Search Results (926)

Chronic atrophic gastritis (CAG) is a pivotal precancerous condition in gastric carcinogenesis, with progression typically following the classic Correa cascade. Although Helicobacter pylori (H. pylori) infection is widely recognized as the principal etiological factor, the persistence of gastric cancer (GC) risk in a subset of patients after successful eradication suggests that gastric microbiota dysbiosis may also contribute to CAG progression. In recent years, high-throughput sequencing technologies have revealed distinct microbial restructuring in patients with CAG, characterized by decreased microbial diversity, depletion of commensal taxa, and enrichment of opportunistic pathogens. These compositional changes are accompanied by metabolic dysfunction, activation of inflammatory signaling pathways, and disruption of immune homeostasis, which may contribute to a microenvironment permissive for precancerous transformation of the gastric mucosa. Probiotics and related microbiome-based therapeutics, including prebiotics, synbiotics, and postbiotics, have emerged as promising adjunctive strategies for H. pylori eradication and disease management. Their beneficial effects are mediated through multiple mechanisms, including remodeling of the microbial community, inhibition of pathogen colonization, modulation of host immune responses, and restoration of mucosal barrier integrity. However, whether these interventions can reverse established atrophic or metaplastic lesions remains unclear. In addition, how strain specificity, dose dependency, and interindividual heterogeneity influence clinical efficacy has yet to be fully elucidated. In this review, we summarize the compositional and functional features of gastric microbiota dysbiosis in patients with CAG, as well as the mechanisms and clinical applications of microbiome-based interventions. We further highlight current limitations in the field and discuss future directions for precision microecological therapies integrating multi-omics approaches, engineered probiotics, and artificial intelligence. These advances may provide a theoretical framework and practical guidance for the diagnosis and management of CAG and the prevention of GC. Full article

The planthopper pests Geisha distinctissima and Ricanula fujianensis are major threats to tea plantations. Although insect endosymbionts are functionally important, their communities in these pests are poorly understood. This study, conducted in the representative tea-growing region of Guiyang in southwestern China, employed high-throughput sequencing to analyze the bacterial and fungal endosymbionts of both species. We found that bacterial communities were dominated by Proteobacteria and Firmicutes, with core genera such as Enterobacter and Rickettsia showing significant interspecific variation. Fungal communities were primarily composed of Ascomycota and Basidiomycota, and key genera like Fusarium exhibited host-specific patterns. Most notably, we discovered an intriguing pattern: bacterial communities differed in structure but showed conserved predicted functions, whereas fungal communities were structurally similar yet functionally divergent. This suggests that bacterial symbionts may underpin core physiological stability, while fungal symbionts could act as key drivers of host-specific adaptation. These results provide critical insights into planthopper–microbe interactions and establish a theoretical basis for developing targeted, microbiome-based pest management strategies. Full article

Carbohydrate-active enzymes (CAZymes) encoded by the human gut microbiome are central mediators of dietary glycan metabolism and host–microbe biochemical homeostasis. Among these, β-glucuronidases represent functionally pivotal hydrolases implicated in metabolism, intestinal physiology, and therapeutic modulation. The present study performs an integrative in silico structural and functional interrogation of β-glucuronidases derived from Acidobacterium capsulatum (3VNY), Bacteroides ovatus (6D8K), and Faecalibacterium prausnitzii (6ED2). An integrated computational framework encompassing physicochemical parameters profiling, hierarchical structural prediction, tertiary-structure validation, salt-bridge energetics, functional domain and motif annotation, protein–protein interaction reconstruction, ligand-binding thermodynamics via molecular docking, and residue-resolved non-covalent interaction network mapping using the Protein Contacts Atlas (PCA) was employed. Physicochemical analyses indicated that all enzymes are thermostable, intracellular, and hydrophilic, while secondary-structure organization revealed a functional balance between helix-mediated rigidity and coil-driven flexibility. Structural validation metrics identified 6ED2 as the most conformationally stable architecture, whereas 6D8K displayed enhanced functional complexity, including enriched motif composition, membrane-associated features, and superior ligand-binding affinity. Docking simulations highlighted castanospermine and calcium saccharate as the most favorable interacting ligands across enzyme variants. Importantly, PCA-based interaction analysis revealed distinct ligand-centered atomic contact networks, with immediate contact counts of 57 (3VNY), 32 (6D8K), and 41 (6ED2), providing residue-level insight into stabilization mechanisms and interaction topology beyond conventional docking metrics. Collectively, these findings establish a multidimensional computational framework linking structural stability, functional diversification, ligand recognition, and atomic interaction networks in gut microbial β-glucuronidases, thereby supporting future biochemical validation, microbiome-targeted therapeutics, and biotechnological or cosmeceutical applications. Full article

