Search Results (108)

Microplastic (MP) contamination has become a defining feature of twenty-first century environmental change, yet the toxicological and ecological consequences for amphibians and reptiles—two vertebrate classes already facing severe extinction pressures—remain fragmented across taxa, regions, and methodological traditions. Here, we synthesize field and experimental evidence from five continents to provide a taxonomically balanced, mechanistically grounded, and geographically explicit assessment of MP exposure, bioaccumulation, and toxicity in herpetofauna, drawing on a structured literature search in Web of Science, Scopus, and PubMed (January 2015—March 2026). Field detection rates of MPs in amphibian larvae range from 26% in conservatively screened Central European populations to 73–80% in anuran tadpoles from high-anthropogenic-pressure Anatolian catchments, with fibrous polyethylene terephthalate (PET), polyethylene (PE), and polypropylene (PP) particles dominating the detected burden. Mechanistic evidence converges on oxidative stress cascades, hypothalamic–pituitary–thyroid axis disruption, gut and cutaneous microbiome dysbiosis, and compromised antiviral and antifungal immunity, with the latter potentially amplifying vulnerability to Batrachochytrium dendrobatidis and to ranavirus. Among reptiles, sea turtles display near-universal MP ingestion with documented maternal transfer to eggs; freshwater turtles, terrestrial squamates, and crocodilians remain critically understudied. Three structural asymmetries constrain current ecotoxicological risk characterization: taxonomic bias toward anurans and sea turtles, geographic bias toward the Global North, and experimental bias toward acute, supra-environmental laboratory exposures using pristine, single-polymer particles that fail to capture the chemical complexity of weathered field mixtures. We argue that MP burden may warrant consideration as a candidate stressor criterion within IUCN Red List assessments and within environmental risk assessment frameworks for freshwater and terrestrial biodiversity once a robust quantitative relationship between MP burden and demographic decline or population-level fitness has been established, and propose six hypothesis-driven research priorities: methodological standardization, reptile toxicokinetics, transgenerational epigenetics, MP–pathogen microbiome interactions and their translation into population viability models, temperature × MP interaction under climate warming, and population-genetic consequences of contemporary MP-driven selection, as the most tractable avenues for ecotoxicological progress and for the development of herpetofauna-specific risk characterization frameworks. Full article

Emerging research highlights the complex interplay between the gut microbiome, skin health, and environmental exposures, forming what is now recognized as the gut–skin–exposome axis. This narrative review explores the role of gut microbiome dysbiosis—a disruption in the balance of intestinal microorganisms—in the pathogenesis and progression of various non-communicable inflammatory skin diseases, including acne, atopic dermatitis, psoriasis, rosacea, systemic lupus erythematosus, chronic spontaneous urticaria, hidradenitis suppurativa, and alopecia areata. This review synthesizes mechanistic studies, clinical trials, and Mendelian randomization data to elucidate how altered gut microbial composition contributes to systemic and cutaneous inflammation. Key modifiable factors, such as diet, antibiotics, stress, and sleep, as well as interventions like probiotics, prebiotics, synbiotics, and fecal microbiota transplantation, are discussed for their potential therapeutic value. By integrating clinical insights with microbiome science, this review underscores the importance of a holistic, systems-based approach in managing inflammatory skin diseases, offering clinicians evidence-based strategies to improve patient outcomes through gut microbiome modulation. Full article

Recent studies have reported skin microbiome dysbiosis in patients with photodermatoses, featuring enriched Staphylococcus aureus colonization and decreased microbiome diversity. We propose that ultraviolet radiation (UVR), along with atypical antimicrobial peptides, may exert selective pressure on the skin microbiome, while cytokine dysregulation and a reduction in commensal bacteria amplify microbial dysbiosis. Dysbiotic microorganisms further release pathogen-associated patterns and virulence factors, and activate tissue-resident memory T cells, which collectively contribute to local inflammation. These mechanisms establish the skin microbiome as a potential target for early intervention. Potential therapeutic strategies may include antibiotics, phototherapy, bleach baths, phage therapy, and microbiota-based therapies. This review integrates current findings from microbial ecology, molecular biology, and host immunology to outline a conceptual framework linking UVR exposure, microbiome alterations, and cutaneous immune responses, while emphasizing the current limitations and evidence gaps in this field. Full article

