Search Results (973)

Background: This study aimed to determine whether osteoporosis is associated with differences in the subgingival microbiome of postmenopausal women, stratified by periodontitis stage. Methods: In this observational, stratified case–control study, 166 postmenopausal women were assigned to six strata defined by bone status (osteoporosis vs. normal BMD) and periodontal category (no periodontitis, Stage I–II, Stage III–IV). Standardized pooled subgingival samples were profiled by 16S rRNA gene sequencing. Community structure was evaluated using Bray–Curtis dissimilarity and tested with PERMANOVA (9999 permutations) and prespecified contrasts comparing osteoporosis versus normal BMD within each periodontal category (Holm adjustment). Alpha diversity (Shannon) was assessed using two-way ANOVA. Results: Periodontal category was strongly associated with community structure (PERMANOVA R² = 0.514, pseudo-F = 86.681, p < 0.0001), whereas bone status (R² = 0.004, p = 0.178) and the bone status × periodontal category interaction (R² = 0.007, p = 0.294) were not. None of the three prespecified within-category contrasts reached significance after Holm adjustment. Shannon diversity differed by periodontal category (p = 1.93 × 10⁻²⁴) but not by bone status (p = 0.200), with similar distributions between osteoporosis and normal BMD within each periodontal category. Conclusions: In postmenopausal women, periodontitis severity dominates variation in the subgingival microbiome, and osteoporosis does not confer an additional community-level or taxonomic signature when periodontal status is held constant. Longitudinal and multi-omic studies incorporating host-response biomarkers and therapy exposures are warranted to clarify whether osteoporosis influences periodontal susceptibility and progression primarily through host-mediated mechanisms. Full article

Inflammatory and autoimmune diseases are now understood to be significantly influenced by the intricate interactions between the microbiome and host physiology. This review investigates the function of epigenetic dysregulation in microbiome–host interaction and its consequences for health and disease. Epigenetic modifications, including DNA methylation, histone modifications, and non-coding RNA-associated regulation, are key mechanisms that control gene expression without altering the underlying DNA sequence. Microbial metabolites and community composition alterations can cause disruptions in these epigenetic processes, resulting in dysregulated immune responses and the initiation of chronic inflammatory conditions. In particular, the diversity of gut microbiota alters host epigenetic patterns, affecting T cell differentiation, inflammatory modulation, and tissue homeostasis. Aberrant epigenetic modifications contribute to the pathogenesis of autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) by promoting inflammation and autoimmunity. Similarly, gut microbiota dysbiosis has been implicated in the development and progression of inflammatory bowel disease (IBD). Identifying the reciprocal interaction between epigenetic alterations and microbiome dynamics provides unique insights into therapeutic options targeted at restoring microbial homeostasis to prevent disease progress. Consequently, understanding the intricacies of epigenetic dysregulation in microbiome–host interactions represents a significant sector in biomedical research and highlights the promise for precision medicine approaches in treating inflammatory and autoimmune diseases. The potential for microbiome-based therapies to affect host epigenetic landscapes requires additional research, paving the way for innovative therapeutic paradigms targeted at improving host resilience and restoring immunological balance. The purpose of this review is to synthesize current knowledge on how epigenetic dysregulation and microbiome–host interactions drive inflammatory and autoimmune diseases and to highlight emerging therapeutic opportunities. Full article

Chronic kidney disease (CKD) is a progressive condition associated with metabolic disturbances, systemic inflammation, and the accumulation of gut-derived uremic toxins. Increasing evidence highlights the role of gut microbiota dysbiosis in the progression of CKD through the gut–kidney axis. Consequently, microbiome-targeted nutritional strategies, including probiotics, prebiotics, and synbiotics, have emerged as promising complementary approaches to modulate intestinal microbial composition and metabolic functions. This review summarizes and critically evaluates the current clinical evidence regarding the use of these interventions in CKD patients. Clinical studies indicate that supplementation with probiotics, prebiotics, and synbiotic formulations may promote beneficial shifts in the composition of the gut microbiota, enhance saccharolytic fermentation, and increase the production of short-chain fatty acids (SCFAs). These changes have been associated with reduced circulating levels of gut-derived uremic toxins such as indoxyl sulfate and p-cresyl sulfate, as well as with the attenuation of systemic inflammation and oxidative stress. However, available trials remain heterogeneous in terms of study design, probiotic strains, prebiotic substrates, dosing regimens, and patient populations, and are frequently limited by small sample sizes and short intervention durations. As a result, evidence for improvements in renal function and long-term clinical outcomes remains inconclusive. While synbiotics may offer theoretical advantages by combining microbial supplementation with targeted substrates that support microbial growth and metabolic activity, current evidence does not consistently demonstrate superior clinical efficacy. Overall, these interventions often improve surrogate biomarkers, but their effects on renal function and hard clinical outcomes remain uncertain. Larger, longer-duration multicenter randomized controlled trials with standardized formulations are needed to establish their clinical utility and to better elucidate microbiota–host interactions in CKD. Advancing this field may support the development of personalized microbiome-based therapeutic strategies aimed at modulating the gut–kidney axis and ultimately improving clinical outcomes in CKD patients. Full article

