@article {pmid42521142,
year = {2026},
author = {Chen, A and Ordinola-Zapata, R and Noblett, WC and Clarke, BC and Baumgardner, KR and Gould, M and Staley, C},
title = {THE EFFECT OF ENDODONTIC DISINFECTION ON MICROBIAL REDUCTION AND BIODIVERSITY OF ROOT CANAL SYSTEMS WITH NECROTIC PULPS.},
journal = {Journal of endodontics},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.joen.2026.07.016},
pmid = {42521142},
issn = {1878-3554},
abstract = {AIM: To analyze microbial reduction and diversity changes after cleaning and shaping procedures, and calcium hydroxide interappointment medication. The influence of clinical and radiographic factors was assessed as well.

METHODOLOGY: Thirty-two teeth diagnosed with pulp necrosis and evidence of apical periodontitis were included. Five samples were collected on each tooth: surface sample before access (C1), before treatment (S1), after cleaning and shaping with ultrasonic irrigant activation (S2), at the second visit after removal of the temporary restoration (C2), and after removal of calcium hydroxide (S3). All samples were processed using quantitative real-time polymerase chain reaction (qPCR) and 16S rRNA next generation sequencing. The Shannon and Chao1 indices were used to measure alpha diversity. Differences in abundances of genera were evaluated using the Kruskal-Wallis test. Differences in community composition (beta diversity) were evaluated using analysis of similarity (ANOSIM) with Bray-Curtis dissimilarity matrices.

RESULTS: The qPCR analysis revealed significant differences between S1 and S2 as well as between S1 and S3 (P =0.0001). No significant differences between S2 and S3 were observed for qPCR (P =0.458) as well as for Chao1 alpha diversity. ANOSIM revealed differences between S1 and S3 (P < 0.001, R = 0.59), and between S1 and S2 (P < 0.001, R = 0.40). The presence of percussion sensitivity (ANOSIM R = 0.07, p < 0.023) and sinus tracts (ANOSIM R = 0.06, p < 0.03) had significant interactions with the results. Most of preoperative taxa (top 20) found before treatment were significantly impacted by root canal procedures except Peptostreptococcus and Clostridiales (P > 0.05). The relative abundance of Schaalia (P = 0.004) and Enterococcus (P = 0.001) increased significantly after treatment.

CONCLUSION: A significant reduction in microbial load after instrumentation (S2) and after calcium hydroxide medication (S3) was observed. The effect on root canal composition (beta diversity) was impacted after the cleaning and shaping. No additional changes were observed after the use of calcium hydroxide. The effects produced by clinical factors although significant were low, the results reinforce the value of robust chemical and mechanical disinfection procedures.},
}

@article {pmid42521216,
year = {2026},
author = {Yaakoub, G and Emna, B and Hfayeth, H and Mohamed Ali, T},
title = {Controlled incubation, leachate, and pot assays of shrimp shell-based compost for suppressing Verticillium dahliae in olive.},
journal = {Pest management science},
volume = {},
number = {},
pages = {},
doi = {10.1002/ps.71158},
pmid = {42521216},
issn = {1526-4998},
abstract = {BACKGROUND: Verticillium wilt of olive (Olea europaea L.), caused by Verticillium dahliae Kleb., is difficult to manage because long-lived microsclerotia persist in soil, and disease risk is influenced by inoculum distribution, irrigation and cultivar susceptibility. This study evaluated mature shrimp shell-based compost (SSC), a chitin-containing circular-economy amendment, for suppressing V. dahliae in naturally infested olive-orchard soil, inhibiting fungal growth in vitro, and reducing disease in a controlled pot assay. Green-waste compost (GWC) was included as a reference amendment.

RESULTS: After 60 days, SSC 5% reduced microsclerotia density by 39.6% and viable microsclerotia by 42.8% relative to unamended soil. Nonsterile SSC leachate inhibited radial growth by 83.7% at 50% (v/v), whereas filter-sterilized leachate retained 58.3% inhibition. In the controlled pot assay, SSC 5% lowered model-estimated final disease incidence from 85% to 30%, and reduced disease severity by 46.5% relative to the infected control. SSC 5% also increased plant height, shoot and root dry weight, leaf area, SPAD index, and rhizosphere chitinase and beta-glucosidase activities.

CONCLUSION: SSC suppressed V. dahliae survival and improved olive plant performance under controlled incubation, in vitro and pot conditions. The results identify SSC as a candidate amendment for further testing, but the proposed inhibitory, chitinolytic, microbiome-mediated, and plant-vigor mechanisms remain hypotheses pending microbiome, pathogen-DNA, metabolite, plant-defense and field validation studies. © 2026 The Author(s). Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.},
}

@article {pmid42521217,
year = {2026},
author = {Markos, S and Praefke, L and Kapetanstatakis, Y and Tsanakas, M and Beletsiotis, E},
title = {Clinical improvement and scalp microbiome restructuring following a 28-day piroctone olamine shampoo intervention.},
journal = {International journal of cosmetic science},
volume = {},
number = {},
pages = {},
doi = {10.1111/ics.70128},
pmid = {42521217},
issn = {1468-2494},
abstract = {OBJECTIVE: To evaluate the clinical efficacy of a piroctone olamine-containing shampoo in individuals with oily dandruff and to characterize associated temporal changes in bacterial and fungal scalp microbiota.

METHODS: An open-label, single-arm, longitudinal study was conducted in 41 volunteers with oily dandruff over 28 days. Participants applied the test shampoo three times weekly. Clinical assessments (erythema, pruritus, desquamation index and sebum levels) were performed at baseline, Day 14, and Day 28. Scalp microbiome samples were collected by standardized swabbing and analyzed using full-length 16S rRNA gene and ITS amplicon sequencing. Microbial community dynamics were evaluated using compositional data analysis, including centred log-ratio transformation, robust Aitchison distance, compositional tensor factorization and linear mixed-effects modelling.

