Search Results (1,244)

Although nanomedicine has enabled significant advances in drug delivery, the clinical translation of conventional synthetic nanocarriers is limited by immune clearance, non-specific biodistribution, and gastrointestinal instability. This poses major challenges for therapy targeting the intestines. Cell membrane-coated nanotechnology (CMCT) and membrane vesicle-based systems have emerged as biomimetic platforms integrating synthetic nanomaterials with naturally derived biological interfaces. These biohybrid systems inherit biological functions originating from cells, including immune evasion, prolonged circulation, lesion homing, and microenvironment-responsive interactions, through the direct transfer of intact membrane components. This review summarizes recent advances in CMCT and membrane vesicle-based strategies for intestinal drug delivery. It covers fabrication methodologies, programmable manufacturing approaches, and functional regulation enabled by diverse membrane sources and hybrid engineering designs. Applications in inflammatory bowel disease, colorectal cancer, and intestinal infections are highlighted, emphasizing key therapeutic mechanisms, such as targeting inflammation, neutralizing toxins, modulating the immune system, and regulating the microbiome. We also discuss the major challenges of translation, such as preserving membrane and coating integrity, ensuring oral stability, achieving batch reproducibility, and ensuring biosafety. Overall, this review establishes a conceptual and engineering framework to guide the transition of membrane-based nanocarriers from passive biomimicry to adaptive, clinically translatable intestinal delivery systems. Full article

Atopic dermatitis (AD) is a chronic inflammatory skin disease with a complex pathogenesis involving epidermal barrier dysfunction, microbiome dysbiosis, and immune dysregulation. Despite significant advances in therapy, including biologics and targeted treatments, their use may be limited by adverse effects, highlighting the need for safe adjunctive strategies. Polyphenols are naturally occurring bioactive compounds that are abundant in plant-based foods and are known for their anti-inflammatory, antioxidant, and immunomodulatory properties, making them promising candidates for supportive AD management. This review integrates current evidence on the effects of polyphenols on epidermal barrier lipids, microbiome interactions, and key inflammatory pathways, including NF-κB and JAK/STAT signaling. Additionally, the role of polyphenols in modulating dendritic cell and neutrophil activity, and reducing reactive oxygen species (ROS) production and neutrophil extracellular trap (NET) formation, as well as their potential involvement in mitophagy regulation, is discussed. Polyphenols support epidermal barrier integrity by modulating the expression of key structural proteins, including filaggrin, involucrin, and loricrin, leading to a reduction in transepidermal water loss (TEWL). Furthermore, they interact bidirectionally with the gut microbiome, acting as metabolic substrates for beneficial bacteria and promoting the growth of short-chain fatty acid (SCFA)-producing species such as Lactobacillus, Bifidobacterium, and Akkermansia, while simultaneously inhibiting pathogenic strains. These findings highlight the role of polyphenols in maintaining microbiome homeostasis and supporting epidermal barrier integrity. The review encompasses findings from clinical studies, animal models, and mechanistic investigations, while also addressing limitations related to polyphenol bioavailability. Overall, polyphenols may represent a valuable adjunctive approach in AD management; however, further well-designed clinical and mechanistic studies are required to confirm their therapeutic potential. Full article

Ototoxicity is traditionally viewed as a local cochlear adverse effect of indispensable therapies such as cisplatin and aminoglycosides. However, emerging evidence suggests that cochlear vulnerability is shaped by systemic physiology, including inflammatory tone, vascular barrier integrity, and metabolic state. In this Review, we propose a Gut–Mito–Ear axis in which gut ecosystem function influences circulating mediator modules that converge on two cochlear mediator nodes: blood–labyrinth barrier (BLB) gating and mitochondrial stress tolerance. We synthesize evidence showing that gut perturbation can alter cochlear outcomes in vivo, that at least one microbiota-derived metabolite signal can directly protect hearing in experimental settings, and that BLB dysfunction and inflammatory trafficking are mechanistically relevant to cisplatin- and aminoglycoside-induced injury. We further organize the literature using an evidence-weighted framework that distinguishes direct cochlear causality from mechanistic plausibility and explicitly retains negative studies as boundary-setting evidence. Finally, we outline a translational roadmap in which microbiome-targeted prevention is pursued through mediator-anchored, non-interference-aware strategies and evaluated across linked state variables spanning exposure context, gut function, defined mediator modules, BLB gating, mitochondrial stress tolerance, and auditory phenotype. The Gut–Mito–Ear axis is not considered an established mechanism. We present it as a falsifiable systems-biology model that organizes the current evidence. Within this model, we define the minimum and ideal standards for A-tier causal evidence, explicit criteria for interpreting boundary-setting negative (A−) studies, and a set of testable predictions for causal validation. Full article