Environmental stressors and host genetics influence gut microbiota and antimicrobial resistance, but their combined effects across intestinal niches remain poorly unexplored. We conducted a metagenomic analysis of 60 jejunal and cecal samples from 30 native Chinese pigs across three altitudes (500 m, 1400 m, and 3850 m). The aim was to disentangle the interactive impacts of altitude, breed, and intestinal site on microbiome structure and antibiotic resistome dynamics. The cecal microbiota was taxonomically conserved and strongly associated with breed. Conversely, while jejunal communities exhibited structural variations among the sampled cohorts, differences in alpha diversity (Shannon index, p < 0.01) appeared to be primarily associated with breed differences rather than an independent altitudinal effect. High-altitude Tibetan pigs showed an enrichment of Bifidobacterium and Pseudomonas, which may be linked to hypoxia adaptation. Despite a shared core resistome (88 ARG types), the cecum harbored significantly higher ARG abundance than the jejunum within-breed comparisons of Tibetan pigs across altitudes; this revealed stable ARG profiles (p > 0.05) suggesting that, although some descriptive differences were observed, the independent effect of altitude weakens when the genetic effect is taken into account. Furthermore, carbohydrate-active enzymes (e.g., CBM13, GH33) correlated positively with ARG abundance. In conclusion, the jejunum appears to act as an environmentally responsive niche, while the cecum exhibits a higher ARG abundance that is closely associated with the host breed. Full article

Cross-kingdom pathogenesis—human and animal pathogens colonizing and persisting in plants—is transforming our understanding of microbial ecology, food safety, and public health. This review translates incoming research that demonstrates plants as more than mute carriers to dynamic ecological interfaces where human and zoonotic pathogens, such as Salmonella enterica, Escherichia coli O157:H7, and Listeria monocytogenes, will adhere, internalize, and, in some cases, potentially evade host defenses. Such pathogens exploit evolutionarily conserved molecular processes like Type III secretion system 1 (TTSS), biofilm formation, quorum sensing, and small RNA-mediated immune sabotage that have allowed them to cross biological kingdom boundaries. To provide an entry point for pathogens, environmental conditions (e.g., contaminated irrigation water, manure application, wildlife access, and mechanical wounding) promote pathogen transfer to and penetration into plant tissues through stomata hydathodes above ground or roots below ground. Once inside, pathogens confront a range of plant immune responses, indigenous microbiota, and abiotic stresses such as UV radiation exposure, nutrient starvation, and osmotic fluctuations. Nonetheless, biofilm production, metabolic versatility, and virulence gene expression contribute to their persistence. Interactions with plant pathogens and microbiomes additionally shape colonization dynamics, for example, through co-survival and niche manipulation. With the acceleration of these processes due to climate change, urbanization, and intensified agriculture, cross-kingdom pathogenesis becomes a rising concern for One Health. Critical knowledge gaps, including seedborne transmission, microbiome engineering, and predictive modeling, are pointed out in the review along with emerging mitigation strategies, including point-of-care diagnostics and microbial biocontrol. In conclusion, this review advocates for interdisciplinary collaboration from microbiology, plant science, and One Health perspectives to predict and mitigate cross-kingdom threats to global food production. Full article

As the predominant native pollinator across Asia, Apis cerana is essential for the maintenance of biodiversity and agricultural productivity. The gut microbiota of honeybees plays a central role in host nutrition, detoxification, and immune function. p-Coumaric acid, a widespread phenolic acid enriched in pollen and nectar, has been reported to promote honeybee health by prolonging lifespan and increasing the expression of detoxification-related genes, hence improving tolerance to pesticides. Its influence on gut microbial communities, however, remains insufficiently characterized in A. cerana. This study evaluated the effects of dietary p-coumaric acid on survival, sucrose solution consumption, and gut microbiome composition in A. cerana workers using absolute quantification sequencing. Bees were provided sucrose solutions containing p-coumaric acid at concentrations of 41.0, 82.0, and 164.0 mg/L for durations of 5 and 10 days. The results indicated no effect on survival but revealed time-dependent changes in sucrose solution consumption. p-Coumaric acid exposure altered the abundance of non-core bacterial taxa, including Bombella and Apilactobacillus, whereas the core gut microbiota (Lactobacillus, Gilliamella, Snodgrassella, Apibacter, and Bifidobacterium) remained stable. These results suggest that p-coumaric acid modulates sucrose solution consumption and selectively influences non-core gut bacteria without disrupting survival or core microbiota stability, underscoring its role in regulating host–microbe interactions in honeybees. Full article