RESULTS: Significant clinical improvement was observed by Day 28, with marked reductions in erythema and pruritus. Sebum levels increased during the study period (p < 0.01), indicating that symptom improvement occurred independently of reduced sebum production. Bacterial community analysis revealed progressive restructuring of the scalp microbiome, becoming most evident by Day 28. This shift was characterized by a descriptive increase in the relative abundance of Cutibacterium acnes together with a numerical decline in Staphylococcus capitis, resulting in an increase in the C. acnes/Staphylococcus ratio from 2.83 to 4.51. Longitudinal compositional analyses further identified several bacterial genera associated with the temporal shift, including Streptococcus, Flavobacterium and Sphingomonas. The fungal community responded earlier to treatment, showing directional reduction of Malassezia-associated dominance together with enrichment of several non-Malassezia genera. Fungal richness increased significantly by Day 14 and remained elevated at Day 28, while beta-diversity analyses confirmed significant temporal restructuring of both bacterial and fungal communities.

CONCLUSION: Use of a piroctone olamine shampoo was associated with significant clinical improvement and measurable shifts in both bacterial and fungal scalp microbiota. These findings suggest that dandruff improvement may coincide with ecological restructuring of the scalp microbiome rather than broad microbial suppression.},
}

@article {pmid42521223,
year = {2026},
author = {Phuong-Nguyen, K and Rivera, LR and Biesiekierski, JR},
title = {Resistant starch as a dietary strategy for metabolic and gut health: Implications for Asia-Pacific populations.},
journal = {Asia Pacific journal of clinical nutrition},
volume = {35},
number = {4},
pages = {577-588},
doi = {10.6133/apjcn.202608_35(4).0003},
pmid = {42521223},
issn = {1440-6047},
mesh = {Humans ; *Gastrointestinal Microbiome ; Animals ; Asia ; *Diet ; *Starch/administration & dosage ; },
abstract = {BACKGROUND AND OBJECTIVES: Metabolic diseases are rising rapidly across the Asia-Pacific region as traditional diets are displaced by refined, low-fibre foods. Resistant starch (RS) is a fermentable dietary component that modulates gut microbial activity and short-chain fatty acid (SCFA) production, representing a promising strategy for metabolic and gut health. However, responses to RS vary according to dose, RS type, and individual context.

METHODS AND STUDY DESIGN: This narrative review synthesised evidence from animal and human studies on RS classification, food sources, microbial interactions, and metabolic regulation. We evaluated how responses differ by dose, RS type, baseline microbiome composition, metabolic phenotype, and habitual diet, with particular attention to traditional Asia-Pacific staple foods and ongoing dietary transitions.

RESULTS: Across studies, RS supplementation at moderate-to-high doses improves insulin sensitivity, hepatic lipid accumulation, and markers of gut barrier function, primarily through SCFA-mediated and gut hormone pathways. However, responses are highly context-dependent, varying with baseline metabolic status, micro-biome composition, habitual fibre intake and RS type. Individuals with metabolic disturbances or low fibre intake tend to show greater metabolic and microbial shifts.

CONCLUSIONS: RS is a promising strategy for supporting metabolic and gut health in Asia-Pacific populations undergoing rapid nutritional transition. Culturally familiar RS-rich foods offer practical, regionally tailored intervention opportunities. Standardised characterisation, microbiome-stratified analyses and long-term human studies are needed to clarify who benefits most, under which conditions and through which mechanisms.},
}

Humans
*Gastrointestinal Microbiome
Animals
Asia
*Diet
*Starch/administration & dosage

@article {pmid42521607,
year = {2026},
author = {Li, Y and Chen, Y and Huang, X and Yang, J and Zhou, Z and Ma, X and Zeng, L},
title = {Causal associations between gut microbiota and inflammatory factors in neonatal jaundice: a Mendelian randomization study.},
journal = {The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians},
volume = {39},
number = {1},
pages = {2709189},
doi = {10.1080/14767058.2026.2709189},
pmid = {42521607},
issn = {1476-4954},
mesh = {Humans ; Mendelian Randomization Analysis ; Infant, Newborn ; *Gastrointestinal Microbiome/genetics ; *Jaundice, Neonatal/microbiology/genetics ; Genome-Wide Association Study ; Inflammation/genetics ; },
abstract = {BACKGROUND: Neonatal jaundice is a common clinical condition, affecting approximately 60% of full-term infants and 80% of preterm infants. The majority of neonatal jaundice represents benign physiological hyperbilirubinemia that resolves spontaneously, yet a subset progresses to clinically significant hyperbilirubinemia (CSH), defined as elevated serum bilirubin requiring phototherapy or exchange transfusion to prevent permanent neurotoxic injury. The gut microbiota plays a crucial role in human health and disease, with inflammatory mediators frequently contributing to the body's response to illness or injury, often through their modulation of immune system function. As a result, the interplay between gut microbiota, inflammatory factors, and neonatal jaundice has garnered considerable research interest. Investigating the involvement of gut microbiota and inflammatory factors in neonatal jaundice holds the potential to inform the development of novel therapeutic strategies.

METHODS: This study employed Mendelian Randomization (MR) to investigate the causal relationships between 418 gut microbiota taxa, 91 inflammatory factors, and clinically significant neonatal hyperbilirubinemia. Instrumental variables (IVs) genetic variants used as proxies for the exposure were selected from genome-wide association study (GWAS) summary statistics according to stringent criteria. Five well-established MR methods-namely, inverse variance weighting (IVW), MR-Egger, weighted median, simple mode, and weighted mode-were applied to evaluate the causal associations between gut microbiota composition and susceptibility to neonatal jaundice. Sensitivity analyses and tests for pleiotropy were performed on the MR results to assess the robustness and reliability of the findings.

RESULTS: Mendelian Randomization analysis identified ten bacterial taxa associated with neonatal jaundice. The consistency in the direction of beta values across nine microbial taxa further substantiates the robustness of these associations. Notably, the genus Slackia (id.825) exhibited a protective effect against neonatal jaundice, while the genus Adlercreutzia (id.812) was linked to an increased risk of this condition. Additionally, significant correlations were observed between Adlercreutzia and three inflammatory markers: β-nerve growth factor (NGF), C-X-C motif chemokine 1 (CXCL1), and interleukin-6 (IL-6).