Aedes aegypti (Ae. aegypti) is the primary vector for dengue, Zika and chikungunya, which represent major global public health concerns. The use of Wolbachia as a biological control agent in Ae. aegypti has gained significant international attention following the successful establishment of field-released mosquitoes in Australia, Malaysia, Brazil, Indonesia and Singapore. This study presents a comprehensive scientometric analysis of the research landscape of Wolbachia and Ae. aegypti. Data comprising 662 English-language publications from 2000 to 2025 were extracted from the Scopus database. Analytic tools, including VOSviewer and R-based Biblioshiny, were employed to quantify author productivity, transcontinental collaboration networks, thematic evolution, research gaps and future directions, while Bradford’s Law of Scattering was used to identify core dissemination channels. Publications have shown a steady upward trajectory since 2000, with an overall relative growth rate of 0.3%, while annual citations peaked in 2009 and 2011 (3337 and 3460 citations, respectively). The dataset strictly conformed to Bradford’s distribution (0.16% error), identifying PLOS Neglected Tropical Diseases (11.9%) and Parasites and Vectors (5.6%) as the core journals. Global research networks are predominantly led by Australia and the United States, supported primarily by the National Institutes of Health (14.8%) and the National Health and Medical Research Council (14.2%). Crucially, thematic analysis using a methodological triangulation approach demonstrates a progressive maturation in the field, shifting from foundational laboratory mechanisms toward large-scale deployment logistics and microbiome dynamics. Overall, this study highlights the intellectual landscape, underscores the vital role of global collaboration, and provides strategic insights to guide future evidence-based policies in Wolbachia–Aedes aegypti research. Full article

Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive lung disease with limited therapeutic options. To investigate the roles of the pulmonary microbiota and metabolism in fibrosis, we established a bleomycin (BLM)-induced mouse model at 14- and 28-day timepoints and performed integrated 16S rRNA gene amplicon sequencing and untargeted metabolomic analyses. Histological and Western blot analyses confirmed significant fibrotic changes and the upregulation of fibrotic markers. Microbiome profiling revealed marked dysbiosis after BLM exposure, characterized by reduced microbial diversity and enrichment of Klebsiella. LC-MS–based metabolomic analysis identified substantial perturbations in the lung tissue metabolome, particularly in lipid metabolism, amino acid metabolism, and energy pathways. Correlation analysis indicated a strong positive association between the abundance of Klebsiella and the levels of specific dipeptides, including Ala-Hyp-Gly, Asp-His, and Asp-Asn. The accumulation of these dipeptides may reflect increased collagen degradation and turnover in fibrotic lungs. Collectively, our findings demonstrate that BLM-induced pulmonary fibrosis is accompanied by coordinated alterations in the lung microbiome and metabolome. Notably, microbial dysbiosis, particularly the expansion of Klebsiella, may be associated with alterations in amino acid metabolism and fibrotic progression. Full article