The rhizosphere is a complex microecosystem where soil, roots, and microbes interact to maintain soil ecological functions. Blueberry (Vaccinium spp.), an economically important fruit, has a shallow, fibrous root system with few root hairs, limiting its nutrient absorption. It thrives in acidic, high-organic matter soils, restricting its cultivation in many soil types worldwide. Enhancing blueberry productivity and adaptation by leveraging beneficial rhizosphere microbial communities offers a sustainable solution. This review summarizes the composition of blueberry rhizosphere microbial community across different microenvironments and the blueberry rhizosphere core microbiome. We detail the functional roles of beneficial microorganisms in stimulating nutrient bioavailability and secreting phytohormones. Furthermore, factors influencing microbiome assembly, including cultivars, planting age, and metabolites, are evaluated alongside agricultural management practices. Despite extensive taxonomic characterization, a critical gap remains in understanding the functional synergism between blueberry and its rhizosphere microbiome, particularly the ecological mechanisms underlying host adaptation to acidic and nutrient-limited environments. Overall, future research should focus on developing targeted agricultural practices and synthetic microbial communities to reshape the rhizosphere microbiome, thereby establishing productive, resilient rhizosphere-based microbial systems that support eco-friendly and sustainable agricultural ecosystems. Full article

Antibiotic therapy represents one of the strongest ecological perturbations of the human gut microbiota, inducing rapid and often prolonged alterations in community structure, metabolic activity, and functional resilience. While the use of probiotics to mitigate antibiotic-associated dysbiosis is widely adopted in clinical practice, probiotic selection is still largely empirical and insufficiently grounded in biological compatibility with specific antibiotic pressures. In this conceptual review, antibiotics are reframed not merely as antimicrobial agents, but as ecological forces that shape microbial survival, quiescence, and recolonization dynamics. We propose a biologically informed framework that distinguishes genetic antibiotic resistance from functional or ecological insensitivity, highlighting how microbial traits, such as the absence or inaccessibility of the antibiotic target, metabolic state, sporulation, and cellular architecture, influence the persistence of probiotics during antibiotic exposure. By integrating the mechanisms of action of antibiotics with key physiological and structural features of probiotic microorganisms, we develop a conceptual framework aimed at rationalizing the compatibility of probiotics and antibiotics. This framework does not imply clinical efficacy but provides an interpretative tool to guide hypothesis generation, experimental validation, and the design of future targeted probiotic strategies. A more ecologically grounded approach to probiotic selection may ultimately improve microbiota support during antibiotic therapy and advance personalized microbiome modulation. Full article

Climate change is intensifying winters in temperate regions, posing a serious threat to Apis mellifera health. The gut microbiome, a distinct community of core bacterial species, is central to overwintering success by supporting immune function, nutrient assimilation, and pathogen resistance, but is highly sensitive to environmental stressors such as cold temperatures and dietary shifts. Stress-induced perturbations can reshape the composition and relative abundance of the gut microbiome in honey bees, leading to adverse effects on host health, physiological functions, and overwinter survival. Cold temperatures and additional stressors further destabilize the microbiome, compounding these effects. This review is the first to synthesize current knowledge on how extrinsic factors, such as diet, antibiotics, and pathogens, and intrinsic factors, including age and strain, influence the composition and function of the honey bee gut microbiota during the overwintering period. Given the increasing severity of winter conditions under climate change, a deeper understanding of microbiome–host–environment interactions is essential for improving honey bee resilience. By integrating evidence on the microbiome’s roles in nutrient utilization, immune modulation, and pathogen defense, this review outlines a framework to guide future research aimed at sustaining pollinator health and nutrition in a changing global climate. Full article

