@article {pmid41198730,
year = {2025},
author = {Garrigós, M and García-Ruiz, O and Enkvist, CR and García-López, MJ and Moreno-Indias, I and Ruiz-López, MJ and Veiga, J and Figuerola, J and Videvall, E and Martínez-de la Puente, J},
title = {Effects of avian Plasmodium exposure on the microbiota of Culex pipiens.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {38898},
pmid = {41198730},
issn = {2045-2322},
support = {PRE2021-098544//Ministerio de Ciencia, Innovación y Universidades/ ; PU19/01925//Ministerio de Ciencia, Innovación y Universidades/ ; FJC2021-048057-I//Ministerio de Ciencia, Innovación y Universidades/ ; PID2020-118205GB-I00//Ministerio de Ciencia, Innovación y Universidades/ ; PTA2022-021854-I//Agencia Estatal de Investigación/ ; PID2020-118921RJ-100/AEI/10.13039/501100011033//Agencia Estatal de Investigación/ ; CPII21/00013//Instituto de Salud Carlos III/ ; 2023-05026//Swedish Research Council/ ; },
mesh = {Animals ; *Culex/microbiology/parasitology ; *Plasmodium/physiology ; RNA, Ribosomal, 16S/genetics ; *Microbiota ; Sparrows/parasitology ; Mosquito Vectors/microbiology/parasitology ; *Malaria, Avian/parasitology/transmission ; },
abstract = {Malaria parasites (Plasmodium spp.) are mosquito-borne parasites that infect humans and wildlife. Several studies support the role of mosquito microbiota as a major driver of Plasmodium transmission, although studies on wildlife malaria are typically neglected. Here, we used a 16S rRNA metabarcoding approach to assess whether the exposure to avian Plasmodium parasites affects the microbiota of their natural vector, Culex pipiens. Mosquitoes, captured in the field as larvae and grown in the laboratory, were allowed to feed on house sparrows (Passer domesticus) naturally infected with Plasmodium relictum (lineage SGS1) and uninfected birds. We analyzed the microbiota composition of the abdomens of individual mosquitoes and found 2,006 Amplicon Sequence Variants (ASVs). Culex pipiens' microbiota was dominated by bacteria of the genus Wolbachia, followed by the genera Stenotrophomonas and Faecalibacterium. We observed no difference in alpha nor beta diversity between mosquitoes that fed on Plasmodium-infected birds (exposed mosquitoes) and those that fed on uninfected birds (unexposed mosquitoes). However, exposed mosquitoes had a higher relative abundance of bacteria of the family Bacteroidaceae and the genus Bacteroides than the unexposed mosquitoes. Excluding the intracellular endosymbiont Wolbachia from the analyses, we obtained similar results, and also found a higher relative abundance of bacteria of the family Rikenellaceae in exposed mosquitoes. A pathway enrichment analysis based on KEGG annotations revealed that the bacterial community in exposed mosquitoes was enriched in pathways mainly related to biosynthesis and metabolism. Our results suggest that Cx. pipiens exposed to avian Plasmodium have slightly different microbiota composition, although further research is needed to establish the causality of these effects.},
}

Animals
*Culex/microbiology/parasitology
*Plasmodium/physiology
RNA, Ribosomal, 16S/genetics
*Microbiota
Sparrows/parasitology
Mosquito Vectors/microbiology/parasitology
*Malaria, Avian/parasitology/transmission

@article {pmid41198444,
year = {2025},
author = {Goryachok, M and Fairbanks-Mahnke, A and Fulte, S and Tamkin, E and McCarty, A and Larson, ED and Planet, PJ and Clark, SE},
title = {Functional CFTR may be required for Prevotella melaninogenica regulation of epithelial cell defense against Staphylococcus aureus.},
journal = {Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jcf.2025.11.002},
pmid = {41198444},
issn = {1873-5010},
abstract = {BACKGROUND: Prevotella melaninogenica is enriched in the lungs of people with cystic fibrosis (pwCF), yet its functional impact on respiratory tract homeostasis remains incompletely understood. Prior studies identified immune modulatory effects following lung exposure to Prevotella, but the relevance of these findings for CF infections is unknown.

METHODS: The impact of P. melaninogenica on infection with the CF pathogen Staphylococcus aureus was evaluated using a mouse lung infection model and by measuring S. aureus adherence to human respiratory tract cystic fibrosis transmembrane conductance regulator (CFTR) mutant and isogenic wild-type (WT)-corrected CFBE41o- epithelial cells. Epithelial cytokine/chemokine secretion and RNA-sequencing were performed to compare P. melaninogenica-induced signaling programs in WT-corrected versus CFTR mutant cells.

RESULTS: P. melaninogenica significantly reduced S. aureus lung infection, associated with elevated S. aureus killing by lung neutrophils and impaired S. aureus adherence to epithelial cells. Live or killed P. melaninogenica were sufficient to mediate these effects, which were dependent on TLR2. P. melaninogenica impairment of S. aureus adherence required functional CFTR, as this effect was lost in CFTR mutant cells but restored by CFTR modulators. RNA-sequencing identified several antibacterial defense pathways selectively upregulated by P. melaninogenica in WT corrected epithelial cells, correlating with higher IL-8 and IL-6 cytokine production.

CONCLUSIONS: P. melaninogenica enhanced neutrophil and epithelial defense against S. aureus, but the benefits of epithelial cell regulation by P. melaninogenica were lost with CFTR dysfunction. CFTR modulators rescued P. melaninogenica responsiveness in epithelial cells, highlighting the potential for synergistic effects of host-microbiome interactions and CFTR targeted therapies.},
}

@article {pmid41198406,
year = {2025},
author = {Adame, MD and Segal, LN and Dickson, RP},
title = {The ensemble approach: integrating microbiome therapeutics into our treatment of pneumonia.},
journal = {The European respiratory journal},
volume = {66},
number = {5},
pages = {},
doi = {10.1183/13993003.01701-2025},
pmid = {41198406},
issn = {1399-3003},
}

@article {pmid41198034,
year = {2025},
author = {Dieter, L and Bowie, K and Luhung, I and Healy, HG and Roberts, SC and Mathew, T and Peaper, D and Martinello, RA and Gerstein, MB and Peccia, J},
title = {Aerosol-based Exposure to Opportunistic Pathogens Originating from Hospital Sink Drains.},
journal = {American journal of infection control},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ajic.2025.10.030},
pmid = {41198034},
issn = {1527-3296},
abstract = {BACKGROUND: Hospital room sink drains contain biofilms that harbor opportunistic pathogens. Exposures to these pathogens may occur from aerosolization and droplet dispersion into patient rooms during sink use. This study characterizes aerosolization and droplet generation of sink drain opportunistic pathogens into operational hospital rooms.

METHODS: Sink drains, sink surfaces, water droplets, aerosols generated during sink use, and settled aerosols were sampled in patient rooms and analyzed via culture-, spectrometry- and genome-based approaches. Opportunistic pathogens were compared across samples via whole-genome sequencing and single-nucleotide polymorphism analysis. Biofilms and settled aerosols underwent 16S ribosomal deoxyribonucleic acid sequencing to assess impacts of sink drain biofilms into room bioaerosols.

RESULTS: Analyses suggested sink drain biofilm bacteria dispersed into hospital rooms. Opportunistic pathogens were identified in sink drains, droplets near sinks, and room aerosols. Stenotrophomonas maltophilia isolates from sink drain biofilm and droplets matched at the single-nucleotide level and microbial community analysis suggested general transmission of bacteria from sink drains into hospital rooms.

DISCUSSION: Viable opportunistic pathogens from sink drains were present in water droplets and aerosols within patient range, suggesting a potential exposure route.

CONCLUSIONS: Hospital sink drain biofilms contributed to the microbiome of hospital room surfaces and air, with microbes generally transmitted from sink drain sources to the room.},
}

@article {pmid41198001,
year = {2025},
author = {Gong, F and Liu, N and Miao, J and Wang, C and Lin, M and Luan, B and Chen, J and Chen, Y and Chen, X and Ge, F and Chen, W},
title = {Vitamin D regulation of gut microbiota-derived butyrate as a potential inhibitor of breast cancer proliferation.},
journal = {Gene},
volume = {},
number = {},
pages = {149872},
doi = {10.1016/j.gene.2025.149872},
pmid = {41198001},
issn = {1879-0038},
abstract = {Vitamin D is a fat-soluble vitamin implicated in the etiology, progression, and prognosis of breast cancer, yet its precise mechanisms of action remain elusive. We have integrated the latest insights from both basic and clinical research to find that in the human body, vitamin D is activated by hydroxylase to form the active form 1,25(OH)2D. 1,25(OH)2D may stimulate the abundance of butyrate-producing bacteria by upregulating their abundance, and butyrate can regulate the intestinal microenvironment and modulate the immune system to inhibit the proliferation of breast cancer. Notably, our investigations reveal a novel role of vitamin D in modulating the gut microbiome, particularly in stimulating the production of butyrate and other metabolites, which exhibit potent anti-proliferative effects on breast cancer cells. These findings open promising avenues for innovative clinical approaches in breast cancer therapy. This review delves into the intricate interplay between vitamin D, butyrate, and breast cancer, aiming to propose novel therapeutic strategies.},
}

@article {pmid41197947,
year = {2025},
author = {Zhou, Y and Li, J and Wang, D and Peng, L and Chen, K},
title = {Multimodal relationships and multifactorial associations between oral microecological and neurodegenerative diseases.},
journal = {Neuropharmacology},
volume = {},
number = {},
pages = {110760},
doi = {10.1016/j.neuropharm.2025.110760},
pmid = {41197947},
issn = {1873-7064},
abstract = {Dysregulation of the oral microbiome can result in inflammation of the oral mucosa and is associated with the development and advancement of numerous local and systemic illnesses, including those triggered by viral infections. The review thoroughly examines how the IL-17/Th17 response contributes to both protective immunity and inflammation in the oral mucosa, as well as its role in the onset of neurodegenerative diseases. A theoretical structure is offered for the possible connections among immune cells and the bacteria in the mouth. Changes in the oral microbiome and its produced pro-inflammatory factors may serve as non-invasive biomarkers for the invasion of potential neurodegenerative pathogens, offering predictive and early warning value for the severity of neurodegenerative diseases. Studying the intricate connection between the oral microbiome and neurodegenerative diseases offers potential for innovative strategies in preventing and treating the advancement of such conditions. Additional investigation is needed to reveal the mechanisms behind this connection and offer important insights for upcoming clinical procedures.},
}

@article {pmid41197919,
year = {2025},
author = {Mohit, and Verma, S and Venkatesh, V and Nityanand, S},
title = {Immuno-Microbial Crosstalk in Aplastic Anemia: Role of Gut and Viral Triggers.},
journal = {Microbial pathogenesis},
volume = {},
number = {},
pages = {108158},
doi = {10.1016/j.micpath.2025.108158},
pmid = {41197919},
issn = {1096-1208},
abstract = {Aplastic anemia (AA) is a rare but life-threatening hematological disorder, manifested in bone marrow failure and pancytopenia, which occurs worldwide due to the preferential immune mediated destruction of hematopoietic stem and progenitor cells. Despite the autoimmune etiology of AA, recent findings emphasize the key role of microbial and viral factors in the pathogenesis of AA by driving the host immune dysregulation. We delve into the immune-microbial crosstalk that is relevant in AA pathogenesis to provide novel insights related to gut microbial ecology, microbial metabolites, viral infections mediated inflammation and cytotoxicity against bone marrow components. Additionally, providing the roadmap of current knowledge for immune-mediated bone marrow failure focusing on activated cytotoxic T cells, altered regulatory T cells and proinflammatory cytokines. Imbalanced immune activation via defects in gut barrier function which promotes pathogen-associated molecular patterns (PAMPs) signaling through Toll-like receptors (TLRs) and other innate sensors. Considering the role of viral trigger such as Parvovirus B19, Epstein-Barr and Hepatitis as inducers of dysregulated immunity and their ability to affect antigen presentation, T cell receptor repertoires, and interferon pathways. We also delineate the potential of targeting the gut-immune axis for personalized AA therapy, including potential microbiome-directed interventions, antiviral and anti-cytokine approaches, as promising complement lines for standard immunosuppression therapy in AA. This cited approach will provide the advanced and novel clinical paradigm for the interconnected immune-microbial signals in pathogenesis of AA which promotes the host immune surveillance and also lead to precision medicine in AA treatment.},
}

@article {pmid41197774,
year = {2025},
author = {Gholamipour-Shirazi, P and Gholamipour-Shirazi, A},
title = {Infant Gut Microbiota and Functional Foods: Opportunities for Early Health Intervention.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.clnesp.2025.10.032},
pmid = {41197774},
issn = {2405-4577},
abstract = {BACKGROUND & AIMS: The infant gut microbiome, established at birth, plays a critical role in immune, metabolic, and neurological development. Early-life exposures, including delivery mode and feeding practices, significantly influence microbial colonization. This review aims to evaluate how functional foods, including probiotics, prebiotics, synbiotics, and human milk oligosaccharides (HMOs), modulate the infant gut microbiota during this critical developmental window and their implications for long-term health.

METHODS: We synthesized findings from clinical trials, systematic reviews, and mechanistic studies exploring the role of functional food components in shaping infant microbiota composition and functionality. The review integrates insights from microbiology, immunology, and nutrition science, with emphasis on interventions during infancy.

RESULTS: Breastfeeding and HMOs promote Bifidobacterium dominance, linked to reduced risks of allergies, obesity, and inflammatory bowel disease. HMO-supplemented formulas approximate the microbial profiles of breastfed infants, and probiotics, such as Lactobacillus rhamnosus GG, reduce the incidence of atopic dermatitis. Synbiotics enhance gut health in preterm infants, thereby reducing morbidity. Despite the demonstrated benefits, challenges persist in probiotic stability, host-specific responses, and regulatory harmonization.

CONCLUSIONS: Functional foods offer a promising, evidence-based strategy to harness early microbial plasticity and promote resilience against chronic disease. Standardized formulations, longitudinal studies, and personalized approaches are needed to optimize their implementation in diverse infant populations.},
}

@article {pmid41197755,
year = {2025},
author = {Wang, XX and Liang, JJ and Duan, X and Chen, G},
title = {Microbial Metabolites for Cancer Immunotherapy: Current Evidence and Future Directions.},
journal = {Seminars in cancer biology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.semcancer.2025.10.005},
pmid = {41197755},
issn = {1096-3650},
abstract = {Immune checkpoint blockade (ICB) therapy has transformed cancer treatment by activating the body's immune defenses to combat malignancies, offering substantial therapeutic outcomes for patients with advanced cancers. However, its efficacy varies considerably across different tumor types and individual patients. Recent studies have identified the human microbiome as a pivotal regulator of host homeostasis and systemic immunity and also found that it is essential for regulating immunotherapy's efficacy. Beyond direct microbial-host interactions, microbiota-derived immunomodulatory products, including metabolites, extracellular vesicles, and polysaccharides, have been shown to profoundly influence tumorigenesis, disease progression, and therapeutic responses. These microbial-derived immunomodulatory products can reshape the tumor microenvironment (TME) and modulate tumor immunity. Notably, emerging therapeutic strategies targeting or utilizing microbial immunomodulators have demonstrated promising efficacy in both preclinical and clinical models. This review provides a comprehensive overview of current research on microbiota-derived immunomodulatory products in cancer immunotherapy, highlighting their mechanistic roles and potential as innovative adjuncts in future tumor treatment strategies.},
}

@article {pmid41197754,
year = {2025},
author = {Xia, F and Yi, Q and Xu, Z and Zhou, Z and Tang, H and Zhang, K and Yan, Y},
title = {Microbial Modulation as a Game Changer: Boosting Immunotherapy Efficacy in Breast Cancer.},
journal = {Seminars in cancer biology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.semcancer.2025.10.006},
pmid = {41197754},
issn = {1096-3650},
abstract = {Breast cancer is generally regarded as an immunologically cold tumor, characterized by limited T cell infiltration and poor responsiveness to immune checkpoint inhibitors. Increasing evidence suggests that the human microbiome, including both gut and tumor-associated microbial communities, serves as a critical regulator of systemic and local antitumor immunity, with potential to convert inert tumors into immune-responsive states. Gut microbiota influence systemic immune homeostasis through metabolites such as lipids, lactic acid, and trimethylamine N-oxide, which modulate T lymphocytes, dendritic cells, leukocytes, and stromal components. Tumor-resident microbiota further shape the tumor immune microenvironment by regulating CD4[+] and CD8[+] T cells, NKT cells, Tregs, and macrophages, thereby impacting the efficacy of immune checkpoint blockade. Emerging strategies to sensitize cold breast tumors through microbiome modulation include dietary phytochemicals, bariatric surgery induced microbial shifts, probiotics and postbiotics, polyvalent microbial antigen vaccines, and nanotechnology-based platforms. Clinical challenges remain, particularly interindividual microbial heterogeneity, safety and regulatory considerations, and the need for reliable microbial and immune biomarkers. This review summarizes current advances in microbiota-immune interactions in breast cancer and discusses opportunities for microbiome-targeted strategies to enhance immunotherapy outcomes.},
}

@article {pmid41197738,
year = {2025},
author = {Acevedo-Fontanez, LA and Sánchez-Feliciano, A and Ershadi, S and Reichenberg, J and Eichenfield, LF and Barbieri, JS},
title = {Periorificial Dermatitis: Pathophysiology, Diagnosis, and Management.},
journal = {Journal of the American Academy of Dermatology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaad.2025.10.138},
pmid = {41197738},
issn = {1097-6787},
abstract = {Periorificial dermatitis is a chronic papulopustular facial dermatitis. Despite being frequently encountered in clinical practice and associated with significant effects on quality of life, its etiology remains incompletely understood, and no therapies are specifically approved by the Food and Drug Administration for its treatment. In this review, the current mechanistic understandings of periorificial dermatitis pathogenesis are discussed including the role of inciting factors, skin barrier dysfunction, inflammation, and the microbiome. In addition, we review the diagnostic features of periorificial dermatitis and how to distinguish it from clinical mimickers. Finally, treatment is discussed including skincare, topical, and systemic therapies.},
}

@article {pmid41197619,
year = {2025},
author = {Forbes, M and Ng, DYK and Boggan, RM and Frick-Kretschmer, A and Durham, J and Lorenz, O and Dave, B and Lassalle, F and Scott, C and Wagner, J and Lignes, A and Noaves, F and Jackson, DK and Howe, K and Harrison, EM},
title = {Benchmarking of human read removal strategies for viral and microbial metagenomics.},
journal = {Cell reports methods},
volume = {},
number = {},
pages = {101218},
doi = {10.1016/j.crmeth.2025.101218},
pmid = {41197619},
issn = {2667-2375},
abstract = {Human reads are a key contaminant in microbial metagenomics and enrichment-based studies, requiring removal for computational efficiency, biological analysis, and privacy protection. Various in silico methods exist, but their effectiveness depends on the parameters and reference genomes used. Here, we assess different methods, including the impact of the updated telomere-to-telomere (T2T)-CHM13 human genome versus GRCh38. Using a synthetic dataset of viral and human reads, we evaluated performance metrics for multiple approaches. We found that the usage of high-sensitivity configuration of Bowtie2 with the T2T-CHM13 reference assembly significantly improves human read removal with minimal loss of specificity, albeit at higher computational cost compared to other methods investigated. Applying this approach to a publicly available microbiome dataset, we effectively removed sex-determining SNPs with little impact on microbial assembly. Our results suggest that our high-sensitivity Bowtie2 approach with the T2T-CHM13 is the best method tested to minimize identifiability risks from residual human reads.},
}

@article {pmid41197616,
year = {2025},
author = {Gao, P and Yuan, H and Mei, Z and Yin, X and Zeng, Y and Liu, Z and Yang, X and Xue, J and Liu, Z and Jiang, Y and Ye, W and Lu, M and Suo, C and Chen, X},
title = {The comprehensive oral microbiome landscape unveils its interplay with poor oral health in esophageal squamous cell carcinoma risk.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {102431},
doi = {10.1016/j.xcrm.2025.102431},
pmid = {41197616},
issn = {2666-3791},
abstract = {Growing evidence links poor oral health to an increased esophageal squamous cell carcinoma (ESCC) risk, with the oral microbiome recognized as a key contributor. However, human-based evidence remains limited. Here, we analyze salivary shotgun metagenomic data from 390 ESCC case-control pairs and 16S rRNA sequencing data from 206 incident esophageal cancer (EC) case-control pairs. We identify 50 bacterial species altered in ESCC (e.g., enriched Porphyromonas catoniae and depleted Campylobacter rectus) and disruptions in 54 biochemical pathways (e.g., inosine 5'-phosphate degradation). These features potentially mediate the association between poor oral health and ESCC. Notably, this association is stronger among individuals with lower Streptococcus mitis levels, implicating pathways related to thiamine salvage and energy metabolism. Consistent findings in the validation dataset further support the interplay between the oral microbiome and oral health in EC risk. Our results highlight the promise of precision-targeted microbial interventions to improve oral health for ESCC prevention and management.},
}

@article {pmid41197352,
year = {2025},
author = {Jhetam, S and Shynkaruk, T and Hamaoka, T and Crowe, TG and Jeffery, A and Rogers, MB and Van Kessel, AG and Schwean-Lardner, K},
title = {Feeding leghorn chicks during simulated transport as an early feeding strategy and the benefits of a single spray probiotic application.},
journal = {Poultry science},
volume = {104},
number = {12},
pages = {106024},
doi = {10.1016/j.psj.2025.106024},
pmid = {41197352},
issn = {1525-3171},
abstract = {This study examined early, interrupted, or no feeding, with (P) or without (N) a spray-on probiotic (Lactobacillus reuteri), on chick stress, growth, gastrointestinal tract (GIT) development, microbiota, and gene expression during and after simulated transport (ST; 24 Hz vibration, 25°C, uncontrolled humidity). Lohmann LSL-Lite chicks (n = 1520) underwent 24 h of ST (5 h post-hatch) with either 24, 16, 8, or 0 h of feed access (FA) during ST with P or N treatment (trt). Following ST, birds were housed in pens for 14 d (5 replications/trt). Body weight, blood chemistry and heterophil-to-lymphocyte (H/L) ratio, relative length, weight and histomorphology of the GIT, quantitative PCR for ileum expression of genes related to inflammation and gut-barrier function, and microbiome analysis were assessed. At d 7 and 14, P birds were heavier. On d 1 (post-ST), H/L ratios were higher in the P trt, possibly from immunostimulation. Blood pH was lowest, and ionized calcium was highest in the 8-h trt. Glucose was higher in the N trt, and more dehydration occurred in the 0- and 8-h trt. The 0-h trt had reduced small intestine length and weight, and jejunum weight was highest in the P trt on d1. On d 7, duodenum and ileum weight were lowest for 8 h and N, respectively. Histomorphology revealed interactions in the ileum and cecum, suggestive of P preventing delayed gut development with interrupted FA. On d 1, ileum IL-6 expression was greater for 0 compared to 24 h. The P trt had a lower microbiome diversity but may have improved gut development with interrupted FA and prevented dehydration in the 0- and 8-h trt. Interrupting FA after 8 h had more negative effects than 0-h FA. With 0-h FA during ST, GIT development was delayed and could have contributed to ileum inflammation. Early FA had a positive effect on leghorn chick health, gut development, and growth. One post-hatch spray application of P may improve chick well-being over long transport durations.},
}

@article {pmid41197206,
year = {2025},
author = {Li, Y and Gao, Y and Wang, L and Si, J},
title = {NK cell adaptation in the tumor microenvironment: Insights for NK cell-based immunotherapy.},
journal = {Cytokine & growth factor reviews},
volume = {86},
number = {},
pages = {181-198},
doi = {10.1016/j.cytogfr.2025.10.003},
pmid = {41197206},
issn = {1879-0305},
abstract = {Natural killer (NK) cells serve as critical first responders within the immune system, orchestrating antitumor responses by directly eliminating malignant cells and modulating broader immune functions. Their capacity to recognize stressed targets without MHC-restricted neoantigen presentation, together with a favorable safety profile, underpins growing enthusiasm for NK cell‑based therapeutics. Nonetheless, the clinical efficacy of NK-cell-based therapies in solid tumor has been hindered by tumor microenvironment (TME)-driven immunosuppression, metabolic competition, and cell-intrinsic exhaustion mechanisms. In this review, we outline the journey from the discovery of NK cells to their role as a breakthrough target in cancer immunotherapy. We then provide a comprehensive framework of NK cell biology, from homeostatic regulation to TME-driven epigenetic, transcriptional, and metabolic adaptations. Notably, we discuss recent investigations into NK cell subset heterogeneity and their interactions with tumor cells, immune cells and the gut microbiome. Finally, we critically evaluated clinical progress while highlighting the imperative for rationally designed, mechanism-based combinations that address tumor escape pathways. The review concludes with a forward-looking perspective on engineering solutions to unlock the full therapeutic potential of NK cells across solid tumors and hematologic malignancies.},
}

@article {pmid41196682,
year = {2025},
author = {Cao, L and Shi, X and Li, T and Zhu, H and Liu, Y and Pei, R and Chen, C and Xu, Q and Zhang, H and Raza, W and Logrieco, AF and Wang, G and Liu, D and Shen, Q},
title = {Fusaric acid detoxification mediates interspecies interactions for sustainable Fusarium wilt disease management.},
journal = {Cell reports},
volume = {44},
number = {11},
pages = {116531},
doi = {10.1016/j.celrep.2025.116531},
pmid = {41196682},
issn = {2211-1247},
abstract = {Microbial biocontrol agents (BCAs) play a critical role in maintaining plant health by antagonizing pathogens. However, most research has focused on direct suppression mechanisms (e.g., antibiosis and competition), while the neutralization of mycotoxin for disease management remains unexplored. Here, we report that a fungal BCA, Trichoderma harzianum (Th), subverts Fusarium verticillioides (Fv) infection via a fusaric acid (FSA) detoxification process in maize. Salicylate hydroxylase was found to detoxify FSA into an almost non-toxic metabolite, 10OH-FSA. This mechanism not only neutralized the pathogenicity of Fv but also mediated interspecies interactions contributing to Fv suppression. Additionally, FSA detoxification exhibited broad applicability in controlling different Fusarium diseases in maize, tomato, and wheat. More profoundly, Th-induced FSA detoxification activity in the rhizosphere could stimulate the growth of other FSA detoxification-capable microbes, amplifying disease suppression through ecological cross-talk. These findings unveil an ecological tactic employed by BCAs to manage soil-borne Fusarium wilt disease.},
}

@article {pmid41196658,
year = {2025},
author = {Verna, G and De Santis, S and Islam, BN and Sommella, EM and Licastro, D and Zhang, L and De Almelda Celio, F and Miller, EN and Merciai, F and Caponigro, V and Xin, W and Campiglia, P and Pizarro, TT and Chieppa, M and Cominelli, F},
title = {A missense mutation in Muc2 promotes gut microbiome- and metabolome-dependent colitis-associated tumorigenesis.},
journal = {The Journal of clinical investigation},
volume = {},
number = {},
pages = {},
doi = {10.1172/JCI196712},
pmid = {41196658},
issn = {1558-8238},
abstract = {Colitis-associated cancer (CAC) arises from a complex interplay between host and environmental factors. In this report, we investigated the role of the gut microbiome using Winnie mice, a UC-like model with a missense mutation in the Muc2 gene. Upon rederivation from a conventional (CONV) to a specific-pathogen-free (SPF) facility, Winnie mice developed severe colitis and, notably, spontaneous CAC that progressively worsened over time. In contrast, CONV Winnie showed only mild colitis but no tumorigenesis. By comparison, when rederived into germ-free (GF) conditions, SPF Winnie mice were protected from colitis and colon tumors, indicating an essential role for the gut microbiome in the development of CAC in these mice. Using shotgun metagenomics, metabolomics, and lipidomics, we identified a distinct pro-inflammatory microbial and metabolic signature that potentially drives the transition from colitis to CAC. Fecal microbiota transplantation (FMT), using either SPF Winnie or WT (Bl/6) donors into GF Winnie recipients, demonstrated that while colitis developed regardless of the donor, only FMT from SPF Winnie donors resulted in CAC. Our studies present a relevant model of CAC, providing strong evidence that the microbiome plays a key role in its pathogenesis, thereby challenging the concept of colon cancer as a strictly non-transmissible disease.},
}

@article {pmid41196474,
year = {2025},
author = {Song, H and Hosain, MM and Park, T},
title = {DeepIMB: Imputation of non-biological zero counts in microbiome data.},
journal = {Genes & genomics},
volume = {},
number = {},
pages = {},
pmid = {41196474},
issn = {2092-9293},
support = {NRF-2022R1A2C1092497//National Research Foundation of Korea/ ; },
abstract = {BACKGROUND: The high prevalence of non-biological zero counts, arising from low sequencing depth and sampling variation, presents a significant challenge in microbiome data analysis. These zeros can distort taxon abundance distributions and hinder the identification of true biological signals, complicating downstream analyses.