Increasing evidence suggests pancreatic cancer develops within a host–microbe ecosystem in which microbial communities across anatomical niches interact with tumour biology, immune regulation, metabolism, and therapeutic response. This review examines pancreatic cancer through the lens of humans as holobionts, integrating evidence from the oral, gut, biliary, and intratumoural microbiomes. Epidemiological and sequencing studies demonstrate consistent microbial alterations across these niches in pancreatic cancer, including oral dysbiosis associated with periodontal pathogens, gut microbial shifts toward pro-inflammatory taxa, disease-specific biliary microbial signatures, and the presence of distinct intratumoural microbial communities. Mechanistic studies indicate that intestinal barrier disruption, microbial translocation, immune and metabolite signalling can influence tumour immune architecture, macrophage polarisation, T-cell infiltration, oncogenic signalling pathways, and chemotherapeutic metabolism, particularly inactivation by tumour-associated bacteria. Microbiome-driven shifts in immunometabolism can reprogramme immune-cell metabolic pathways, impairing effective T-cell activation, promoting tumour-supportive macrophage phenotypes. Emerging therapeutic strategies aim to modulate the microbiome–tumour axis, including dietary interventions, probiotics and immunonutrition, faecal microbiota transplantation, engineered microbial therapies, and microbiome-informed antibiotic strategies. While pre-clinical findings are compelling and early-phase clinical studies suggest feasibility, most evidence remains associative and heterogeneous across cohorts and methodologies. Understanding pancreatic cancer as a multi-site ecological system may help explain inter-patient variability in disease progression and treatment response. This could usher in a new era for therapeutic manipulation where future progress will depend on longitudinal, multi-omic, and interventional studies to determine whether microbiome-targeted strategies can produce clinically meaningful improvements in pancreatic cancer outcomes. Full article

Microbiome-based therapies are reshaping the therapeutic landscape for ulcerative colitis (UC), offering new avenues for disease management beyond conventional immunomodulatory and biologic treatments. UC remains a chronic, relapsing condition with significant unmet clinical needs, as many patients fail to achieve sustained remission or experience adverse effects with current therapies. The gut microbiome has emerged as a central contributor to UC pathogenesis, influencing epithelial barrier integrity, immune homeostasis, and metabolic signaling. Interventions such as fecal microbiota transplantation (FMT) and defined microbial consortia have demonstrated proof-of-concept efficacy in early-phase clinical trials, each leveraging distinct mechanistic strategies. FMT, as a broad ecological intervention, restores microbial diversity and functional redundancy, potentially addressing multiple pathogenic mechanisms simultaneously. In contrast, defined consortia enable precise targeting of specific metabolic and immunological pathways, including short-chain fatty acid production, bile-acid remodeling, epithelial barrier reinforcement, immune modulation, and succinate degradation. Recent clinical evidence suggests that consortia with broader mechanistic coverage may achieve more consistent biological activity than narrowly focused designs. This review synthesizes mechanistic and clinical insights across broad and defined microbial consortia, integrates evidence from randomized controlled trials and early-phase LBP studies, and outlines a precision-medicine framework to guide therapy selection. We highlight the importance of aligning therapeutic mechanisms with patient-specific microbial, metabolic, and immune profiles, and discuss future directions including biomarker-guided stratification, hybrid consortia, and adaptive trial designs. Advancing both broad and defined approaches, while incorporating ecological principles, mechanistic understanding, and patient stratification, will be essential to realizing the full therapeutic potential of microbiome-based therapies in UC. Full article