CONCLUSION: This study provides evidence supporting associations between specific gut microbiota taxa and neonatal jaundice, as well as potential links with inflammatory markers. These findings are hypothesis-generating and should be interpreted cautiously, especially because the gut microbiome instruments were derived from adult cohorts rather than neonatal cohorts. They do not support immediate clinical recommendations regarding probiotics or antibiotics in newborns, but may help guide future mechanistic and pediatric validation studies.},
}

Humans
Mendelian Randomization Analysis
Infant, Newborn
*Gastrointestinal Microbiome/genetics
*Jaundice, Neonatal/microbiology/genetics
Genome-Wide Association Study
Inflammation/genetics

@article {pmid42521687,
year = {2026},
author = {Mahmoudi, M and Hu, Y and Almario, J and Stincone, P and Tenzer, LM and Chaudhry, V and Braun, L and Quinzer, S and Nieselt, K and Kemen, E},
title = {Machine learning reveals biocontrol agents shaping disease outcome in natural Arabidopsis populations.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42521687},
issn = {2041-1723},
support = {DeCoCt ERC-2018-COG 820124//EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council)/ ; SPP 2125 DECRyPT//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; TRR 356 PlantMicrobe//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; Germany's excellence strategy-EXC 2124-390838134//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; },
mesh = {*Arabidopsis/microbiology/genetics ; *Plant Diseases/microbiology/prevention & control ; *Machine Learning ; Microbiota/genetics ; *Oomycetes/physiology/pathogenicity ; Plant Leaves/microbiology ; Host-Pathogen Interactions ; },
abstract = {Plants recruit antagonistic microbes to defend against phytopathogens, offering a route to rational biocontrol beyond empirical screening. Here, using six generations of leaf-microbiome data from natural Arabidopsis populations infected by the oomycete Albugo laibachii, we show that microbial diversity is driven by infection, site, and host genotype, and that infected plants form modular networks with increased inter-kingdom antagonism. We train four machine-learning models to discriminate infected from uninfected plants by microbiota composition and identify microbes enriched in diseased (disease-associated) or healthy (health-associated) plants. Testing the most predictive bacteria, fungi, and cercozoa in planta, we find all confer varying protection against Albugo, with health-associated microbes outperforming disease-associated taxa. The best candidate, a Cystofilobasidium fungus, is validated in a synthetic community, where genomic and community assays indicate biocontrol acts mainly through microbe-microbe interactions rather than plant immune activation. This work shows that pairing microbiome data with machine learning identifies effective biocontrol agents.},
}

*Arabidopsis/microbiology/genetics
*Plant Diseases/microbiology/prevention & control
*Machine Learning
Microbiota/genetics
*Oomycetes/physiology/pathogenicity
Plant Leaves/microbiology
Host-Pathogen Interactions

@article {pmid42521792,
year = {2026},
author = {Mekadim, C and Kristeková, D and Mikuška, P and Buchtová, M and Mrázek, J},
title = {Inhalation of cadmium oxide nanoparticles alters intestinal and pulmonary microbiomes in mice.},
journal = {Applied microbiology and biotechnology},
volume = {110},
number = {1},
pages = {},
pmid = {42521792},
issn = {1432-0614},
support = {24-10051S//Czech Science Foundation/ ; },
mesh = {Animals ; *Lung/microbiology/drug effects ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Oxides/administration & dosage/toxicity ; *Cadmium Compounds/administration & dosage/toxicity ; *Microbiota/drug effects ; Bacteria/classification/drug effects/genetics ; Male ; Colon/microbiology ; *Nanoparticles/administration & dosage ; *Inhalation Exposure ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Exposure to cadmium (Cd), a toxic heavy metal, is a severe threat to organismal health, causing a wide range of pathological alterations in various tissues and organs. Alterations in the composition and function of the gut microbiome have been indicated across numerous animals exposed to Cd. However, the impact of Cd inhalation exposure on the pulmonary microbiome has not been well investigated yet. Therefore, in this study, we investigated the effects of exposure to CdONPs and its clearance on both colonic and pulmonary microbiomes in mice. The diversity of both colonic and pulmonary microbiomes of exposed mice was significantly affected after 9 weeks of CdONPs inhalation. The effects of CdONPs exposure on bacterial composition and function were more pronounced in the colonic microbiome than in the pulmonary microbiome. The clearance was more efficient in the restoration of gut microbiome composition in comparison to the lung microbiome. Moreover, we evaluated a bidirectional interaction between Cd exposure and gut microbiota. Duncaniella, Odoribacter, and Pontibacter were the prominent biomarkers that significantly positively correlated with dysregulated functions in the colonic microbiome of exposed mice. Based on the PICRUSt2 prediction analysis, our results suggested that perturbations in the gut microbiota balance due to Cd exposure were associated with the increase in the proportion level of bacteria with excessive membrane transporters, which may potentially augment the absorption of this metal by intestinal microbiota thereby leading to the accumulation of Cd in intestinal bacteria and the potential alleviation of the Cd toxicity effect. Furthermore, genes related to metal chelators were consistent with the colonic microbiome of exposed mice, suggesting possible promotion of Cd excretion and its eventual fecal elimination. However, these observations derived from 16S rRNA profiling and PICRUSt2 predictions would need to be verified experimentally to establish any functional or mechanistic implications. This could be considered a key factor in determining the intestinal bacterial species able to minimize the toxicity of heavy metals in future therapeutic approaches. KEY POINTS: • Inhalation of CdO nanoparticles significantly alters both gut and pulmonary microbiome composition and diversity in mice. • Microbiome changes are more pronounced in the gut than in the lungs following inhalation exposure. • Partial recovery of microbiome composition occurs after the clearance period, with greater restoration in the gut than in the lung. • Predicted functional profiles indicate shifts in microbial metabolic potential associated with Cd exposure. • The findings support a potential interaction between inhaled Cd exposure and the gut microbiome, highlighting the relevance of the gut-lung axis.},
}