OBJECTIVE: To address the challenges of non-biological zeros in microbiome datasets, we propose DeepIMB, a deep learning-based imputation method for microbiome data, specifically designed to accurately identify and impute non-biological zero counts while preserving biological integrity.

METHODS: DeepIMB operates in two main phases. First, it identifies non-biological zeros using a gamma-normal mixture model applied to the normalized, log-transformed taxon count matrix. Second, it imputes these zeros with a deep neural network model that integrates diverse sources of information, including taxon abundances, sample covariates, and phylogenetic distances, thereby learning complex, nonlinear relationships within microbiome data.

RESULTS: By leveraging integrated information from multiple data types, DeepIMB accurately imputes non-biological zeros while preserving true biological signals. In our two simulation studies, DeepIMB outperformed existing imputation methods in terms of mean squared error, Pearson correlation coefficient, and Wasserstein distance.

CONCLUSION: DeepIMB effectively addresses the challenges posed by non-biological zeros in microbiome data. By improving the quality of the data and the reliability of downstream analyses, DeepIMB represents a significant advancement in microbiome research methodologies.},
}

@article {pmid41196415,
year = {2025},
author = {He, Y and Yang, T and Mi, J and He, S and Yang, Z and Lu, S and Yue, K and Huang, Y and Song, L and Xiao, Y and Ren, Z},
title = {B.uniformis IM01-derived IAA alleviates asthma via AhR/NLRP3 pathways in mice.},
journal = {Cellular and molecular life sciences : CMLS},
volume = {82},
number = {1},
pages = {388},
pmid = {41196415},
issn = {1420-9071},
support = {2023YFC0871200//the National Key R&D Program of China/ ; 33054//the National Institute for Communicable Disease Control and Prevention, Chinese Center for Disease Control and Prevention/ ; 29172//the National Institute for Communicable Disease Control and Prevention, Chinese Center for Disease Control and Prevention/ ; },
mesh = {Animals ; *Receptors, Aryl Hydrocarbon/metabolism ; *Asthma/pathology/metabolism/immunology/drug therapy ; *NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; *Indoleacetic Acids/metabolism/pharmacology ; Mice ; *Signal Transduction/drug effects ; Disease Models, Animal ; NF-kappa B/metabolism ; Mice, Inbred BALB C ; T-Lymphocytes, Regulatory/immunology ; Female ; Lung/pathology ; Interleukin-22 ; Tryptophan/metabolism ; Th2 Cells/immunology ; Interleukins/metabolism ; *Basic Helix-Loop-Helix Transcription Factors/metabolism ; },
abstract = {Symbiotic flora exhibits a strong association with the pathogenesis of allergic disorders. Certain Bacteroides species have demonstrated potential in ameliorating allergic conditions. However, the specific role of Bacteroides uniformis in allergic asthma and its underlying mechanisms remain incompletely understood. This study demonstrates that oral administration of B.uniformis IM01 significantly enhanced the production of indole-3-acetic acid (IAA), suppressed airway inflammatory cell airway infiltration and aberrant T helper 2 (Th2) immune responses, and improved the epithelial barrier function in a murine model of asthma. Mechanistically, B.uniformis IM01 upregulated tryptophan metabolism, elevating IAA levels in both colon and serum, which activated the aryl hydrocarbon receptor (AhR) and induced interleukin-22 (IL-22) production. Activated AhR may inhibit NF-κB/NLRP3 signaling pathway and facilitate the splenic differentiation of Foxp3[+] regulatory T cells (Tregs), thus attenuating lung barrier dysfunction and improving allergic asthma symptoms. In summary, our results revealed that B.uniformis IM01 upregulated production of IAA to activate AhR leading to inhibited NF-κB/NLRP3-mediated immune responses, and ameliorated allergic asthma through the gut-lung axis.},
}

Animals
*Receptors, Aryl Hydrocarbon/metabolism
*Asthma/pathology/metabolism/immunology/drug therapy
*NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
*Indoleacetic Acids/metabolism/pharmacology
Mice
*Signal Transduction/drug effects
Disease Models, Animal
NF-kappa B/metabolism
Mice, Inbred BALB C
T-Lymphocytes, Regulatory/immunology
Female
Lung/pathology
Interleukin-22
Tryptophan/metabolism
Th2 Cells/immunology
Interleukins/metabolism
*Basic Helix-Loop-Helix Transcription Factors/metabolism

@article {pmid41196286,
year = {2025},
author = {Ni, Z and Ye, D},
title = {The impact of gut microbiota modulation on responses to immune checkpoint inhibitors in cancer.},
journal = {Acta microbiologica et immunologica Hungarica},
volume = {},
number = {},
pages = {},
doi = {10.1556/030.2025.02719},
pmid = {41196286},
issn = {1588-2640},
abstract = {The gut microbiota has emerged as a critical determinant of antitumor immunity and a potential modulator of responses to immune checkpoint inhibitors (ICIs). Although pre-clinical and clinical studies suggest that specific bacterial taxa may influence both efficacy and immune-related adverse events (irAEs). However, the magnitude and consistency of these associations remain unclear. A systematic search of PubMed, Embase, Web of Science, and the Cochrane Library was conducted through March 2025. Eligible studies evaluated baseline gut microbiota composition, fecal microbiota transplantation (FMT), probiotic/prebiotic interventions, or antibiotic exposure in cancer patients treated with ICIs. Pooled hazard ratios (HRs) for overall survival (OS) and progression-free survival (PFS), and odds ratios (ORs) for response rates and irAEs, were estimated using random-effects models. Across 38 studies involving 5,642 patients were included. Pooled analysis demonstrated that enrichment of Akkermansia muciniphila, Bifidobacterium longum and Faecalibacterium prausnitzii was significantly associated with improved OS (HR 0.62, 95% CI 0.51-0.76) and PFS (HR 0.69, 95% CI 0.55-0.83). Conversely, antibiotic exposure before or during ICI treatment was associated with worse OS (HR 1.84, 95% CI 1.45-2.34). Patients undergoing FMT from responders exhibited higher objective response rates (OR 2.91, 95% CI 1.48-5.73). Microbiota diversity indices were consistently higher in responders than in non-responders. Collectively, gut microbiota composition and its modulation significantly impact the therapeutic efficacy and toxicity profile of ICIs. These findings highlight the translational potential of microbiome-based biomarkers and interventions in optimizing immunotherapy.},
}

@article {pmid41196057,
year = {2025},
author = {Fait Kadlec, T and Ilett, EE and da Cunha-Bang, C and Sengeløv, H and Brieghel, C and Gulay, A and Rafiq, S and Ravn, HB and Zheng, C and Nielsen, RV and Sørensen, SS and Zargari Marandi, R and Niemann, CU},
title = {Explainable machine learning to identify chronic lymphocytic leukemia and medication use based on gut microbiome data.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0094425},
doi = {10.1128/spectrum.00944-25},
pmid = {41196057},
issn = {2165-0497},
abstract = {Medication, particularly antibiotics, significantly alters gut microbiome composition, often reducing microbial diversity and affecting host health. Given that the gut microbiome may influence cancer progression, we integrated clinical, shotgun metagenomic, and medication data to assess microbiome composition across diseased and healthy cohorts, as well as the impact of medication on microbiome variation. The study cohorts included patients with chronic lymphocytic leukemia (CLL, n = 85), acute myeloid leukemia (AML, n = 61), myeloid dysplastic syndrome (MDS), and other severe hematological malignancies (n = 104); patients scheduled for elective cardiac surgery (n = 89); and kidney donors (n = 9), all collected as part of a consecutive microbiome sampling effort at Copenhagen University Hospital, Denmark; and healthy individuals (N = 59). First, our analyses revealed similarities in both diversity and composition between microbiomes of patients with CLL and patients prior to elective cardiac surgery, whereas patients with AML and MDS exhibited the least diverse and most distinct microbiomes. Second, when we quantified sources of microbiome variation, the combination of medication, disease, age, and sex accounted for 4% of variation between all cohorts and 10.4% of variation between CLL and pre-cardiac surgery patients only; the two cohorts selected for comparison due to their similar microbiomes. Notably, this left 90%-95% of the variation unexplained, emphasizing the need for better identification of the parts of the microbiome variation impacting health and disease. Third, using a machine learning approach, we validated and further refined the CLL-associated microbiome pattern from our previous studies. Overall, our data provide a foundation for further investigation into disease-specific microbial signatures and the potential interactions between medication, underlying disease, and the microbiome, with the ultimate goal to improve our understanding and clinical management of CLL.IMPORTANCEThis study reveals how disease and medication influence the gut microbiome in patients with chronic lymphocytic leukemia (CLL) when compared to other more severe hematological malignancies, a cohort of patients scheduled for elective cardiac surgery representing a severely diseased nonhematological cohort, and a cohort of healthy individuals. We found that patients with CLL and those scheduled for cardiac surgery had the most similar microbiome diversity and composition. Similarities across very different disease contexts suggest that disease status alone has limited impact. Consistently, across all cohorts, medication, disease, age, and sex together explained only less of microbiome variation, leaving 90%-95% unexplained. This underscores the important need for better identification of factors shaping the microbiome. In addition, we validated a previously published, machine learning-based CLL-associated microbiome signature, demonstrating the robustness of our previous findings differentiating the microbiome signature for CLL as compared to healthy individuals. The findings expand knowledge on how disease states and medical treatments shape gut microbiome composition and diversity, potentially leading to new ways of managing CLL and improving patient outcomes through microbiome signatures.},
}

@article {pmid41196055,
year = {2025},
author = {Plaza Oñate, F and Quinquis, B and Thirion, F and Gilles, M and Morabito, C and Valeille, K and Martin, R and Guidet, B and Kern, C and Pécastaings, S},
title = {Assessment of protocols for characterization of the human skin microbiome using shotgun metagenomics and comparative analysis with 16S metabarcoding.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0173225},
doi = {10.1128/spectrum.01732-25},
pmid = {41196055},
issn = {2165-0497},
abstract = {The skin microbiome includes bacteria, fungi, and viruses, with composition varying significantly across body sites. Although 16S rRNA gene sequencing is common, it excludes non-prokaryotic taxa and offers limited functional data. Shotgun metagenomics provides broader taxonomic and functional insights but is challenging for low-biomass skin samples due to limited microbial DNA and high host contamination. In this study, we characterized the microbiome of the forehead and armpits in healthy individuals using shotgun metagenomics and assessed the strategies to improve sequencing success. We compared collection kits, DNA extraction protocols, and tested multiple displacement amplification (MDA). We found that sampling with D-Squame discs followed by an in-house DNA extraction protocol was the most effective combination to maximize DNA yields. MDA introduced significant compositional biases and is not recommended. Shotgun sequencing, without MDA, produced microbial compositions and diversity indices broadly consistent with 16S rRNA metabarcoding, although it showed discrepancies in the relative abundance of some genera. Consistent with prior studies, the armpit microbiome was dominated by Staphylococcus spp., whereas the forehead microbiome was dominated by Cutibacterium spp. Critically, shotgun sequencing provided additional insights into viral and eukaryotic microorganisms and revealed the functional potential of microbial communities, demonstrating its clear advantages over 16S rRNA metabarcoding for comprehensive skin microbiome research.IMPORTANCEWith growing evidence of the role of microorganisms in maintaining healthy skin, accurately characterizing the skin microbiome remains a significant challenge. In this study, we demonstrate that shotgun sequencing, carried out with adapted wet lab protocols, provides deep insights into the microbiome composition of specific areas, such as the forehead or the armpits. Notably, it enables the characterization of fungi and viruses while offering direct functional insights into microbial communities, providing a clear advantage over 16S ribosomal RNA gene sequencing. Our findings highlight the potential of shotgun metagenomics as a powerful tool for comprehensive skin microbiome analysis. They emphasize the importance of tailored protocols for low-biomass samples, improving the reliability of shotgun sequencing and paving the way for more robust clinical studies focused on the skin microbiome.},
}

@article {pmid41196050,
year = {2025},
author = {Lee, S and Raza, S and Lee, E-J and Chang, Y and Ryu, S and Kim, H-L and Kang, S-H and Kim, H-N},
title = {Metagenome-assembled genomes reveal microbial signatures and metabolic pathways linked to coronary artery disease.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0095425},
doi = {10.1128/msystems.00954-25},
pmid = {41196050},
issn = {2379-5077},
abstract = {Gut microbiota has emerged as a critical factor influencing cardiovascular disease (CVD) risk, particularly coronary artery disease (CAD) development. Using fecal metagenomic shotgun sequencing, we investigated gut microbiota signatures associated with CAD and provided strain-resolved insights through metagenome-assembled genome (MAG) reconstruction. We analyzed 14 patients with CAD and 28 propensity score-matched healthy controls. Differential abundance analysis identified 15 CAD-associated bacterial species. Members of the Lachnospiraceae family, previously associated with trimethylamine-N-oxide production, were significantly enriched in patients with CAD. Conversely, short-chain fatty acid-producing bacteria Slackia isoflavoniconvertens and Faecalibacterium prausnitzii were depleted, suggesting a potential contribution to gut-mediated inflammation and metabolic dysregulation. Metabolic pathway analysis revealed significant urea cycle and L-citrulline biosynthesis enrichment in CAD cases, with Alistipes and Coprococcus as key contributors. Among predicted metabolites, inosine, which is implicated in coronary artery relaxation, was elevated in patients with CAD, whereas C18:0e MAG and α-muricholate were depleted. A random forest model achieved a mean AUC of 0.89 for CAD classification, with improved performance when integrating microbial taxa and metabolites. CAD-derived MAGs showed metabolic signatures linked to inflammatory dysbiosis and cardiovascular dysfunction, such as enriched N2 fixation and sulfite reduction. Strain-resolved comparative genomic analysis of MAGs revealed distinctive functional characteristics between CAD-derived and control-derived strains of Akkermansia muciniphila and Megamonas fumiformis. F. prausnitzii MAG from the control group carried non-trimethylamine-producing gene, mtxB, suggesting its potential protective role in CAD pathophysiology. These findings provide insights into gut microbial alterations in CAD and highlight potential targets for microbiome-based therapeutic interventions to reduce CVD risk.IMPORTANCEGut microbiota plays a pivotal role in cardiovascular disease; however, its specific contribution to coronary artery disease (CAD) remains underexplored. This study identified distinct microbial signatures associated with CAD, including the enrichment of pro-inflammatory bacterial taxa and depletion of short-chain fatty acid-producing bacteria, which may contribute to systemic inflammation and metabolic dysregulation. Perturbations in key pathways, such as the urea cycle and glycolysis, suggest metabolic links between the gut microbiota and CAD. Additionally, the metagenome-assembled genome-based analysis revealed strain-resolved functional heterogeneity that shapes host-microbe interactions and may contribute to CAD pathophysiology. These findings provide novel insights into gut dysbiosis in CAD and highlight the potential of microbiome-targeted therapeutic strategies in precision medicine.},
}

@article {pmid41196042,
year = {2025},
author = {Lesani, M and Middleton, CE and Feng, T-Y and Urbán Arroyo, JC and Casarez, E and Ewald, SE and McCall, L-I},
title = {Spatially divergent metabolic impact of experimental toxoplasmosis: immunological and microbial correlates.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0112625},
doi = {10.1128/msystems.01126-25},
pmid = {41196042},
issn = {2379-5077},
abstract = {Maladaptive host metabolic responses to infection are emerging as major determinants of infectious disease pathogenesis. However, the factors regulating these metabolic changes within tissues remain poorly understood. In this study, we used toxoplasmosis, as a prototypical example of a disease regulated by strong type I immune responses, to assess the relative roles of current local parasite burden, local tissue inflammation, and the microbiome in shaping local tissue metabolism during acute and chronic infections. Toxoplasmosis is a zoonotic disease caused by the parasite Toxoplasma gondii. This protozoan infects the small intestine and then disseminates broadly in the acute stage of infection, before establishing chronic infection in the skeletal muscle, cardiac muscle, and brain. We compared metabolism in 11 sampling sites in C57BL/6 mice during the acute and chronic stages of T. gondii infection. Strikingly, major spatial mismatches were observed between metabolic perturbation and local parasite burden at the time of sample collection for both disease stages. By contrast, a stronger association with indicators of active type I immune responses was observed, indicating a tighter relationship between metabolic perturbation and local immunity than with local parasite burden. Loss of signaling through the IL1 receptor in IL1R knockout mice was associated with reduced metabolic impact of infection. In addition, we observed significant changes in microbiota composition with infection and candidate microbial origins for multiple metabolites impacted by infection. These findings highlight the metabolic consequences of toxoplasmosis across different organs and potential regulators.IMPORTANCEInflammation is a major driver of tissue perturbation. However, the signals driving these changes on a tissue-intrinsic and molecular level are poorly understood. This study evaluated tissue-specific metabolic perturbations across 11 sampling sites following systemic murine infection with the parasite Toxoplasma gondii. Results revealed relationships between differential metabolite enrichment and variables, including inflammatory signals, pathogen burden, and commensal microbial communities. These data will inform hypotheses about the signals driving specific metabolic adaptation in acute and chronic protozoan infection, with broader implications for infection and inflammation in general.},
}

@article {pmid41195911,
year = {2025},
author = {Pai, YC and Huang, CY and Lin, LY and Li, YH and Yu, LC},
title = {Infectious Carcinogens Derived from Intestinal Microflora: Mechanisms of Microbial Transitions from Eubionts to Pathobionts.},
journal = {Journal of physiological investigation},
volume = {},
number = {},
pages = {},
doi = {10.4103/ejpi.EJPI-D-25-00045},
pmid = {41195911},
issn = {2950-6344},
abstract = {A diverse community of microorganisms inhabits the gastrointestinal tract in a physiological state. While a symbiotic relationship exists between commensal bacteria and the healthy host, an imbalanced microbial population (dysbiosis) is associated with the development of colitis-associated colorectal cancers. The decline of beneficial microbes (eubionts) and the expansion of commensal-derived opportunistic pathogens (pathobionts) are widely recognized as key factors in the microbial etiology of various diseases. In particular, certain bacteria with emerging virulence elements are present in the gut microbiome and have been implicated as contributors to the development of colon cancer, such as Escherichia coli, Bacteroides fragilis, and Fusobacterium nucleatum. Bacterial virulent factors, including lipopolysaccharide, fimbriae and adhesins, and toxins, promote oncogenesis through direct or indirect mechanisms. These microbial products modify host cellular functions, resulting in DNA damage, increased epithelial proliferation, and intensified inflammation, all of which ultimately contribute to tumor formation. Although the existence of pathobionts is generally accepted nowadays, an open question remains regarding why bacteria shift from harmless commensals to disease-causing pathobionts. Accumulating evidence suggests that host epithelial functions influence the composition of the intestinal microbiota by regulating oxygen availability in the lumen, providing antimicrobial defense, activating innate immune responses, synthesizing mucin glycoproteins, and establishing a physical barrier through the organization of microvilli. This review examines the various aspects of mucosal drivers that shape microbiota and provides evidence that intraepithelial stress plays a significant role in configuring colitogenic and tumorigenic microflora. Understanding the mechanisms by which microbes transition from eubionts to pathobionts that promote cancer progression is crucial for developing bacterial precision medicine. Identifying the roles of intestinal pathobionts and the critical time point for host-microbe interactions in tumorigenesis could lead to the development of new strategies for prevention and therapy.},
}

@article {pmid41195700,
year = {2025},
author = {Crestani, E and Harb, H and Benamar, M and Kaddurah-Daouk, R and Phipatanakul, W and Chatila, TA},
title = {Metabolomic and immunological signatures of asthma severity in children.},
journal = {Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology},
volume = {36},
number = {11},
pages = {e70242},
doi = {10.1111/pai.70242},
pmid = {41195700},
issn = {1399-3038},
support = {//National Institute of Allergy and Infectious Diseases/ ; /AG/NIA NIH HHS/United States ; },
mesh = {Humans ; *Asthma/immunology/metabolism/blood/diagnosis ; Child ; Female ; Male ; Severity of Illness Index ; *T-Lymphocytes, Regulatory/immunology/metabolism ; Metabolomics ; Child, Preschool ; Cytokines/blood ; Adolescent ; Growth Differentiation Factor 15/blood ; Biomarkers/blood ; Metabolome ; },
abstract = {BACKGROUND: Multiple risk factors for asthma severity have been identified by epidemiological studies. Yet, the pathophysiological mechanisms driving the severity of clinical asthma manifestations remain incompletely understood. In asthmatic children, Notch4 expression on circulating Treg cells and levels of circulating GDF15 have been shown to be increased as a function of disease severity, suggesting a contribution of Treg dysfunction to disease phenotype.

METHODS: 126 children with asthma (intermittent = 40; mild persistent = 43; moderate persistent = 29, and severe persistent = 14) and 83 non-asthmatic controls were recruited in the Allergy clinic at Boston Children's Hospital and from asthma cohorts. Untargeted metabolomic analysis and cytokine profiling were performed in plasma and results correlated with disease severity, Notch4 expression, and presence of other atopic comorbidities.

RESULTS: Children with moderate/severe asthma had higher levels of select lipids (triglycerides, ceramides) and carboxylic acids (lactic acid, aconitic acid) and lower levels of amino acids (sarcosine and arginine) and of IFNλ 2/3 compared to children with intermittent/mild asthma. Treg Notch4 expression and GDF15 levels, which increase with disease severity, correlated positively with lactic acid and xanthine levels and inversely with sarcosine and arginine. The concomitant presence of food allergy was associated with alterations in microbiome-related metabolites and allergic rhinitis with marked triglyceride dysregulation.