Background/Objectives: Mushroom-derived phenolic compounds are gaining attention as bioactive molecules with potential roles in gut microbiota modulation, intestinal health, and metabolic regulation. Although mushroom polysaccharides are well established as fermentable substrates, the contribution of fungal phenolics to microbiota–host interactions remains less defined. This review aimed to critically analyse the evidence supporting mushroom-derived phenolic compounds as emerging prebiotic-like modulators of gut microbiota, intestinal function, and host metabolism. Methods: A narrative critical review was conducted using scientific literature retrieved from PubMed, Scopus, Web of Science, and Google Scholar. Studies addressing phenolic profiling in edible and medicinal mushrooms, gastrointestinal digestion, colonic fermentation, microbial biotransformation, gut microbiota modulation, intestinal barrier function, inflammation, and metabolic outcomes were considered. Particular attention was given to chromatographic and mass spectrometry-based studies, in vitro digestion/fermentation models, mechanistic studies, animal experiments, clinical trials, systematic reviews, and meta-analyses. Results: Current evidence shows that mushrooms contain diverse phenolic compounds, mainly phenolic acids such as gallic, protocatechuic, caffeic, p-coumaric, ferulic, vanillic, syringic, and cinnamic acids. Due to limited small intestine absorption, a substantial fraction of these compounds may reach the colon, where they undergo microbial biotransformation into smaller phenolic metabolites. These metabolites may influence microbial ecology, support beneficial taxa, modulate short-chain fatty acid production indirectly, attenuate oxidative stress and inflammatory signaling, and contribute to intestinal barrier integrity. However, most evidence derives from in vitro and preclinical studies, while human data remain limited and are mainly based on whole-mushroom interventions. Conclusions: Mushroom-derived phenolic compounds are promising prebiotic-like modulators within the microbiota–metabolite–host axis. Nevertheless, their specific contribution cannot yet be quantitatively distinguished from that of other mushroom constituents, particularly β-glucans, chitin, and other fungal polysaccharides, because most available evidence derives from whole-mushroom matrices, crude extracts, or polysaccharide-rich preparations rather than isolated phenolic fractions. Future studies should compare whole mushroom preparations, polysaccharide-rich fractions, and standardized phenolic-rich extracts, integrating metabolomics, microbiome profiling, and well-designed clinical trials to clarify the relative mechanistic and therapeutic relevance of mushroom phenolics. Future studies should use standardized phenolic-rich extracts, metabolomics, microbiome analysis, and well-designed clinical trials to clarify their mechanistic relevance, clinical significance, and translational potential. Full article

Background/Objectives: Chemotherapy-induced peripheral neuropathy (CIPN) affects up to 85% of patients receiving neurotoxic regimens, often leading to dose reduction and impaired quality of life, yet effective preventive or therapeutic options remain scarce. Emerging evidence implicates chemotherapy-induced gut microbiota dysbiosis in CIPN pathogenesis via a gut–nerve axis. Concurrently, rectal ozone insufflation (ROI) has been shown to modulate the gut microbiota and reduce inflammation in preclinical models. This article critically examines the evidence on the role of gut dysbiosis in CIPN, evaluates the microbiota-modulating capacity of rectal ozone therapy (OT), and assesses the biological plausibility of ozone as a microbiota-targeting intervention for CIPN, while explicitly distinguishing between established evidence and hypothetical mechanisms. Evidence synthesis: Neurotoxic agents induce dysbiosis marked by reduced microbial diversity, loss of short-chain fatty acid-producing bacteria, and expansion of pro-inflammatory taxa. Preclinical models demonstrate a causal role for specific microbial communities in CIPN, with microbiota depletion or fecal transplantation modulating neuropathic phenotypes. In human cohorts, dysbiosis severity correlates with CIPN symptoms. Preclinical studies show that ROI restores microbial balance, enhances short-chain fatty acid levels, and strengthens intestinal barrier function via Nrf2/HO-1 and SIRT1 pathways. Preliminary retrospective data from small case series (n = 7 and n = 15) report sustained symptom improvement in CIPN patients receiving OT. However, no human study has directly linked ozone-induced microbiota changes to clinical outcomes, and the clinical evidence for OT in CIPN remains limited to uncontrolled observations. Conclusions: Convergent preclinical evidence supports a biological rationale for investigating ROI as a microbiota-targeting intervention in CIPN. However, this rationale remains largely hypothetical in the clinical setting. High-quality randomized controlled trials with longitudinal microbiome profiling are urgently needed to establish mechanistic causality and to determine whether the promising preclinical findings translate into clinically meaningful benefits. Until such evidence is available, the framework presented here should be regarded as hypothesis-generating rather than as a basis for clinical practice. Full article