Animals
*Lung/microbiology/drug effects
*Gastrointestinal Microbiome/drug effects
Mice
*Oxides/administration & dosage/toxicity
*Cadmium Compounds/administration & dosage/toxicity
*Microbiota/drug effects
Bacteria/classification/drug effects/genetics
Male
Colon/microbiology
*Nanoparticles/administration & dosage
*Inhalation Exposure
RNA, Ribosomal, 16S/genetics

@article {pmid42522116,
year = {2026},
author = {Rahayu, ID and Iswahyudi, I and Sutanto, A and Garfansa, MP and Meylanzharie, Z and Nurfadilah, LR and Amani, SA and Hidayati, A and Ekalaturrahmah, YAC and Gafur, MAA and Chanan, M and Budiyono, A},
title = {Earthworm Gut Microbiota as a Biological Driver of Plastic Degradation: Implications for Microplastic Mitigation.},
journal = {Environmental microbiology},
volume = {28},
number = {8},
pages = {e70387},
doi = {10.1111/1462-2920.70387},
pmid = {42522116},
issn = {1462-2920},
support = {E.2.a/275.10/RPK/UMM/2025//Universitas Muhammadiyah Malang/ ; },
mesh = {Animals ; *Oligochaeta/microbiology/metabolism ; *Biodegradation, Environmental ; *Microplastics/metabolism ; *Gastrointestinal Microbiome ; Bacteria/metabolism/classification/genetics/isolation & purification ; *Soil Pollutants/metabolism ; Soil Microbiology ; },
abstract = {Microplastic pollution in terrestrial environments has emerged as a growing threat to agricultural sustainability. Earthworms and their gut microbiota have recently attracted attention as potential nature-based agents for microplastic mitigation. This study systematically synthesizes empirical evidence on the role of earthworm intestinal microorganisms in the transformation and potential biodegradation of microplastics. A literature synthesis was conducted using Scopus-indexed, peer-reviewed publications published between 2018 and 2025 that examined interactions among microplastics, earthworms, and gut microbiota. The synthesis indicates that microplastic degradation within the earthworm digestive system is a multifactorial process involving mechanical fragmentation, selective microbial enrichment, and biological and metabolic activity. Across different earthworm species and polymer types, the phyla Actinobacteria, Proteobacteria, and Firmicutes consistently dominated the gut microbiome. Several genera, including Bacillus, Paenibacillus, Rhodococcus and Streptomyces, were repeatedly associated with microplastic transformation. Earthworm activity may also improve nutrient availability, stabilize soil microbial communities and enhance plant tolerance to microplastic-induced stress. However, major gaps remain in quantifying biodegradation rates, determining microbial removal efficiency and identifying enzymes directly involved in plastic degradation. Overall, this synthesis positions vermiremediation as a promising strategy for managing terrestrial microplastic contamination, while underscoring the need for stronger mechanistic evidence to support practical application.},
}

Animals
*Oligochaeta/microbiology/metabolism
*Biodegradation, Environmental
*Microplastics/metabolism
*Gastrointestinal Microbiome
Bacteria/metabolism/classification/genetics/isolation & purification
*Soil Pollutants/metabolism
Soil Microbiology

@article {pmid42522258,
year = {2026},
author = {Curias, C and Wieme, AD and Joossens, M and Vandamme, P},
title = {The microbiome of the wood-dwelling Cossus cossus (Lepidoptera: Cossidae): a functional approach.},
journal = {Environmental entomology},
volume = {55},
number = {4},
pages = {},
doi = {10.1093/ee/nvag081},
pmid = {42522258},
issn = {1938-2936},
mesh = {Animals ; *Moths/microbiology/growth & development ; *Bacteria/classification/isolation & purification/genetics ; RNA, Ribosomal, 16S/analysis/genetics ; Wood ; Larva/microbiology/growth & development ; *Microbiota ; *Gastrointestinal Microbiome ; Lignin/metabolism ; },
abstract = {Microorganisms associated with insects can offer diverse benefits to their host, but the degree to which hosts rely on them varies across insect groups. Although research has increasingly focused on Lepidoptera, many of which are important pest species, key aspects of their microbiome's stability and functional importance remain ambiguous and seem context-dependent. The caterpillars of the goat moth, Cossus cossus (Linnaeus), which develop over 2 to 5 years within trunks of deciduous trees and consume a wood-based diet rich in recalcitrant lignin, provide an intriguing model to examine potential microbial contributions to lignocellulose degradation. Full-length 16S rRNA gene sequencing revealed a gut microbiome dominated by Enterococcus spp. and a high Leuconostoc spp. presence in the mandibular glands. Concurrent culturomics approaches recovered 64 taxa identified by sequencing and uncovered additional diversity, such as Brevibacterium spp. and Streptomyces spp. Notably, several isolates, including strains of Acinetobacter johnsonii, Citrobacter gillenii, Leucobacter sp., and Pseudomonas sp., demonstrated growth on minimal media supplemented with wood, lignin, or lignin-derived aromatics as the sole carbon and energy sources. These findings provide the first evidence that specific bacterial members of the goat moth caterpillar's microbiome may contribute to wood digestion, suggesting a functional symbiosis suited to a challenging dietary niche.},
}

Animals
*Moths/microbiology/growth & development
*Bacteria/classification/isolation & purification/genetics
RNA, Ribosomal, 16S/analysis/genetics
Wood
Larva/microbiology/growth & development
*Microbiota
*Gastrointestinal Microbiome
Lignin/metabolism

@article {pmid42522515,
year = {2026},
author = {Khan, S and Hussain, D and Ahmad, H and Ahmed, S},
title = {Microbiome dysbiosis in psoriatic skin among Asian populations: Insights from a systematic review and meta-analysis.},
journal = {Dermatology online journal},
volume = {32},
number = {3},
pages = {},
pmid = {42522515},
issn = {1087-2108},
mesh = {Humans ; *Psoriasis/microbiology/drug therapy ; *Skin Microbiome ; Asian People ; *Dysbiosis/microbiology ; Malassezia/isolation & purification ; *Skin/microbiology ; },
abstract = {BACKGROUND: Psoriasis is a chronic immune-mediated skin disease increasingly associated with microbial dysbiosis.