This study evaluated the effects of a host-specific multi-lactic acid bacterial (MLAB) probiotic and sex on performance, carcass traits, meat quality, and gut microbiota in fattening pigs. Thirty-two crossbred pigs (10 ± 0.80 weeks; 23.43 ± 0.17 kg) were assigned to a 2 × 2 factorial design with diet (control or MLAB probiotics) and sex (barrow or female). The MLAB supplement consisted of seven lactic acid bacterial strains mixed in equal proportions (≈14.3% each)—Lactobacillus brevis, Lactobacillus reuteri, Weissella cibaria, Lactobacillus paraplantarum, Lactococcus lactis, Lactobacillus pentosus, and Pediococcus pentosaceus—administered at 1 × 10⁹ CFU/kg feed for 12 weeks. MLAB probiotic supplementation reduced bone proportion while increasing skin and fat content (p < 0.05), with a treatment × sex interaction for loin eye area (p < 0.05). Meat quality improved in the MLAB group, showing higher ultimate pH and lower cooking loss (p < 0.05), indicating improved water-holding capacity. Female pigs exhibited higher early postmortem pH and protein content (p < 0.05). Microbiome analysis revealed increased abundances of Oxalobacteraceae and Paludibacteraceae and reduced Clostridium sensu stricto 6 (p < 0.05). These results suggest that host-adapted probiotics may support gut microbial balance and improve certain pork quality traits. Full article

Background: Patients with diabetes mellitus exhibit increased susceptibility to peri-implant inflammation and implant failure due to systemic metabolic dysfunction, impaired immunity, and delayed tissue healing. The oral microbiome is increasingly recognized as a key intermediary in these pathogenic processes. Aims: This review aims to systematically evaluate the available literature examining the relationships among the oral microbiome, biomaterial biocompatibility, and inflammatory changes in peri-prosthetic tissues in insulin-dependent diabetic patients. Methods: A systematic search of PubMed and Scopus databases identified studies published between January 2000 and July 2025. Eligible studies (25 in total) included clinical, histological, microbiological, or immunohistochemical investigations involving diabetic patients rehabilitated with dental implants or prostheses. Study selection and reporting followed PRISMA 2020 guidelines. Results: Diabetic cohorts showed consistent microbial alterations, including a higher relative abundance of periopathogenic species (P. gingivalis, T. forsythia, and F. nucleatum), lower microbial diversity, and greater biofilm-forming potential. Histological analyses frequently described increased inflammatory infiltrates, higher cytokine expression, and reduced soft-tissue integration. Biomaterial surface characteristics were also associated with differences in microbial adhesion, while hyperglycemia was linked to microbial and host-response patterns suggestive of greater pathogenicity and inflammation. Collectively, these findings suggest that diabetes-associated dysbiosis may be associated with increased peri-implant inflammatory changes and altered peri-implant homeostasis. Conclusions: The oral microbiome may be involved in inflammatory activity and biocompatibility at the tissue–implant interface in diabetic patients. A better understanding of host–microbe–material interactions may support risk assessment and help inform future personalized management strategies, such as targeted antimicrobial approaches, probiotic modulation, and biomaterial surface optimization, although these implications should be interpreted cautiously given the predominantly observational and heterogeneous nature of the available evidence. Full article

The cervicovaginal microbiome (CVMB) is pivotal in maintaining the homeostasis of the lower female genital tract and has emerged as a significant modulator of cervical carcinogenesis. Although persistent infection with high-risk human papillomavirus (HR-HPV) is a prerequisite for the development of cervical intraepithelial neoplasia (CIN) and subsequent cervical carcinoma, it remains insufficient alone to drive oncogenesis. Accumulating evidence suggests that alterations in the CVMB composition profoundly impact HPV persistence, local immune responses, and disease progression. A vaginal microbiota dominated by Lactobacillus species, most notably Lactobacillus crispatus, correlates with low microbial diversity, robust immune regulation, and facilitated HPV clearance. Conversely, microbial dysbiosis—characterized by Lactobacillus depletion and a concomitant proliferation of anaerobic taxa, typical of Community State Type (CST) IV and Lactobacillus iners-dominated profiles—is strongly associated with chronic inflammation, oxidative stress, epithelial barrier compromise, and an elevated risk of CIN progression. This review synthesizes current evidence regarding the multifaceted interactions among the cervicovaginal microbiome, HPV pathogenesis, immune dysregulation, and oxidative stress in the etiology of CIN. Elucidating these intricate host–microbiome dynamics may precipitate the discovery of novel microbiome-derived biomarkers, ultimately informing innovative prophylactic and therapeutic interventions for cervical cancer. Full article