CONCLUSIONS: Untargeted metabolomic profiling identified both shared and unique pathways associated with known asthma severity contributors, Notch4 dysregulation and GDF15 elevation, suggesting that different mechanisms may both converge or independently contribute to determining clinical manifestations of asthma severity in asthmatic children.},
}

Humans
*Asthma/immunology/metabolism/blood/diagnosis
Child
Female
Male
Severity of Illness Index
*T-Lymphocytes, Regulatory/immunology/metabolism
Metabolomics
Child, Preschool
Cytokines/blood
Adolescent
Growth Differentiation Factor 15/blood
Biomarkers/blood
Metabolome

@article {pmid41195400,
year = {2025},
author = {Zhili, G and Jie, L and Peihao, Y},
title = {Macro- and metabolome-based characterization between gut microbiota and metabolites in patients with colorectal adenomas.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1628315},
pmid = {41195400},
issn = {1664-302X},
abstract = {OBJECTIVE: The gut microbiota has been recognized as a significant regulator in the development and progression of colorectal adenoma (CRA). However, few studies have investigated the presence and association of resident microbial species and metabolites in patients with CRA. Our aim was to analyze differences in gut microbiome composition and metabolites, as well as to evaluate their diagnostic potential for CRA.

METHODS: We conducted metagenomic and metabolomic analyses on fecal samples from 90 subjects, including 60 patients with CRA (CRA group) and 30 healthy subjects who served as normal controls (NC group). By integrating fecal metagenomic and metabolomic data, we identified gut microbiota-associated metabolites that showed significant abundance changes in CRA patients. Furthermore, we explored whether these metabolites and microbial species could distinguish CRA patients from healthy individuals.

RESULTS: 16S rRNA gene sequencing and untargeted metabolomics analysis revealed microbial changes that distinguished CRA patients from controls. Microbial population analysis showed that the CRA group formed distinct clusters from the controls, with significant β-diversity (PCA and PCoA analyses, p < 0.05). At the phylum level, the dominant taxa in terms of relative abundance included Firmicutes, Ascomycota, Mycobacteria, Actinobacteria, and Clostridia. Differential analysis of the gut flora based on species abundance revealed significant differences in taxonomic composition between healthy individuals and CRA patients. KEGG functional enrichment analysis indicated that the differential flora were primarily involved in metabolic pathways, including metabolic pathways, biosynthesis of secondary metabolites, microbial metabolism in diverse environments, amino acid biosynthesis, and cofactor biosynthesis. In this study, three microbial species-Fusobacterium mortiferum, Alistipes, and Bacteroides fragilis-were validated as discriminators between healthy individuals and CRA patients, with Alistipes showing higher classification efficacy. Metabolomic analysis revealed differences in tryptophan metabolism, protein degradation products, amides, and phenolic acid metabolites. KEGG enrichment results indicated that metabolic pathways were the most significantly enriched. Differential metabolites were mainly associated with the biosynthesis of plant secondary metabolites. Procrustes and Venn analyses were performed on functional entries of the two omics datasets, highlighting enriched pathways including Metabolic pathways, Glycerophospholipid metabolism, Sphingolipid metabolism, and Alpha-linolenic acid metabolism. A review of the literature confirmed that the differential flora and metabolites are associated with adenoma growth.

CONCLUSION: In this study, metagenomic and metabolomic analyses were conducted in subjects with CRA. The findings based on fecal metagenomic and metabolomic assays suggest that intestinal microecology is altered in CRA patients, leading to changes in gut cellular structure.},
}

@article {pmid41195399,
year = {2025},
author = {, },
title = {Correction: Metagenomic insights reveal the differences in the community composition and functional characteristics of the sea turtle microbiomes based on host species and tissue region.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1721706},
doi = {10.3389/fmicb.2025.1721706},
pmid = {41195399},
issn = {1664-302X},
abstract = {[This corrects the article DOI: 10.3389/fmicb.2025.1652229.].},
}

@article {pmid41195394,
year = {2025},
author = {Sun, Q and Fei, S and Huang, S and Tan, R and Chen, H and Song, S and Wang, B},
title = {Wilt disease reshapes rhizosphere microbiota in small yellow ginger soils.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1670956},
pmid = {41195394},
issn = {1664-302X},
abstract = {INTRODUCTION: Continuous cropping obstacles, particularly the prevalent ginger wilt disease (bacterial wilt), severely constrain the sustainable development of the small yellow ginger (Zingiber officinale Roscoe) industry in Rucheng County, China. However, the primary pathogen responsible for this disease in the local cultivar and the associated microbiome shifts within the rhizosphere remain unidentified. This study aimed to elucidate the distinctive rhizosphere microbial community changes induced by ginger wilt disease, identify the potential key pathogen responsible for this disease in Rucheng, and provide a scientific basis for overcoming continuous cropping obstacles in small yellow ginger cultivation.

METHODS: Soil samples were collected from an uncultivated plot and from the rhizosphere of healthy and wilted small yellow ginger plants. Microbial community structure and composition were analyzed using 16S rRNA gene high-throughput sequencing. Linear Discriminant Analysis (LDA) effect size (LEfSe) was employed to identify differential biomarkers, and functional prediction was performed using BugBase.

RESULTS: Ginger wilt disease significantly altered the rhizosphere soil bacterial community structure and composition: the relative abundance of Proteobacteria increased significantly, primarily due to the enrichment of the genus Ralstonia; conversely, the relative abundance of Acidobacteriota, Firmicutes, and Chloroflexi significantly decreased. Ginger wilt disease also significantly reduced the diversity of the rhizosphere soil bacterial community. LEfSe further confirmed Ralstonia as a diagnostic biomarker for ginger wilt disease. BugBase phenotypic prediction indicated that the microbiota enriched in the diseased ginger rhizosphere exhibited higher capabilities for oxidative stress resistance, pathogenic potential, and mobile element content, attributed to a functional consortium of multiple genera, such as Ralstonia as the dominant contributor alongside major contributors such as Rhodanobacter and Dokdonella.

DISCUSSION: Our findings highlight that the enrichment of Ralstonia is strongly associated with ginger wilt in Rucheng County and concomitant with profound changes in the rhizospheric microbiota of wilted ginger, involving alterations in both community structure and functional potential.},
}

@article {pmid41195389,
year = {2025},
author = {Li, J and Diao, L and Li, M and Huang, F and Sun, K},
title = {Unraveling the mysteries of the gut-kidney axis: the protective role of traditional Chinese medicine in chronic kidney disease.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1642377},
pmid = {41195389},
issn = {1664-302X},
abstract = {Chronic kidney disease (CKD) constitutes a globally progressive nephropathy orchestrating inexorable deterioration of renal architecture. The paradigmatic gut-kidney axis unveils sophisticated bidirectional interplay between enteric microbiome and renal homeostatic equilibrium. Dysbiotic perturbations catalyze aberrant accumulation of gut-derived uremic metabolites, attenuate intestinal epithelial fortification, and propagate subclinical inflammatory cascades, synergistically precipitating CKD trajectory acceleration. Contemporary therapeutic arsenals targeting this axis encompass probiotic reconstitution, prebiotic orchestration, synbiotic hybridization, precision nutritional calibration, and enteral sequestrants including AST-120. Traditional Chinese Medicine (TCM) paradigms deploy multifaceted strategies through meticulous microbiota choreography, mucosal barrier reinforcement, and renal fibrogenesis attenuation. Distinguished phytotherapeutics including Rhubarb (Rhei Radix et Rhizoma), Salvia miltiorrhiza, and Poria cocos, synergized with bioactive constituents curcumin and punicalagin, orchestrate nephroprotective virtuosity via intricate microbiome-metabolome networks. Sophisticated polyherbal architectures, exemplified by YQHG and YSHS, harmoniously fortify intestinal impermeability while nullifying uremic translocation. These revelations substantiate the transformative potential of integrative paradigms amalgamating TCM-based phytomedicine with microbiota-directed precision therapeutics for CKD stewardship.},
}

@article {pmid41195143,
year = {2025},
author = {Ducrocq, F and Hafidi, O and Grosjean, J and Hehn, A and Piutti, S},
title = {Influence of genotype and soil on specialized metabolites production and bacterial microbiota associated to wild hop (Humulus lupulus L.): an early-stage study.},
journal = {Frontiers in plant science},
volume = {16},
number = {},
pages = {1702956},
pmid = {41195143},
issn = {1664-462X},
abstract = {Hop (Humulus lupulus L.) is a dioecious climbing plant that is emblematic for the brewing industry because of its specialized metabolites. Many studies have focused on hop metabolism without considering the microbiota associated with hop tissues, although over the past decade, a paradigm shift has redefined plants as holobionts, with complex associations between the plant host and its associated microbial communities. In this study, we investigated the effects of three wild hop genotypes cultivated in two different agricultural soils under controlled conditions on specialized metabolite production and on bacterial community composition across different hop compartments (rhizosphere soil, roots, and leaves). Phytochemical analysis of leaf contents revealed distinct metabolic profiles across the six 'genotype×soil' interactions, driven by variations in the biosynthesis of prenylated chalcones, α- and β-type bitter acids, and their derivatives. PERMANOVA results demonstrated that both 'genotype' and 'soil' factors significantly influenced leaf metabolite composition, each explaining approximately 28% of the observed variance. However, the strongest effect was observed for the 'genotype×soil' interaction, which accounted for 66% of the variance. In parallel, soil type, hop genotype, and their interaction significantly shape hop-associated bacterial communities, with a predominant interaction effect in each compartment (rhizosphere soil, roots and leaves) (R[2] = 0.74, 0.74 and 0.32, respectively). Furthermore, Spearman microbiome-metabolome correlation analysis revealed that bacterial families were positively correlated with the biosynthesis of key metabolites, particularly bitter acids. Our findings further suggest that the hop-associated microbiota may contribute to metabolic biosynthesis, opening new perspectives for optimizing metabolite biosynthesis through microbiome manipulation.},
}

@article {pmid41195064,
year = {2025},
author = {Sun, W and Xue, N and Zhang, Q},
title = {Integrated multi-omics analysis reveals the mechanisms of naringin in ameliorating high-fat diet-induced metabolic dysfunction-associated steatotic liver disease.},
journal = {Frontiers in nutrition},
volume = {12},
number = {},
pages = {1694191},
pmid = {41195064},
issn = {2296-861X},
abstract = {INTRODUCTION: Naringin (Nar), the predominant flavonoid in citrus fruits, shows therapeutic potential against metabolic dysfunction-associated steatotic liver disease (MASLD). However, its underlying mechanisms remain largely elusive.

METHODS: In this study, we investigated the efficacy and underlying mechanisms of Nar in a mouse model of high-fat diet (HFD)-induced MASLD using integrated analyses of network pharmacology, molecular docking, hepatic lipidomics, and gut microbiota.

RESULTS: Treatment with Nar markedly ameliorated MASLD phenotypes, as evidenced by reduced body and liver weights, lower hepatic triglycerides (TGs), and improved serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Network pharmacology analysis revealed that Nar targets associated with MASLD are primarily enriched in proteins such as SRC, AKT1, STAT3, FOS, ESR1, and NFKB1, which exert their effects through the PI3K-AKT signaling pathway. Molecular docking simulations further elucidated the interaction mechanisms. Lipidomic analysis revealed that Nar restored hepatic lipid homeostasis, significantly decreasing levels of TGs and diglycerides (DGs), with 20 differentially abundant lipid species identified as potential biomarkers. Additionally, Nar profoundly altered the gut microbial community, promoting the enrichment of beneficial genera including Oscillibacter, Allisonella, and Flavonifractor.

DISCUSSION: Our findings indicate that Nar prevents MASLD by harmonizing hepatic lipid metabolism and modulating the gut microbiome, providing a multifaceted mechanistic insight into its therapeutic potential.},
}

@article {pmid41194963,
year = {2025},
author = {Chen, L and Wang, F and Zhang, H and Qin, S and Sui, M and Ishigami, T},
title = {Lactulose for prevention of cardiovascular events after myocardial infarction: A retrospective cohort study.},
journal = {JRSM cardiovascular disease},
volume = {14},
number = {},
pages = {20480040251393767},
pmid = {41194963},
issn = {2048-0040},
abstract = {BACKGROUND: Acute myocardial infarction (AMI) remains a major cause of global mortality, with post-infarction cardiovascular events significantly contributing to poor outcomes. Emerging evidence suggests that gut microbiome dysbiosis may influence cardiovascular risk through increased intestinal permeability and systemic inflammation. Although lactulose-a prebiotic known to modulate gut microbiota-has shown beneficial effects in experimental models, its impact on major adverse cardiovascular events (MACEs) after AMI remains unclear.

METHODS: In this single-center retrospective cohort study, we analyzed 165 AMI patients hospitalized between 2016 and 2019. Participants were stratified by lactulose use during hospitalization. The primary outcome was in-hospital MACEs. Multivariable logistic regression was used. Secondary outcomes included pneumonia incidence and length of hospital stay.

RESULTS: After adjustment for confounders, lactulose use was independently associated with a reduced risk of MACEs (adjusted odds ratio (OR) 0.40, 95% confidence interval (CI) 0.16-0.95; p = 0.038). The overall incidence of MACEs was 18.2% in the lactulose group versus 30.0% in controls, though this difference was not statistically significant in unadjusted analysis (χ² = 2.41, p = 0.12), likely reflecting limited statistical power. No significant associations were observed for pneumonia (OR = 0.17, p = 0.09) or hospital stay duration (p = 0.60).

CONCLUSIONS: In this retrospective analysis, lactulose supplementation was associated with reduced in-hospital cardiovascular events following AMI. However, these preliminary findings require validation in larger prospective studies to establish causality and elucidate underlying gut-mediated mechanisms. If confirmed, lactulose may represent a simple and accessible adjunct therapy in post-infarction care.},
}

@article {pmid41194669,
year = {2025},
author = {Schleiss, MR},
title = {The urgent search for predictive biomarkers in the emerging era of universal congenital cytomegalovirus screening.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {380},
number = {1938},
pages = {20240434},
pmid = {41194669},
issn = {1471-2970},
support = {/TR/NCATS NIH HHS/United States ; //NIH/ ; //CDC/ ; },
mesh = {Humans ; *Cytomegalovirus Infections/congenital/diagnosis/complications ; Biomarkers/analysis ; *Cytomegalovirus/physiology ; Infant, Newborn ; Developmental Disabilities/virology ; Pregnancy ; Female ; },
abstract = {In utero acquisition of cytomegalovirus (CMV) represents the most common infectious cause of paediatric developmental disability. With a global prevalence of approximately 0.7%, congenital CMV (cCMV) infection can produce wide-ranging injury to the developing fetal and neonatal central nervous system, leading to microcephaly, intracranial calcifications, neuronal migration defects and damage to the developing cochlea and retina. Clinical sequelae include cerebral palsy, seizure disorder, intellectual disabilities, developmental delay, autism spectrum disorders, sensorineural hearing loss (SNHL) and visual impairment. It has been generally believed that most cCMV infections are asymptomatic in nature, and are not associated with long-term neurodevelopmental impairment. This dogma, however, has been called into question in the context of several state and provincial universal cCMV screening programmes that have been implemented in recent years in the United States and Canada. Moreover, the full spectrum of neurodevelopmental sequelae amongst asymptomatic cCMV cases is just starting to be recognized. Host and/or viral factors that predict which asymptomatic infants will have sequelae, including SNHL, are unknown. This review summarizes the current state of the art with respect to the search for predictive biomarkers that can inform the prognosis of asymptomatic cCMV, and aid in decision-making about therapeutic intervention.This article is part of the discussion meeting issue 'The indirect effects of cytomegalovirus infection: mechanisms and consequences'.},
}

Humans
*Cytomegalovirus Infections/congenital/diagnosis/complications
Biomarkers/analysis
*Cytomegalovirus/physiology
Infant, Newborn
Developmental Disabilities/virology
Pregnancy
Female

@article {pmid41194539,
year = {2025},
author = {Rolhion, N and Sokol, H},
title = {Targeting the gut microbiome in inflammatory bowel disease: from concept to clinical reality.},
journal = {Intestinal research},
volume = {23},
number = {4},
pages = {396-404},
doi = {10.5217/ir.2025.00104},
pmid = {41194539},
issn = {1598-9100},
support = {ERC-2021-COG-101043802/ERC_/European Research Council/International ; //MSDAVENIR/ ; },
abstract = {The gut microbiota, a complex community of trillions of microorganisms inhabiting the human gastrointestinal tract, has emerged as a critical regulator of immune homeostasis and gastrointestinal health. In the context of inflammatory bowel disease (IBD), comprising primarily Crohn's disease and ulcerative colitis, disruptions to this microbial ecosystem-collectively termed dysbiosis-have been increasingly recognized as central to disease pathogenesis. Recent research has established that alterations in gut microbiota not only reflect disease states but may actively drive immune dysregulation, barrier dysfunction, and mucosal inflammation. This review synthesizes current knowledge on the role of the gut microbiota in IBD and evaluates the therapeutic landscape of microbiota-modulating strategies using selected examples. Fecal microbiota transplantation, while offering proof-of-concept validation, is hindered by standardization challenges and variable clinical outcomes. As a response, microbiome-based therapeutics have evolved toward defined live biotherapeutic products including bacterial consortia and single-strain products, postbiotics, and metabolite-centered approaches targeting specific pathways. Groundbreaking research into rationally designed synthetic microbiomes and next-generation probiotics is driving a paradigm shift in microbiota-based treatment for IBD from empirical to precision-guided interventions.},
}

@article {pmid41194479,
year = {2025},
author = {Das, S and Patel, M and Khandelwal, S and Rawat, R and Shukla, S and Kumari, AP and Singh, K and Kumar, A},
title = {From Mutations to Microbes: Investigating the Impact of the Gut Microbiome on Repeat Expansion Disorders.},
journal = {Journal of neurochemistry},
volume = {169},
number = {11},
pages = {e70278},
doi = {10.1111/jnc.70278},
pmid = {41194479},
issn = {1471-4159},
mesh = {*Gastrointestinal Microbiome/physiology/genetics ; Humans ; Animals ; *Mutation/genetics ; Dysbiosis/genetics ; *DNA Repeat Expansion/genetics ; },
abstract = {Repeat expansion disorders (REDs) are a diverse array of genetic disorders characterized by the expansion of specific DNA sequences. These expansions are frequently dynamic and are susceptible to further expansion across generations. They contribute to disease progression by leading symptoms to become more severe and manifest earlier in subsequent generations. Despite a substantial understanding of their molecular mechanisms, the exact etiology of REDs remains tricky. Emerging evidence indicates that gut microbiome dysbiosis significantly impacts REDs by regulating various biochemical pathways. Alterations in microbial diversity and composition have been observed across multiple REDs; however, a comprehensive understanding of the complete scenario remains a significant challenge. To elucidate these dynamic interactions, future research should utilize multifaceted approaches. This review focuses on the key modifications in the gut microbiome that contribute to the pathogenesis of REDs and discusses potential gut microbiome-targeted therapeutic strategies that could be effectively employed to treat these disorders.},
}

*Gastrointestinal Microbiome/physiology/genetics
Humans
Animals
*Mutation/genetics
Dysbiosis/genetics
*DNA Repeat Expansion/genetics

@article {pmid41194405,
year = {2025},
author = {Cheng, Z and Wang, X and Yu, J and Li, X and Tang, Q and Qu, C and Yang, D and Li, Y and Xia, Y and Guo, Y},
title = {Trigonelline Improves Metabolism and Cardiac Function of HFpEF Mice Via Gut Microbiome Alterations-Mediated AMPK Activation.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e13956},
doi = {10.1002/advs.202513956},
pmid = {41194405},
issn = {2198-3844},
support = {CYYY-BSHPYXM-202204//Postdoctoral Incubation Project of The First Affiliated Hospital of Chongqing Medical University/ ; CYYY-BSYJSCXXM-202306//Doctoral Innovation Project of The First Affiliated Hospital of Chongqing Medical University/ ; CSTB2022NSCQ-MSX0913//Natural Science foundation of Chongqing/ ; CSTB2022NSCQ-BHX0712//Natural Science foundation of Chongqing/ ; 2022CQBSHTBT003//Chongqing Postdoctoral Science Foundation/ ; KJQN202300480//Chongqing education committee/ ; WZSTC-20220133//Chongqing Wanzhou district/ ; 2022YJKYXM-039//Chongqing University Three Gorges Hospital & Chongqing Three Gorges Central Hospital/ ; W0168//Program for Youth Innovation in Future Medicine, Chongqing Medical University/ ; 2022M720601//China Postdoctoral Science Foundation/ ; 82200422//National Natural Science Foundation of China/ ; },
abstract = {Heart failure with preserved ejection fraction (HFpEF) is a prevalent end-manifestation of cardiovascular diseases currently lacking effective treatment. Using a high-fat diet and L-NAME-induced mouse model, untargeted metabolomic profiling is performed and trigonelline is identified as a markedly reduced metabolite in HFpEF hearts. Oral trigonelline supplementation alleviates metabolic syndromes, including obesity, insulin resistance, and hepatic injury, leading to improved cardiac function in HFpEF mice. AMPK inhibition blunts the protective effects of trigonelline despite trigonelline per se not activating AMPK directly. Gut microbiota is required in AMPK activation and consequent beneficial effects on HFpEF mice by trigonelline. Further investigations demonstrate that trigonelline significantly restores HFpEF mouse gut microbiome dysbiosis by decreasing Firmicutes and increasing Bacteroidetes. In conclusion, the studies demonstrate that trigonelline supplementation mitigates HFpEF-associated metabolic disorders and improves cardiac function via gut microbiome alterations-mediated AMPK activation. These findings suggest that trigonelline has therapeutic potential for HFpEF.},
}

@article {pmid41194195,
year = {2025},
author = {Cansado-Utrilla, C and Saldaña, MA and Golovko, G and Khanipov, K and Watson, RK and Wild, AL and Brettell, LE and Weaver, SC and Heinz, E and Hughes, GL},
title = {Mosquito host background impacts microbiome-Zika virus interactions in field- and laboratory-reared Aedes aegypti.},
journal = {Animal microbiome},
volume = {7},
number = {1},
pages = {116},
pmid = {41194195},
issn = {2524-4671},
abstract = {UNLABELLED: Mosquito microbiota abundance and composition are modulated by a variety of factors, including pathogen exposure. The microbiome can also influence pathogen infection of the host and thus harbours considerable potential to impact transmission of pathogens. As such, there is a growing interest in using particular bacterial members of the microbiota for novel vector-control strategies. However, before novel microbiota-based approaches can move towards translation, a more complete understanding of the interactions between mosquitoes, their microbiome, and the pathogens they transmit, is required to better appreciate how variation in the microbiome of field mosquitoes affects these interactions. To examine the impact of the mosquito background and the associated diversity of bacterial microbiota within distinct hosts, we exposed several laboratory-reared and field-collected Aedes aegypti mosquito lines to Zika virus (ZIKV) and examined their bacterial load and composition in response to pathogen exposure and viral infection success. Intriguingly, we show that ZIKV exposure and infection had distinct impacts on microbiome composition and density within different mosquito lines. In one laboratory-reared line ZIKV exposure and infection reduced the bacterial load, while conversely in another line load was increased by the virus. Distinct responses of the microbiome were also seen in mosquitoes collected from the field. Sampling site-specific differences in the microbiome of mosquitoes were observed as virus infection altered microbiome alpha and beta diversities in one cohort, while in mosquitoes from other sampling sites, viral progression through the mosquito had minimal effect on the microbiome. We also identified bacterial taxa correlating with either ZIKV infection or a lack of infection. These taxa are potential candidates for future follow-up studies disentangling functional mechanisms and directionality of interactions. Overall, our study highlights that interactions between mosquito, virus, and microbiota are variable and context dependent, and that tripartite interactions among distinct mosquito cohorts and their microbiomes are not universal.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s42523-025-00482-0.},
}

@article {pmid41194006,
year = {2025},
author = {Ivanova, A and Buzova, V},
title = {A novel enzymatic approach for a targeted fungal growth inhibition.},
journal = {BMC microbiology},
volume = {25},
number = {1},
pages = {719},
pmid = {41194006},
issn = {1471-2180},
support = {03-ZP23-087//SkyLab AG/ ; 03-ZP23-087//SkyLab AG/ ; },
mesh = {*Malassezia/drug effects/growth & development/genetics ; Humans ; *Antifungal Agents/pharmacology ; *Chitinases/pharmacology ; *Glycoside Hydrolases/pharmacology ; Dandruff/microbiology/drug therapy ; Microbial Sensitivity Tests ; Chitosan/metabolism ; Scalp/microbiology ; Dermatomycoses/microbiology/drug therapy ; Fibroblasts/drug effects ; Female ; Male ; Cell Line ; Adult ; Middle Aged ; },
abstract = {BACKGROUND: Dandruff represents a complex, multifactorial disorder characterized by impaired barrier function, altered lipid composition, and microbial imbalance. The principal pathogenic mechanism, however, involves excessive colonization by Malassezia species, notably M. furfur, M. restricta and M. globosa, on the scalp. Standard antifungal options often lead to undesirable effects, including itching and irritation, and may negatively impact the scalp microbiome. This study evaluates combination of chitinase and chitosanase, targeting fungal cell wall chitin and chitosan, as a promising targeted approach for scalp Malassezia spp.

METHODS: The in vitro antifungal activities of chitinase (100 U/g) and chitosanase (200 U/g) were evaluated against Malassezia furfur, Malassezia restricta, and Malassezia globosa at concentrations ranging from 0.125% to 5% w/w. Their efficacy was compared to that of conventional antifungal agents, including climbazole, piroctone olamine, selenium sulfide, zinc pyrithione, and propanediol caprylate. Cytotoxicity was assessed using fibroblast cell lines via MTT assay and fluorescence microscopy. A clinical study (n = 18) evaluated the impact of a solution containing 0.25% chitinase and 0.25% chitosanase on scalp M. furfur and M. restricta DNA and RNA levels using quantitative PCR (qPCR). A metagenomic analysis was conducted to assess the impact of enzymatic treatment on bacterial composition and diversity.

