Search Results (72)

Attention-deficit/hyperactivity disorder (ADHD) is a complex neurodevelopmental disorder increasingly discussed within the microbiota-gut–brain axis. This narrative review synthesizes evidence on bacterial and fungal dysbiosis in ADHD, with emphasis on Candida spp., diet, probiotics, synbiotics, and health-related quality of life. A structured narrative search of PubMed/MEDLINE, Scopus, and KoBSON-accessible sources was performed for studies addressing ADHD, gut microbiota, mycobiome, Candida, nutrition, microbiome-targeted interventions, and quality of life. Evidence was synthesized thematically because of methodological heterogeneity. Available studies suggest that ADHD may be associated with altered gut microbial diversity, changes in taxa such as Faecalibacterium, Blautia, Odoribacter, and Enterococcus, and immune–metabolic alterations. However, findings are heterogeneous and do not support a single ADHD-specific microbial signature. The fungal component remains insufficiently investigated, although evidence indicates increased Candida, particularly Candida albicans, in children with ADHD and a possible link with intestinal permeability. Dietary quality, micronutrient status, probiotics, and synbiotics may modulate microbiota–gut–brain pathways, but should be considered complementary and individualized, particularly in patients with gastrointestinal, dietary, immune, or metabolic vulnerability. Bacterial and fungal dysbiosis may represent biologically plausible, primarily associative components of ADHD-related pathophysiology. Evidence remains preliminary, exploratory, non-causal, and requires cautious interpretation in future research and clinical settings. Full article

Autoimmune and immune-mediated inflammatory diseases (IMIDs) develop when genetically and environmentally susceptible hosts lose stable immune tolerance. The gut ecosystem is increasingly recognized as a biologically active interface in this process. Its bacterial, fungal, and viral components may shape mucosal and systemic immunity through antigenic stimulation, barrier regulation, and metabolite-dependent signaling, although the strength of evidence is uneven: bacteriome data are currently the most mature, whereas mycobiome, virome, and phageome findings remain more disease-specific and emerging. Dysbiosis may influence autoimmunity through overlapping routes, including epithelial barrier failure, altered short-chain fatty acid, bile acid, and tryptophan metabolism, molecular mimicry, and cross-kingdom microbial interactions. Nutrition is central to this network because dietary substrates determine microbial growth, metabolic output, epithelial integrity, and immune-cell differentiation. In this narrative review, we integrate evidence on disease-associated bacteriome, mycobiome, and virome patterns in systemic autoimmune diseases, with emphasis on rheumatoid arthritis, systemic lupus erythematosus, Sjögren’s syndrome, systemic sclerosis, spondyloarthritis, vasculitides, and idiopathic inflammatory myopathies. COVID-19 is considered not as a proven causal driver of autoimmunity, but as an example of an environmental and infectious insult capable of perturbing microbiome–barrier–immune communication. Finally, we discuss diet-based and microbiome-targeted approaches, including probiotics, prebiotics, synbiotics, and postbiotics, as adjunctive strategies that may help restore microbial resilience and immune balance. A better understanding of the diet–microbiome–host immunity axis may support more personalized preventive and therapeutic concepts in autoimmune disease. Full article

Background: Cutaneotrichosporon jirovecii is an under-characterized basidiomycetous yeast within the family Trichosporonaceae. Its taxonomic placement, ecological distribution, and functional potential remain incompletely understood because genome-scale resources for C. jirovecii and closely related lineages are limited. Methods: We characterized strain H0426_7, a C. jirovecii-related yeast recovered from a human fecal sample, using ITS-based type-strain comparison, ITS phylogenetic analysis, whole-genome sequencing, average nucleotide identity analysis, read-level assessment of public C. jirovecii-labeled datasets, and comparative functional annotation. Antifungal susceptibility was assessed using the Sensititre YeastOne plate. Results: The ITS sequence of H0426_7 closely matched type-strain material of C. jirovecii, including CBS 6864 and its equivalent deposits. The ITS-based tree placed H0426_7 adjacent to CBS 6864 with bootstrap support of 87%. The final draft genome comprised 38.66 Mb in 1974 contigs, with a GC content of 63.76% and BUSCO completeness of 80.0%. ANI analysis showed that H0426_7 was genomically distinct from the recognized Cutaneotrichosporon species included in the ANI analysis but highly similar to two unclassified feces-derived strains, P10-008 and PK4640, with ANI values exceeding 98.8%. Two public datasets labeled as C. jirovecii showed anomalously low ANI values with H0426_7; read-level taxonomic profiling indicated low target-fungal read proportions, suggesting that these datasets are unsuitable as definitive genome-level references. CAZyme annotation identified 285 family assignments in H0426_7, representing 278 non-redundant predicted proteins, including relatively high GH5 and GH31 counts, suggesting candidate carbohydrate-utilization features shared with the H0426_7/P10-008/PK4640 lineage. Conclusions: H0426_7 is best described as a C. jirovecii-related Cutaneotrichosporon isolate pending availability of a high-quality genome assembly from the C. jirovecii type strain. This study expands genome-scale resources for underrepresented basidiomycetous yeasts and provides a comparative framework for future taxonomic, ecological, and functional studies of feces-associated Cutaneotrichosporon lineages. Full article