OBJECTIVE: To clarify patterns of skin microbiome alteration in psoriasis.

METHODS: We conducted a systematic review and meta-analysis of Asian cohort studies. Eleven studies were included.

RESULTS: Results for α-diversity were inconsistent, with Shannon and Simpson indices showing heterogeneous outcomes. In contrast, genus-level analysis revealed consistent taxonomic trends: psoriatic lesions demonstrated enrichment of Staphylococcus and Streptococcus with concurrent depletion of Cutibacterium. Fungal analyses showed redistribution of Malassezia species, with increased burden reported in Japanese, Chinese, and Iranian cohorts. Funnel plots indicated limited publication bias, and sensitivity analyses confirmed that exclusion of therapeutic cohorts did not alter results. Importantly, IL-17A inhibitor studies demonstrated partial restoration of microbial balance following treatment. These findings provide reproducible evidence of microbiome shifts in psoriatic skin across Asian populations. The results suggest that specific bacterial and fungal taxa may serve as biomarkers of disease activity and therapeutic response.

CONCLUSION: Future mechanistic work should integrate microbiome and host immune pathways to advance development of microbiome-targeted interventions in psoriasis.},
}

Humans
*Psoriasis/microbiology/drug therapy
*Skin Microbiome
Asian People
*Dysbiosis/microbiology
Malassezia/isolation & purification
*Skin/microbiology

@article {pmid42522607,
year = {2026},
author = {Guo, X and Mo, N and Fu, T and Lai, Y and Hou, X and Zhou, Y},
title = {[Artificial intelligence-based mining of antimicrobial peptides in the microbiome].},
journal = {Sheng wu gong cheng xue bao = Chinese journal of biotechnology},
volume = {42},
number = {7},
pages = {2881-2901},
doi = {10.13345/j.cjb.250842},
pmid = {42522607},
issn = {1872-2075},
support = {32402702//the National Natural Science Foundation of China/ ; LMS25C170002//the Natural Science Foundation of Zhejiang Province/ ; 2024-2026QNRC001//the Young Elite Scientists Sponsorship Program by CAST/ ; },
mesh = {*Artificial Intelligence ; *Antimicrobial Peptides ; *Microbiota ; Humans ; Drug Discovery ; *Data Mining ; },
abstract = {Antimicrobial peptides (AMPs) are small-molecule polypeptides with broad-spectrum antimicrobial activity that are induced by the innate immune system of organisms and constitute a crucial component of the innate immune defense. With the misuse of antibiotics and other antimicrobial agents, the problem of bacterial resistance has become increasingly severe. Naturally occurring AMPs derived from the microbiome, owing to their broad availability, stable physicochemical properties, relatively low propensity to induce resistance, and capacity to contribute to the maintenance of commensal microbiota homeostasis, are regarded as beneficial supplements and adjuvant therapeutic strategies to traditional antibiotics. In recent years, the rapid advancement of artificial intelligence (AI) technologies has facilitated their application in the field of drug discovery, thereby opening new avenues for the large-scale screening of AMPs and substantially accelerating the overall research progress. This review summarizes the developmental trajectory of AMP research methodologies from early approaches to the present day and provides a comparative overview of AI-based AMP screening tools and databases. In addition, the criteria for AMP screening and the recent progress in AI-assisted AMP development, both domestically and internationally, are systematically compiled. The aim of this review is to provide a systematic synthesis of the methodological framework for AI-based mining of microbiome-derived AMPs, thereby offering theoretical references and technical guidance for the efficient identification of novel AMPs. It is anticipated that this review will stimulate further consideration regarding AMP screening and design, and will promote advancements in the field of human health in the era of AI.},
}

*Artificial Intelligence
*Antimicrobial Peptides
*Microbiota
Humans
Drug Discovery
*Data Mining

@article {pmid42522811,
year = {2026},
author = {Sindhughosa, DA and Mariadi, IK and Lesmana Dewi, PIS and Pamungkas, KMN and Yunia Dewi, NLP and Dewi, NNGK and Alamsyah, AZ and Widiada, PA},
title = {Microbial Composition Study in Cholangiocarcinoma: Stage-Specific Diversity Analysis in Bile and Tumor Microbiome.},
journal = {Asian Pacific journal of cancer prevention : APJCP},
volume = {27},
number = {7},
pages = {2509-2518},
doi = {10.31557/APJCP.2026.27.7.2509},
pmid = {42522811},
issn = {2476-762X},
mesh = {Humans ; *Cholangiocarcinoma/microbiology/pathology ; *Bile Duct Neoplasms/microbiology/pathology/genetics ; *Microbiota ; Female ; Male ; *Bile/microbiology ; Prognosis ; RNA, Ribosomal, 16S/genetics ; Middle Aged ; Neoplasm Staging ; *Bacteria/genetics/classification/isolation & purification ; Follow-Up Studies ; Aged ; },
abstract = {OBJECTIVE: Cholangiocarcinoma (CCA) is an aggressive malignancy of the biliary tract with poor prognosis and limited early diagnostic tools. Microbial dysbiosis has been implicated in carcinogenesis, yet microbial signatures across disease stages and anatomical sites in CCA remain poorly defined. This study aimed to characterize the microbial diversity in bile and tumor tissue of CCA patients and evaluate association with disease stage.

METHODS: Microbiome profiles were analyzed from 36 subjects using 16Sr RNA gene sequencing data from the Sequence Read Archive (SRA). Alpha diversity (Chao1 index) and beta diversity (Bray-Curtis dissimilarity) were assessed across bile and intratumoral samples. Linear discriminant analysis effect size (LEfSe) was employed to identify stage-specific microbial taxa.

RESULT: Alpha diversity did not differ significantly between disease stages (ANOVA, F = 0.385, p = 0.816), suggesting stable microbial richness throughout progression. However, beta diversity analysis (PERMANOVA, R² = 0.279, p = 0.013) revealed distinct clustering by sample type and tumor stage. LEfSe identified enrichment of Fusobacterium, Escherichia-Shigella, and Enterococcus in advanced-stage tumor samples, while Lactobacillus and Streptococcus were more abundant in early-stage bile samples.