RESULTS: Individually, 0.25% chitinase and 0.25% chitosanase inhibited Malassezia spp. growth by 23.85% and 26.15%, respectively (p < 0.05). When combined at 0.25%, they achieved 98.38% inhibition (p < 0.05), with complete suppression observed at 0.5%. In a clinical study, a 3-hour scalp treatment with a solution containing 0.25% chitinase and 0.25% chitosanase followed by quantitative PCR of post-treatment samples demonstrated significant reductions in DNA and RNA levels of M. furfur and M. restricta. DNA content decreased 2.4- and 1.9-fold, and RNA levels declined 2.4- and 4.6-fold, respectively. Cytotoxicity was detected only at concentrations ≥ 7.6%, well above the effective antifungal doses. The metagenomic analysis demonstrated that a three-hour scalp treatment with chitinase - chitosanase solution increased alpha diversity (Chao1 index) and doubled the number of identifiable operational taxonomic units (OTUs).

CONCLUSIONS: The chitinase-chitosanase combination offers a promising targeted approach for scalp Malassezia spp. control without broad antimicrobial effects.},
}

*Malassezia/drug effects/growth & development/genetics
Humans
*Antifungal Agents/pharmacology
*Chitinases/pharmacology
*Glycoside Hydrolases/pharmacology
Dandruff/microbiology/drug therapy
Microbial Sensitivity Tests
Chitosan/metabolism
Scalp/microbiology
Dermatomycoses/microbiology/drug therapy
Fibroblasts/drug effects
Female
Male
Cell Line
Adult
Middle Aged

@article {pmid41193988,
year = {2025},
author = {Zhang, W and Xu, S and Bai, T and Aman, BO and Wang, Y and Li, S and Wang, J and Qin, Y and Wang, YY and Zheng, SJ},
title = {Banana genotype-associated microbiomes play an essential role in suppressing Fusarium wilt.},
journal = {BMC plant biology},
volume = {25},
number = {1},
pages = {1513},
pmid = {41193988},
issn = {1471-2229},
support = {YNWR-QNBJ-2020-298//The Provincial Xingdian Talent Program "Young Talent" Project/ ; XDYC-QNRC-2022-0243//The Provincial Xingdian Talent Program "Young Talent" Project/ ; D23033//Funded in part by Seedqual Initiative of One CGIAR, and the International Atomic Energy Agency, under project "An Integrative Approach to Enhancing Disease Resistance Against Fusarium Wilt (Foc TR4) in Banana - Phase II/ ; D23033//Funded in part by Seedqual Initiative of One CGIAR, and the International Atomic Energy Agency, under project "An Integrative Approach to Enhancing Disease Resistance Against Fusarium Wilt (Foc TR4) in Banana - Phase II/ ; 202301AT070008//General Program of Yunnan Provincial Natural Science Foundation/ ; 202401BD070001-096//Yunnan Fundamental Research Projects/ ; NSFC32161143001//National Natural Science Foundation of China/ ; YNWR-YLXZ-2018-018//Yunling Scholar Programme of Yunnan Provincial Government/ ; },
abstract = {BACKGROUND: Fusarium wilt of banana (FWB) seriously threatens the banana industry’s sustainable development. Recent evidence indicates that FWB occurrence and development are not only regulated by host resistance genes, but are also significantly influenced by host microbiomes. However, the link between banana genotypes and genotype-associated microbiomes remains unclear.

RESULTS: In this study, we used the amplification sequencing method to characterize the bacterial and fungal communities in three root compartments (root peripheral, rhizosphere, and endosphere) of six banana genotypes with different levels of FWB resistance. Sequence analysis showed that the banana host’s resistance to FWB significantly correlated with its associated bacterial and fungal communities in the root peripheral and rhizosphere. The FWB highly resistant group (RG) have more stable cross-kingdom microbial networks than FWB moderately resistant group (MG) and susceptible group (SG). The relative abundance of potential beneficial microorganisms differs significantly between RG and SG in the root periphery and rhizosphere. Bacillus, Penicillium, and Trichoderma are enriched in the root periphery of RG, whereas Flavobacterium, Sphingobium, and Pseudomonas are enriched in the root periphery and rhizosphere of SG. Inoculation with the RG biomarker Penicillium sp., which showed high relative abundance in the root periphery, significantly reduced the FWB disease index in the susceptible banana genotypes Brazilian and Guijiao No.1 by 51.67% and 51.72%, respectively.

CONCLUSIONS: The outcome of this study provides solid data that banana genotype-linked, root-associated microbiomes can play a highly significant role in suppressing FWB. This provides a promising basis for microbiome-based interventions in FWB management.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12870-025-07565-9.},
}

@article {pmid41193778,
year = {2025},
author = {Pirouzbakht, M and Hamzeh, S and Soleimani Samarkhazan, H},
title = {Beyond single biomarkers: multi-omics strategies to predict immunotherapy outcomes in blood cancers.},
journal = {Clinical and experimental medicine},
volume = {25},
number = {1},
pages = {355},
pmid = {41193778},
issn = {1591-9528},
mesh = {Humans ; *Immunotherapy/methods ; *Biomarkers, Tumor ; *Hematologic Neoplasms/therapy/genetics/immunology ; Genomics/methods ; Proteomics/methods ; Metabolomics/methods ; Treatment Outcome ; Multiomics ; },
abstract = {Immunotherapy has revolutionized hematologic cancer treatment, yet responses remain unpredictable due to primary resistance, relapse, and life-threatening toxicities. Conventional biomarkers fail to capture the complexity of tumor-immune interactions, necessitating integrative approaches. This review explores how multi-omics technologies, genomics, transcriptomics, proteomics, metabolomics, spatial omics, and microbiome profiling, decode the molecular drivers of immunotherapy efficacy and adverse events in hematologic malignancies. We highlight key advances: genomics reveals neoantigen landscapes and HLA diversity shaping checkpoint inhibitor responses; transcriptomics identifies T-cell exhaustion signatures predictive of CAR-T failure; metabolomics uncovers lactate-driven immunosuppression in AML; and spatial omics maps immune architectures linked to Hodgkin lymphoma outcomes. Supervised machine learning algorithms (e.g., random forest, support vector machines) integrate these layers to build predictive models for cytokine release syndrome (CRS) and resistance, while longitudinal ctDNA monitoring enables dynamic therapy adaptation. Emerging frontiers like CRISPR-based epitope editing, digital twins for in silico clinical trials, and non-coding RNA biomarkers further refine precision strategies. Despite challenges in data integration, tumor plasticity, and ethical frameworks, multi-omics is accelerating biomarker-driven trial designs (e.g., basket trials with omics stratification) and patient-centric tools (wearable sensors for real-time metabolite tracking). This review distinguishes itself by synthesizing these rapid technological advances not only to predict outcomes but also to chart a forward-looking roadmap for their clinical translation, offering a unique perspective on overcoming the current barriers to precision immuno-oncology. Together, these advances promise to transform immunotherapy from empirical to precision medicine, optimizing outcomes for leukemia, lymphoma, and myeloma patients.},
}

Humans
*Immunotherapy/methods
*Biomarkers, Tumor
*Hematologic Neoplasms/therapy/genetics/immunology
Genomics/methods
Proteomics/methods
Metabolomics/methods
Treatment Outcome
Multiomics

@article {pmid41193697,
year = {2025},
author = {Chica Cardenas, LA and Leonard, MM and Baldridge, MT and Handley, SA},
title = {Gut virome dynamics: from commensal to critical player in health and disease.},
journal = {Nature reviews. Gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
pmid = {41193697},
issn = {1759-5053},
abstract = {The gut virome is a complex ecosystem characterized by the interplay of diverse viral entities, predominantly bacteriophages and eukaryotic viruses. The gut virome has a critical role in human health by shaping microbial community profiles, modulating host immunity and influencing metabolic processes. Different viral metagenomics approaches have revealed the remarkable diversity of the gut virome, showing individual-specific patterns that evolve over time and adapt dynamically to environmental factors. Perturbations in this community are increasingly associated with chronic immune and inflammatory conditions, metabolic disorders and neurological conditions, highlighting its potential as a diagnostic biomarker and therapeutic target. The early-life gut virome is particularly influential in establishing lifelong health trajectories through its interactions with diet, immune pathways and others, thereby contributing to inflammatory and metabolic regulation. This Review synthesizes current knowledge of gut virome composition, dynamics and functional relevance, critically evaluating evidence distinguishing causal from correlative roles in disease pathogenesis. The interactions of the virome with other microbiome components and host immunity are examined, and emerging translational applications, including phage therapy and biomarker development, are discussed. Integrating these insights while acknowledging methodological challenges provides a comprehensive framework for understanding the complex roles of the gut virome in health and disease.},
}

@article {pmid41193636,
year = {2025},
author = {Hug, LA and Hatzenpichler, R and Moraru, C and Soares, AR and Meyer, F and Heyder, A and , and Probst, AJ},
title = {Author Correction: A roadmap for equitable reuse of public microbiome data.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41564-025-02212-3},
pmid = {41193636},
issn = {2058-5276},
}

@article {pmid41193635,
year = {2025},
author = {Weinheimer, AR and Brown, JM and Thompson, B and Leonaviciene, G and Kiseliovas, V and Jocys, S and Munson-McGee, J and Gavelis, G and Mascena, C and Mazutis, L and Poulton, NJ and Zilionis, R and Stepanauskas, R},
title = {Single-particle genomics uncovers abundant non-canonical marine viruses from nanolitre volumes.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {41193635},
issn = {2058-5276},
support = {991222//Simons Foundation/ ; },
abstract = {Viruses and other extracellular genetic elements play essential roles in marine communities. However, methods to capture their full diversity remain limited by the constraints of bulk sequencing assemblers or pre-sorting throughput. Here we introduce environmental micro-compartment genomics (EMCG), which vastly improves the throughput and efficiency of single-particle genomic sequencing obtained from nanolitre volumes by compartmentalizing particles of a sample into picolitre-sized, semi-permeable capsules for in-capsule DNA amplification and barcoding. From 300 nanolitres of seawater, EMCG obtained genomic sequences of 2,037 particles. The microbiome composition agreed with other methods, and the virus-like assembly lengths indicated that most were near complete. Many viral assemblies belonged to the Naomiviridae, lacked metagenomic representation and aligned to outlier contigs of abundant, putative host lineages, suggesting their use of non-canonical DNA and overlooked ecological importance. This approach provides opportunities for high-throughput, quantitative and cost-effective genome analyses of individual cells and extracellular particles across complex microbiomes.},
}

@article {pmid41193561,
year = {2025},
author = {Chen, TY and Huang, WY and Liu, KH and Lin, S and Wu, HM},
title = {Circulating endotoxin is correlated with fatty acid binding protein 2 and leukocyte nuclear factor-κB activation in menopausal women.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {38693},
pmid = {41193561},
issn = {2045-2322},
support = {111-CCH-IRP-086//Changhua Christian Hospital/ ; MOST 108-2314-B-371-004-MY3//National Science and Technology Council, Taiwan/ ; },
mesh = {Humans ; Female ; *Fatty Acid-Binding Proteins/blood/metabolism ; Middle Aged ; *Endotoxins/blood ; *Leukocytes/metabolism ; *NF-kappa B/metabolism ; *Menopause/blood ; Inflammation/blood ; Endotoxemia/blood ; Fasting/blood ; Glucose Tolerance Test ; Biomarkers/blood ; },
abstract = {Circulating endotoxin is mainly derived from gut microbiome and is frequently increased after meals. However, the interplay between endotoxemia and innate immune cells in systemic inflammation remains unclear. The aim was to investigate the role of endotoxemia in systemic inflammation, focusing on the immune responses in innate immune cells. Menopausal women (n = 174) were divided into 2 groups. Blood samples were collected from the participants of group 1 (n = 80), who fasted for at least 8 h, to analyze the correlation between endotoxin levels, fatty acid-binding protein 2 (FABP2), markers of systemic inflammation, and nuclear factor-κB (NF-κB) activation in leukocytes. The participants of group 2 (n = 94) fasted for at least 8 h and received oral glucose tolerance test (OGTT). Their fasting and post-OGTT blood samples were also collected to evaluate the impact of postprandial endotoxemia on the expression of NF-κB target genes in leucocytes. The study revealed that circulating endotoxin level was significantly associated with FABP2 level and NF-κB activation in leukocytes after fasting and within a 2 h-OGTT period. Variation in endotoxin levels (about 1 EU/ml) was sufficient to modulate NF-κB activation in leukocytes. These results provide clues for understanding the effects of postprandial endotoxemia on immune cell activation and inflammation induction. Our findings suggest that an increase in intestinal barrier permeability might be linked to endotoxemia-induced systemic inflammation in menopausal women.},
}

Humans
Female
*Fatty Acid-Binding Proteins/blood/metabolism
Middle Aged
*Endotoxins/blood
*Leukocytes/metabolism
*NF-kappa B/metabolism
*Menopause/blood
Inflammation/blood
Endotoxemia/blood
Fasting/blood
Glucose Tolerance Test
Biomarkers/blood

@article {pmid41193447,
year = {2025},
author = {Baskaran, N and V, M and S, S and Ranjan, J and Islam, A and Hussain, MS and Debnath, B and Ashique, S},
title = {Applications of Artificial Intelligence and Machine Learning in Microbiome and Colorectal Cancer Research: Diagnostic Advances, Prognostic Tools, and Forensic Implications.},
journal = {Current pharmaceutical design},
volume = {},
number = {},
pages = {},
doi = {10.2174/0113816128405592251004061813},
pmid = {41193447},
issn = {1873-4286},
abstract = {Artificial Intelligence (AI) and Machine Learning (ML) are rapidly transforming microbiome and colorectal cancer (CRC) research by enabling high-throughput data analysis and predictive modelling. This review highlights the current applications of AI/ML tools, such as Convolutional Neural Networks, Random Forest classifiers, and Support Vector Machines, in CRC diagnostics and microbiome profiling. It discusses how AI-integrated endoscopic and imaging systems improve polyp detection accuracy and reduce diagnostic delays. The manuscript also introduces the novel use of AI and microbial fingerprints in forensic science, including postmortem interval estimation and individual identification. Lastly, emerging trends in microbiotabased precision medicine and ethical considerations surrounding AI deployment are explored. These insights underscore AI/ML's potential in reshaping clinical diagnostics, prognostics, and forensic practices related to CRC. This review emphasizes the translational impact of AI/ML in CRC, from bench to bedside to the courtroom, highlighting both current challenges and future research directions.},
}

@article {pmid41192778,
year = {2025},
author = {Tabata, K and Ikarashi, N and Yoshida, R and Shinozaki, Y and Kato, Y and Kon, R and Iwasaki, Y and Yokoyama, K and Saito, R and Sakai, H and Hosoe, T},
title = {High-fat diet exacerbates atopic dermatitis through alterations in the gut microbiome.},
journal = {The Journal of nutritional biochemistry},
volume = {},
number = {},
pages = {110164},
doi = {10.1016/j.jnutbio.2025.110164},
pmid = {41192778},
issn = {1873-4847},
abstract = {Atopic dermatitis (AD) is a chronic, relapsing skin disorder characterized by pruritic eczema. In addition to genetic predispositions, environmental factors such as diet are thought to contribute to the exacerbation of AD. The aim of this study was to provide scientific evidence on how environmental factors, particularly a high-fat diet (HFD), influence the pathogenesis of AD. AD was induced in NC/Nga mice fed an HFD through the application of 2,4-dinitrochlorobenzene. In the AD-HFD group, the expression levels of inflammatory markers (Tnfa, Il1b, Ptgs2, and Nos2) and AD-related factors (Il4, Ccl17, and Tslp) in the skin were significantly elevated compared with those in the AD group (mice fed a normal diet). Alteration of gut microbiota was observed in the AD-HFD group, characterized by a reduction in the abundances of Bacteroides acidifaciens and Parabacteroides distasonis, bacteria involved in short-chain fatty acid (SCFA) production. Moreover, the levels of acetate, propionate, and butyrate in the cecal contents were significantly decreased in the AD-HFD group. Fecal microbiota transplantation experiments revealed that alterations in the gut microbiota were associated with the exacerbation of AD symptoms. Furthermore, the administration of acetate alleviated the increase in the expression of skin inflammation markers and AD-related factors and the overall exacerbation of AD-like symptoms induced by the HFD. HFD intake exacerbates AD-like symptoms, and this exacerbation is linked to alteration of gut microbiota and a decrease in SCFA levels. These results suggest that acetate and acetate-producing bacteria may serve as potential tools for the prevention and treatment of AD.},
}

@article {pmid41192743,
year = {2025},
author = {Ueyama, M and Ohue-Kitano, R and Kimura, I and Kimura, H},
title = {Association between Gut Actinobacteria and Obstructive Sleep Apnoea Severity in Japanese Adults.},
journal = {Respiratory medicine},
volume = {},
number = {},
pages = {108472},
doi = {10.1016/j.rmed.2025.108472},
pmid = {41192743},
issn = {1532-3064},
abstract = {BACKGROUND: Gut microbiota are known to mediate human health and are affected by physiological conditions, including hypoxia. Although studies involving animal models have shown that intermittent hypoxia alters gut microbiota, its effects in adult Japanese patients with obstructive sleep apnoea (OSA) remain unclear. We investigated the association between OSA severity and gut microbiota composition in Japanese adults with OSA.

METHODS: This cross-sectional study included 74 Japanese diagnosed with OSA via polysomnography. The average body mass index was 30.5 ± 3.8 kg/m[2] and the average 3% oxygen desaturation index (ODI) was 39.9 ± 20.0. No control group was included. Faecal samples were collected in a fasting period of >10 h. The association between 3% ODI and gut microbiota were analysed at the phylum, family and genus level.

RESULTS: At the phylum level, 3% ODI significantly positively correlated with Actinobacteria (r = 0.3151, p = 0.0126) and negatively correlated with Firmicutes (r = 0.3150, p = 0.0126). No significant correlations were found with Proteobacteria or Bacteroidetes. At the family level, 3% ODI significantly positively correlated with Bifidobacteriaceae in Actinobacteria (r = 0.2373, p = 0.0418). At genus level, Bifdobacterium was prominently increased compared with other group.

CONCLUSION: This study showed that the gut microbiome in Japanese with OSA showed an increase in Bifdobacterium. Although our cohort was biased towards moderate obesity and severe OSA severity, intermittent hypoxia might contribute to the change of gut microbiome. These findings suggest that increased Bifdobacterium may help maintain gut homeostasis under hypoxic stress, especially in Japanese.},
}

@article {pmid41188868,
year = {2025},
author = {Duan, S and Wang, Y and Zhan, S and Ye, Z and Luo, T and Zhou, Y and Xu, H and Huang, H},
title = {Engineered probiotics: a new era in treating inflammatory bowel disease.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {1223},
pmid = {41188868},
issn = {1479-5876},
support = {82100124//National Natural Science Foundation of China/ ; 2024A1515220138//Basic and Applied Basic Research Foundation of Guangdong Province/ ; A2025164//Guangdong Medical Science and Technology Research Fund/ ; B2025093//Guangdong Medical Science and Technology Research Fund/ ; 2025A03J4148//Science and Technology Projects in Guangzhou/ ; },
abstract = {Inflammatory bowel disease (IBD) is a chronic, relapsing condition that is often refractory to treatment. Data from the Global Burden of Disease Study (GBD) indicate that the incidence and disease burden of this condition continue to rise globally, posing a significant public health challenge. With advancements in synthetic biology, engineered probiotics constructed using gene-editing tools like CRISPR-Cas9 have offered a groundbreaking strategy for treating IBD. These engineered probiotics modulate the intestinal microenvironment with high precision through multiple mechanisms, including the targeted delivery of anti-inflammatory factors, scavenging of excess reactive oxygen species (ROS), restoration of barrier integrity, and regulation of microbial homeostasis. Preclinical studies indicate that, in terms of therapeutic precision and functionality, these probiotics may provide advantages over traditional medications. In addition, advances in delivery systems have improved acid resistance and targeted colonization at lesion sites. Engineered smart, responsive engineered probiotics can monitor inflammation in real-time and dynamically release therapeutic molecules. Their use in combination with conventional drugs can significantly improve mucosal healing. This study summarizes recent research progress of engineered probiotics in IBD diagnosis and treatment, aiming to provide insights into the application of microbiome-driven curative interventions in IBD.},
}

@article {pmid41192727,
year = {2025},
author = {Lai, J and Yang, B and Ju, P and Sun, Y and Sun, X and Cheng, W and Chen, J},
title = {Gut microbiota from adolescents with social anxiety disorder is associated with behavioral alterations and metabolic changes in the medial prefrontal cortex.},
journal = {Journal of affective disorders},
volume = {},
number = {},
pages = {120597},
doi = {10.1016/j.jad.2025.120597},
pmid = {41192727},
issn = {1573-2517},
abstract = {BACKGROUND: Social anxiety disorder (SAD) is a prevalent and burdensome neuropsychiatric disorder characterised by pronounced and persistent fear and anxiety in social situations. While evidence links gut microbiota to neuropsychiatric disorders, its role in SAD remains poorly understood.

AIM: In this study, we aimed to investigate the potential involvement of gut microbiota in SAD pathophysiology through fecal microbiota transplantation.

METHOD: We collected demographic data and fecal samples from 40 first-episode, comorbidity-free, and drug-naive adolescent patients with SAD, along with 32 demographically matched healthy controls. Fecal samples underwent 16S rDNA amplicon sequencing and were pooled for transplantation into neonatal rats from postnatal day 1 through late adolescence. Recipient rats were evaluated with behavioral tests, microbiota detection, and non-targeted metabolomics of the medial prefrontal cortex.

RESULT: Patients with SAD displayed alterations in gut microbiota composition. Rats colonized with SAD-associated microbiota exhibited anxiety-like behaviors and reduced social novelty preference, alongside microbial profiles partially overlapping with those of patients. These behavioral changes were correlated with microbiota differences, and distinct metabolic alterations were detected in the medial prefrontal cortex of SAD-colonized rats.