Intestinal fungal overgrowth (IFO) is an increasingly recognized yet underexplored component of gut dysbiosis with potential implications for gastrointestinal and systemic disease. While bacterial microbiota have historically garnered research attention, recent advances in sequencing technologies have highlighted the importance of the gut mycobiome in maintaining intestinal homeostasis. Disruption of fungal–bacterial balance, particularly involving Candida albicans, C. tropicalis, and C. glabrata, may contribute to symptom generation through immune activation, epithelial barrier dysfunction, biofilm formation, and the production of toxic metabolites such as acetaldehyde and candidalysin. Emerging clinical evidence suggests that IFO is associated with persistent gastrointestinal symptoms, including bloating, abdominal discomfort, and altered bowel habits, particularly in patients who do not respond to conventional therapies targeting bacterial overgrowth. Furthermore, fungal dysbiosis involving Malassezia restricta and Saccharomyces cerevisiae has been associated with inflammatory bowel disease, metabolic disorders, and systemic immune dysregulation; however, the nature and directionality of these relationships remain incompletely understood. Despite increasing recognition, the diagnosis of IFO remains challenging due to a lack of standardized criteria and validated non-invasive tools. Therapeutic strategies, including antifungal agents such as fluconazole and nystatin, as well as microbiome-targeted interventions, show promise but require further validation. This review provides a comprehensive synthesis of current evidence regarding the epidemiology, pathophysiology, clinical manifestations, diagnostic challenges, and therapeutic implications of IFO, with particular emphasis on species-specific mechanisms. Recognition of the intestinal mycobiome as a potentially important component of gut health may provide new perspectives for understanding gastrointestinal disorders and inform future precision medicine approaches. Full article

Type 1 Diabetes (T1D) is a complex autoimmune disorder characterized by immune-mediated destruction of pancreatic β cells, driven by genetic susceptibility and modulated by environmental factors, notably the gut microbiome. Dysbiosis, manifested as reduced microbial diversity, perturbations in the Firmicutes/Bacteroidetes ratio, and compromised short-chain fatty acid production, contributes to T1D pathogenesis through mechanisms involving immune system dysregulation and heightened intestinal permeability. Emerging evidence indicates a relationship between the gut and oral microbiomes, as well as the potential influence of the virome and mycobiome. This narrative review synthesizes the current literature on the intricate interplay between the gut microbial ecosystem, the host immune response, and the development of T1D, highlighting the potential for targeted microbiome-based interventions to ameliorate disease progression. A more nuanced understanding of these multi-kingdom interactions is essential for developing precise therapeutic strategies to prevent or delay T1D onset and to improve patient outcomes through restoration of immune tolerance and gut homeostasis. Full article

Sewage sludge management poses major environmental challenges due to increasing production and concerns about contaminants and microbial risks. Vermicomposting offers a sustainable biological treatment, yet the extent to which different earthworm species shape microbial outcomes remains poorly understood. Here, we examined how gut transit by three epigeic (Eisenia andrei, E. fetida, and Dendrobaena hortensis) and two anecic (Lumbricus friendi and L. terrestris) earthworm species alters bacterial and fungal communities in fresh sewage sludge. Using 16S rRNA and ITS amplicon sequencing combined with multivariate, differential-abundance, and functional prediction analyses, we compared sludge and earthworm cast bacteriomes and mycobiomes. Earthworm gut transit caused pronounced species-specific restructuring of bacterial and fungal community composition, diversity, and functional profiles, with clear separation between sludge and cast communities. Functional analyses indicated coordinated shifts in bacterial metabolic potential and fungal trophic modes consistent with enhanced biosynthetic and decomposer functions. Pathogen profiles were reshaped in a host-dependent manner, with low overall abundances and selective changes rather than uniform suppression. These findings demonstrate that vermicomposting outcomes depend strongly on earthworm species and microbial kingdom, highlighting the importance of earthworm lifestyle diversity when evaluating the ecological safety and agronomic potential of sludge-derived amendments. Full article