Psoriasis is a chronic immune-mediated disease driven by genetic susceptibility and environmental factors, including microbial exposure. While HLA-C-linked variants represent the strongest genetic risk factors, their relationship with the cutaneous microbiome remains incompletely understood. This study aimed to investigate host–microbiome interactions in psoriasis through integrative multi-omics analysis. Skin microbiome profiling using 16S rRNA sequencing and targeted genotyping of psoriasis-associated single-nucleotide polymorphisms (SNPs) was performed in lesional and non-lesional skin from patients with plaque psoriasis and in healthy controls. Integrated analysis was conducted using supervised multivariate modeling (DIABLO) to identify coordinated genetic and microbial features associated with disease status. Combined genetic and microbial signatures differentiated lesional, non-lesional, and healthy skin. Variants within the HLA-C susceptibility region, including rs12191877, rs10484554, and rs4406273, showed contributions to group separation and demonstrated positive associations with Peptostreptococcus anaerobius. Associations involving ERAP1 variants linked antigen-processing pathways with inflammation-associated microbial taxa in lesional skin. Importantly, genotype–microbiome correlations were also detected in clinically non-lesional skin, where an increased psoriasis risk allele dosage co-varied with a higher relative abundance of P. anaerobius and Aerococcus urinae. In contrast, commensal-associated taxa were enriched in healthy controls and formed genotype-linked clusters only in non-lesional skin. These findings suggest that psoriasis is characterized by coordinated host genetic and microbial interaction patterns centered on antigen presentation pathways. The presence of a genotype–microbiome coupling in non-lesional skin may indicate that genetically determined immune configurations could shape microbial community structure prior to visible lesion development. Rather than reflecting uniform dysbiosis, psoriasis may represent a dynamic host–microbe ecosystem in which genetic susceptibility influences microbial persistence and inflammatory readiness. Full article

Hidradenitis suppurativa (HS) is a chronic inflammatory dermatosis characterized by recurrent nodules, abscesses, and sinus tract formation in intertriginous skin. Although HS is increasingly recognized as an autoinflammatory condition rather than a classical infection, antimicrobial therapies remain central to disease management, implicating a potential role for the cutaneous microbiome in disease activity. Recent advances in culture-independent sequencing techniques have enabled more detailed characterization of microbial communities in HS, revealing consistent alterations in microbial composition and diversity. Compared with healthy skin, HS lesions exhibit reduced microbial diversity, depletion of commensal organisms such as Cutibacterium acnes, and enrichment of anaerobic bacteria including Prevotella, Porphyromonas, and Finegoldia. These alterations are more pronounced in chronic, tunnel-forming disease and are frequently associated with biofilm formation, which may contribute to treatment resistance and persistent inflammation. Microbiome changes have also been observed beyond overtly lesional skin, suggesting a broader field effect. Evidence regarding extracutaneous microbial compartments, particularly the gut microbiome, remains limited and heterogeneous, while methodological variability in sampling, sequencing, and treatment exposure continues to complicate cross-study comparisons. Emerging data further suggest that immune-targeted therapies, including biologic and small-molecule agents, may indirectly influence microbial community structure through modulation of the inflammatory milieu. Collectively, the available evidence supports cutaneous dysbiosis as a characteristic feature of HS that may potentially interact bidirectionally with immune dysfunction. Future longitudinal, multi-omic studies integrated with clinical phenotyping will be critical to clarify causal relationships and to determine whether microbiome modulation can be leveraged to improve therapeutic outcomes in HS. Full article

Cutaneous disorders such as atopic dermatitis, psoriasis, acne vulgaris, and rosacea, together with UV-induced skin injury and photoaging, are highly prevalent conditions that involve varying contributions from dysregulated immune responses, cutaneous inflammation, oxidative stress, barrier dysfunction, microbiome alteration, and exogenous injury. However, these conditions are biologically heterogeneous and should not be regarded as a single mechanistic class. Sulforaphane, a naturally occurring isothiocyanate found primarily in broccoli and other cruciferous vegetables, has attracted interest in dermatology because of its antioxidant, cytoprotective, and context-dependent anti-inflammatory properties. Sulforaphane exerts its biological effects by modulating key signaling pathways, particularly the Keap1/Nrf2 pathway and, in some settings, NF-κB-related signaling, thereby reducing oxidative stress and inflammation, regulating immune responses, enhancing skin barrier function, and potentially influencing the cutaneous microbiome. Preclinical studies and limited human data suggest that sulforaphane may reduce erythema, edema, and other markers of cutaneous damage in selected settings. This comprehensive review explores the role of sulforaphane across heterogeneous cutaneous conditions, with emphasis on molecular mechanisms, disease-specific differences, current evidence, and discusses key translational constraints including formulation, delivery, lack of standardized dosing, and the limitations of cell culture and animal models for predicting human efficacy. Overall, sulforaphane should presently be regarded as a promising but still early-stage translational candidate in dermatology. Robust human efficacy data remain lacking for chronic inflammatory dermatoses such as psoriasis, atopic dermatitis, acne, and rosacea, whereas the strongest current human evidence relates to UV-associated skin outcomes and photoprotection. Full article