Transitioning to sustainable, plant-forward diets, such as the Planetary Health Diet is a global priority; however, the palatability gap remains a formidable barrier, as consumers often perceive low-sodium, plant-centric diets as sensory-deficient. While aromatic herbs could bridge this gap, the current literature rarely integrates their sensory, ecological, phytochemical, and cultural dimensions. This narrative review explores how Mediterranean aromatic plants indigenous to the Maltese Islands function as sensory and molecular catalysts to bridge this gap. Through a thematic synthesis (2005–2026) integrating ethnobotanical evidence with molecular nutrition and sensory science, the Maltese archipelago is examined as a small-island ecological model. Chronic abiotic stressors, including high salinity and intense solar exposure, induce phytochemical priming, significantly enhancing secondary metabolites like polyphenols and terpenoids. These compounds establish a folk–medicine bridge, where traditional culinary practices align with modern biochemical validation. These bioactives demonstrate a capacity to modulate the NF-κB inflammatory axis, mitigate systemic inflammaging, and support the gut–microbiome–brain axis. Furthermore, these aromatics serve as translational tools for EAT-Lancet 2025 targets by facilitating cross-modal sensory compensation for sodium reduction and improving nutrient bioaccessibility via the culinary entourage effect. The TASTE-MED framework positions culinary nutrition as a vital translational bridge, asserting that flavour is a prerequisite for dietary sustainability and aligning individual molecular resilience with broader planetary health goals. Full article

Background: Rosacea is a chronic inflammatory dermatosis characterized by vascular dysregulation, immune dysfunction, neurovascular alterations, and microbial involvement. Recent advances in understanding its pathophysiology have led to the development of targeted therapeutic strategies addressing multiple disease mechanisms. This systematic review aimed to evaluate contemporary evidence regarding emerging and established treatment approaches for rosacea. Methods: A systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. PubMed, Scopus, and Web of Science were searched for studies published between 2016 and 2025. Original human studies evaluating therapeutic interventions for rosacea were included. Study selection, data extraction, and risk-of-bias assessment were performed independently by two reviewers. Methodological quality was assessed using Joanna Briggs Institute (JBI) critical appraisal tools appropriate for each study design. Results: Fifteen studies involving 537 patients with rosacea and 77 controls (614 participants in total) met the eligibility criteria. Evaluated interventions included vascular-targeted therapies, topical anti-inflammatory agents, systemic and immunomodulatory treatments, and microbiome-oriented approaches. Oxymetazoline, pulsed-dye laser, platelet-rich plasma, ivermectin, azelaic acid, dapsone, sulfur preparations, and metronidazole demonstrated clinical benefits in reducing erythema, inflammatory lesions, or overall disease severity. Emerging therapies, including tofacitinib and oral ivermectin, showed promising results in refractory disease. Microbiome-related interventions, particularly Demodex-targeted therapies and Helicobacter pylori eradication, were also associated with clinical improvement. Risk-of-bias assessment identified two studies with low risk of bias, twelve with moderate risk of bias, and one study with high risk of bias. Conclusions: Current evidence supports a multimodal and mechanism-based approach to rosacea management, integrating vascular, inflammatory, immunological, and microbiological targets. However, the available evidence remains limited by small sample sizes, heterogeneous methodologies, short follow-up periods, and a predominance of non-randomized study designs. Large, well-designed randomized controlled trials are needed to establish optimal evidence-based treatment strategies and define the long-term efficacy and safety of emerging therapies. Full article

Chronic wounds represent a substantial and growing clinical burden, yet durable healing remains difficult to achieve in a large proportion of patients. The skin microbiome plays a central role in this challenge: in healthy tissue, resident microorganisms support barrier integrity and calibrate immune responses, whereas in chronic wounds, community disruption—often combined with persistent biofilm formation—drives non-resolving inflammation, impairs re-epithelialisation, and increases antimicrobial tolerance. As antibiotic resistance escalates, these features strengthen the rationale for microbiome-directed strategies that target wound ecology while reducing reliance on conventional antimicrobials. Current evidence is still dominated by mechanistic and preclinical studies, with only early clinical signals for selected approaches; therefore, next-generation probiotics, including Lactiplantibacillus/Lactobacillus spp., as well as defined prebiotic and postbiotic formulations, should be interpreted as promising adjuncts rather than clinically established therapies. Causal mechanisms, optimal formulations, reproducibility, and patient-level determinants of response remain insufficiently defined, representing a critical knowledge gap that limits translation. Here, we synthesise current evidence linking microbial ecology to key wound-healing pathways and propose a precision framework that integrates metagenomics, transcriptomics, metabolomics, and spatial profiling to map host–microbe interactions, identify predictive biomarkers, and guide stratified therapy. We further highlight combinatorial approaches pairing ecological engineering with biofilm-disruptive materials and immune-modulatory molecules. Realising the potential of these interventions will require mechanism-resolved clinical trials, standardised outcome frameworks, and patient stratification tools—advances that could improve chronic wound management while reducing selective pressure for antimicrobial resistance. Full article