CONCLUSION: Gut microbiota from adolescents with SAD is associated with behavioral and metabolic alterations in a rodent model, suggesting a potential role of the gut-brain axis in SAD. Further studies are warranted to establish causality and elucidate underlying mechanisms.},
}

@article {pmid41192697,
year = {2025},
author = {Forton, C and DeVries, J and Lou, M and Brundin, S and Cave, T and Anis, E and Madaj, Z and Isaguirre, C and Johnson, A and Sheldon, RD and Smart, L and Bohnert, KM and Kassien, J and Holzgen, O and Youssef, NA and Khan, T and Brundin, L},
title = {Gut microbiome-derived tryptophan metabolites predict relapse in alcohol use disorder.},
journal = {Brain, behavior, and immunity},
volume = {},
number = {},
pages = {106161},
doi = {10.1016/j.bbi.2025.106161},
pmid = {41192697},
issn = {1090-2139},
abstract = {Relapse is common in alcohol use disorder (AUD), a condition that affects nearly 11 % of adults in the US. Excessive alcohol consumption causes gut dysbiosis, which may in turn alter the production of bacterial-derived tryptophan metabolites. These metabolites impact the intestinal enteroendocrine environment and modulate neuroinflammation. This can ultimately affect behavior. However, the role of bacterial-derived tryptophan metabolites in AUD is not well-understood. Thus, in this study, we enrolled 40 patients admitted for severe AUD (26 males, 14 females) to investigate whether bacterial-derived indoles could predict AUD relapse. Upon enrollment, alcohol use as well as depression and anxiety symptoms were assessed. Peripheral blood samples were collected and analyzed for cytokines, bacterial-derived as well as endogenous tryptophan metabolites, and hematological factors. At three months after discharge, 25 patients completed follow-up and were re-assessed for clinical symptoms to identify AUD relapse. Ten patients relapsed and 15 patients were in early remission. Two bacterial tryptophan metabolites, indole-3-carboxaldehyde (IAld) and indole-3-acetic acid (IAA), significantly predicted relapse versus remission using logistic regression models (p = 0.019, SGPV = 0, and p = 0.035, SGPV = 0 respectively). These findings remained significant after adjustment for age, sex, BMI, and when additionally adjusting for nicotine use and depression severity. Moreover, higher IAld levels correlated with increased serotonin levels (Pearson's R; 0.592, p < 0.001) and fewer white blood cells (Pearson's R; -0.318, p < 0.05) in all 40 patients. Our data indicate significant interactions between microbiome-derived metabolites and host metabolism, and that IAld specifically may have a protective role in AUD, potentially through serotonin modulation.},
}

@article {pmid41192621,
year = {2025},
author = {Carpani, JM and Barta, JR and Guy, RA},
title = {Suppression/competition PCR: A novel method to minimize unwanted amplicons in metabarcoding, with applications to parasite detection in fecal samples.},
journal = {Journal of microbiological methods},
volume = {},
number = {},
pages = {107320},
doi = {10.1016/j.mimet.2025.107320},
pmid = {41192621},
issn = {1872-8359},
abstract = {Metabarcoding is widely used for detecting microorganisms in fecal samples, but its effectiveness is often limited by the co-amplification of abundant non-target DNA. In this study, a novel metabarcoding assay was developed to amplify a near-complete 18S rRNA gene fragment suitable for long-read nanopore sequencing, enhancing taxonomic resolution. The primers were optimized to maximize detection of parasitic taxa while minimizing off-target amplification of bacterial and archaeal sequences, thereby improving assay specificity. In this study, the 18S metabarcoding assay worked well on clinical fecal samples containing clinically relevant levels of parasites. However, analysis of ungulate fecal samples revealed that fungal and plant sequences vastly outnumbered other eukaryotic taxa in many samples, obscuring the detection of low-abundance protozoan and helminth parasites. To address this, Suppression/Competition PCR was developed, a novel method that selectively reduces amplification of unwanted DNA. This approach reduced fungal and plant reads by over 99 %, enabling sequences from other taxa to comprise an average of over 98 % of total reads as opposed to an initial 36 %. Utilizing this newly-developed metabarcoding assay in either the standard or Suppression/Competition configuration on fecal DNA extracts from a range of host species, parasites of interest such as Cryptosporidium sp., Cyclospora cayetanensis, Blastocystis sp., Entamoeba sp., Eimeria sp., Ancylostoma sp., and Toxocara sp. were detected, demonstrating its broad applicability.},
}

@article {pmid41192424,
year = {2025},
author = {Li, P and Sun, J and Geng, Y and Jiang, Y and Li, YZ and Zhang, Z},
title = {Assessment of enzyme diversity in the fermented food microbiome.},
journal = {Cell systems},
volume = {},
number = {},
pages = {101430},
doi = {10.1016/j.cels.2025.101430},
pmid = {41192424},
issn = {2405-4720},
abstract = {Microbial bioactivity is essential for the flavor, appearance, quality, and safety of fermented foods. However, the diversity and distribution of enzymatic resources in fermentation remain poorly understood. This study explored 10,202 metagenome-assembled genomes from global fermented foods using machine learning, identifying over 5 million enzyme sequences grouped into 98,693 homologous clusters, representing over 3,000 enzyme types. Functional analysis revealed that 84.4% of these clusters were unannotated in current databases, with high novelty in terpenoid and polyketide metabolism enzymes. Peptide hydrolases exhibited broad environmental adaptability based on predicted optimal temperatures and pH, and niche breadth calculations indicated 31.3% of enzyme clusters displayed food-type specificity. Additionally, we developed a machine learning model to classify fermented food sources by enzyme clusters, highlighting key enzymes differentiating habitats. Our findings emphasize the untapped potential of fermented food environments for enzyme resource exploration, offering valuable insights into microbial functions for future food research. A record of this paper's transparent peer review process is included in the supplemental information.},
}

@article {pmid41192300,
year = {2025},
author = {Ge, Y and Shi, R and Liu, W and Li, X and Shi, X and Zeb, A and Zhao, Y and An, J and Sun, Y},
title = {Foliar exposure to 6PPD-Q disturbs photosynthetic processes and induces oxidative stress in Eichhornia crassipes.},
journal = {Journal of environmental management},
volume = {395},
number = {},
pages = {127919},
doi = {10.1016/j.jenvman.2025.127919},
pmid = {41192300},
issn = {1095-8630},
abstract = {Air pollution is a currently common global concern issue. The widespread occurrence of N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-Q), a transformation product of tire additives detected on airborne particular matter, necessitates an urgent assessment of its environmental risks. This study investigated the phytotoxic effects of atmospheric 6PPD-Q deposition via foliar exposure on water hyacinth through integrated metabolomic, microbiomic, and spectroscopic analyses. 6PPD-Q exposure severely damaged chloroplast ultrastructure and suppressed Rubisco activity by 21.09 % at high concentrations, driving concentration-dependent reductions in net photosynthetic rate (28.95 %, 41.83 %, and 55.88 %). Concurrent oxidative stress and nutrient uptake limitations further impaired carbohydrate metabolism. Molecular docking and spectral analyses revealed structural perturbations in key functional proteins, while phyllosphere microbiome disruption manifested through simplified fungal-bacterial co-occurrence networks and depletion of beneficial taxa. These collective impacts exacerbated plant physiological dysfunction. Our findings demonstrate the systemic phytotoxic mechanisms of airborne 6PPD-Q, highlighting the urgent need to investigate its ecological risks in ecosystems.},
}

@article {pmid41192182,
year = {2025},
author = {Lei, J and Zhang, S and Zhao, C and Zhang, L and Li, Y and Zhou, W},
title = {Engineering microbiome for carbonate precipitation in heavy oil produced water: Hot-zone identification of ion accumulation and crystallization.},
journal = {Journal of hazardous materials},
volume = {500},
number = {},
pages = {140317},
doi = {10.1016/j.jhazmat.2025.140317},
pmid = {41192182},
issn = {1873-3336},
abstract = {Microbially induced carbonate precipitation (MICP) presents a promising strategy for the softening and purification of produced water. However, produced water from heavy oil reservoirs exhibits high salinity, refractory organics, particularly with hardness ions such as Ca[2+] and Mg[2+], all of which substantially inhibit microbial mineralization activity. Industrially viable continuous-flow operational strategies remain underdeveloped, and the underlying biomineralization mechanisms are not yet fully elucidated. Here, we report the successful construction of an engineering microbiome through substrate gradient acclimation, achieving continuous and stable precipitation of Ca[2+] (87.28 %) and Mg[2+] (84.16 %). The process also revealed the sequential transformation of organic functional groups under high salinity perturbation. Hydroxyl groups (-OH) in extracellular polymeric substances preferentially bound divalent cations under neutral conditions, whereas carboxyl groups (-COO[-]) served as nucleation sites for carbonate formation under alkaline conditions. Extracellular carbonate precipitation predominated, while a minor fraction of amorphous magnesium carbonate was accumulated intracellularly. The engineering microbiome, dominated by urease-positive and hydrocarbon-degrading taxa, tolerated extreme salinity and hardness through metabolic complementarity and coordinated gene regulation. These findings demonstrate a robust, continuous-flow MICP process for HPW treatment, offering a foundation for industrial-scale integration with improved stability, efficiency, and microbiome resilience in complex environments.},
}

@article {pmid41192153,
year = {2025},
author = {Ma, X and Ju, L and Zheng, J and Li, Z and Gao, L},
title = {Japanese encephalitis virus infection modulates gut microbiota of immunocompetent mice.},
journal = {Veterinary microbiology},
volume = {311},
number = {},
pages = {110779},
doi = {10.1016/j.vetmic.2025.110779},
pmid = {41192153},
issn = {1873-2542},
abstract = {Japanese encephalitis virus (JEV), a neurotropic pathogen, causes severe encephalitis in humans and animals. It invades the central nervous system, and triggers neuroinflammation leading to neuronal damage. However, the impact of JEV on the gut microbiome of adult immunocompetent hosts remains unclear. Here, we characterized JEV-induced gut microbiota alterations in C57BL/6 J mice using 16S rRNA sequencing of the V3-V4 region and cytokine/chemokine profiling. Alpha diversity analysis showed a higher Shannon index and lower Simpson index in JEV-infected group. Relative abundance of bacterial groups revealed increased Deferribacteres and Spirochaetes and decreased Actinobacteria and Firmicutes at phylum level. LEfSe analysis demonstrated enhanced relative abundance of Lachnospiraceae_NK4A136_group, norank_f_Lachnospiraceae and Lachnoclostridium, whereas that of Turicibacter, Coriobacteriaceae_UCG-002 and Romboutsia decreased at genus level. At 14dpi, IL-6, IL-10, TNF-α, CCL2, IFN-γ, and IFN-β were upregulated in the brain, while only IFN-γ was elevated in colon tissue, accompanied by mild pathological damage in colonic epithelium. These findings demonstrate that JEV infection remodels gut microbiota composition and disrupts colonic homeostasis in immunocompetent adult mice, suggesting that gut microbial alterations may be mediated by brain-derived IFN-γ-producing lymphocytes via the brain-gut axis.},
}

@article {pmid41192073,
year = {2025},
author = {McDonagh, F and Kovarova, A and Tumeo, A and O'Connor, A and McEvoy, N and Lonappan, AM and Venkateswaran, K and Murray, EK and Hallahan, B and Miliotis, G},
title = {Complete genome and comparative genomic analysis of cefpodoxime resistant Pantoea septica strain GABEPS69 isolated from saliva of a patient diagnosed with treatment resistant schizophrenia.},
journal = {International journal of medical microbiology : IJMM},
volume = {321},
number = {},
pages = {151681},
doi = {10.1016/j.ijmm.2025.151681},
pmid = {41192073},
issn = {1618-0607},
abstract = {OBJECTIVES: This study aims to generate the first complete genome of Pantoea septica and provide a thorough genomic characterisation of this under-documented species. The study seeks to enhance understanding of P. septica, clarifying features relevant to opportunistic infection in vulnerable cohorts.

METHODS: P. septica GABEPS69 was an opportunistic coloniser isolated from the saliva of a patient prescribed the antipsychotic clozapine, leading to a dysbiotic oral microbiome. A hybrid sequencing approach yielded a closed genome comprising a 4.1 Mb chromosome and six plasmids. Phenotypic susceptibility was determined by disk-diffusion and minimum inhibitory concentration (MIC) assays. Its chromosomal and plasmidic content was bioinformatically analysed alongside all canonical GenBank available P. septica genomes and the type strains of taxonomic neighbours Pantoea piersonii and "Pantoea latae", with focus on virulence-factors (VFs), antimicrobial-resistance-genes (ARGs), metal-resistance-genes (MRGs) and biosynthetic gene clusters.

RESULTS: GABEPS69 exhibited a narrow resistance spectrum, displaying resistance to the third-generation cephalosporin cefpodoxime. Plasmid pGABEPS69_1 harboured an aerobactin pathogenicity island homologue; a locus implicated in enhanced virulence, that was also identified across most other P. septica genomes and in the closely related human-pathogen Pantoea piersonii. A conserved chromosomal class-A β-lactamase homologue was also identified. Additionally, a universal presence of bioactive thiopeptide biosynthetic-gene-clusters was observed in P. septica genomes, suggesting a potential role in microbiome modulation.

CONCLUSION: This study presents a first complete genome of P. septica, revealing its genomic architecture, resistance, and virulence potential. Detailed plasmid analysis and comparative genomics enhance our understanding of the species clinical relevance and microbiome-modulating capacity. These findings motivate surveillance of transient oral microbiota in at-risk populations, including patients receiving clozapine.},
}

@article {pmid41192043,
year = {2025},
author = {Kumar, A and Xu, C and Dakal, TC},
title = {Microbiome based precision medicine through integrated multiomics and machine learning.},
journal = {Microbiological research},
volume = {303},
number = {},
pages = {128384},
doi = {10.1016/j.micres.2025.128384},
pmid = {41192043},
issn = {1618-0623},
abstract = {Gut microbiome (GME) is a dynamic ecosystem composed of diverse microorganisms with extensive functional potential that influence host physiology, endocrinology, and neurology. This review explores how multiomics (m[OMICS]) and machine learning (ML) enhance understanding of the GME and its implications for human disease and therapy. Integrating metagenomics, metatranscriptomics, metaproteomics, and metabolomics with ML enables the linkage of microbial composition and function to clinical outcomes. Combined m[OMICS] approaches elucidate species and strain dynamics, metabolic pathways, and metabolite production within the gut environment. Techniques such as shotgun metagenomics, metagenome-assembled genomes, and pathway mapping reveal associations between dysbiosis and diseases including inflammatory bowel disease, colorectal cancer, cardiometabolic, and neurological disorders. Mechanistic insights highlight short-chain fatty acids in immune regulation, bile acid transformations in metabolic signaling, and trimethylamine N-oxide in cardiovascular risk. ML models trained on heterogeneous datasets identify disease-related microbial modules, improve patient stratification, and predict therapeutic responses, such as differentiating IBD subtypes and detecting cancer-linked microbial signatures. Network analyses uncover gut microbial interaction patterns influencing host physiology. Emerging integrative tools like MOFA+ , DIABLO, and MintTea strengthen cross-modal analysis and biomarker discovery. Standardized workflows addressing quality control, assembly, binning, annotation, and visualization ensure reproducibility. Together, m[OMICS] and ML establish a robust framework for translating GME ecology into clinically relevant biomarkers and precision interventions. To enhance reliability, GME studies should adopt uniform sampling protocols, correct compositional biases, employ interpretable models, and validate findings across multi-site cohorts to advance microbiome-based diagnostics and therapeutics in precision medicine.},
}

@article {pmid41191730,
year = {2025},
author = {Chen, Y and Aldrich, CG},
title = {Digestibility and Palatability of Extruded Dog Food with Aspergillus oryzae Fermented Soybean Meal and its Influence on Colonic Fermentation Indicators.},
journal = {Journal of animal science},
volume = {},
number = {},
pages = {},
doi = {10.1093/jas/skaf392},
pmid = {41191730},
issn = {1525-3163},
abstract = {This study aimed to compare Aspergillus oryzae fermented soybean meal with traditional soybean products in extruded diets on digestibility, colonic fermentation and palatability when fed to dogs. Four diets using differed soybean products (30% soybean meal, SBM; 30% soybean meal + 1% dry A. oryzae biomass product, AMF; 30% fermented soybean meal, FSBM; and 18% soybean protein isolate, SPI) were fed to 12 adult dogs in a replicated 4 x 4 Latin square design. Dogs were adapted to diets for 9 days followed by a 5-day total fecal collection and fresh fecal collection. Apparent total tract digestibility (ATTD) was calculated by total fecal collection method and indirect marker (titanium dioxide) method. Data were analyzed with a generalized linear mixed model (GLIMMIX; SAS version 9.4) with diet as fixed effect and dog and period as random effects. Dogs fed with SPI had lower (P＜0.001) fecal output and defecation frequency than dogs fed with other diets. Dogs fed with FSBM had ATTD of organic matter, crude protein and gross energy similar to dogs fed with SBM, but lower (P＜0.05) than those fed with SPI regardless of estimation method. The ATTD of dry matter, as calculated by the marker method, was greater (P＜0.001) in dogs fed with FSBM diet compared to those fed with SBM. Fecal pH was greater (P＜0.05) in dogs fed with SPI than in those fed with SBM and AMF, with dogs fed with FSBM intermediate. While fecal ammonia content was similar across dogs, short-chain fatty acid (SCFA) content was the lowest (P＜0.05) in dogs fed with SPI and the highest (P＜0.05) in those fed with AMF. Acetate, propionate, and total volatile fatty acid (the sum of SCFA and BCFA) contents mirrored the ranking of SCFA. Percentage of propionate and SCFA to total volatile fatty acids were lower (P＜0.05), whereas those for butyrate, isovalerate, and branched-chain fatty acids (BCFA) were higher (P＜0.05) in dogs fed with SPI diet compared to dogs on other diets. Palatability trials were conducted with 20 dogs over 2 days. Data were analyzed with a 1-way ANOVA, a paired t-test and a Chi2 test at significance level of α = 0.05. Dogs showed preference (P＜0.05) for SBM over FSBM, but differences between SBM, AMF, and SPI were insignificant. In conclusion, the A. oryzae fermented soybean meal-based diet was less palatable than regular soybean meal-based diet but they induced similar stool quality, nutrient digestibility and colonic fermentation pattern in dogs.},
}

@article {pmid41191616,
year = {2025},
author = {Maretto, L and Deb, S and Squartini, A and Concheri, G and Stevanato, P and Nardi, S and Cocco, S and Corti, G},
title = {Evaluation of the soil microbiome of three raised beaches in the Devon Island Lowland, High Arctic, Canada.},
journal = {PloS one},
volume = {20},
number = {11},
pages = {e0336235},
doi = {10.1371/journal.pone.0336235},
pmid = {41191616},
issn = {1932-6203},
mesh = {*Soil Microbiology ; *Microbiota/genetics ; Arctic Regions ; RNA, Ribosomal, 16S/genetics ; Canada ; Bacteria/genetics/classification ; Soil/chemistry ; DNA, Bacterial/genetics ; Islands ; Ecosystem ; },
abstract = {The Arctic region is characterized by severe temperatures and a unique ecosystem with largely unexplored microbiomes. Whereas soil microbiomes in temperate regions play key roles in nutrient cycling, organic matter decomposition, greenhouse gas fluxes, and overall ecosystem functioning, Arctic microbiomes remain poorly understood, highlighting the need for a thorough characterization to better predict and manage soil health and resilience. In this study, we compared the microbial profiles of three raised beaches on Devon Island (Nunavut, Canadian Arctic Archipelago), which emerged sequentially between eight and two thousand years ago, to assess their similarities and differences. Samples were collected by genetic horizons along excavations from the top layer to the permafrost. For each horizon, total soil DNA, 16S gene copies dPCR quantification, 16S metabarcoding, and functional prediction were carried out. Total DNA quantification revealed a consistently comparable concentration of genetic material across the three soil beaches (AB2 μ = 2.28 ± 5.44 μg ∙ g-1, AB1 μ = 4.71 ± 2.35 μg ∙ g-1, AB3 μ = 5.44 ± 2.91 μg ∙ g-1), regardless of site age (AB2 = 2,360 YBP, AB1 = 6,726 YBP, AB3 = 8,410 YBP). Conversely, clear differences emerged by comparing the different horizons at each site. The hierarchical cluster analysis based on the Bray-Curtis dissimilarity matrix revealed a clear separation between surface and deep horizons. The core microbiome analysis highlighted Actinobacteria, Proteobacteria, and Firmicutes as the three predominant phyla accounting for relative abundances of 42%, 22%, and 18%, respectively. Remarkable evidence was the unexpectedly high taxonomic diversity that was recorded in these sites and that surprisingly matched with the commonly observed values in soils of temperate regions. Since these stony shores developed under cold, life-limiting conditions, their apparent microbial richness raises doubts about the potential biases in inferring physiological contexts and active biodiversity directly inferred from culture-independent DNA-based studies. The reason is that such inventories can be possibly inflated, in all environments, by chronically accumulated cells from passive immigration events through atmospheric discharge.},
}

*Soil Microbiology
*Microbiota/genetics
Arctic Regions
RNA, Ribosomal, 16S/genetics
Canada
Bacteria/genetics/classification
Soil/chemistry
DNA, Bacterial/genetics
Islands
Ecosystem

@article {pmid41191542,
year = {2025},
author = {Millick, DD and Ghosh, S and Wu, G and Krzyzanowska, AK and Osorio, LJ and Zhao, L and Strair, R and Sant'Angelo, DB},
title = {Dietary animal fat disrupts gut microbiota and aggravates Scl-cGVHD after allogeneic hematopoietic stem cell transfer.},
journal = {Blood advances},
volume = {},
number = {},
pages = {},
doi = {10.1182/bloodadvances.2024014831},
pmid = {41191542},
issn = {2473-9537},
abstract = {Allogeneic Hematopoietic Stem Cell Transplant (allo-HCT) is an effective treatment for high-risk or relapsed acute leukemia. However, the frequent occurrence of graft-versus-host disease (GVHD) poses significant complications. Modifiable factors such as the gut microbiome and dietary regimen have the potential to influence the frequency and severity of GVHD. Previous studies in mouse models have shown a direct link between obesity and increased severity of GVHD. Analysis of human data has not suggested a causal relationship, however. We hypothesized that dietary fat content prior to transplantation, rather than obesity itself, might affect outcomes, given that increased dietary fat is associated with reduced gut microbiome diversity. In our study, we evaluated the effects of an animal fat-based diet (AFD) and a plant fat-based diet (PFD) in a mouse model of sclerodermatous chronic GVHD (Scl-cGVHD). Mice initially fed normal chow (~10% kcal from fat) were switched to either AFD or PFD (each with ~25% kcal from fat) two weeks before allo-HCT. Mice on the AFD had an elevated serum cytokine response, more severe skin inflammation, and greater intestinal immune dysregulation compared to mice on the PFD. Although both diets reduced gut microbial diversity, the fat source led to distinct microbiota compositions that included two co-abundance guilds (CAGs) that differentiated between the AFD and PFD groups. Our findings demonstrate that even short-term consumption of diets with equivalent macronutrient content, but different fat sources, can modulate the gut microbiome, disrupt intestinal homeostasis, and influence Scl-cGVHD outcomes.},
}

@article {pmid41191326,
year = {2025},
author = {Bongers, KS and Flott, TL and Yeomans, L and Maynard, L and Adame, MD and Falkowski, NR and McDonald, RA and Petouhoff, A and Baker, JM and McLellan, M and Aragones, LL and Kaniaru, J and Singer, BH and Dickson, RP and Stringer, KA},
title = {"Gut microbiome-mediated nutrients alter opportunistic bacterial growth in peritonitis".},
journal = {American journal of physiology. Gastrointestinal and liver physiology},
volume = {},
number = {},
pages = {},
doi = {10.1152/ajpgi.00132.2025},
pmid = {41191326},
issn = {1522-1547},
support = {K08AR083015//HHS | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)/ ; F31HL158033//HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)/ ; R01AG074968//HHS | NIH | National Institute on Aging (NIA)/ ; T32HL007749//HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)/ ; K24HL159247//HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)/ ; R01HL144599//HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)/ ; R35GM136312//HHS | NIH | National Institute of General Medical Sciences (NIGMS)/ ; },
abstract = {Peritonitis is a well-known complication of bowel perforation and abdominal surgery, leading to sepsis and high mortality. Despite its prevalence and severity, the pathogenesis of peritonitis remains incompletely understood, limiting our ability to develop targeted medical therapies. Specifically, little is known about the determinants of the peritoneal nutrient environment for pathogens. The gut microbiome is a well-established source of infectious bacteria in peritonitis, but whether it also modulates levels of nutrients that enable and sustain these infections remains unknown. Using multiple murine models of peritonitis (lipopolysaccharide, cecal slurry), multiple methods of microbiome modulation (germ-free mice and antibiotic-treated mice), novel ex vivo modeling of peritonitis, and nuclear magnetic resonance (NMR) metabolomics of the peritoneal microenvironment, we performed a series of experiments to determine how the gut microbiome influences peritoneal metabolite concentration during peritonitis. We found that both lipopolysaccharide and cecal slurry peritonitis caused consistent changes in high-abundance peritoneal metabolites, and that many of these changes were blunted or completely abrogated in antibiotic-treated and germ-free mice. Moreover, we found that peritoneal washings from septic, microbiome-depleted animals supported less bacterial growth of common intra abdominal pathogens compared to washings from septic conventional animals. We identified the peritoneal nutrients consumed by two common pathogens from the Enterobacteriaceae family, and found that supplementation of gut microbiome-mediated nutrients was sufficient to alter bacterial growth in an ex vivo model. Taken together, we identify the gut microbiome as a key driver of the peritoneal nutrient environment, mediating pathogen growth. These findings suggest microbiome-targeted therapies could mitigate peritonitis risk.},
}

@article {pmid41191152,
year = {2025},
author = {Kaur, S and Thakur, R},
title = {Gut microbiota and inflammatory bowel disease: mechanisms, clinical implications, and future directions.},
journal = {Molecular biology reports},
volume = {53},
number = {1},
pages = {47},
pmid = {41191152},
issn = {1573-4978},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Dysbiosis/microbiology ; *Inflammatory Bowel Diseases/microbiology/therapy ; Probiotics/therapeutic use ; Prebiotics ; Animals ; Colitis, Ulcerative/microbiology ; },
abstract = {The gut microbiota plays a vital role in intestinal homeostasis and the regulation of the immune system, thereby influencing overall well-being. Disruption of this microbial ecosystem, termed dysbiosis, has been implicated in the aetiology of a large number of human diseases, including inflammatory bowel diseases (IBD). IBD is classified into Crohn's disease (CD) and ulcerative colitis (UC). Several factors, such as genetic predisposition and gut microbiota, cause IBD. It has been suggested that there is a significant correlation between the development of IBD and alterations in the gut microbiome. This disproportion between healthy gut microbiota and their metabolites has recently been revealed by clinical studies, with the development of screening, sequencing, and multiomics technology. Therefore, gut microbiome dynamics studies and their interaction with the host can have essential results on the pathogenesis of IBD. Hence, this review highlights the recent findings on the role of the gut microbiota in IBD, the mechanisms by which microbial dysbiosis leads to inflammation, and the development of novel therapeutic strategies targeting the microbiome. In addition, we talked about potential interventions involving the microbiome, such as probiotics, prebiotics, and microbiome-directed therapies as well.},
}

Humans
*Gastrointestinal Microbiome/physiology
Dysbiosis/microbiology
*Inflammatory Bowel Diseases/microbiology/therapy
Probiotics/therapeutic use
Prebiotics
Animals
Colitis, Ulcerative/microbiology