Comano thermal water (CTW) is a hypotonic, bicarbonate–calcium–magnesium mineral water traditionally used to manage chronic inflammatory and relapsing skin diseases. This review summarises and discusses the available clinical, experimental, and translational evidence on CTW, with a particular focus on dermatological indications. The physicochemical properties of CTW, along with the presence of a stable, non-pathogenic microbial community, are examined in relation to their potential biological activity. Clinical studies indicate that CTW-based balneotherapy, alone or in combination with narrowband Ultraviolet B (UVB) phototherapy, is associated with improvements in disease severity, symptom burden, and quality of life in patients with psoriasis and atopic dermatitis, and has a favourable safety and tolerability profile. Experimental data further suggest that CTW may exert anti-inflammatory and immunomodulatory effects, modulate keratinocyte function, support skin barrier restoration, and influence the cutaneous microenvironment, including microbiome-related pathways. The review also outlines emerging evidence for CTW in skin regeneration and in upper airway inflammatory conditions treated via inhalation-based approaches. Overall, this review suggests that CTW may serve as a biologically active therapeutic resource, warranting further investigation as a complementary approach within integrative management strategies for inflammatory and barrier-related conditions. Full article

Atopic dermatitis (AD) is a chronic inflammatory skin disease influenced by several factors, including immune system imbalance, impairment of the epidermal barrier, and alterations in the composition of the gut and skin bacterial and fungal microbiota. This study combines metagenomic sequencing and culture-based methods to explore the impact of probiotic supplementation on the cutaneous microbiota and mycobiota of AD patients. Twenty-five adults diagnosed with AD were enrolled, and skin swabs were analyzed to characterize microbial diversity and load. Culturomic analyses identified 42 bacterial and 6 fungal species, confirming Staphylococcus aureus and Candida parapsilosis as predominant taxa. High-throughput sequencing revealed Staphylococcus spp. and Malassezia spp. as dominant genera, with notable interindividual variability. While probiotic use did not significantly influence bacterial diversity, it was associated with higher richness and evenness in fungal communities, as shown by alpha and beta diversity metrics. Malassezia restricta was more prevalent among probiotic users, whereas Candida parapsilosis and Rhodotorula mucilaginosa were enriched in non-users. These findings indicate an association between probiotic use and differences in the composition and diversity of the skin mycobiota compared with the bacterial microbiota, suggesting that fungal communities may be more responsive to probiotic-associated factors. Integrating metagenomic and culturomic approaches offers valuable insights into the complex interactions among host factors, microbial communities, and probiotic use in AD, paving the way for targeted microbiome-based therapeutic strategies. Full article

The accumulated ammonia within the recirculating aquaculture systems threaten fish health, while little is known about the influences during early fish ontogeny. Using larval and juvenile yellow catfish (Pelteobagrus fulvidraco) as a model, a comprehensive experiment exposing fish to varying total ammonia nitrogen concentrations (0, 10, 20 mg/L for larvae; 0, 25, 125 mg/L for juveniles) was conducted to evaluate the effects on gill transcriptome and microbiota along with the serotonergic regulation. First, the serotonin (5-HT) signal, which controls oxygen chemoreception and ventilation, was mainly detected in the surface of the body of the larvae, and then shifted to gill filaments of juveniles, showing a transition from cutaneous to branchial respiration. Both larval and juvenile yellow catfish exhibited reduced survival, damaged gill structure, and elevated 5-HT expression after ammonia exposure, as well as upregulated tph1b, slc6a4b, scgn and lama5 expression with the increased ammonia concentration, indicating the effects on respiratory function via serotonergic regulation. Further transcriptome analysis was conducted in juveniles to identify the differentially expressed genes (DEGs) and thus, to illustrate more detailed responses after ammonia exposure; KEGG enrichment analysis of DEGs indicated the coping strategy shifted from metabolic buffering to metabolic elimination via glutamine synthesis with the increased ammonia level. The qRT-PCR experiment also identified the increased expression of genes involved in the urea cycle—such as ass1, asl and glula—with the increased ammonia level. Considering the potential contributary role of microbiome to gill health, 16S sequencing was conducted on the gill in the control and the 125 mg/L ammonia-exposed group. Ammonia exposure at 125 mg/L induced significant variation in Simpson index and a marked decline in β diversity. Notably, the abundance of opportunistic pathogens such as Pseudomonadota increased, while the abundance of Deinococcota and Deinococcus—which were renowned for exceptional stress resistance capacity—decreased after ammonia exposure. Thus ammonia exposure disrupts the transcriptomic and microecological balance within gill mucosa, which may elevate the risk of pathogenic infection. Overall, our study provided the first evidence of serotonergic regulation on early fish respiration during ammonia exposure, and also offered new theoretical insights into the involvement of microorganisms in ammonia toxicity. Full article