Driven by increasingly severe drought stress associated with global warming, this study investigated a synthetic microbial community, SynCom-SASW01, with strong stress tolerance and plant growth-promoting potential, and systematically elucidated its mechanisms for enhancing drought resistance in wheat (Triticum aestivum L.). Dual-site field trials demonstrated that SynCom-SASW01 significantly alleviated drought-induced growth suppression, increasing grain yields by 10.42% and 8.52% at the Hohhot and Hulunbuir sites, respectively. This improvement was primarily associated with increased effective tiller number and enhanced root vigor. Physiologically, inoculation promoted root proline and glutathione accumulation and enhanced antioxidant enzyme activities, including superoxide dismutase, thereby reducing malondialdehyde levels. Environmental analyses showed that the consortium established rhizosphere “micro-reservoirs” through exopolysaccharide secretion, improving soil relative water content and the availability of alkali-hydrolyzable nitrogen and phosphorus. High-throughput sequencing revealed that SynCom-SASW01 reshaped the endosphere microbiome through early colonization priority effects, selectively enriching beneficial taxa such as Pseudomonas. Functional prediction indicated upregulated branched-chain amino acid biosynthesis, promoting osmotic adjustment and redox homeostasis. These findings provide a microbiome-based strategy for stabilizing wheat productivity in arid regions. Full article

Background/Objectives: Ultra-processed foods (UPFs) are increasingly recognized as dietary exposures associated with cardiometabolic, hepatic, and neurocognitive outcomes. However, UPFs are often treated mainly as nutrient-poor foods, whereas their processing-related features may perturb gut–liver–brain communication. This review examines whether metabolic dysfunction-associated steatotic liver disease (MASLD) can be conceptualized as a hepatic metabolic amplifier linking UPF exposure to cognitive aging. Methods: We conducted a structured narrative search of PubMed/MEDLINE, Web of Science Core Collection, and Scopus from January 2010 to 11 May 2026 across four evidence modules: UPFs and MASLD/NAFLD; UPFs and cognitive aging or dementia; UPFs and gut–liver–brain mechanisms; and MASLD/NAFLD and cognitive aging. Representative studies were prioritized according to direct relevance to the proposed axis, study design, exposure and outcome validity, mechanistic specificity, and contribution to major evidence gaps. Results: Observational and mechanistic evidence links higher UPF consumption with liver steatosis, MASLD/NAFLD-related outcomes, cognitive decline, cognitive impairment, stroke, and dementia-related outcomes, although causality remains incompletely established and residual confounding is important. Candidate pathways include food-matrix disruption, rapid eating, displacement of microbial substrates, selected additives and processing-derived compounds, intestinal barrier dysfunction, metabolic endotoxemia, bile acid signaling, hepatic lipotoxicity, systemic inflammation, vascular dysfunction, and neuroimmune activation. Many pathways overlap with general cardiometabolic dysfunction; the processing-centered contribution lies in positioning industrial formulation as an upstream exposure and MASLD as a hepatic node that may amplify gut-derived and metabolic signals relevant to brain aging. Conclusions: A processing-centered gut–liver–brain framework integrates UPFs, MASLD, and cognitive aging as linked metabolic-aging phenomena. Future studies should test UPF substitution using liver imaging, microbiome profiling, metabolomics, bile acid and inflammatory biomarkers, neuroimaging, and cognitive assessment. Full article