Obesity represents a heterogeneous metabolic disorder characterized by substantial interindividual variation in inflammatory status, insulin sensitivity, and cardiometabolic risk. Traditional anthropometric measures fail to capture this metabolic diversity, limiting risk stratification and personalized intervention strategies. This review critically examines nutritional and metabolic biomarkers that reflect the physiological dysregulation underlying obesity, including adipokines (leptin, adiponectin, resistin), inflammatory markers (C-reactive protein, interleukin-6, TNF-α), insulin resistance indices (HOMA-IR, fasting insulin, HbA1c), and lipid metabolism indicators (LDL cholesterol, triglycerides, HDL cholesterol, and liver enzymes such as ALT and GGT). Among these, elevated CRP, reduced adiponectin, and increased HOMA-IR have demonstrated the strongest clinical utility for early metabolic risk identification. We further evaluate emerging biomarkers—including circulating microRNAs, gut microbiota-derived metabolites (short-chain fatty acids, TMAO, lipopolysaccharides), and bile acid profiles—which offer additional mechanistic insight into diet–microbiome–host interactions. We systematically assess the mechanistic basis, clinical relevance, and nutritional modulation of each biomarker class, emphasizing how dietary composition—particularly fatty acid quality, fiber intake, and overall dietary patterns such as the Mediterranean diet—influences biomarker profiles and metabolic outcomes. Furthermore, we explore how biomarker-based phenotyping enables precision nutrition approaches by identifying individuals most likely to benefit from specific dietary interventions. Integration of multi-biomarker panels with clinical and genetic data holds promise for advancing from population-based dietary guidelines toward individualized nutrition strategies that optimize metabolic health and prevent obesity-related complications. Future research should prioritize validating biomarker-guided intervention frameworks, establishing standardized thresholds across diverse populations, and developing clinically implementable tools for personalized nutritional medicine. Full article

Advances in sequencing technologies have transformed human microbiome research, yet most analyses still rely on species-level profiles. However, strains rather than species represent the true ecological and functional units of the microbiome. Individual strains can vary substantially in gene content, metabolic capacity, virulence factors, antimicrobial resistance, and host-interaction properties. These differences critically influence immune responses, epithelial barrier integrity, disease susceptibility, and therapeutic outcomes. Here, we synthesize recent human microbiome studies that provide robust strain-resolved evidence, focusing on three major themes: (i) the emergence and long-term persistence of personalized strain repertoires, (ii) strain-specific pathobiont traits that drive host pathology, and (iii) the implications of strain-level ecology for the development of next-generation microbiome therapeutics. We also highlight key methodological innovations including high-resolution amplicon profiling, advanced metagenomic and single-cell genomics, and culture-based functional approaches that collectively enable strain-level resolution and are reshaping the field. Full article

Fish host complex intestinal bacterial communities that contribute to a wide range of functions, from nutrient assimilation to modulation of the immune system. Understanding how environmental and host-related factors shape the fish gut microbiota is essential for advancing sustainable aquaculture practices. This study compared the intestinal microbiota of gilthead sea bream (Sparus aurata) between wild and aquaculture populations in western Greece using 16S rRNA gene amplicon sequencing targeting the V3–V4 region, combined with culture-based methods. The analysis was based on a 97% similarity threshold and included 141 gastrointestinal samples of fish collected at two aquaculture facilities and two wild fisheries, representing two different growth phases (150 g and 300 g body weight). High-throughput sequencing data revealed a clear separation of gut microbial communities according to origin (wild vs. aquaculture), geographic location, and body growth phase, with most wild fish groups exhibiting higher microbial diversity than their farmed counterparts, except for group MES_150 which showed similar or lower values. The gut microbiota was dominated by Pseudomonadota (53%), Bacillota (29%), Actinomycetota (7%), Deinococcota (5%), and Bacteroidota (4%). A shared core microbiome, comprising Psychrobacter, Staphylococcus, Geobacillus, Aeromonas, Enterobacter, Pantoea, Bacillus, and Acinetobacter, was detected across all populations. Wild fish were enriched in Psychrobacter, Aeromonas, and Photobacterium, while aquaculture fish displayed higher abundances of Vibrio, Allomeiothermus, and Staphylococcus. Network analysis revealed mostly mutually exclusive interactions in both groups but distinct patterns of co-occurrence, driven mainly by Paenibacillus, Enterobacter, and Staphylococcus in wild samples, and by Vibrio, Aeromonas, and Pseudomonas in farmed fish. Culture-based assays demonstrated greater diversity in wild fish, dominated by Pseudomonas, Staphylococcus, and Vibrio strains, in contrast to the frequent occurrence of Staphylococcus and Psychrobacter in aquaculture samples. The findings suggest that aquaculture practices significantly alter gut microbial community structure and reduce diversity, with potential implications for fish health and disease resistance. The identified core and differentially abundant taxa provide candidates for probiotic development to improve aquaculture sustainability. Full article