Probiotics, live microorganisms that confer health benefits when administered in adequate amounts, are increasingly recognized as modulators of interconnected microbiome–host networks that extend beyond gastrointestinal function. This review synthesizes evidence on classical probiotic roles in maintaining gut homeostasis, immune regulation, and infection prevention, while integrating emerging systemic effects across the gut–brain, gut–skin, gut–oral, and metabolic axes. Rather than presenting isolated outcomes, we adopt a systems-level framework that links probiotic actions to shared mechanisms, including microbial metabolite signaling (e.g., SCFAs), competitive exclusion of pathobionts, barrier reinforcement, and immune–neuroendocrine pathway modulation. We further discuss translational advances that enable rational probiotic design, including targeted delivery platforms (encapsulation and protective matrices), engineered/next-generation strains, and postbiotic-inspired strategies, alongside sustainability considerations and regulatory/labeling challenges. Finally, we outline future directions emphasizing precision microbiome-centered interventions, synthetic biology, and AI-assisted multi-omics analysis to support strain- and context-specific probiotic strategies. Collectively, this review provides an integrated, systems-oriented synthesis to guide future research and accelerate safe clinical and industrial applications of probiotics. Full article

Rheumatoid arthritis (RA) is a chronic inflammatory disease of autoimmune background and unknown etiology. The importance of genetic factors in RA development is well-established. Environmental factors have also been extensively researched in relation to risk of RA and managing its symptoms. Smoking, physical activity, diet, and gut microbiota are considered to be the most essential modifiable factors in RA. Among dietary interventions, the most researched is Mediterranean diet, monounsaturated fatty acids, fish consumption, and fish oil (EPA, eicosapentaenoic acid and DHA, that is, docosahexaenoic acid). Others concerned gluten-free and vegan or vegetarian diet, salt intake, supplementation with vitamin D, antioxidants, prebiotics, and probiotics. Diet modifications can alter the gut environment, and the association between RA development or severity and the composition of gut bacteria has already been shown. This review focuses on effectiveness and usefulness of various dietary approaches and supplements in RA prevention and management, including the influence on disease activity and inflammatory status. The composition of gut microbiota and its changes in response to dietary factors are also considered. There is a great need for further research into mutual dependencies of diet, microbiome, and RA activity. The current state of knowledge provides promising evidence for future nutrition and microbial therapies. Full article

Objective: Hepatitis B virus (HBV) is a globally distributed infectious disease affecting the liver. This literature review aims to summarize all available relevant information on the PubMed database about HBV’s connection to the microbiome and to consider possible treatment adjuncts. Materials and methods: Database used: PubMed. Keywords used: “HBV”, “Hepatitis B”, “microbiome”. In the PubMed database, 179 research publications were identified using these keywords; 69 studies were excluded as they were irrelevant or retracted. Of the remaining, 110 were analyzed in this literature review, and four additional literature sources were used to supply background information and context. Information was summarized. The analysed studies in total included 14,814 participants (excluding animal studies), of whom 8564 were HBV-infected individuals. Results: Results characterizing abundance or decrease in specific bacterial, viral, and fungal species are heterogeneous; multiple studies support that the HBV patient oral and fecal microbiome is different from that in healthy controls (HCs) and varies throughout disease progression. The HBV seems to transform the microbiome negatively, leading to dysbiosis and decreased microbial diversity in most studies. Evidence links HBV microbiome changes with influence on HbeAg seroconversion, HBV-DNA load, metabolic pathways, liver cirrhosis, and hepatocellular carcinoma. The research proposes that members of microbiota could potentially promote or protect against liver injury in HBV. Four studies proposed that the plasma virome in HBV patients was primarily composed of members of the Anelloviridae. One study researched a parasite (Entamoeba gingivalis) in HBV patients. Two studies analyzed HBV patients’ fungal profiles. Conclusions: Microbiota research, although promising, at the present moment is heterogeneous. HBV patients’ microbiota is distinguishable from HCs, and multiple studies have tried to identify the HBV characteristic microbiome; however, more precise information is needed to draw conclusions. Fecal microbiota transplantation and probiotics have the potential to be therapy adjuncts for HBV patients, but more research is needed. Full article