@article {pmid41191139,
year = {2025},
author = {Boussageon, R and Lemaitre, JP and Vaccaro, F and Gourrat, K and Perrotte, J and Garnier-Mugneret, M and Mengoni, A and Wipf, D and Courty, PE},
title = {The volatile profiles of three strawberry varieties exhibit common and distinct responses to the inoculation with Rhizophagus irregularis and different Pseudomonas fluorescens strains.},
journal = {Mycorrhiza},
volume = {35},
number = {6},
pages = {63},
pmid = {41191139},
issn = {1432-1890},
mesh = {*Fragaria/microbiology/chemistry/genetics/metabolism ; *Pseudomonas fluorescens/physiology ; *Volatile Organic Compounds/metabolism/analysis ; *Glomeromycota/physiology ; *Mycorrhizae/physiology ; Fruit/chemistry/microbiology ; Phylogeny ; Gas Chromatography-Mass Spectrometry ; },
abstract = {Cultivated strawberry dominates fruit production of the northern hemisphere and provide essential nutrients for human health. However, strawberry production has still a negative impact on agricultural soil and fruit quality does not always meet consumer expectations. Plant-microorganism interactions engineering involving arbuscular mycorrhizal fungi and rhizobacteria is known to alter plant's metabolic pathways and shape fruit quality (flavour and nutrient content). In our study, 21 Pseudomonas fluorescens strains were isolated from a two-year strawberry cultivation system and screened for their plant growth promoting activities. Four P. fluorescens were selected based on their activity and phylogenetic groups and inoculated in association or not with Rhizophagus irregularis DAOM 197198 on 3 different strawberry genotypes. The volatile profiles of the harvested strawberries were analysed by GC-MS. The abundance of hexanal, a compound used to extend shelf-life and reduce post-harvest diseases, was found more abundant in strawberry fruit from plants inoculated with the AMF R. irregularis than in non-Ri plants. The study showed that metabolite content of strawberries is significantly different between cultivars but exhibits a distinct and consistent pattern in response to P. fluorescens in association or not with the AMF R. irregularis. Our results suggest that the inoculation with P. fluorescens and R. irregularis improves strawberry quality and fine-tunes taste to consumer preference. Broadly, microbiome engineering has the potential to tailor fruit flavour to consumer taste while increasing nutritional benefits and food safety.},
}

*Fragaria/microbiology/chemistry/genetics/metabolism
*Pseudomonas fluorescens/physiology
*Volatile Organic Compounds/metabolism/analysis
*Glomeromycota/physiology
*Mycorrhizae/physiology
Fruit/chemistry/microbiology
Phylogeny
Gas Chromatography-Mass Spectrometry

@article {pmid41190871,
year = {2025},
author = {Liang, W and Chen, G and Zheng, B and Zhou, H and Ouyang, Y and Wang, X and He, Z and Wu, D and Lan, P and Huang, R},
title = {Biocompatible Nanozyme Shell-Armed Probiotic with Inflammation Targeting and Scavenging Properties Enables Effective Treatment of Colitis.},
journal = {Advanced materials (Deerfield Beach, Fla.)},
volume = {},
number = {},
pages = {e08532},
doi = {10.1002/adma.202508532},
pmid = {41190871},
issn = {1521-4095},
support = {2022YFA1304000//National Key Research and Development Program of China/ ; 22271320//National Natural Science Foundation of China/ ; 52372057//National Natural Science Foundation of China/ ; 2021B1212040017//Science and Technology Planning Project of Guangdong Province/ ; 2023B0303000025//Guangdong Major Project of Basic and Applied Basic Research/ ; //Fundamental Research Funds for the Central Universities/ ; 23yxqntd002//Sun Yat-sen University/ ; JCYJ20240813150654069//Shenzhen Science and Technology Program/ ; //Guangdong Basic Research Center of Excellence for Functional Molecular Engineering/ ; //National Key Clinical Discipline/ ; },
abstract = {Coupling probiotics with lesion targeting and inflammation control properties without complex chemical modifications is crucial for preserving their native bioactivity, but remains challenging. Herein, metformin as a functional self-modulated alkaline reagent is incorporated to achieve the rapid and biocompatible construction of a polydopamine-based nanozyme shell (DMCe) on the surface of probiotics, thus avoiding the biological toxicity caused by traditional triggering methods. DMCe can not only serve as a robust physical barrier to protect probiotics from the invasion of digestive juices and antibiotics, but also synergistically scavenge reactive oxygen species (ROS) at colitis lesions via the intrinsic antioxidant property of catechol and the catalase-mimicking activity of cerium oxide. It is worth noting that during the process of scavenging ROS, the originally harmful ROS can be utilized by DMCe as reactive components to facilitate chemical reactions between the modified probiotics and colitis lesions, thus achieving prolonged inflammation targeting for up to 7 days. In addition, nanozyme shell-armed probiotics can improve microbial community composition and increase the levels of short-chain fatty acids. By integrating inflammation targeting, ROS scavenging, and microbiome remodeling, nanozyme shell-armed probiotics can significantly reduce inflammation levels and promote healing of the mucosal barrier in a mouse colitis model.},
}

@article {pmid41190831,
year = {2025},
author = {Lefimil, C and Bustamante, P},
title = {Insights into toxin-antitoxin systems in the genus Bifidobacterium.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0193425},
doi = {10.1128/aem.01934-25},
pmid = {41190831},
issn = {1098-5336},
abstract = {Toxin-antitoxin (TA) systems are widespread genetic modules in prokaryotes, implicated in diverse functions including stress adaptation, genome stability, and virulence. While extensively studied in pathogenic bacteria, their presence and roles in beneficial gut microbes like Bifidobacterium remain underexplored. This review consolidates current knowledge on type II TA systems within the Bifidobacterium genus, highlighting their diversity, genomic context, and potential functional roles. Genomic analyses reveal a predominance of MazEF and RelBE families, with other systems such as VapBC, YefM-YoeB, and PumAB also identified, albeit less frequently. Experimental validation is limited, with most studies focused on B. longum strains. Emerging evidence suggests that these systems may contribute to acid and osmotic stress responses and mobile genetic element maintenance. The species- and strain-specific distribution of TA loci suggests their potential utility as molecular markers for strain-level microbiome analysis. Given their multifaceted roles, further functional studies are warranted to elucidate the biological significance of TA systems in Bifidobacterium and their implications for gut health and probiotic efficacy.},
}

@article {pmid41190815,
year = {2025},
author = {Hung, Y-T and Tuan, S-J and Wong, AC-N},
title = {Systematic analysis of nutrient-microbiome interactions and their effects on host phenotypes in Drosophila.},
journal = {mBio},
volume = {},
number = {},
pages = {e0248025},
doi = {10.1128/mbio.02480-25},
pmid = {41190815},
issn = {2150-7511},
abstract = {Diet and the gut microbiome are interconnected forces shaping host physiology and behavior. However, disentangling their independent and combined effects on phenotypic variation remains a major challenge. Here, we systematically assessed 120 combinations of nutrient and microbiome conditions to evaluate their effects on Drosophila melanogaster phenotypes. By varying dietary yeast-to-sucrose ratios (Y:S) and concentrations, coupled with five defined microbiome configurations, we disentangled the complex diet-microbiome interplays on metabolic, reproductive, and behavioral traits. Our analyses show that abundances of the major gut bacteria Acetobacter pasteurianus and Levilactobacillus brevis are differentially shaped by macronutrient components. A. pasteurianus exhibits a linear positive association with dietary yeast, whereas L. brevis displays a non-linear response driven more strongly by the yeast-sucrose ratio. In the host phenotypes, body protein and triglyceride levels are primarily determined by the nutrient environment, while the microbiome exerts a more notable influence on glucose metabolism. Microbial species exhibited context-dependent effects: A. pasteurianus facilitated protein assimilation and weight gain under high-yeast conditions, whereas co-colonization with L. brevis synergistically amplified fecundity. Critically, microbiome influences on locomotion and sleep varied by dietary Y:S, which helps explain discrepancies in prior studies that did not account for dietary variability when assessing microbiome-behavior relationships. By conceptualizing diet as a multidimensional nutrient environment, our study introduces a framework to better predict how dietary and microbial variation shape host phenotypes. These findings highlight that microbial contributions to host phenotypes are not fixed but emerge from interactions with the nutritional environment, thus advancing a more ecologically realistic framework for studying diet-microbiome relationships.IMPORTANCEThe interplay between diet and the gut microbiome is fundamental to shaping host physiology and behavior; however, their interactions remain poorly understood. Most studies treat diet as a single-dimensional variable (e.g., high-fat or high-sugar), overlooking the complexity of nutrient balance and density. This oversimplification neglects how diet and microbes function as an integrated system. This study addresses this gap by testing 120 different nutrient-microbiome combinations in Drosophila melanogaster, systematically varying yeast and carbohydrate levels and microbiome configurations. Our results show that dietary nutrient composition drives body protein and fat storage, whereas the microbiome plays a notable role in glucose metabolism and buffers against excess fat accumulation. Microbial effects on reproduction, locomotion, and sleep depend on nutrient composition, and our model reveals specific diet-microbiome patterns driving these outcomes. By treating diet as a dynamic, multidimensional factor, we provide a novel, ecologically relevant framework for understanding how diet and microbiome shape host.},
}

@article {pmid41190528,
year = {2025},
author = {Teo, KWE and Liew, YJM and Mazumdar, P and Suhaimi, NSM and Chan, KG and Chua, KO},
title = {Phyllosphere microbiome shifts reveal Gluconobacter japonicus T12B as a biocontrol agent against Xanthomonas in tomato through genomic and functional characterization.},
journal = {Journal of applied microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/jambio/lxaf273},
pmid = {41190528},
issn = {1365-2672},
abstract = {AIMS: Bacterial spot disease caused by Xanthomonas spp. is a major threat to tomato production that leads to significant yield losses. As these pathogens invade through stomata and wounds, understanding the phyllosphere microbiome dynamics during infection is critical for identifying potential biocontrol agents. In this study, we profiled the tomato phyllosphere microbiome shift during Xanthomonas infection, assessed the antagonistic activity of a phyllosphere bacterium and characterized its genetic features through whole genome analysis.

METHODS AND RESULTS: Phyllosphere microbiome analysis was performed on control and Xanthomonas-infected tomato plants using the leaf swabbing method and 16S rRNA gene amplicon sequencing with various primer sets. A significant increase in the abundance of Acetobacteraceae in infected plants prompted the targeted cultivation of the taxon, which subsequently led to the isolation of strain T12B. It exhibited strong in vitro and in vivo antagonistic activity against Xanthomonas, primarily through organic acid production. Whole genome analysis confirmed T12B as Gluconobacter japonicus subsp. japonicus. The genome of T12B encodes 2 792 coding DNA sequences, including complete pathways for acetic, gluconic, and ketogluconic acid biosynthesis, as well as other putative genes that may contribute to its antagonistic activity against Xanthomonas.

CONCLUSIONS: Tomato phyllosphere microbiome profiling facilitated the targeted isolation of G. japonicus T12B that demonstrated potential for disease suppression and biocontrol applications in tomato.},
}

@article {pmid41190323,
year = {2025},
author = {Choi, EM and Park, SK},
title = {The efficacy of lactic acid bacteria-based toothpaste on oral health: a systematic review and meta-analysis.},
journal = {Frontiers in oral health},
volume = {6},
number = {},
pages = {1668943},
pmid = {41190323},
issn = {2673-4842},
abstract = {INTRODUCTION: Lactic acid bacteria (LAB) have emerged as promising adjunctive agents for oral health management due to their antimicrobial and immunomodulatory properties. With the increasing incorporation of probiotics into oral care products, it is critical to evaluate their clinical efficacy. This systematic review and meta-analysis aimed to assess the effectiveness of LAB-based toothpaste in improving oral health outcomes.

METHODS: Following PRISMA guidelines, five databases (MEDLINE, EMBASE, Scopus, Web of Science, and CENTRAL) were searched through February 2025. Randomized controlled trials (RCTs) evaluating toothpastes containing probiotic, prebiotic, synbiotic, or postbiotic agents were included. Primary outcomes included plaque index (PI), gingival index (GI), bleeding on probing (BOP), probing pocket depth (PPD), and clinical attachment level (CAL). Secondary outcomes assessed oral microbiota changes. Risk of bias was evaluated using the RoB 2 tool.

RESULTS: Twelve RCTs were included, with four studies suitable for meta-analysis. Meta-analysis demonstrated significant plaque reduction at 3 months [Mean Difference (MD) = -0.64; 95% confidence interval (CI): -1.14 to -0.15; p = 0.01] and BOP improvement (MD = -1.49; 95% CI: -2.42 to -0.56; p = 0.002). Longer interventions (≥6 months) in periodontitis patients revealed significant PPD reduction (MD = -1.32; 95% CI: -1.81 to -0.84; p < 0.00001) and CAL improvement (MD = -0.79; 95% CI: -1.25 to -0.33; p = 0.0007). Streptococcus mutans levels were significantly reduced across multiple studies.

CONCLUSIONS: LAB-based toothpaste demonstrates beneficial effects on plaque control and gingival inflammation. However, substantial heterogeneity (I[2] > 75% for most outcomes) limits effect estimate precision. Lactobacillus paracasei strains showed consistent benefits, while sustained use (≥6 months) appears necessary for periodontal improvements.

https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD420250650340, PROSPERO CRD420250650340.},
}

@article {pmid41190273,
year = {2025},
author = {Akdur-Öztürk, E and Al-Adilee, YMS and Edwards, W and Gentekaki, E and Tsaousis, AD and Dogruman-Al, F},
title = {Blastocystis across humans, animals and the environment in rural Türkiye, and relationships with the human intestinal microbiome.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1665966},
pmid = {41190273},
issn = {1664-302X},
abstract = {Blastocystis is a globally prevalent intestinal protist commonly found in humans and animals, yet its role in health and disease remains ambiguous. This is a cross-sectional study of Blastocystis in rural Türkiye, examining 124 human, 305 livestock (cattle, sheep, goats), and 40 environmental samples using culture/microscopy, qPCR, and sequencing. We further explored associations between Blastocystis and population parameters, along with gut microbiota profiles. Using a combination of sequencing and microscopy, the overall prevalence was high, at 76.6% in humans, 71%-78% in livestock, and 38% in environmental samples. Subtypes ST1-ST4 were detected in humans, with ST3 being most frequent. Livestock harbored ST10 predominantly, with goats showing high carriage of ST24. Several subtypes (e.g., ST25, ST26) were recorded in livestock for the first time in Türkiye. Body mass index (BMI) was significantly associated with Blastocystis colonization, with lean individuals having higher carriage. Contrary to other studies, individuals with ST4 exhibited reduced bacterial diversity and altered microbial composition, suggesting subtype-specific interactions. By combining parasitology, microbiome, and environmental analysis, this study offers an overview of Blastocystis diversity and distribution in rural Türkiye. This work provides a foundation for future integrative research approaches to explore the ecological role of Blastocystis and its subtypes, potential health implications, and interactions with other microbes in rural and global contexts.},
}

@article {pmid41190270,
year = {2025},
author = {Li, W and Li, X and Cheng, J and Liu, J and Liu, J and Wang, Y and Yuan, W and Ren, E},
title = {Lung microbiota of raccoon dogs (Nyctereutes procyonoides) using high-throughput sequencing.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1677761},
pmid = {41190270},
issn = {1664-302X},
abstract = {Pneumonia frequently causes mass mortality in raccoon dogs, resulting in significant economic loss. Additionally, raccoon dogs carry various zoonotic pathogens. This study systematically assessed pulmonary pathogens in raccoon dogs and their potential public health implications utilizing 2bRAD microbiome sequencing (2bRAD-M) and viral metagenomics. We analyzed 30 lung tissue samples for microbial composition. Sequencing revealed Pseudomonadota, Ascomycota, and Actinobacteria as dominant phyla and Acinetobacter, Escherichia, and Klebsiella as predominant genera. The most abundant species were Acinetobacter baumannii, Escherichia coli, and Klebsiella pneumoniae. In total, 158 species across 84 genera were identified, including 49 potentially zoonotic species. Viral metagenomics revealed Peduoviridae, Rountreeviridae, and Parvoviridae as dominant families, with Valbvirus ValB1MD2, Andhravirus andhra, and Amdoparvovirus carnivoran3 comprising over 80% of the viral composition. These findings highlight the pathogenic complexity of raccoon dog pneumonia and its zoonotic risks, providing crucial insights for disease control and public health management.},
}

@article {pmid41190207,
year = {2025},
author = {You, Y and Liu, X and Wang, L and Khalid, M and Wang, X and Jiang, L and Wang, F and Pang, Z and Peng, Y and Zhao, X},
title = {Integrated metagenomic and soil chemical analyses revealed shifts of microbial nutrient cycling with poplar plantation age.},
journal = {Frontiers in plant science},
volume = {16},
number = {},
pages = {1513281},
pmid = {41190207},
issn = {1664-462X},
abstract = {INTRODUCTION: Poplar (Populus spp.) is widely recognized as an ideal model system for studying plant-microbial interactions due to its rapid growth, genetic tractability, and ecological importance in afforestation programs. Leveraging these advantages, we investigated how poplar cultivation reshapes soil microbial communities and their nutrient cycling functions. Although plant roots are known to profoundly influence microbial community structure and functionality, comprehensive studies systematically linking poplar-induced microbiome shifts to nutrient cycling remain limited.

METHODS: Here, we employed an integrative approach combining metagenomic sequencing with soil nutrient analyses to assess poplar-induced changes in microbial community and metabolic activities at the root-soil interface.

RESULTS: Our analyses revealed three major findings: (1) poplar cultivation significantly altered the composition of microbial communities-including bacteria, fungi, and archaea-and reduced the complexity of microbial interaction networks, as revealed by co-occurrence analysis; (2) poplar cultivation enhanced microbial genetic potential related to degradation pathways for starch, lignin, and aromatic compounds, as well as carbon (C) fixation, while suppressing cellulose/hemicellulose decomposition; and (3) soil nutrient cycling processes involving nitrogen (N), phosphorus (P), and sulfur (S) were reprogrammed through changes in both gene abundance (e.g., nifH, pqqC, aprA) and nutrient availability (e.g., NO3-, P). Moreover, specific microbial taxa showed strong correlations with these functional shifts, i.e., Bacteroidota correlated with P metabolism in roots/soil, Actinobacteria and Firmicutes with organic C turnover, and Gemmatimonadetes and Nitrospirae with nitrate cycling dynamics.

DISCUSSION: By integrating poplar's roles as both a model species and a driver of ecological change, this study elucidates how afforestation shapes soil ecosystems through complex plant-microbe-environment interactions. These findings provide critical insights for sustainable land management strategies.},
}

@article {pmid41190158,
year = {2025},
author = {Yu, X and Liu, X and Li, H},
title = {Nutrient metabolism and complications of type 2 diabetes mellitus: implications for rehabilitation and precision care.},
journal = {Frontiers in nutrition},
volume = {12},
number = {},
pages = {1699259},
pmid = {41190158},
issn = {2296-861X},
abstract = {Systemic disruptions in the metabolism of carbohydrates, fats, proteins, and micronutrients cause micro- and macro-vascular damage and impede recovery, which is the driving force behind type 2 diabetes mellitus (T2DM). Neuropathy, nephropathy, foot ulcers, and sarcopenia are symptoms of persistent hyperglycemia, lipotoxicity, excess branched-chain amino acids, and deficiencies in magnesium, zinc, and vitamin D that impair insulin signaling, mitochondrial integrity, and tissue repair. Functional decline is accelerated in skeletal muscle and peripheral nerves due to advanced glycation end-product deposition, ectopic lipid accumulation, and impaired glucose uptake. Micronutrient deficiency hinders wound healing and immune function, while altered nitrogen handling and progressive albuminuria intensify catabolism in the kidney. Controlled protein intake, micronutrient replacement, and microbiome-informed precision diets are targeted nutritional interventions that reduce complications by preserving renal function, restoring nerve integrity, and promoting wound closure. By combining machine learning analytics with continuous glucose monitoring, macronutrient ratios can be changed in real time, improving individualized care. Improved mobility, less neuropathic pain, and better glycaemic control are the results of integrating systematic nutritional assessment and treatment into multidisciplinary rehabilitation protocols. The translation in standard practice continues to be obstructed by inconsistent evaluation tools, lack of availability of omics technologies and few nurse-led randomized trials. Future studies must comprehensively evaluate the long-term effectiveness, cost-effectiveness, and scalability of tailored nutrition in rehabilitation frameworks to lessen the burden of complications and restore functional autonomy in people suffering from type-2 diabetes.},
}

@article {pmid41189901,
year = {2025},
author = {Bautista, J and Maldonado-Noboa, I and Maldonado-Guerrero, D and Reinoso-Quinga, L and López-Cortés, A},
title = {Microbiome influence in gastric cancer progression and therapeutic strategies.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1681824},
pmid = {41189901},
issn = {2296-858X},
abstract = {Gastric cancer (GC) remains a major global health burden, ranking as the fifth most commonly diagnosed malignancy and the fourth leading cause of cancer-related death worldwide. While Helicobacter pylori is established as the primary microbial risk factor, emerging evidence underscores the broader oncogenic potential of gastric microbiome dysbiosis. This review synthesizes recent advances in understanding how microbial communities, both within the stomach and along the gut-stomach axis, contribute to gastric carcinogenesis. We explore how alterations in microbial diversity, virulence, and metabolic output disrupt mucosal homeostasis, drive chronic inflammation, and reshape local immune surveillance. Special attention is given to the molecular mechanisms by which H. pylori virulence factors cytotoxin-associated gene A (CagA) and VacA, vacuolating cytotoxin, induce epithelial transformation, immune evasion, and epigenetic reprogramming. We also highlight the oncogenic roles of non-H. pylori taxa such as Fusobacterium nucleatum, Streptococcus anginosus, and Lactobacillus fermentum, which synergize with host and environmental factors to sustain tumor-promoting microenvironments. Multi-omics studies reveal microbial signatures predictive of disease progression, therapeutic response, and prognosis, laying the foundation for microbiome-informed precision oncology. Furthermore, we examine how microbiota-targeted interventions, probiotics, prebiotics, dietary modulation, and fecal microbiota transplantation, can enhance chemotherapy and immunotherapy efficacy while mitigating treatment-related toxicity. Lastly, we discuss the implications of early H. pylori eradication, the impact of antibiotic resistance, and the need for global surveillance strategies.},
}

@article {pmid41189884,
year = {2025},
author = {Tyc, O and Kraus, N and Wiedemann, T and Erasmus, HP and Ortiz, C and Vasseur, J and Hourfar, K and Seidl, C and Mücke, MM and Storf, H and Dahmer, I and Herrmann, E and Zeuzem, S and Kempf, VAJ and Trebicka, J and Welsch, C and Brieger, A},
title = {Enterococcus faecium DNA in acute decompensated cirrhosis: a key player in inflammation and kidney dysfunction.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1629210},
pmid = {41189884},
issn = {2296-858X},
abstract = {Liver cirrhosis is a major global health burden, with acute-on-chronic liver failure (ACLF) being a severe complication associated with high mortality. Systemic inflammation (SI) plays a crucial role in ACLF development, yet indicators for predicting disease progression remain limited. Enterococcus faecium (EF) has been implicated in bacterial translocation and SI, but its clinical relevance in ACLF remains unclear. We analyzed sera of 197 patients from a prospective observational study with acutely decompensated liver cirrhosis versus 234 healthy controls for the presence of EF DNA using RT-qPCR and cytokine analysis of serum samples. Overall, EF DNA was detected in 26% (n = 51, p = 0.001) of the patients, and only in 1.28% (n = 3, p = 0.001) in the control cohort. The positive patient samples were distributed as follows: 12% of patients were with stable decompensated cirrhosis (SDC), 5% of patients were with unstable decompensated cirrhosis (UDC) and 10% in patients were with ACLF. In the latter group, EF positivity significantly correlated with significant elevated leukocyte counts, increased C-reactive protein (CRP), Interleukin-6, and increased bilirubin, Aspartate Aminotransferase (AST), as well as creatinine levels. These findings suggest that the translocation of EF or its DNA, into the systemic circulation may reflect increased intestinal permeability, which is thought to be a key driver of SI and subsequent organ failure in ACLF. Taken together, our findings demonstrate that the presence of EF DNA in serum may contribute to the pathophysiological cascade of ACLF by promoting SI and organ dysfunction, particularly affecting renal function. We therefore propose and hypothesize that the presence of EF DNA in patients' serum could serve as an indicator of intestinal barrier dysfunction and further underscores the critical role of the gut-liver axis in the development and progression of ACLF.},
}

@article {pmid41189723,
year = {2025},
author = {Fineberg, D and Moreau, A and Schneider-Futschik, EK and Armstrong, CW},
title = {A Perspective on the Role of Metformin in Treating Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Long COVID.},
journal = {ACS pharmacology & translational science},
volume = {8},
number = {10},
pages = {3411-3431},
pmid = {41189723},
issn = {2575-9108},
abstract = {Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and Long COVID (LC) are increasingly recognized as debilitating postinfectious conditions that impact both individuals and society. Recent research highlights the potential of metformin, an antidiabetic agent, as a treatment for these syndromes by targeting their underlying mechanisms. This review assesses the effectiveness of metformin in ME/CFS and LC, which involve complex dysfunctions related to cytokines, glycolysis, ATP generation, oxidative stress, gastrointestinal microbiomes, and vascular endothelial function. Metformin, traditionally known for its antihyperglycemic properties may offer broader therapeutic benefits by influencing these pathological pathways. It works by inhibiting complexes I and IV of the electron transport chain, which reduces the strain on malfunctioning complex V and decreases the production of harmful free radicals. Additionally, metformin's impact on mTOR signaling could improve energy metabolism in ME/CFS and LC by downregulating an overactive but underperforming protein, thereby alleviating symptoms. Beyond the impact on cellular metabolism, metformin has shown to have anti-inflammatory, vascular, gastrointestinal, neuroprotective and epigenetic effects. We explore this impact of metformin and the potential role it could play to help people with ME/CFS. While metformin shows promise, it is unlikely to be a stand-alone solution. Instead, it may be part of a broader treatment strategy that includes other therapies targeting neurocognitive and autonomic impairments.},
}

@article {pmid41189709,
year = {2025},
author = {Chen, Y and Zhang, R and Wen, J and Zhao, J and Zhang, J},
title = {Metagenomic analysis of blood microbiota alterations: insights into HIV progression and immune restoration.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1619059},
pmid = {41189709},
issn = {2235-2988},
mesh = {Humans ; *HIV Infections/immunology/drug therapy/microbiology/blood/virology ; Metagenomics ; Male ; Female ; Adult ; *Microbiota ; Middle Aged ; Disease Progression ; Viral Load ; *Bacteria/classification/genetics/isolation & purification ; *Immune Reconstitution ; *Blood/microbiology ; CD4-CD8 Ratio ; },
abstract = {INTRODUCTION: Emerging evidence suggests that the blood microbiome may influence the progression of HIV infection and immune restoration. This study aims to comprehensively characterize blood microbiota alterations associated with HIV infection and antiretroviral therapy (ART), and to evaluate their potential as microbial indicators for assessing infection status and immune restoration.