Chronic inflammatory skin diseases, including atopic dermatitis (AD) and psoriasis, are systemic immune-mediated disorders driven by dysregulated immune responses. The gut–skin axis is a bidirectional network linking intestinal microorganisms, their metabolites, and host immunity. It connects microbiome composition and function with systemic inflammation and cutaneous pathology, shaping disease-specific mechanisms such as Th2/IL-4/IL-13-mediated barrier dysfunction in AD and Th17/IL-23/IL-17-driven hyperproliferation in psoriasis. Microbiota-derived metabolites, including short-chain fatty acids, tryptophan-derived aryl hydrocarbon receptor ligands, and bile acid-dependent FXR/TGR5 signaling, modulate immune homeostasis and epithelial integrity. Gut dysbiosis, impaired metabolite production, and barrier dysfunction disrupt regulatory networks, amplifying inflammation. Microbiota-targeted interventions, including probiotics, synbiotics, postbiotics, and precision nutrition, may serve as adjunctive therapies, although further well-controlled clinical studies are needed. Integrating multi-omics, metabolomics, and functional microbial profiling, alongside investigations of the gut mycobiome and virome, will be critical to identify predictive biomarkers and optimize therapeutic strategies. These concepts remain mechanistically compelling but largely theoretical, requiring validation in longitudinal and interventional studies. Full article

Recent findings suggest that the gut microbiome significantly influences cancer outcomes, including responses to immune checkpoint inhibitor (ICI) treatments. Although early research focused on gut bacteria, it is now understood that the microbiome includes a bacteriome, virome, and mycobiome, all of which can modulate host immunity. Some commensal bacteria enhance anti-tumor immune responses and improve ICI efficacy, as demonstrated in both mice and patients. Fecal microbiota transplants (FMT) from patients responding to ICI have successfully reversed resistance in certain non-responders. In addition to bacteria, gut fungi and viruses are gaining attention as further factors influencing ICI effectiveness and toxicity. Recent multi-omics studies across cancer cohorts show that fungal and viral populations in the gut vary between ICI responders and non-responders. Commensal fungi may shape anti-cancer immunity by inducing inflammatory or tolerogenic pathways, while viral components can stimulate innate immune sensors that promote tumor surveillance. On the other hand, gut dysbiosis marked by expansion of pathobionts (including opportunistic fungi) and reduction in beneficial microbes is linked to serious immune-related adverse events (irAEs) such as ICI-induced colitis. This review discusses the multi-kingdom gut microbiome–bacteria, fungi, and viruses–and their interactions with the immune system in cancer therapy. We emphasize known mechanisms linking these microbes to anti-tumor immunity, overview human studies associating gut microbiome profiles with ICI outcomes and explore strategies to modulate the microbiome to enhance ICI efficacy while reducing toxicity. Understanding and utilizing the gut mycobiome and virome in conjunction with the bacteriome could pave the way for new biomarkers and therapeutic adjuvants in cancer immunotherapy. Full article

Prior studies in people with cystic fibrosis (CF) demonstrated a positive impact of ivacaftor on the stool microbiome. However, studies evaluating the impact of elexacaftor–tezacaftor–ivacaftor (ETI) on gut dysbiosis are limited. In this prospective, observational study, we evaluated the differences in stool microbiome in children (aged 2–17 years) with CF who were treated with ETI for at least two months and compared with children with CF who did not receive ETI. We also included healthy siblings as controls. There were no significant differences in the demographics between the groups. There were no significant differences in alpha diversity between the groups for both bacteriome and mycobiome. Alpha diversity showed a negative trend with the duration of ETI therapy for both bacteriome and mycobiome. Firmicutes and Proteobacteria were the most abundant phyla and core members across all samples, regardless of disease status or treatment. Ascomycota and Basidiomycota were the most abundant and core members across all samples, regardless of disease status or treatment. Alpha diversity showed a negative trend with the duration of ETI therapy for both bacteriome and mycobiome in children with CF treated with ETI. Future studies are needed to confirm or refute our preliminary findings. Full article