CONCLUSION: This study demonstrates distinct microbial composition patterns across disease stages and anatomical sites in CCA. Enrichment of specific pathogenic taxa in advanced stages supports a role for microbiome alterations in CCA pathogenesis. Microbial markers may serve as potential tools for staging and prognosis, warranting further functional and prospective validation studies.},
}

Humans
*Cholangiocarcinoma/microbiology/pathology
*Bile Duct Neoplasms/microbiology/pathology/genetics
*Microbiota
Female
Male
*Bile/microbiology
Prognosis
RNA, Ribosomal, 16S/genetics
Middle Aged
Neoplasm Staging
*Bacteria/genetics/classification/isolation & purification
Follow-Up Studies
Aged

@article {pmid42523014,
year = {2026},
author = {Shie, ZH and Chang, HX},
title = {Spatial microbiome and synthetic community analyses reveal Trinickia sclerotiorum sp. nov. promotes sclerotia mortality of Sclerotinia sclerotiorum.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag201},
pmid = {42523014},
issn = {1751-7370},
abstract = {Bulk microbiome analysis obscures the spatial heterogeneity of microbial communities, limiting the understanding of bacterial distribution inside fungal sclerotia, which are the survival structures of the plant pathogen Sclerotinia sclerotiorum. Although studies have profiled microbiomes of different fungal structures, sclerotia microbiome remains largely unexplored. We applied bulk microbiome using PacBio full-length 16S rRNA sequencing, synthetic community (SynCom), and 10x Genomics Xenium platform to resolve the spatiotemporal contribution of soil bacteria to sclerotia mortality. In the bulk microbiome, the relative abundance of soil bacteria such as Massilia and Trinickia were enriched when sclerotia mortality increased under flooding conditions. Twelve enriched sclerotia-associated bacteria were assembled into a SynCom to study their causality for sclerotia mortality. Spatial microbiome analysis revealed the temporal dynamics and distribution pattern of each SynCom member. Among them, Trinickia sclerotiorum sp. nov. type strain MC (TsMC) was found to reach the most interior sclerotia and its relative abundance coincided with sclerotia mortality. TsMC exhibits the highest importance in four antagonistic assays and SynCom drop-out test. Whole genome sequencing confirmed TsMC as a novel species with antifungal potentials. Collectively, we document a novel bacterium for sclerotia mortality and demonstrate the advantage of spatiotemporal distribution in microbiome research.},
}

@article {pmid42523065,
year = {2026},
author = {Sarjit, A and Hall, AM and Sellapperumage, N and Makings, C and Dykes, GA},
title = {The faecal microbiome and carriage of Salmonella in Australian captive pythons.},
journal = {FEMS microbiology ecology},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsec/fiag084},
pmid = {42523065},
issn = {1574-6941},
abstract = {There is a growing interest in keeping exotic pets such as pythons in Australia. Reptiles are known asymptomatic carriers of Salmonella in their digestive tract. This study investigated the microbiome and carriage of Salmonella in faeces from captive Australian pythons (n=28). This study also aimed to determine the effect of temperature and nutrient availability on monospecies biofilm formation of python-associated Salmonella isolated in this study (n=10) as a possible indicator of persistence. A total of 23 Salmonella strains were identified from 28 captive Australian pythons, representing diverse serovars of subspecies enterica, namely S. Bergedorf, S. Havana, S. Jangwani, S. Java, S. Kottbus, S. Muenchen, and S. Umbadah, as well as subspecies S. diarizonae and S. salamae. The composition of the microbial communities differed according to sampling location, diet and Salmonella serovars or subspecies. Bacillota, Bacteroidota, and Pseudomonadota were the most abundant taxa across the faecal microbiome. Strains belonging to subspecies enterica were generally poorer biofilm formers than strains belonging to subspecies salamae and diarizonae. This study shows that microbial communities are variable depending on the environmental factors, which could increase the risk of acquiring reptile-associated salmonellosis whilst handling captive pythons.},
}

@article {pmid42523106,
year = {2026},
author = {Xu, S and Yang, L and Gao, J and Shi, Y and Tang, X and Cai, H and Yang, L and Han, Y and Lin, L and Meng, R and Sun, J and Guan, W-j and Tang, T and Shu, W and Cao, C and Zheng, X-y and Wang, Z and Yi, X},
title = {The associations of human genetic variations with airway microbiome, environmental exposures, and respiratory health.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0044226},
doi = {10.1128/msystems.00442-26},
pmid = {42523106},
issn = {2379-5077},
abstract = {UNLABELLED: The intricate interactions between environmental exposures, the respiratory microbiome, and host genetic variations remain inadequately understood in the context of respiratory health. This study utilized sputum metagenomic data from 1,651 individuals in our previous cohort to elucidate these associations. Mendelian randomization indicated that air pollutants (e.g., SO2, CO, and PM2.5) were associated with lung function, which is potentially mediated by microbes, such as Actinomyces, Haemophilus influenzae, and Veillonella spp. Several genetic loci associated with respiratory microbiome variation were found to be linked to genotype-dependent associations between environmental exposures and lung function. For bacteria, the MEOX1 locus (rs1973191819) was associated with lower Filifactor alocis abundance under air pollutant exposure. The FAM110D (1:26157175) and USP36 (rs1343834070) loci showed associations with higher levels of certain pathogenic taxa (e.g., Ralstonia pickettii, Neisseria) and lower levels of the commensal Oribacterium, increasing chronic obstructive pulmonary disease (COPD) risk. For fungi, DNAJC18 and CCDC57 loci exhibited associations with Candida and Penicillium abundance, respectively. These genotype-dependent associations between the microbiome and environmental exposures provide insights into airway dysbiosis and susceptibility to respiratory diseases.