Basal cell carcinoma (BCC) is the most common malignancy worldwide, yet the role of the skin microbiome in BCC remains poorly defined. In this cross-sectional observational case series, we compared the cutaneous microbiome of BCC lesions with matched perilesional and control skin using whole-genome shotgun sequencing in an intra-patient, multi-site sampling design. BCC samples demonstrated reduced microbial richness and significant shifts in community composition compared with matched control skin. Specifically, BCC lesions exhibited significantly lower Chao1 diversity (β = −484.6, 95% CI: −772.1 to −197.2, p = 0.003). Differences in overall microbial composition were confirmed by PERMANOVA analysis based on Bray–Curtis and Jaccard distance metrics (R² = 12.6% and 9.7%, respectively; both p = 0.01). At the species level, Cutibacterium acnes was significantly reduced in BCC samples compared with controls (β = −0.31, 95% CI: −0.45 to −0.16, p = 0.0004), corresponding to an approximately 27% lower geometric mean relative abundance. Functional profiling suggested shifts in microbial metabolic potential, with pathways related to redox balance and lipid-associated processes differentially represented in BCC samples relative to controls. Together, these findings demonstrate that BCC lesions are associated with localized alterations in microbial diversity, community composition, and inferred functional potential. These results support the presence of a tumor-associated microbiome signature in BCC; however, further studies in larger and more diverse cohorts are needed to determine whether these changes contribute to tumor development or reflect adaptation to the tumor microenvironment. 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

Cancer is a major health concern, with its incidence rate continuing to increase. There is growing interest in the microbiota and its role in carcinogenesis, as it significantly influences physiological and pathological processes. Various aspects of the microbiome have been shown to have both anti-tumor and pro-tumor effects. Advances in techniques such as high-throughput DNA sequencing have greatly improved our understanding of microbial populations in the human and canine gut. We aimed to (1) characterize the intestinal microbiota of healthy dogs and dogs with cutaneous mast cell tumors (MCTs), (2) assess changes in the intestinal microbiota of dogs undergoing electrochemotherapy (ECT) combined with gene electrotransfer (GET) of the IL-12 plasmid (IL-12), and (3) explore possible associations with the expression of immune markers Programmed cell death protein 1 (PD-1), Programmed death-ligand 1 (PD-L1), and Granzyme B (GZMB) in MCT tissue. Stool samples were collected from healthy dogs (n = 24) and dogs with MCTs (n = 24) before and after ECT and IL-12 GET. DNA was extracted from the samples, and shallow shotgun sequencing was performed. Immunohistochemistry was performed on the tumors to assess the expression of PD-1, PD-L1, and GZMB. The dysbiosis index, alpha diversity, and beta diversity did not differ between groups. Regarding microbial composition, Bifidobacterium animalis, Corynebacterium variabile, Lactobacillus johnsonii, Pediococcus pentosaceus, Streptococcus anginosus, Streptococcus equinus, Streptococcus intermedius, Clostridium thermobutyricum, Megasphaera elsdenii, and Anaerobiospirillum sp. were found in lower relative abundance in feces of dogs with MCTs, while Bacteroides togonis, Lactobacillus amylolyticus, Prevotella sp. CAG:279, and Megamonas hypermegale were more abundant compared to healthy dogs. Our study provides further insight into the composition of the gut microbiota in dogs with MCTs, where ECT and IL-12 GET did not lead to major shifts. We were unable to establish any association between the expression of immune markers and the microbiota. Full article