Modern dentistry increasingly relies on light-curing units (LCUs) and lasers in essential clinical procedures such as composite resin polymerization, caries treatment, and periodontal therapy. This review aims to outline the evolution of light-emitting technologies and to assess their potential biological risks, with particular emphasis on effects on the visual system, oral tissues, and microbiome. The development of curing devices is presented chronologically, from the first-generation ultraviolet (UV-A) lamps introduced in the 1970s to current light-emitting diode (LED-LCU) systems and dental lasers (e.g., Er:YAG, Nd:YAG). The progressive increase in light intensity—now exceeding 3000 mW/cm²—has shortened curing times but simultaneously raised safety concerns. Major hazards include the so-called blue-light hazard, where exposure to high-energy visible (HEV) blue light may accelerate macular degeneration, and temperature elevations in the pulp chamber, which may damage the dentin–pulp complex. Laser radiation also exerts significant microbiological effects: Er:YAG and diode lasers demonstrate bactericidal activity against biofilms and oral pathogens (e.g., P. gingivalis), although therapeutic outcomes depend on wavelength, dose, and exposure time. Suboptimal parameters may lead to microbiome disturbances, whereas low-level laser therapy (LLLT; 600–1200 nm) supports tissue regeneration and helps restore microbial balance. The individualization of irradiation parameters, combined with thorough theoretical knowledge, operator expertise, and technical understanding of LCUs and lasers, is essential for maximizing clinical benefits while minimizing health risks and preserving oral microbiome homeostasis. Full article

Inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn’s disease (CD), are consistently associated with alterations in gut microbial communities, although the extent and characteristics of these alterations vary across studies, supporting a potential role of the microbiota in disease pathogenesis and therapeutic modulation. We conducted a systematic review to synthesize current evidence on microbiota alterations in IBD and the clinical application of fecal microbiota transplantation (FMT). A total of 118 studies were included (76 focused on microbiota profiling and 42 evaluated FMT as therapy). Across heterogeneous study designs and microbial characterization methods, reduced microbial diversity was the most consistently reported alteration, generally more pronounced in CD than in UC. Depletion of Faecalibacterium prausnitzii—a key butyrate producer with anti-inflammatory properties—was commonly reported, often accompanied by functional impairment in short-chain fatty acid production. Microbial patterns were frequently associated with mucosal inflammation and varied across disease phenotypes; these patterns have been increasingly explored as predictors of treatment response and relapse, although mechanistic interpretation remains limited and causal relationships are difficult to establish. Evidence from randomized controlled trials suggests potential efficacy of FMT in UC, particularly with intensive or repeated protocols, whereas data in CD remain limited and heterogeneous, with signals of benefit often appearing transient. FMT was generally well tolerated, but long-term safety data remain scarce. Emerging multi-omic approaches are reshaping the field by integrating taxonomic and functional insights, with potential implications for risk stratification, diagnosis, prognosis, and therapeutic optimization. Further standardized, longitudinal, and mechanistically oriented studies are required to translate microbiome research into clinically actionable strategies in IBD. Full article

The prevalence of Crohn’s disease has increased over the last few decades, even in developing countries, whereas that of intestinal tuberculosis has decreased, which places both diseases at an epidemiological crossroads. Crohn’s disease and intestinal tuberculosis share many clinical, endoscopic, imaging, and pathological features, which sometimes make differential diagnosis very difficult; an accurate diagnosis is, however, very important since an erroneous treatment can worsen the evolution or delay proper therapy. The association between past TB infection and Crohn’s disease can make the diagnosis especially hard. This review summarizes current data on specific features that allow differentiation between Crohn’s disease and intestinal tuberculosis, paying particular attention to the microbiome, clinical signs, endoscopy, cross-sectional imaging, bacteriological, and immunological findings detailed. The importance of computerized models and scores for the differentiation is also detailed, because common features may make the differentiation based on a single criterion difficult. Full article

Obstructive sleep apnea (OSA) is the most common sleep-related breathing disorder and is increasingly recognized as a contributor to cognitive decline and a potential risk factor for neurodegeneration. Previous studies have also identified various associated comorbidities such as vascular dysfunction, metabolic alterations, and neuroinflammatory changes. Positive airway pressure (PAP) therapy has been associated with cognitive improvement in some studies, but its long-term effects on cognitive function remain uncertain. This study employs a prospective, observational, longitudinal cohort design to examine longitudinal associations between disease severity, PAP therapy and cognition. Additionally, we aim to examine the relationships between cognitive dysfunction, brain structure and associated OSA-related risk factors. A total of 100 eligible participants with mild to severe OSA will be recruited. All participants will undergo comprehensive assessments at baseline and after 12 months, including neurological, pulmonary, and ear, nose and throat clinical examinations, polysomnography, neuropsychological testing, brain magnetic resonance imaging with volumetry, anthropometric measurements, blood and saliva sampling for the assessment of the selected laboratory parameters, gut microbiome analysis, and evaluation of endothelial function and baroreflex sensitivity. This study may improve understanding of how PAP therapy and OSA-related pathophysiological processes influence cognitive outcomes. Full article