IMPORTANCE: This study reveals why individuals exposed to identical air pollution exhibit varying degrees of respiratory severity, pointing to a critical missing link: our genetics. While pollution is a known disease trigger, our findings demonstrate that host genetic variation actively regulates and shapes the respiratory microbiome under environmental stress. By mapping specific genetic loci to pollutant-driven bacterial shifts, this work elucidates how host genetics filters environmental risks to govern microbial homeostasis. These results underscore the necessity of incorporating host-microbiome genetic regulation into environmental health research. Ultimately, this study shifts the paradigm toward personalized medicine, enabling the early identification of at-risk individuals and the development of targeted, microbiome-informed interventions.},
}

@article {pmid42523201,
year = {2026},
author = {Kananen, K and Tran, N and Bradley, PH},
title = {Phylogenize2: robust phylogenetic methods link genes to phenotypes across host-associated and environmental microbiomes.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.15.738685},
pmid = {42523201},
issn = {2692-8205},
abstract = {UNLABELLED: In microbiome studies, associations between microbial functions and the environment are often confounded by phylogeny. While some methods explicitly account for this confounder, they require information about genome content, limiting their use in biomes where few genomes have been available. To make these methods more universally accessible, we have developed Phylogenize2, a redesigned phylogeny-aware tool for linking microbial gene families to abundance phenotypes. Phylogenize2 integrates large metagenome-assembled genome collections, including both biome-specific collections from MGnify and a broadly sampled general purpose database, GlobDB, to substantially expand species coverage, allowing its application in environments like the mouse gut and ocean. In addition, by default, Phylogenize2 uses a new robust phylogenetic testing framework that has been optimized for microbial abundance data, while also allowing the use of other comparative methods such as POMS. In an experimental mouse study, Phylogenize2 identifies that Muribaculaceae with higher abundance on a high-fat diet are enriched for proteins in the thioredoxin family, with likely roles in oxidative stress. When we apply Phylogenize2 to a polar ocean study, we find that a molybdenum-dependent PaoABC/YagTSR-like aldehyde oxidoreductase system differentiates mesopelagic from surface-dwelling Flavobacteriaceae , suggesting that aldehyde detoxification may be important for organisms that degrade marine snow. Together, these results show that Phylogenize2 expands phylogeny-aware microbiome analysis beyond the human gut and can provide insight into the genetic basis of microbiome-encoded traits in diverse environments.

IMPORTANCE: Microbiome studies often set out to identify which microbes are more or less abundant across environments, but these patterns can be difficult to interpret. Phylogenize2 is an open-source software package that allows researchers to ask whether individual microbial gene families are associated with the environment across independent branches of the microbial tree of life. By incorporating large collections of genomes from uncultivated microbes, as well as modern statistical methods designed for microbial abundance data, Phylogenize2 makes this approach practical for microbiomes beyond the human gut, including in model organisms like lab mice and free-living environments like the ocean. We also provide a pipeline that allows the use of new genome collections. In two case studies, we demonstrate that Phylogenize2 effectively prioritizes specific genes and pathways from metagenomic data, thereby leading researchers from changes in microbial abundance to more biologically interpretable explanations.},
}

@article {pmid42523245,
year = {2026},
author = {Smedshammer, S and Baxter, B and Briceno, GJ and Morales, KE and Lizcano, A and Clark, T and Willard, D and Riestra, AM},
title = {Study of microbe-microbe interactions between the sexually transmitted parasite Trichomonas vaginalis with the cervicovaginal bacteria Lactobacillus iners.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.14.738301},
pmid = {42523245},
issn = {2692-8205},
abstract = {Trichomonas vaginalis is the leading cause of non-viral sexually transmitted infections and it is associated with comorbidities that affect female health. Lactobacillus iners is one of the most predominant bacteria in the cervicovaginal microbiome. As so, both microbes are likely to encounter one another upon T. vaginalis infection. To our knowledge, the interaction of both microbes has not been previously investigated. Here, we report that T. vaginalis and L. iners bind to one another at early time points of co-incubation. Using imaging flow cytometry and scanning electron microscopy, we capture the dynamics of this microbe-microbe association. We observed active remodeling of the T. vaginalis cell surface leading to thin-membrane protrusions that make contact with L. iners . Larger T. vaginalis membrane extensions that surround and engulf L. iners were also visible. These T. vaginalis - L. iners interactions ultimately lead to a reduction of L. iners viability while T. vaginalis viability was unaffected by exposure to L. iners . Inhibition of actin polymerization blocked T. vaginalis antibacterial activity against L. iners . Together our findings reveal novel insight about T. vaginalis - L. iners interactions and highlight a new T. vaginalis pathogenic effect.},
}

@article {pmid42523308,
year = {2026},
author = {Dover, CE and Tamrakar, K and Dwivedi, B and Roberts, ER and Chudal, S and King, S and Chavez, ES and de Crécy-Lagard, V and Shields, RC},
title = {Deciphering the Streptococcus mutans essentialome: multi-omic resolution of hypothetical genes and identification of a functional RocS equivalent.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.15.738700},
pmid = {42523308},
issn = {2692-8205},
abstract = {UNLABELLED: Genome-wide viability catalogs produced by transposon sequencing (Tn-seq) and CRISPR interference (CRISPRi) have successfully mapped the essential genome of Streptococcus mutans . However, particularly for genes annotated as "hypothetical" or uncharacterized, translating these findings into mechanistic biological functions remains a significant bottleneck. In this study, we developed an integrated functional genomics pipeline combining predictive bioinformatics, tunable CRISPRi transcriptional silencing, transmission electron microscopy, transcriptomics, and genetic suppressor screens to characterize nine legacy hypothetical essential genes in S. mutans . Comparative transcriptomics and proteomics revealed a conserved baseline stress signature across diverse essential pathways, marked by the coordinated downregulation of the citZ - citB - idh metabolic locus and insoluble matrix synthesis enzymes (gtfBC), paired with the robust activation of the integrative and conjugative element Tn Smu1 . Against this backdrop of systemic stress, we successfully resolved the function of SMU_393, defining it as a functional equivalent of the pneumococcal regulator of chromosome segregation, RocS. Depletion of SMU_393 resulted in abnormal cell widening, hypersensitivity to DNA damage, and a significant subpopulation of anucleate cells. Remarkably, these phenotypes were bypassed by a spontaneous surface-exposed missense mutation (dnaA [Q197E]) within the AAA+ ATPase domain of the replication initiator. Together, this work uncovers an important cell cycle regulator and provides a framework for exploring uncharacterized essential genes of the oral microbiome.

