoxic metabolites, altering bile acid metabolism, and disrupting epithelial barrier integrity. At the same time, the gut microbiome significantly modulates the host response to oncotherapies including chemotherapy, radiotherapy, and especially immunotherapy, where microbial diversity and specific taxa determine treatment efficacy and toxicity. This review synthesizes current evidence on the role of the gut microbiome in both oncogenesis and oncotherapies, focusing on thirteen cancers with the strongest and most clinically relevant microbiome associations, colorectal cancer, gastric cancer, hepatocellular carcinoma, gallbladder cancer, esophageal cancer, pancreatic cancer, oral squamous cell carcinoma, cervical cancer, prostate cancer, breast cancer, lung cancer, brain cancer, and melanoma. These cancers were selected based on robust mechanistic data linking microbial alterations to tumor initiation, progression, and therapy modulation, as well as their global health burden and translational potential. In addition, we have provided mechanistic insights or clinical correlations between the microbiome and cancer outcomes. Across cancers, common microbial mechanisms included pro-inflammatory signaling (e.g., NF-κB and STAT3 pathways), DNA damage from bacterial toxins (e.g., colibactin, nitrosating species), and metabolite-driven tumor promotion (e.g., secondary bile acids, trimethylamine N-oxide). Conversely, beneficial commensals such as Faecalibacterium prausnitzii and Akkermansia muciniphila supported antitumor immunity and improved responses to immune checkpoint inhibitors. In conclusion, the gut microbiome functions as both a driver of malignancy and a modifiable determinant of therapeutic success. Integrating microbiome profiling and modulation strategies such as dietary interventions, probiotics, and fecal microbiota transplantation into oncology practice may pave the way for personalized and more effective cancer care. Full article

Background: Amoxicillin, clindamycin and azithromycin are the most frequently prescribed antibiotics for odontogenic infections, but their comparative effects on gut microbiota and intestinal homeostasis remain insufficiently understood. Disruption of gut microbiota, short-chain fatty acid (SCFA) production, and mucosal barrier integrity may contribute to gastrointestinal symptoms. We aimed to compare the impacts of these antibiotics on gut microbiota, SCFA levels, and colonic goblet cells. Methods: C57BL/6N mice were treated with oral amoxicillin, clindamycin, or azithromycin at clinically relevant dosages. Cecal index, fecal water content, and diarrhea index were assessed during treatment and recovery. Gut microbiota composition and absolute bacterial abundance were determined using 16S rRNA amplicon absolute quantification sequencing. SCFAs in cecal contents were quantified by gas chromatography–mass spectrometry. Goblet cell abundance and Muc2 mRNA expression in colon tissues were evaluated using Alcian blue staining and RT-PCR. Results: Amoxicillin caused moderate increases in cecal index, reduced Ligilactobacillus abundance, increased Escherichia-Shigella, lowered SCFA levels, and decreased goblet cells and Muc2 expression, with partial recovery after two weeks. Clindamycin induced more severe dysbiosis, including sustained Proteobacteria expansion, persistent loss of beneficial taxa, 86–90% reduction in SCFA production, and lasting decreases in goblet cells and Muc2 expression without recovery during the observation period. Azithromycin caused mild and reversible changes across all parameters. Conclusions: Among the three antibiotics, azithromycin had the least detrimental effects on gut microbiota, SCFA production, and mucosal barrier function, whereas clindamycin caused profound and persistent intestinal disruption. These findings provide comparative evidence to inform antibiotic selection in clinical practices. Full article

As a major export crop in China, Saccharina japonica cultivation suffers from significant economic losses due to disease outbreaks, with pathogen identification remaining a critical bottleneck for mariculture. In this study, a dominant bacterial strain, LJ53, was isolated from the diseased farmed S. japonica. Artificial challenge assay confirmed that this strain is the direct causative agent of bleaching symptoms on sporophytes. Based on morphological characteristics and 16S rRNA gene-based phylogeny, it was identified as Pseudoalteromonas agarivorans LJ53. Ultrastructural observation revealed that this strain destroyed host cells and caused typical pathological changes such as chloroplast disintegration. Interestingly, metagenomic analysis showed no significant difference in the relative abundance of this pathogen between healthy and diseased S. japonica tissues. However, the co-occurrence network of the disease community exhibited increased connectivity, altered modularity, and features characteristic of microbial dysbiosis. This dysbiosis disrupts the water ecological balance by destabilizing microbial symbiosis and nutrient cycling, which are essential for overall ecosystem resilience. As a result, these imbalances can exacerbate disease transmission and weaken the self-regulating capacity of marine environment, highlighting the need for integrated management strategies to restore equilibrium. These findings provide a theoretical basis for elucidating the mechanisms of bacterial diseases in S. japonica and developing future control strategies. Full article