Acute myeloid leukemia (AML) remains a highly morbid malignancy in which outcomes are constrained not only by disease refractoriness and relapse, but also by therapy-related toxicity—particularly infections, mucosal injury, and delayed hematopoietic reconstitution. The gut microbiota has emerged as a potentially modifiable layer of host vulnerability and resilience during AML treatment. Microbiome disruption is detectable already at diagnosis, even in antibiotic-naïve patients, and is often characterized by reduced community diversity, depletion of anaerobic taxa linked to short-chain fatty acids (SCFAs) production, and enrichment of pathobiont-associated profiles. During induction, cytotoxic therapy and antimicrobials precipitates diversity loss, domination events, and persistent shifts beyond discharge. Clinically, the most consistent translational signal is the association between baseline or early-treatment microbiome features and infectious outcomes, while emerging data suggest that diagnosis-time microbiome structure may also relate to hematologic recovery kinetics. Mechanistic models converge on pathways linking barrier integrity, microbial metabolites (notably butyrate and other SCFAs), immune calibration, and inflammatory translocation of microbial products. These insights support hypotheses: antimicrobial stewardship may preserve microbiome function; ecosystem repair strategies such as autologous fecal microbiota transfer (A-FMT) are feasible and can restore community structure; and metabolite or nutritional interventions merit evaluation in immunocompromised hosts. Regimen-specific microbiome effects and microbiome–drug interactions suggest that treatment choice could have downstream microbiome-mediated consequences. We synthesize evidence, outline interventional concepts, and define methodological priorities for next-generation trials assessing causality and clinical benefit. Progress will require longitudinal sampling, multi-omic integration (metabolomics, resistomics, and barrier/inflammatory biomarkers), and interventional designs linking microbiome dynamics to clinically meaningful outcomes. Full article

Pancreatic ductal adenocarcinoma (PDAC), which remains undetected till advanced stages of progression, is becoming a more common and aggressive PC with high mortality rates. Trending unhealthy dietary habits, sedentary life, obesity, diabetes, high body mass index (BMI), and perturbed gut microbiota, also known as dysbiosis, increase the PDAC incidences. There is an urgent need to delve into reliable and cost-effective biomarkers and strategies to diagnose and prevent the disease. Microbial remedies and dietary phytonutrients that restore gut microbial balance may be the prospective preventive measures. This article intends to recommend the hypothesis that PDAC is incepted and characterized by microbial signatures and can be managed by integrating evidenced-based complimentary approaches entailing diet, nutraceuticals, microbial interventions and life style modifications with standard therapies. The futuristic longitudinal and mechanistic studies to unravel host–microbiota and the host–microbiome interactions will allow deeper aetiologic and mechanistic insights into PDAC to evolve therapies and recommendations for better pancreatic health. Full article

Necrotizing enterocolitis (NEC) and sepsis/late-onset sepsis (LOS) are significant contributors to preterm infant morbidity and mortality, with prematurity and low birth weight representing major risk factors for these interconnected conditions. Although the pathogenesis of NEC and LOS is not fully understood, there is a clear association with an immature intestinal mucosal barrier, which may enable bacterial invasion and translocation, resulting in an inflammatory cascade. Increasing recognition of the gut microbiome as a marker for health and disease has driven interest in probiotics, particularly Bifidobacterium spp. and Lactobacillus spp., as potential adjunctive agents for the prevention and management of NEC and LOS in preterm infants, which is the area of focus of this review. The focus of this paper was to analyze clinical studies using different probiotic strains, and compare single-strain versus multi-strain probiotic formulations. Several studies support that probiotic supplementation in preterm infants has the potential to decrease NEC incidence and, to a lesser extent, sepsis/LOS. Nonetheless, inconsistent results due to strain differences and clinical heterogeneity limit the widespread adoption of this mode of therapy, as do safety concerns in this vulnerable population. Further high-quality standardized studies are necessary to establish consistent guidelines for probiotic use in preterm infants. Full article