METHODS: We recruited 91 participants, including 31 treatment-naïve HIV-infected individuals, 30 ART-treated individuals with undetectable viral loads, and 30 healthy controls. Blood samples were collected for metagenomic sequencing and immunological profiling.

RESULTS: HIV infection profoundly disrupted blood microbiota diversity and composition, with a marked reduction in α-diversity and enrichment of opportunistic pathogens such as Pseudomonas aeruginosa, Acinetobacter baumannii and Stenotrophomonas maltophilia, alongside depletion of beneficial taxa like Bifidobacterium longum. ART partially restored microbial diversity but did not fully reestablish a healthy microbiota. Correlation analysis revealed that Acinetobacter pittii, Xanthomonas campestris and Diaphorobacter nitroreducens were significantly associated with viral load, suggesting their potential role in HIV progression. Additionally, after ART, Acinetobacter junii and Pseudomonas putida were significantly correlated with the CD4/CD8 ratio, indicating their potential role in immune restoration.

DISCUSSION: These findings provide new insights into the interactions between blood microbiota and HIV progression. The identified blood microbiota may serve as potential indicators for evaluating HIV infection status and treatment efficacy, offering a basis for microbial-based diagnostic and therapeutic strategies.},
}

Humans
*HIV Infections/immunology/drug therapy/microbiology/blood/virology
Metagenomics
Male
Female
Adult
*Microbiota
Middle Aged
Disease Progression
Viral Load
*Bacteria/classification/genetics/isolation & purification
*Immune Reconstitution
*Blood/microbiology
CD4-CD8 Ratio

@article {pmid41189707,
year = {2025},
author = {Han, S and Rajitha, K and Park, S and Lim, J and Jung, HY and Kim, J and Kim, D},
title = {Unveiling the impact of allulose on oral microbiota and biofilm formation via a cariogenic potential assessment platform.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1670139},
pmid = {41189707},
issn = {2235-2988},
mesh = {*Biofilms/drug effects/growth & development ; Streptococcus mutans/drug effects/growth & development/physiology ; Saliva/microbiology ; *Microbiota/drug effects ; Humans ; *Dental Caries/microbiology ; Streptococcus oralis/drug effects/growth & development ; *Mouth/microbiology ; Sucrose/metabolism ; *Fructose/pharmacology/metabolism ; Polysaccharides, Bacterial/metabolism ; Virulence ; },
abstract = {INTRODUCTION: The increased consumption of refined carbohydrates, particularly sucrose, has contributed to metabolic disorders and oral diseases such as dental caries by promoting dysbiotic biofilm formation and reducing microbial diversity. Allulose, a rare sugar with physicochemical properties similar to sucrose, has been suggested to offer metabolic health benefits; however, its impact on oral biofilm ecology remains unclear.

METHODS: We evaluated the cariogenic potential of allulose using a multi-tiered in vitro platform consisting of single-species planktonic and biofilm models, a dual-species biofilm model involving Streptococcus mutans (pathogen) and Streptococcus oralis (commensal), and a saliva-derived microcosm biofilm model. Key virulence indicators, including bacterial growth, acid production, biofilm biomass, exopolysaccharide (EPS) synthesis, and microbial community composition, were quantitatively assessed.

RESULTS: Compared to sucrose, glucose, and fructose, allulose supported reduced bacterial growth and acid production, showing a profile similar to non-fermentable sugar alcohols such as xylitol and erythritol. Biofilms developed under allulose conditions lacked the dense EPS-enmeshed microcolonies and dome-shaped architecture characteristic of sucrose-induced S. mutans-dominant biofilms. In the saliva-derived microcosm model, allulose-treated biofilms maintained higher microbial diversity and preserved health-compatible genera such as Neisseria, Haemophilus, Veillonella, and Granulicatella.

DISCUSSION: These findings demonstrate that allulose supports lower bacterial virulence activity and minimal biofilm formation compared to common dietary sugars while preserving microbial diversity. This highlights its potential as a non-cariogenic sugar alternative with microbiome-conscious benefits and provides ecological insight into how allulose may modulate oral biofilm structure and function.},
}

*Biofilms/drug effects/growth & development
Streptococcus mutans/drug effects/growth & development/physiology
Saliva/microbiology
*Microbiota/drug effects
Humans
*Dental Caries/microbiology
Streptococcus oralis/drug effects/growth & development
*Mouth/microbiology
Sucrose/metabolism
*Fructose/pharmacology/metabolism
Polysaccharides, Bacterial/metabolism
Virulence

@article {pmid41189614,
year = {2025},
author = {Carlone, J and Parisi, A and Fasano, A},
title = {The performance gut: a key to optimizing performance in high-level athletes: a systematic scoping review.},
journal = {Frontiers in sports and active living},
volume = {7},
number = {},
pages = {1641923},
pmid = {41189614},
issn = {2624-9367},
abstract = {INTRODUCTION: The gut microbiome represents a key ecosystem influencing athletic performance through energy metabolism modulation, inflammatory response regulation, and recovery optimization in high-level athletes. However, the relationship between performance and gut microbiome composition in high-level athletes remains poorly understood.

OBJECTIVES: This systematic scoping review aims to map the current evidence on the relationship between training and gut microbiome in high-level athletes, identify specific patterns in microbial response to different training and sports, analyse the effects of nutritional interventions and highlight some methodological and knowledge gaps in the current literature.

METHODOLOGY: Following the PRISMA-ScR framework, a systematic search was conducted on PubMed, Scopus and Web of Science (2015-2025). Studies were selected according to defined criteria, including a population of high-level athletes, interventions through training and/or nutritional protocols and based on outcomes related to performance and health.

RESULTS: Nineteen studies met the inclusion criteria, comprising 12 experimental studies and 7 systematic/narrative reviews. The analysis of the studies revealed possible sport-specific patterns in microbiome modulation, with distinctive alterations in metabolic profiles, significant correlations between microbial stability and athletic performance, synergistic effects between training and probiotic supplementation and significant impacts of nutritional strategies and hormonal contraceptives on microbiome composition. The heterogeneity in analysis methodologies and the limited duration of studies emerge as the main limitations of the present study.

CONCLUSIONS: The evidence suggests that the significant role of the gut microbiome in athletic performance optimization may be considered in the future, highlighting the importance of implementing an integrated approach between training and nutrition. Further studies are needed to define specific microbiome trends for different types of sports, competition levels and supplementation targeted at implementing performance outcomes in high-level athletes.

https://osf.io/yh49t, identifier YH49T.},
}

@article {pmid41189593,
year = {2025},
author = {Huang, Y and Wei, X and Huang, X and Peng, C and Lin, B and Ren, X and He, G and Zhang, X and Jiang, C and Huang, L and Gu, S},
title = {Pneumocystis jirovecii associated with Lung Virome in patients with severe pneumonia.},
journal = {iScience},
volume = {28},
number = {11},
pages = {113710},
pmid = {41189593},
issn = {2589-0042},
abstract = {Pneumocystis jirovecii (P. jirovecii) threatens immunocompromised patients, yet its role in the lung microbiome remains unclear. We performed metagenomic sequencing on bronchoalveolar lavage fluid from two retrospective cohorts: a multicenter study of 1,737 patients with pneumonia and a validation cohort of 72 intubated ICU patients. Participants were categorized into P. jirovecii infection, colonization, or negative groups based on qPCR and clinical characteristics. Our analysis revealed minimal bacterial differences but significant viral and fungal variations. Notably, negative patients with P. jirovecii exhibited the lowest viral diversity. Even after adjusting for potential confounders, including immunosuppression and disease severity, P. jirovecii status remained most strongly associated with virome alterations. Furthermore, in cytomegalovirus-positive individuals, P. jirovecii positivity was significantly associated with higher 28-day mortality. These findings suggest that P. jirovecii colonization represents a distinct intermediate state in the lung microbial ecosystem between infection and negative, shedding light on its potential role in pneumonia pathogenesis and outcomes.},
}

@article {pmid41189581,
year = {2025},
author = {Healy, C and Campbell, C and Hoffman, K and Butler, JJ and Opron, K and Erb-Downward, JR and Zhang, WZ and Barjaktarevic, I and Han, MK and Kaner, RJ and Curtis, JL and Freeman, CM and Barr, RG and Comellas, AP and Doerschuk, C and Putcha, N and Moore, W and Wells, JM and Keane, R and O'Beirne, S and Cooper, CB and Raman, S and Hastie, A and Paine, R and Hansel, NN and Woodruff, P and Bowler, RP and Ballman, KV and Martinez, FJ and Huang, YJ and Sulaiman, I and Cloonan, SM and , },
title = {Extracellular iron and the lung microbiome in smoking and COPD.},
journal = {ERJ open research},
volume = {11},
number = {6},
pages = {},
pmid = {41189581},
issn = {2312-0541},
abstract = {BACKGROUND: Most microorganisms that make up the lung microbiome use several iron acquisition strategies for survival. Iron levels and iron-associated proteins are higher in the bronchoalveolar lavage fluid (BALF) of smokers with and smokers without COPD associating with disease severity. In this study we assessed whether or not smokers with and smokers without COPD who have increased airway iron display a specifically altered airway microbiome.

METHODS: 16S ribosomal RNA gene sequencing of BALF from individuals (n=181) enrolled in the bronchoscopy substudy of the SubPopulations and InteRmediate Outcome Measures In COPD Study (SPIROMICS) was paired with measured levels of BALF iron, the iron storage protein ferritin (ex-ferritin) and the host-iron siderophore lipocalin-2 (LCN-2) in matched participants.

RESULTS: Overall, iron, ex-ferritin and LCN-2 levels were not associated with ecological diversity metrics in the BALF of participants enrolled in this cohort. However, in a differential analysis, specific taxa were found to be enriched in never-smokers with low BALF ex-ferritin levels and also in smokers with high BALF iron levels. Of participants with COPD, an unclassified taxon, Bacteroidetes-OTU0063, was enriched in those with a high BALF iron level and those with a low BALF LCN-2 level. Furthermore, COPD participants with a high number of historical exacerbations and a high BALF LCN-2 level showed enrichment for Streptococcus and Leptotrichia. Leptotrichia was also enriched in participants with COPD and a high number of historical exacerbations with elevated BALF iron and BALF ex-ferritin levels. In addition, symptomatic individuals with COPD who had a high BALF ex-ferritin level had enrichment with Moraxella.

CONCLUSION: The above data suggest that abundance of iron and iron-binding proteins may be linked to the presence of both oral commensals and potentially pathogenic microorganisms in the lower airways of individuals with COPD.},
}

@article {pmid41189529,
year = {2025},
author = {Green, EM and Harishchandra, A and Lickwar, CR and Kim, YJ and Rawls, JF and Di Giulio, RT and Jayasundara, N},
title = {Environmental Microbial Cues Alter Embryonic Development and Stress Responses in Vertebrates: Insights From the Zebrafish (Danio rerio) Model.},
journal = {Molecular ecology},
volume = {},
number = {},
pages = {e70168},
doi = {10.1111/mec.70168},
pmid = {41189529},
issn = {1365-294X},
support = {P42ES010356/ES/NIEHS NIH HHS/United States ; T32ES021432/ES/NIEHS NIH HHS/United States ; },
abstract = {Host-microbiome interactions shape key physiological processes, including bioenergetics, neurodevelopment and xenobiotic metabolism, and strongly influence the ecological fitness of the host. However, our understanding of host-microbiome interactions is primarily derived from post-embryonic free-living life stages, when the organism is in direct contact with microbes. Whether environmental microbial communities influence embryogenesis-particularly in oviparous organisms where embryos are encased in a protective chorion-remains unknown. Using zebrafish (Danio rerio) embryos reared germ-free or conventionalized with a defined microbial community at 6 and 24 h post-fertilisation, we demonstrate that environmental microbiota influence embryonic development prior to hatching, altering transcriptomic, proteomic and metabolomic pathways linked to energy metabolism, neurodevelopment and xenobiotic responses, including cytochrome P4501A (cyp1a) activation. Furthermore, embryos exposed to benzo(a)pyrene, a CYP1A-activator, exhibited microbiome-dependent changes in embryonic mitochondrial function and larval behaviour, revealing persistent developmental effects. These findings challenge the long-held assumption that embryonic development is insulated from microbial influence. Instead, our results reveal that host-microbe interactions begin earlier than previously recognised, with implications for developmental plasticity, xenobiotic stress responses and environmental sensitivity likely affecting the ecological fitness of the host. Our results advance understanding of molecular adaptation to microbial environments and provide a foundation for investigating how microbiota shape the developmental origins of host resilience and vulnerability in microbially-dynamic natural habitats.},
}

@article {pmid41189477,
year = {2025},
author = {Hager, N and Gindt, ME and Hövels, M and Dorne, JCM and Deppenmeier, U},
title = {Distribution and activity of nitrate and nitrite reductases in the microbiota of the human intestinal tract.},
journal = {The FEBS journal},
volume = {},
number = {},
pages = {},
doi = {10.1111/febs.70299},
pmid = {41189477},
issn = {1742-4658},
support = {OC/EFSA/MESE/2022/04//European Food Safety Authority/ ; EMA/2020/46/L1.02//European Medicines Agency/ ; },
abstract = {The human intestinal microbiota plays a vital role in health. One of the most protective benefits is the bacterial nitrogen metabolism of gut bacteria, which reduces nitrate (NO3 [-]) and nitrite (NO2 [-]) to ammonia or nitric oxide, preventing the formation of carcinogenic nitrosamines. In this study, we shed light on the gut bacterial NO2 [-]/NO3 [-] degradation, its efficacy, and the effects on the steady-state NO2 [-] concentration in the human colon. Highly abundant gut bacteria that represent the most prominent phyla were analyzed for their potential to reduce NO2 [-] or NO3 [-]. Escherichia coli showed the greatest efficiency, which indicates a key role in the detoxification and prevention of nitrosamine formation. Species of the genera Bacteroides and Phocaeicola also contributed to NO2 [-] reduction due to their high abundance. The total activity of stool samples was about 620 μmol NO2 [-] h[-1], indicating that NO2 [-] concentration in the human stool should be very low. We also show that bacterial NO2 [-] reduction is necessary to allow NO2 [-]-sensitive microorganisms to colonize the intestine, preventing a pathological shift in the composition of the intestinal microbiota. The results illustrate that the gut microbiota plays a central role in NO2 [-] detoxification, ensuring microbiota integrity and potentially preventing nitrosamine formation and gut-associated cancers.},
}

@article {pmid41189393,
year = {2025},
author = {Bilici, K and Gerlach, D and Camus, L and Heilbronner, S},
title = {Competitive fitness of Staphylococcus aureus against nasal commensals depends on biotin biosynthesis and acquisition.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wraf248},
pmid = {41189393},
issn = {1751-7370},
abstract = {The human nasal microbiome can serve as a reservoir for pathogens. In particular, the opportunistic pathogen Staphylococcus aureus can be a member of the nasal microbiome increasing the risk of subsequent infections. The nasal carriage of S. aureus is known to be positively and negatively impacted by non-pathogenic species, suggesting interactions between the pathogen and commensals, but the underlying molecular mechanism remains largely unclear. Herein we demonstrate that S. aureus competes with nasal commensals for the coenzyme biotin. Biotin is crucial for all living organisms and we show that depletion of biotin impairs S. aureus growth and membrane integrity. We found the nasal cavity to be a biotin-limited environment, suggesting competition for the coenzyme within the microbiome. For some nasal commensals and S. aureus, we observed biotin prototrophy and all strains released biotin into the environment. In contrast, other commensals and especially coagulase-negative staphylococci (CoNS) were found to be biotin auxotrophs and strongly reliant on prototrophic strains under biotin-limited conditions. We show that high-affinity biotin uptake systems are used by prototrophic and auxotrophic strains alike and represent crucial factors to optimize competitive fitness of species in co-culture. Together, our data show that biotin-mediated interactions occur between the species of the human nasal microbiome and provide evidence for interspecies competition and co-dependency.},
}

@article {pmid41188729,
year = {2025},
author = {Jiang, D and Tang, X and Zheng, M and Niu, D and Zuo, S and Guan, E and Xu, C},
title = {Mechanistic insights into fungal succession mediated by Pichia kudriavzevii during aerobic deterioration of ensiled total mixed ration.},
journal = {BMC microbiology},
volume = {25},
number = {1},
pages = {714},
pmid = {41188729},
issn = {1471-2180},
support = {32302790//National Natural Science Foundation of China/ ; },
mesh = {*Pichia/metabolism/physiology ; Aerobiosis ; *Silage/microbiology/analysis ; Fermentation ; *Fungi/classification/metabolism/genetics ; Animals ; },
abstract = {BACKGROUND: Aerobic deterioration of ensiled total mixed ration (ETMR) represents a critical challenge in livestock feed preservation, yet the microbial drivers of this process remain poorly characterized. Although Pichia kudriavzevii has been identified as the predominant spoilage yeast in ETMR, its ecological role in fungal community assembly and succession during aerobic deterioration remains unclear. This study elucidates the impact of P. kudriavzevii on aerobic stability and fungal succession in alfalfa and oat based ETMR, inoculated with or without P. kudriavzevii and analyzed after 42 days ensiling.

RESULTS: Chemical analyses and high-throughput sequencing demonstrated that P. kudriavzevii inoculation significantly reduced aerobic stability (P<0.05) without affecting fermentation quality. P. kudriavzevii substantially altered fungal communities during both ensiling and aerobic exposure, displaying increased relative abundancewhile suppressing Saccharomyces cerevisiae and Monascus purpureus. Although interspecific fungal interactions were generally weak, a strong negative correlation was identified between P. kudriavzevii abundance and lactic acid concentration (R=-0.789, P<0.001), coinciding with progressive pH elevation during aerobic exposure.

CONCLUSION: The findings establish that P. kudriavzevii drives aerobic deterioration mainly through lactic acid catabolism, with its effects depending on intraspecific diversity. This study provides fundamental insights into fungal-driven spoilage mechanisms in ETMR, highlighting potential microbiome-based targets for enhancing silage preservation. Specifically, the results suggest that controlling P. kudriavzevii proliferation or its metabolic activity could represent an effective strategy for preventing aerobic spoilage in ensiled feeds.},
}

*Pichia/metabolism/physiology
Aerobiosis
*Silage/microbiology/analysis
Fermentation
*Fungi/classification/metabolism/genetics
Animals

@article {pmid41188517,
year = {2025},
author = {Hettiarachchi, A and Tuerlings, T and Weekers, T and Marshall, L and Leclercq, N and Wood, TJ and Cejas, D and Gerard, M and Vereecken, NJ and Michez, D and Smagghe, G and Joossens, M and Vandamme, P},
title = {The Gut Microbial Community of Solitary Bees is Acquired through Host and Location Filtering.},
journal = {Microbial ecology},
volume = {88},
number = {1},
pages = {114},
pmid = {41188517},
issn = {1432-184X},
support = {3094785//Fonds Wetenschappelijk Onderzoek/ ; 3094785//Fonds De La Recherche Scientifique - FNRS/ ; },
mesh = {Animals ; Bees/microbiology/physiology ; *Gastrointestinal Microbiome ; *Fungi/classification/isolation & purification/genetics ; *Bacteria/classification/genetics/isolation & purification ; Europe ; Biodiversity ; },
abstract = {Species traits and environmental conditions are among the many factors that shape bee communities. Their effective conservation is currently challenged due to global changes. The gut microbiome likely contributes to bee plasticity and resilience but is largely understudied in solitary bees. A stable core microbiome in social bees has been identified to be important for health and survival in changing environmental conditions, but knowledge on a host-specific core microbiome in solitary bees is very scarce. In the present study, we analyzed the gut bacterial and fungal communities of eight solitary bee species commonly found in apple orchards along a latitudinal gradient throughout Europe. We aimed to understand the intra- and interspecific variations in the gut microbial communities and the extent to which host species and local environment shape the solitary bee gut microbiota. The bacterial community showed strong host effects, with each bee species having a distinct core bacterial community that was mostly stable across locations. The fungal community was most strongly influenced by the local environment, while different environmental variables were responsible for the variation in bacterial and fungal communities. Our study demonstrated that the examined solitary bee species harbor a distinct microbial diversity and composition, which undergoes host- and location-specific filtering.},
}

Animals
Bees/microbiology/physiology
*Gastrointestinal Microbiome
*Fungi/classification/isolation & purification/genetics
*Bacteria/classification/genetics/isolation & purification
Europe
Biodiversity

@article {pmid41188334,
year = {2025},
author = {Kang, R and Yu, Z and Kim, H and Seo, J and Kim, M and Park, T},
title = {Manually weighted taxonomy classifiers improve species-specific rumen microbiome analysis compared to unweighted or average weighted taxonomy classifiers.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {38587},
pmid = {41188334},
issn = {2045-2322},
mesh = {*Rumen/microbiology ; Animals ; RNA, Ribosomal, 16S/genetics ; *Microbiota/genetics ; *Gastrointestinal Microbiome/genetics ; Species Specificity ; Metagenomics/methods ; *Bacteria/classification/genetics ; },
abstract = {Previous research has demonstrated that applying taxonomic weights to shotgun metagenomic data can improve species identification in 16S rRNA gene-based microbiome analysis. However, such an approach does not allow for accurate analysis of samples collected from less studied habitats, such as rumen. In the present study, we developed a method to incorporate taxonomic weights based on relative abundance of species identified from shotgun sequencing and amplicon sequencing data derived from rumen. Using this weighting method, we evaluated latest versions of five prominent databases-SILVA, Greengenes2 (GG2), RDP, NCBI RefSeq, and GTDB-against the BLAST 16S rRNA database, assessing classification counts, fully classified ratios (proportion of ASVs classified to a known genus and species), and error rates. Our results indicated that providing taxonomic weights partially increased classification counts and fully classified ratios, although the extent of improvement varied across databases. A reduction in error rates was also observed compared to the unweighted taxonomy classifier (P < 0.05). While GG2 and SILVA struggled with accurate classification at the species level owing to their inherent database characteristics, GTDB consistently improved all metrics using the manually weighted taxonomy classifier, achieving up to an 8% error rate reduction at the species level. NCBI RefSeq and RDP also exhibited remarkable improvement in the classification counts and fully classified ratios, along with error rate reductions by up to 47% at the species level. These findings demonstrate that amplicon sequencing datasets can enhance rumen microbiome analyses through effective weighting methods. While SILVA is commonly used in metataxonomic analyses of the rumen microbiome, we recommend NCBI RefSeq for species-level classification due to its superior accuracy and minimal ambiguous classification (e.g., "uncultured" or "sp.") in future metataxonomic studies.},
}

*Rumen/microbiology
Animals
RNA, Ribosomal, 16S/genetics
*Microbiota/genetics
*Gastrointestinal Microbiome/genetics
Species Specificity
Metagenomics/methods
*Bacteria/classification/genetics

@article {pmid41188324,
year = {2025},
author = {Kwak, MS and Cha, JM and Kim, CW and Won, KY and Hwang, CI},
title = {Integrative multi-omics deciphers the potential mechanism and microbial biomarkers for lymph node metastasis in colorectal cancer.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {38611},
pmid = {41188324},
issn = {2045-2322},
support = {NRF- 2022R1A2C100309913//National Research Foundation of Korea/ ; 2022//Medical Science Research Institute grant, Kyung Hee University Hospital at Gangdong/ ; R37CA249007/CA/NCI NIH HHS/United States ; },
mesh = {Humans ; *Colorectal Neoplasms/genetics/pathology/microbiology ; *Lymphatic Metastasis/genetics ; DNA Methylation ; Male ; Female ; *Biomarkers, Tumor/genetics ; Middle Aged ; *Gastrointestinal Microbiome ; Aged ; Transcriptome ; Gene Expression Regulation, Neoplastic ; Gene Expression Profiling ; Multiomics ; },
abstract = {Understanding and accurate diagnosis of lymph node metastasis (LNM) for patients with colorectal cancer (CRC) is essential to determine treatment and follow-up strategies. Therefore, in this study, we aimed to elucidate the biological process and identify the potential biomarker for LNM in CRC.A total of 30 patients who received a histologically confirmed diagnosis of CRC with Stage I to III and a curative surgery between November 2020 and July 2021 at Kyung Hee university hospital at Gangdong were included. We performed multi-omics approach integrating the data on somatic mutation, transcriptomic expression, DNA methylation, and microbiome with tumor and adjacent matched normal tissues of each patient. In total, 12 significant DEGs between the patients with and without LNM were identified, consisting of significantly upregulated S100A8 gene, a proinflammatory gene. The GSEA revealed that gene sets involving "MULTI CANCER INVASIVENESS" in terms related to epithelial-mesenchymal transition was significantly upregulated in the patients with LNM. Integrated functional analysis of DNA methylation with transcriptome profile shows that significantly hypomethylated promoters of the genes are enriched for LNM. The phylum Proteobacteria, unassigned (p_PU) presented significantly higher proportions in cancer tissues from the adjacent normal tissues. Notably, when compared to the patients without LNM, the gut microbiota of those with LNM appears to exhibit a significantly lower abundance of the p_PU, indicating its potential as promising biomarker for LNM in CRC. We explained the mechanism of tumor spreading using multi-omics analysis and identified the relevant metagenomic biomarker to predict the LNM in CRC by the recognition of host-microbial interaction, thereby can make the cancer surveillance of the patients more individualized and convincing.},
}