The aim of this pilot study was to comprehensively evaluate the gut microbiota, mycobiome, and metabolomic profile of six 4-month-old crossbred pigs (A–F) originating from the same litter and from a specific breeding facility intended for preclinical transplantation experiments, in order to assess their physiological uniformity and identify potential health-related risks prior to inclusion in a kidney transplantation study. The results demonstrated an overall high degree of microbial and metabolic uniformity among the animals, confirming the stability and suitability of the selected breeding source for experimental purposes. At the same time, several individual differences of potential clinical relevance were observed. Animals A, E, and F exhibited signs of microbial and metabolic imbalance, including reduced diversity, increased oxidative activity, and the presence of potentially pathogenic taxa (Porphyromonadaceae bacterium DJF B175, Aspergillus). In contrast, animals B, C, and D showed a balanced metabolic and microbial profile without pathological deviations. The obtained results highlight the importance of preoperative assessment of the gut bacteriome, mycobiome, and metabolome when selecting animals for transplantation experiments. Such a selective screening approach may contribute to the early identification of physiological deviations, reduction of interindividual variability, and increased reliability and translational potential of preclinical studies. Full article

This study applied a guided culturomics workflow to isolate and characterize gut-associated yeasts as probiotic candidates. Culture conditions were optimized using Dixon agar and Modified Schädler Agar with a moderate antibiotic cocktail (colistin, chloramphenicol, vancomycin) to suppress bacteria without impairing yeast growth, combined with incubation at 37 °C under anaerobic conditions to mimic the intestinal environment. From three healthy donors, 305 isolates were recovered (MSA: 193; Dixon: 112). After excluding pseudohyphal morphotypes and PCR positive Candida isolates, 127 non-Candida strains remained. Safety screening (hemolysis, DNase, coagulase) reduced the pool to 26 safe isolates. Simulated gastrointestinal stress tests showed that 20 out of 26 exhibited at least 50 percent survival under pH 2.0 or 0.5% bile salts. Functional assays revealed strain-specific antimicrobial activity against Staphylococcus aureus, Escherichia coli including O157:H7 and Salmonella species, with several isolates (Y6, Y22, Y42, Y48, Y55, Y56, Y73, Y105, Y127) showing broad and strong inhibition. Two isolates Y44 and Y55 further demonstrated robust bile and acid tolerance (>50% survivability) in both conditions. All isolates displayed intracellular but not extracellular bile salt hydrolase activity, indicating a viability dependent cholesterol lowering potential. Overall, the workflow minimized bacterial interference while enriching for safe and functional yeasts. Full article

Background/Objectives: Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by persistent social communication difficulties and restricted, repetitive behaviors, with prevalence estimates continuing to rise worldwide. The gut–brain axis has been proposed as a potential contributor to ASD, yet human studies yield inconsistent findings, partly due to confounding effects of diet and behavior. Methods: Here, we investigated the gut bacteriome and mycobiome of children with ASD (n = 17) compared with their non-ASD siblings (n = 9) and parents without ASD (n = 27), alongside detailed assessment of dietary intake (n = 79) using 7-day food diaries. Results: Multi-kingdom microbiome profiling revealed no significant differences in α- or β- diversity across ASD, sibling, and parental groups, with only minor taxonomic variation observed. Similarly, fungal community composition showed negligible group-level differences. By contrast, dietary patterns strongly differentiated ASD from non-ASD participants: children with ASD consumed higher levels of sweets and sugary foods, lower portions of vegetables, and exhibited reduced overall dietary diversity. Statistical analyses confirmed that dietary factors, rather than microbial composition, explained variation in ASD diagnosis. Conclusions: These findings suggest that selective and repetitive eating behaviors are characteristic of ASD shape dietary intake, which in turn influences gut microbial diversity. Thus, in humans, the directionality may run primarily from behavior to diet to microbiome, rather than from microbiome to behavior. Our results underscore the importance of incorporating dietary variables into microbiome research and highlight the need for targeted nutritional interventions to improve health outcomes in individuals with ASD. Full article