Oral mucosa healing is a complex process that involves the innate wound healing system, including the coagulation cascade, extracellular matrix remodeling, immune cell responses, and fibroblast and epithelial responses, within the context of a dynamic resident microbiome. Unlike cutaneous wounds, oral wounds heal rapidly with minimal scarring despite constant exposure to diverse microbial communities, saliva, and mechanical stress. Emerging evidence highlights the critical interplay between microbiome-mediated signaling and macrophage plasticity in shaping wound outcomes, suggesting that similar mechanisms operate within the oral cavity. Inflammation is an essential component of wound repair, and its resolution is necessary to promote tissue remodeling and functional regeneration. Macrophages play a central role in this transition through phenotype switching from a pro-inflammatory (M1) to a pro-resolving, anti-inflammatory (M2) state. This review synthesizes current understanding of the oral microbiome’s influence on macrophage polarization across distinct stages of oral wound healing and examines microbial-based strategies that modulate the immune response to enhance repair. Significant knowledge gaps remain, including limited clinical translation, inter-individual variability in microbiome composition, and complete mechanistic insight into host–microbe immune interaction. Addressing these challenges enables the development of precision microbiome-based therapeutics that restore microbial balance, direct macrophage-driven regeneration, and improve outcomes in oral wounds and chronic inflammatory conditions. Full article

Acne vulgaris is a chronic inflammatory dermatosis where conventional therapies often face limitations in efficacy and safety, necessitating the development of microbiome-targeted interventions. This study investigated the immunomodulatory potential of microbiome-derived tryptophan metabolites as a novel therapeutic strategy for Cutibacterium acnes (C. acnes)-induced inflammation, focusing on the aryl hydrocarbon receptor (AHR) pathway. We evaluated indole-3-lactic acid (ILA), indole-3-acrylic acid (IAA), and indole-3-propionic acid (IPA) in comparison to tapinarof, utilizing C. acnes-stimulated human epidermal keratinocytes and a C. acnes-induced acne mouse model. In vitro, ILA and IPA significantly suppressed C. acnes-driven inflammatory mediators, including Tumor Necrosis Factor-alpha (TNF-α), Interleukin (IL)-1β, and Cyclooxygenase-2 (COX2), whereas IAA demonstrated limited efficacy. In vivo, ILA treatment exhibited superior therapeutic activity, markedly reducing inflammatory cell infiltration, epidermal hyperplasia, and IL-1β expression. Transcriptomic analysis confirmed that ILA attenuates inflammatory signaling (e.g., IL-17 and TNF pathways) while upregulating AHR-responsive genes such as Cytochrome (CYP) 1A1 and CYP1B1. Collectively, these findings establish ILA as a potent postbiotic that mitigates cutaneous inflammation through selective activation of the AHR. Future studies should prioritize the clinical translation of ILA-based topical formulations, with rigorous evaluation of their efficacy and safety in well-designed human trials, to support their development as a non-antibiotic therapeutic alternative for acne management. Full article

Background: The scalp represents a distinct ecological niche within the skin, and the structure of its microbiota, together with the factors shaping it, is considered important for the maintenance of scalp health. Methods: This study systematically analyzed the bacterial and fungal community structures on the scalps of 63 healthy Chinese women aged 18–25, and examined their associations with scalp type, sensitivity, and lifestyle factors. Scalp samples were collected, questionnaire surveys were administered, scalp physiological parameters were measured, and high-throughput sequencing of 16S rRNA and ITS genes was performed. Results: The results showed that, in this unique scalp skin niche, the dominant bacterial phylum was Actinobacteria, while the dominant fungal phylum was Ascomycota. The predominant bacterial genera were Cutibacterium and Staphylococcus, and the fungal community was dominated by Malassezia. When scalp types were categorized according to sebum content, dry scalps showed enrichment of Micrococcus, Streptococcus, Delftia, Staphylococcus aureus, and Staphylococcus hominis, whereas oily scalps, on the other hand, are primarily colonized by Cutibacterium and Staphylococcus species. In addition, we observed microbial interactions under different physiological conditions. The relative abundance of Cutibacterium decreased with increasing scalp sensitivity. Higher psychological stress, insufficient sleep, and high-sugar/high-fat dietary patterns tended to coincide with shifts in the relative abundance of Malassezia, implying that these influences may act through fungal rather than bacterial components of the scalp microbiota. Scalp sensitivity showed the strongest association with β-diversity among the variables examined, although the effect size was modest and did not reach conventional significance in the multivariable PERMANOVA. Conclusions: In young women, the scalp constitutes a distinct cutaneous niche whose microbiota is jointly shaped by sebum level, barrier sensitivity, and lifestyle factors, with sensitivity emerging as one of the more influential dimensions of community variation. These findings provide guidance for future in-depth research on the scalp microbiome network and offer a foundational reference for preventing suboptimal and pathological scalp conditions. Full article