Humans
*Colorectal Neoplasms/genetics/pathology/microbiology
*Lymphatic Metastasis/genetics
DNA Methylation
Male
Female
*Biomarkers, Tumor/genetics
Middle Aged
*Gastrointestinal Microbiome
Aged
Transcriptome
Gene Expression Regulation, Neoplastic
Gene Expression Profiling
Multiomics

@article {pmid41188256,
year = {2025},
author = {Leon-Sampedro, R and Boumasmoud, M and Reichlin, M and Pfrunder-Cardozo, KR and Noll, N and Egli, A and Hall, AR},
title = {Multi-layered ecological interactions determine growth of clinical antibiotic-resistant strains within human microbiomes.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {9733},
pmid = {41188256},
issn = {2041-1723},
mesh = {Humans ; *Anti-Bacterial Agents/pharmacology ; *Escherichia coli/drug effects/genetics/growth & development ; *Gastrointestinal Microbiome/drug effects/genetics ; Plasmids/genetics ; *Drug Resistance, Bacterial/genetics ; beta-Lactamases/genetics/metabolism ; Gene Transfer, Horizontal ; *Microbiota/drug effects ; Phylogeny ; },
abstract = {The spread of antibiotic-resistant bacteria in the gut depends on their ability to establish within complex microbial communities. However, the role of various ecological factors in modulating this process, particularly in the absence of antibiotic selection, remains poorly understood. We hypothesize that different strains within the same species vary in their ability to colonize due to distinct interactions with resident microbiota. Using human gut-microbiome samples in replicated anaerobic microcosms with and without antibiotics, we test multiple clinically relevant and phylogenetically distinct Escherichia coli strains carrying extended-spectrum beta-lactamase (ESBL) or carbapenemase plasmids. While antibiotics influence the growth of incoming resistant strains, some are successful even without antibiotics. Growth outcomes depend on a combination of intrinsic growth capacities in relevant abiotic conditions, competition with resident E. coli, and strain-specific shifts in resident community composition. We also detect horizontal transfer of resistance plasmids in some conditions, but transconjugants remain rare across treatments. Here, we show that the success of antibiotic-resistant bacteria depends on strain-specific ecological interactions, helping to explain the spread and persistence of resistance in human microbiomes.},
}

Humans
*Anti-Bacterial Agents/pharmacology
*Escherichia coli/drug effects/genetics/growth & development
*Gastrointestinal Microbiome/drug effects/genetics
Plasmids/genetics
*Drug Resistance, Bacterial/genetics
beta-Lactamases/genetics/metabolism
Gene Transfer, Horizontal
*Microbiota/drug effects
Phylogeny

@article {pmid41188219,
year = {2025},
author = {Ndiaye, M and Bonilla-Rosso, G and Mazel, F and Engel, P},
title = {Phage diversity mirrors bacterial strain diversity in the honey bee gut microbiota.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {9738},
pmid = {41188219},
issn = {2041-1723},
mesh = {Animals ; *Bacteriophages/genetics/classification/physiology ; *Gastrointestinal Microbiome/genetics ; Bees/microbiology/virology ; *Bacteria/genetics/classification/virology ; Biodiversity ; Metagenomics ; Metagenome ; },
abstract = {Bacteriophages (phages) play a crucial role in shaping bacterial communities. Documenting the relationship between phage and bacterial diversity in natural systems is fundamental to understand eco-evolutionary dynamics that shape community composition, such as host specificity, emergence of phage resistance and phage-driven microbial diversification. However, our current understanding of this relationship is still limited, particularly in animal-associated microbiomes. Here, we analyze paired bacterial and viral metagenomics data from the gut microbiota of 49 individual honeybees and reconstruct the phage-bacteria interaction network by leveraging CRISPR spacer matches and genome homology. The resulting interaction network displays a highly modular structure with nested phage-bacteria interactions within each module. Viral and bacterial alpha and beta diversity are correlated, particularly at the bacterial strain level and when considering the interaction network. Overall, our results suggest that the most relevant approach to study phage-bacteria diversity patterns should rely on strain-level resolution and the explicit use of the interaction network. This may explain why previous studies have obtained mixed results when testing for phage-bacteria diversity correlations. Finally, we call for further studies building up on these correlation patterns to probe the underlying mechanisms by considering both bottom-up and top-down regulatory mechanisms in microbiome assembly.},
}

Animals
*Bacteriophages/genetics/classification/physiology
*Gastrointestinal Microbiome/genetics
Bees/microbiology/virology
*Bacteria/genetics/classification/virology
Biodiversity
Metagenomics
Metagenome

@article {pmid41188062,
year = {2025},
author = {Liu, J and Liu, Z and Geng, X and Wu, Y and Mo, L and Liao, Y and Liu, Y and Yang, P},
title = {KDM5A: A Master Epigenetic Regulator of Th2 Immunity and Allergic Disease Pathogenesis.},
journal = {Immunology},
volume = {},
number = {},
pages = {},
doi = {10.1111/imm.70061},
pmid = {41188062},
issn = {1365-2567},
abstract = {Interleukin-4 (IL-4) drives Th2 polarisation and allergic inflammation, yet the epigenetic mechanisms regulating Il4 transcription in CD4[+] T cells remain unclear. While STAT6 and GATA3 are canonical transcriptional regulators, lysine-specific demethylase 5A (KDM5A), an H3K4-specific demethylase, has not been linked to Th2 immunity. Here, we investigate KDM5A's role in IL-4 production and allergic airway disease (AA). Using DO11.10 TCR-transgenic mice and CD4[+] T cell-specific Kdm5a-knockout models, we assessed KDM5A's role in IL-4 transcription. Chromatin immunoprecipitation (ChIP)-qPCR evaluated H3K4 demethylation at the Il4 promoter. Cross-ELISA quantified IL-4 secretion, and ubiquitination assays analysed KDM5A stability. Lactobacilli-derived DNA (LgDNA) was administered to disrupt the USP7-KDM5A axis in AA models. The results showed that KDM5A deficiency abolished TCR activation-induced IL-4 production, impairing Th2 polarisation. Mechanistically, KDM5A maintained H3K4 hypomethylation at the Il4 promoter, facilitating STAT6/GATA3 recruitment. TCR signalling enhanced KDM5A promoter occupancy via USP7-mediated deubiquitination. USP7 stabilisation of KDM5A elevated H3K4 demethylation and IL-4 transcription, driving AA pathogenesis. LgDNA suppressed USP7 activity, reducing KDM5A promoter binding by 65% and airway inflammation by 72%. In summary, KDM5A acts as an epigenetic rheostat of Th2 immunity, where USP7-dependent stabilisation licenses STAT6/GATA3 access to the Il4 promoter during TCR activation. Targeting the USP7-KDM5A axis with LgDNA selectively suppresses pathogenic Th2 responses while preserving physiological IL-4 functions. Our findings define a novel epigenetic mechanism for allergic disease and establish microbiome-derived LgDNA as a precision therapeutic strategy.},
}

@article {pmid41187907,
year = {2025},
author = {Marrec, L and Bank, C},
title = {Drivers of diversity within and between microbial communities during stochastic assembly.},
journal = {Journal of the Royal Society, Interface},
volume = {22},
number = {232},
pages = {20250329},
doi = {10.1098/rsif.2025.0329},
pmid = {41187907},
issn = {1742-5662},
support = {//HORIZON EUROPE European Innovation Council/ ; //Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung/ ; },
mesh = {*Microbiota/physiology ; *Models, Biological ; Stochastic Processes ; *Biodiversity ; },
abstract = {No two microbial communities share the same species richness and abundance profiles. Experiments have shown that the assembly of new microbial communities from the same environmental pool is sufficient to generate diversity within and between communities: when microbial dispersal is slower than division, communities exhibit low richness but high between-community dissimilarity; when dispersal is faster, richness increases while dissimilarity decreases. Here, we study a minimal stochastic model that recovers these empirically observed assembly regimes. Our mathematical framework yields explicit expressions for the abundance fluctuation distributions across low-, intermediate- and high-dispersal regimes, providing a quantitative lens on microbiome assembly. We derive analytical predictions for the bimodality coefficient that quantifies the transition between assembly regimes, which appears as a robust metric to predict community richness and dissimilarity. Additionally, we highlight the mean relative abundance as a complementary metric sensitive to differences in microbial traits (e.g. dispersal or division rates). Applying these metrics to experimental data indicates their practical value for the rapid identification of assembly regimes and trait asymmetries. Overall, our study provides general predictions about how stochasticity, timescales and microbial traits influence both within-community diversity (richness) and between-community diversity (dissimilarity) during the assembly of new microbial communities. Our work thus contributes to a better understanding of the factors driving variation in microbiome formation.},
}

*Microbiota/physiology
*Models, Biological
Stochastic Processes
*Biodiversity

@article {pmid41187889,
year = {2025},
author = {Sousa, T and Yeung, C and De Monsales, CB and Sangfuang, N and Borde, A and Abrahamsson, B and Basit, A},
title = {Unexpected effects of antibiotics on microbiota-mediated drug metabolism in a fistulated dog model.},
journal = {European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences},
volume = {},
number = {},
pages = {107360},
doi = {10.1016/j.ejps.2025.107360},
pmid = {41187889},
issn = {1879-0720},
abstract = {The human gut microbiome plays a crucial role in the metabolism of drugs, with various bacterial species catalysing the biotransformation of pharmaceutical compounds. In vitro microbiota models, typically derived from faecal material, have been employed to study this phenomenon. However, they often do not fully capture the complex and dynamic environment of the living colon. This study aimed to evaluate whether in vitro models accurately reflect in vivo microbiota-drug interactions by comparing both approaches within the same individual animal via a fistulated dog model. We investigated the metabolism of metronidazole and sulindac, two structurally and pharmacologically distinct drugs, before and after broad-spectrum antibiotic treatment. Prior to antibiotics, in vitro biotransformation was observed for both drugs: metronidazole (t1/2 = 22.89 ± 1.19 min) and sulindac (t1/2 = 104.21 ± 1.01 min). Following antibiotic treatment, no measurable degradation occurred in vitro. However, in the fistulated dog model plasma concentrations decreased following antibiotic treatment compared to pre-treatment levels, indicating a lack of correlation between microbiota metabolism observed in vitro and systemic drug levels in vivo. These findings underscore the complexity of microbiota-host-drug interactions and provide important insights for the development of translational microbiome-pharmacology models. Additionally, the drawbacks over the use of antibiotic-treated animal models to study microbiota-drug interactions are discussed due to antibiotic-induced changes in intestinal permeability and efflux that may influence drug absorption and metabolism.},
}

@article {pmid41187761,
year = {2025},
author = {Bachem, A and Clarke, M and Kong, G and Tarasova, I and Dryburgh, L and Kosack, L and Lee, AR and Newland, LD and Wagner, T and Bawden, E and Yap, KM and Wilson, MD and Engel, S and Wilson, KR and Russ, BE and Tandon, K and Lau, PKH and McArthur, G and Marcelino, VR and Beavis, PA and Turner, SJ and Waithman, J and Stinear, TP and Sandhu, S and Schröder, J and Gebhardt, T and Bedoui, S},
title = {Microbiota-derived butyrate promotes a FOXO1-induced stemness program and preserves CD8[+] T cell immunity against melanoma.},
journal = {Immunity},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.immuni.2025.10.004},
pmid = {41187761},
issn = {1097-4180},
abstract = {A range of microbiota species correlate with improved cancer outcomes in patients and confer protection in pre-clinical mouse models. Here, we examined how microbiota regulate CD8[+] T cell immunity against melanoma. Spontaneous control of cutaneous melanoma in mice correlated with metabolic pathways required for microbial synthesis of short-chain fatty acids (SCFAs) shared between several microbiota species. Diet-induced enforcement of SCFA production by the gut microbiota reduced melanoma progression and enriched tumor-specific stem-like CD127[+]CD8[+] T cells in the tumor-draining lymph node (tdLN). The SCFA butyrate induced a FOXO1-driven stemness program and directly promoted the differentiation of tumor-specific CD127[+]CD8[+] T cells in the tdLN. Metabolic flux modeling predicted enhanced microbial production of butyrate in melanoma patients with complete therapeutic responses to immune checkpoint blockade (ICB), and butyrate induced transcriptional features of ICB responsiveness in CD8[+] T cells. Our findings suggest a critical role for metabolite production shared across several microbiota species in the preservation of stem-like tumor-specific CD8[+] T cells.},
}

@article {pmid41184817,
year = {2025},
author = {Do, KH and Ryu, DH and Ahn, HJ and Kim, MG and Choe, SJ and Lee, SH and Lee, SM and Seo, KW},
title = {Gut microbiota in diarrheic and healthy calves: comparative analysis of 16S rRNA gene full-length sequences.},
journal = {BMC veterinary research},
volume = {21},
number = {1},
pages = {641},
pmid = {41184817},
issn = {1746-6148},
support = {RS-2025-02633155//Rural Development Administration/ ; },
abstract = {BACKGROUND: Neonatal calf diarrhea (NCD) is a leading cause of morbidity and mortality in the dairy industry. Although multiple pathogens have been identified, widespread alterations in gut microbiota composition associated with diarrhea remain poorly understood. This study aimed to characterize the fecal microbiota and potential metabolic pathways in diarrheic and healthy neonatal calves using 16S rRNA gene full-length sequencing. A total of 40 fecal samples (20 normal and 20 diarrheic) were collected, and 16S rRNA gene full-length sequencing was performed.

RESULTS: Alpha diversity measures (Chao1, Shannon, and Simpson indices) were significantly reduced in diarrheic calves (p < 0.01), indicating marked dysbiosis. Principal coordinate analyses, a beta diversity method used to assess difference in microbial composition between groups, revealed distinct clustering of diarrheic versus healthy samples based on both Bray–Curtis and Jensen–Shannon divergences, underscoring a major compositional shift. Taxonomic profiling showed elevated levels of opportunistic/pathogenic bacteria (e.g., Escherichia coli, Salmonella spp., Klebsiella spp.) in diarrheic calves, while beneficial taxa (e.g., Faecalibacterium) were depleted. Functional predictions indicated increased carbohydrate metabolism, notably the N-acetylneuraminate degradation, Entner–Doudoroff, and hexitol fermentation pathways, in diarrheic calves (all adjusted p < 0.05). These findings highlight multifaceted dysbiosis in NCD, including both taxonomic imbalances and heightened carbohydrate metabolic pathways.

CONCLUSIONS: Identifying key bacterial species and metabolic signatures may facilitate the development of diagnostic biomarkers and targeted microbiome-based therapies. Conclusively, the findings emphasize the prospective efficacy of interventions aimed at restoring microbial diversity and metabolic balance to mitigate illness severity and enhance calf health.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12917-025-05094-z.},
}

@article {pmid41187758,
year = {2025},
author = {Yilmaz, B and Baertschi, I and Meier, KHU and Le Gac, C and Jordi, SBU and Black, C and Li, J and Lindholm, AK and , and König, B and Sauer, U and Stelling, J and Macpherson, AJ},
title = {A global survey of taxa-metabolic associations across mouse microbiome communities.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2025.10.010},
pmid = {41187758},
issn = {1934-6069},
abstract = {Host-microbiota mutualism is rooted in the exchange of dietary and metabolic molecules. Microbial diversity broadens the metabolite pool, with each taxon contributing distinct compounds in varying proportions. In the human microbiome, high variability in consortial composition is largely compensated by similar metabolic functions across different taxa. However, the extent of compensation in lower diversity mouse models, and whether vivaria are metabolically equivalent, is unknown. We provide a searchable resource of microbiome composition variability across 51 murine vivaria and 12 wild mouse colonies worldwide, with vivarium-specific variants mapped according to predicted 3D structures for each microbial species. Our matched metabolomics data show that realized metabolic potential has relatively low variability, providing functional evidence for metabolic compensation. Additionally, variability is related to taxonomic composition rather than vivarium, revealing taxa-metabolite associations that are potentially relevant to phenotypic differences between vivaria. Collectively, this resource offers tools to strengthen microbiome studies and collaborative science.},
}

@article {pmid41187701,
year = {2025},
author = {Li, N and Yin, L and Wang, J and Zhang, J and Tong, Y},
title = {Programmable probiotics as next-generation living therapeutics: bridging synthetic biology and precision medicine.},
journal = {Current opinion in biotechnology},
volume = {96},
number = {},
pages = {103375},
doi = {10.1016/j.copbio.2025.103375},
pmid = {41187701},
issn = {1879-0429},
abstract = {Engineered probiotics are rapidly redefining what's possible for living therapeutics. Instead of acting passively, these microbes can now home to disease sites, sense local signals, and deliver precisely the therapeutic activities our patients need - directly in situ and for extended periods. With the help of modular genetic circuits, synthetic biology is transforming once-commensal bacteria into sophisticated, programmable medicines. In this review, we highlight how these designer microbes are tackling inflammatory bowel disease, metabolic conditions, and cancer, and we offer a critical look at the strategies underpinning their safety, efficacy, and clinical translation. We also discuss the translational bottlenecks, such as biocontainment, regulatory complexity, and microbiome variability, that must be overcome as these living medicines move from concept toward routine clinical use. Ultimately, programmable probiotics stand poised to reshape pharmaceutical biotechnology, sitting squarely at the intersection of microbiology, engineering, and precision medicine.},
}

@article {pmid41187575,
year = {2025},
author = {Fooladi, AAI and Cho, WC and Reiter, RJ and Alimohammadi, M and Farahani, N and Hushmandi, K},
title = {Staphylococcal enterotoxins in cancer immunotherapy: An overview of translational advances and targeting strategies.},
journal = {Pathology, research and practice},
volume = {276},
number = {},
pages = {156283},
doi = {10.1016/j.prp.2025.156283},
pmid = {41187575},
issn = {1618-0631},
abstract = {Staphylococcal enterotoxins (SEs) are superantigens that polyclonally activate T cells by cross-linking MHC class II on antigen-presenting cells with T cell receptor (TCR) Vβ regions, generating potent IL-2/IFN-γ/TNF responses distinct from conventional peptide-MHC-restricted activation. This review synthesizes mechanistic and translational evidence for SEs in oncology, emphasizing disease-relevant contexts and advanced engineering strategies that improve therapeutic index. Preclinical studies demonstrate antitumor activity across melanoma, glioblastoma, renal cell carcinoma, bladder cancer, hepatocellular carcinoma, colorectal cancer, breast cancer, squamous cell carcinoma, and hematologic malignancies (e.g., acute myeloid leukemia, lymphoma). Tumor-targeted superantigen platforms, such as antibody or ligand-SE fusion proteins and oncolytic vectors encoding Ses, concentrate activity intratumorally, increase intratumoral IFN-γ/TNF, reduce proliferation and angiogenesis, and enhance necrosis while limiting systemic exposure. Engineered SE variants (for example, SEB with attenuated pyrogenicity) and localized delivery further mitigate risks associated with cytokine release. Early clinical experiences with SE-based constructs and SE-modified tumor vaccines report feasibility and signals of activity in head and neck cancer, glioma, renal cell carcinoma, and myeloma, but small, heterogeneous studies limit definitive conclusions. Although SEs can trigger cytokine storm and off-target activation via MHC II on healthy tissues, risk can be reduced through intratumoral/regional dosing, tumor-targeted fusions, dose-schedule optimization, and indication selection informed by MHC II biology; paradoxical, disease-specific effects (e.g., in cutaneous T-cell lymphoma) highlight the importance of microbiome-aware protocols. Priorities for translation include disease-focused development in MHC II-II-permissive tumors, combinations with immune checkpoint inhibitors, and biomarker-anchored trials integrating multi-omics and patient selection. With targeted engineering and controlled delivery, SEs can evolve from broadly inflammatory agents into precise immuno-oncology tools with meaningful clinical impact. This review underscores that, with targeted engineering, controlled delivery, and biomarker-guided patient selection, SEs can be advanced from broadly inflammatory agents to precise immuno-oncology platforms ready for rigorous clinical evaluation.},
}

@article {pmid41187545,
year = {2025},
author = {Al-Huqail, AA and Darwish, DBE and Melebari, DM and Osman, HES and Alasimi, SM and Alghanem, SMS and Alhaithloul, HAAS and Khan, KA and Abeed, AHA and Peijnenburg, W},
title = {Nanoparticle-driven defense in wheat (Triticum aestivum L.): Enhancing antioxidant and rhizosphere responses under arsenic and microplastic stress.},
journal = {Ecotoxicology and environmental safety},
volume = {306},
number = {},
pages = {119334},
doi = {10.1016/j.ecoenv.2025.119334},
pmid = {41187545},
issn = {1090-2414},
abstract = {Soil contamination with toxic heavy metals such as arsenic (As) and microplastics (MPs) is becoming a serious global problem due to rapid industrial and agriculture expansion. Although nanoparticles (NPs) are the major protectants to alleviate metal toxicity. A pot-based study was conducted to evaluate the effects of silicon (Si-NPs), silicon dioxide (SiO2-NPs), and silver (Ag-NPs) nanoparticles on wheat (Triticum. Aestivum L.) exposed to As and MPs stress, focusing on key physiological, biochemical, and molecular assessments including oxidative stress responses, antioxidant activities, proline metabolism, and rhizosphere microbiome dynamics. Our results depicted that As and MPs exposure significantly reduced plant biomass (by 42-46 %), photosynthetic efficiency (by 38 %), mineral uptake (by 35 %), and rhizosphere microbiome diversity (by 30 %), while increasing malondialdehyde (MDA) and H2O2 contents (by 55-60 %), indicating oxidative stress, health risk indices, and molecular mechanisms. Antioxidant enzymes (SOD, POD, CAT, and APX) were enhanced at 100 mg kg[-1] As and 2 mg L[-1] MPs but declined at 200 mg kg[-1] As and 4 mg L[-1] MPs. As and MPs stress also suppressed anthocyanins and soluble proteins while increasing As accumulation in roots and shoots (by up to 48 %). Application of Si-NPs, SiO2-NPs, and Ag-NPs mitigated these adverse effects by improving growth (30-40 %), photosynthesis (25-33 %), antioxidant defenses (40-50 %), regulating AsA-GSH cycle, proline metabolism, and cellular fractionation, mineral uptake, reducing oxidative damage and HI indices (25-30 %). These treatments also lowered As retention in plant tissues (by 35-40 %). Research findings, therefore, suggested that application of Si-NPs, SiO2-NPs, and Ag-NPs can ameliorate As toxicity in T. aestivum seedlings and resulted in improved plant growth and composition under metal stress.},
}

@article {pmid41187543,
year = {2025},
author = {Lan, W and Zhou, Y and Duan, S and Yang, F and Xiao, Y and Yang, H},
title = {Rhizosphere microbiome-mediated cadmium and lead mobilization in Erigeron canadensis across a regional contamination gradient: Trade-offs between diversity loss and functional gene enrichment.},
journal = {Ecotoxicology and environmental safety},
volume = {306},
number = {},
pages = {119341},
doi = {10.1016/j.ecoenv.2025.119341},
pmid = {41187543},
issn = {1090-2414},
abstract = {Erigeron canadensis, an invasive plant with significant biomass and heavy metal tolerance, has the potential for phytoremediation of soil heavy-metal contaminants. This study aimed to screen the key factors for improving the phytoremediation capacity of E. canadensis by examining rhizospheric ecological characteristics under varying levels of heavy metal pollution. Results showed that E. canadensis exhibited greater ability to enrich Cd and Pb in mildly polluted environments, with distinct mechanisms driving this pattern across three groups: HX (Huayuan County), LX (Liuyang City), and YX (Yueyang City), which represented different levels of pollution. Soil properties such as pH, total nitrogen, alkaline-hydrolyzed nitrogen (readily available nitrogen), and organic matter significantly influenced heavy metal uptake. Furthermore, the rhizosphere environment facilitated the adaptation of plant and enrichment of heavy metals by altering the microbial community, specifically by reducing overall diversity while increasing the relative abundance of key taxa characterized by metal resistance and plant growth-promoting abilities, including Lysobacter, Corynebacterium, Humicola, and Colletotrichum. These microorganisms adapted to Cd/Pb stress with some specific genes (e.g., Fur, PerR, and CueR) and enzymes (e.g., P-type ATPases, catalase, and alcohol dehydrogenase) related to heavy metal transport and uptake. This study elucidated the relationship between rhizospheric ecological factors and the regulatory mechanisms of phytoremediation. Selected microbial taxa might be developed as bioinoculants, improving phytoremediation efficiency and enhancing the ecological restoration capacity while also providing insights for the management of invasive species.},
}