Background: Lung cancer is the leading cause of cancer-related mortality globally, with lung adenocarcinoma (LUAD) as the most common subtype. Dysbiotic intratumoral mycobiomes drive LUAD pathogenesis, and Aspergillus sydowii (A. sydowii) acts as a key oncogenic fungal species. Ginseng polysaccharides (GPs), bioactive phytochemicals with immunomodulatory and oncostatic properties, counteract fungal infections and restore immunosurveillance in LUAD. Methods: Subcutaneous and orthotopic LUAD murine models were established by implanting Lewis lung carcinoma (LLC) cells. Subcutaneous tumors were infected intratumorally and orthotopic models via nasal inoculation. GPs (200 mg/kg/day) were orally administered to evaluate tumor growth. Metagenomic and targeted bile acid metabolomic profiling of fecal and tumor tissues was performed, with Spearman correlations analyzed using R packages. Results: GPs significantly inhibited A. sydowii-induced tumor growth in both models. In subcutaneous tumors; GPs reduced volume (p < 0.05) and weight vs. infected controls. In orthotopic models, GPs decreased pathological nodules and lung weight, with micro-CT/H&E confirming attenuated hyperplasia. Metagenomics showed GPs restored gut homeostasis by enriching Lactobacillus/Muribaculum intestinale and suppressing pro-inflammatory Alistipes. Targeted metabolomics revealed reduced β-Hyodeoxycholic Acid (3β-HDCA), Chenodeoxycholic acid 24-acyl-b-D-glucuronide (CDCA-24G) and 3β-hydroxychol-5-en-24-oic acid (5-isoLCA) after GP treatment. Network analysis confirmed significant microbe–bile acid interactions. Conclusions: GPs exert antitumor effects against A. sydowii-induced LUAD by modulating gut microbiota and bile acid metabolism. This identifies GPs as a promising therapy for mycobiome-influenced cancers, with dual targeting of fungal infection and metabolic reprogramming. Full article

Patients with cystic fibrosis (CF) are frequently exposed to antibiotic treatments, which can alter the fungal communities (mycobiome) across their mucosal sites. This pilot study investigated the impact of antibiotic exposure on the mycobiome by analyzing fungal community dynamics in the upper respiratory- (nasal lavage) and gastrointestinal- (stool samples) tracts of 12 patients with CF following (a) long-term antibiotic treatment over a three-year period and (b) short-term antibiotic therapy during acute pulmonary exacerbations. Mycobiome profiles of the samples obtained from 38 healthy individuals were also analyzed and used for comparison purposes. The ITS1 region of the fungal rRNA gene cluster was sequenced to characterize and quantify the fungal community composition in both cohorts. Compared to healthy controls, samples from the patients with CF who had undergone long-term antibiotic treatment revealed a significantly increased fungal biomass in both sino-nasal and stool samples. Moreover, diversity metrics revealed significant differences in nasal lavage samples, whereas the stool samples showed no significant variation. Candida spp. was significantly enriched in both nasal and stool samples from CF patients. Further analyses demonstrated a strong positive correlation between the relative abundance of Candida spp. and the cumulative antibiotic intake over the three-year period in sino-nasal samples, but not in stool samples. Acute antibiotic treatment during a pulmonary exacerbation episode also led to a marked increase in the abundance of Candida spp. in sino-nasal samples. These findings highlight the increased sensitivity of the sino-nasal mycobiome to both chronic and acute antibiotic exposure in CF patients, as characterized by a site-specific fungal overgrowth, particularly of Candida spp. Full article

Rosacea is a chronic inflammatory skin disorder with multifactorial pathogenesis involving immune dysregulation and microbial alterations. This study compared the mycobiomes of skin, blood, and stool samples in rosacea patients and healthy controls to assess fungal diversity, abundance, and possible translocation, as well as associations with bacterial microbiomes. Internal transcribed spacer (ITS) region sequencing was performed on samples from 14 rosacea patients and 8 controls. While distinct fungal community compositions were observed across sample types, no significant differences in fungal diversity or genus abundance were found between the patient and control groups in any compartment. Malassezia dominated the skin mycobiome, while stool samples showed higher abundances of Candida and Saccharomyces, which were inversely correlated. Patients with high skin and blood Malassezia also exhibited increased Cutibacterium abundance, suggesting a potential role in impaired skin barrier integrity. Stool samples with elevated Saccharomyces correlated with higher levels of anti-inflammatory bacteria Prevotella and Agathobacter, whereas Candida dominance showed the opposite. These findings suggest that fungal dysbiosis, in the interplay with bacterial communities, may influence rosacea pathogenesis through the gut–skin axis. This work underscores the significance of integrated microbiome research across multiple biological compartments in order to enhance our understanding and potential targeting of microbial factors in rosacea. Full article