Clonal hematopoiesis of indeterminate potential (CHIP) and the gut microbiota-derived metabolite trimethylamine N-oxide (TMAO) are both linked to NLRP3-mediated cardiovascular inflammation, but their interaction has not previously been explored. This work proposes the CHIDT axis (clonal hematopoiesis–dysbiosis–TMAO), a feed-forward mechanism in which TET2 loss-of-function CHIP- and TMAO-generating Gram-negative gut dysbiosis mutually enhance cardiovascular risk. The model proceeds in three nodes. CHIP-associated intestinal immune dysregulation promotes luminal expansion of Gammaproteobacteria, which produce both trimethylamine via CntA/CntB-mediated L-carnitine oxidation and ADP-heptose as an obligate LPS biosynthetic intermediate. TMAO amplifies NLRP3 inflammasome activation through the SIRT3 → SOD2 → mtROS pathway. The evidence base of the CHIDT model is strongest for TET2-CHIP; the proposed extension to DNMT3A-CHIP rests on indirect, associative data and requires dedicated experimental confirmation before it can be considered established. TXNIP cascade, with predicted disproportionate potency in macrophages epigenetically primed by TET2 haploinsufficiency. High concentrations of TMAO have also been shown to suppress TET2 expression in endothelial cells through CYTB promoter hypermethylation, inducing NLRP3–GSDMD-dependent pyroptosis, although it remains unclear whether physiological TMAO levels can trigger this effect. Concurrently, ADP-heptose activates the ALPK1–TIFA–NF-κB pathway in bone marrow progenitors, favoring the expansion of mutant hematopoietic stem and progenitor cells. The model identifies three potential therapeutic strategies: NLRP3 inhibition, microbial TMA lyase inhibition, and microbiome-targeted reduction in Gram-negative bacteria. None has been tested in CHIP carriers stratified by plasma TMAO. Further studies in preclinical models and human cohorts integrating CHIP genotyping and TMAO quantification are needed to validate the CHIDT axis as a target for precision cardiovascular prevention. Full article

Acute exacerbation of interstitial lung disease (AE-ILD) represents sudden, severe deterioration in patients with pre-existing ILD and is associated with high morbidity and mortality. Our work presents a case series of AE-ILD in patients with idiopathic pulmonary fibrosis (IPF), idiopathic non-specific interstitial pneumonia (iNSIP), and connective tissue disease-associated ILD (CTD-ILD) managed at our institution and provides a narrative review of AE-ILD. Across cases, AE-ILD manifested as rapid progression of dyspnea and extensive ground-glass opacities (GGOs) on imaging, often triggered by infections or immune-mediated processes. Despite treatment, all cases were fatal, confirming that mortality remains high in AE-ILD. In our literature review, we focus on dysregulated innate immunity, an altered microbiome, potential microaspiration, surgical procedures, and autoantibody-mediated inflammation as triggers, as well as the risk factors for and prevalence of AE-ILD. We also examine pharmacological and non-pharmacological interventions, with particular emphasis on the role of antifibrotic agents as a key protective factor. Evidence for and against corticosteroid use in AE-IPF and non-IPF AE-ILD is discussed, highlighting the radically different treatment approach for AE in melanoma differentiation-associated gene 5 (MDA5)-positive dermatomyositis (DM)-associated ILD compared to AE-IPF. Our findings underscore the heterogeneous presentation and poor prognosis of AE-ILD, emphasizing the urgent need for standardized diagnostic criteria, risk stratification, and prospective studies with larger cohorts to establish evidence-based therapeutic strategies. Full article

De novo granulation of autochthonous microorganisms of water and wastewater reduces the start-up periods for cultivating aerobic granular sludge (AGS) and enrichment of degrading strains. However, it has not been demonstrated using refractory carbon compounds. This work investigated the formation of AGS from the seawater microbiome and establishment of pollutant removal pathways by feeding acetonitrile as the sole carbon and nitrogen source. Use of acetonitrile at an organic loading rate of 0.124 kg/m³/day enabled rapid emergence of aggregates and then stable granules (size: 1.3 mm; SVI5: 68 mL/g) within two weeks. TOC removal accompanied by ammonium nitrogen release was consistent and stable at 93% during the 50 days of bioreactor operation. Formation of acetamide and ammonium indicated involvement of nitrile hydratase and amidase enzymes in acetonitrile biodegradation. Ammonium released during acetonitrile biodegradation was removed by partial nitrification and the nitrite denitrification pathway. However, incomplete ammonium removal led to accumulation of up to 120 mg/L NH₄⁺-N by day 50. Phosphate was removed via the enhanced biological phosphate removal pathway. This study shows that de novo granulation permits cultivation of AGS via the de novo granulation approach for simultaneous biodegradation of refractory acetonitrile and biological nutrient removal under saline conditions. Full article