IMPORTANCE: Although genome sequencing has identified thousands of genes required for bacterial survival, the precise biological roles for many of them remain completely unknown. This study implements an integrated functional genomics pipeline to resolve the molecular functions of legacy uncharacterized essential genes in the oral pathogen Streptococcus mutans . We discovered a critical molecular checkpoint that acts as a physical anchor, linking the bacterial chromosome to the cell envelope to ensure that chromosome replication is synchronized with cell division. Remarkably, a single mutation in the replication machinery can fully bypass the loss of this anchor, maintaining proper genetic inheritance even during severe cellular stress. Ultimately, this study provides a pipeline for uncovering highly specific physiological vulnerabilities that can be exploited for targeted therapeutics against oral pathogens.},
}

@article {pmid42523323,
year = {2026},
author = {Hite, CR and Zhao, C and Hoffman, K and Hurst, JH},
title = {Perinatal exposures and upper respiratory tract microbiome composition are associated with age at first acute otitis media episode.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.13.738158},
pmid = {42523323},
issn = {2692-8205},
abstract = {UNLABELLED: Acute otitis media (AOM) is the most common bacterial infection of childhood and the leading indication for antibiotic prescriptions and healthcare consultations globally. Colonization of the upper respiratory tract (URT) microbiome by bacterial respiratory pathogens precedes AOM episodes; however, the factors that influence colonization susceptibility and subsequent AOM are not well understood. We hypothesized that perinatal exposures, including mode of delivery, intrapartum antibiotic exposure, and infant feeding influence the composition of the URT microbiome at birth, modifying risk of AOM in infancy. We characterized the URT microbiome in nasopharyngeal swabs collected from 163 infants at birth. Swabs were generally collected within two days of delivery (median [IQR] collection time: 25 [17, 45] hours) and microbiome composition was evaluated with 16S rRNA V4 sequencing. Exposures evaluated included birth mode, intrapartum antibiotic exposures, and feeding type at hospital discharge. AOM episodes were identified through electronic health records data. We built Cox proportional hazards models to determine if perinatal exposures and/or microbiome characteristics at birth were associated with the time to first AOM episode in the first two years of life. URT microbiome diversity and composition were associated with feeding type at hospital discharge, wherein exclusive formula feeding was associated with increased diversity and the presence of Staphylococcus and Haemophilus spp. Increased URT microbiome diversity was associated with younger age at first AOM episode. Our findings suggest that perinatal exposures may influence the composition of the birth URT microbiome, and that this early composition may be related to AOM susceptibility in infancy.

IMPORTANCE: Ear infections are the most common bacterial infection of childhood and the leading indication for healthcare consultation and antibiotic receipt. Previous studies have demonstrated that the microbes that inhabit the upper respiratory tract, known as the microbiome, influence risk of ear infection. This study sought to understand how exposures around the time of birth, including delivery type, maternal antibiotic exposures, and infant feeding, influence the development of the infant microbiome, and in turn, how the microbiome is related to ear infections. An analysis of nasal swabs collected from infants shortly after birth demonstrated that increased microbial diversity is associated with earlier age at first ear infection episode. Overall, this study demonstrates that exposures in early life influence respiratory microbiome development, which contributes to infection susceptibility.},
}

@article {pmid42523339,
year = {2026},
author = {Tran, N and Kananen, K and Bradley, PH},
title = {A robust, sensitive phylogenetic method enables gene-level metagenomic analyses.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.15.738679},
pmid = {42523339},
issn = {2692-8205},
abstract = {UNLABELLED: A key goal in the microbiome field is to move from taxonomic associations towards mechanistic hypotheses about microbial gene function. However, most methods for linking microbiome changes to specific genes are biased towards finding marker genes, with weak evidence for functional relevance. Phylogenetic regression can address this issue and has been previously applied to changes in microbial prevalence, but many environments (such as the gut in health vs. disease) are characterized more by changes in abundance, which presents unique statistical challenges. We show that when applied to real differential abundances from metagenomes, phylogenetic regression has an anti-conservative bias, indicating inflated false positives. We develop an alternative non-parametric method called "robust permutration," designed specifically for differential abundance data, and evaluate its performance against phylogenetic regression as well as several other phylogenetic comparative methods in realistic simulations of metagenomic data. These results show that robust permutration is the most powerful method that appropriately controls the false positive rate. We further apply robust permutration to a human case-control study of liver cirrhosis, revealing that Lachnospiraceae abundance in disease is linked to a previously uncharacterized iron- sulfur transcription factor encoded near homologs of the butyryl-CoA oxygen oxidoreductase system, a recently discovered system for oxygen detoxification. This illustrates how robust, sensitive phylogenetic methods can enable the generation of new molecular hypotheses directly from metagenomic case-control data.

IMPORTANCE: Previously, we showed that phylogenetic regression can effectively detect genes associated with microbial presence or absence while correcting for evolutionary relationships. Unexpectedly, however, we here observe that this method can lead to high false positive rates when applied to microbial abundance data. In realistic simulations, other methods we test either have similar problems with false positives, or display very low power. We outline a new statistical test that better accounts for measurement uncertainty, outliers, and model violations, achieving more balanced sensitivity and accuracy than competing methods. Applying this test to a cirrhosis study reveals an uncharacterized transcription factor enriched in disease, with an apparent role in oxidative stress based on its sequence and gene neighborhood. This suggests a functional explanation for the observed taxonomic shifts, and demonstrates how improved phylogenetic methods could help inform future microbiome-targeted treatments.},
}

@article {pmid42523359,
year = {2026},
author = {Uwamanzu-Nna, A and Olagoke, O and Shi, CX and Mengistie, HD and Asfaha, K and Read, TD and Dean, D},
title = {Ocular community state types reveal distinct microbial compositions among microbiomes with implications for trachoma control.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42523359},
issn = {2692-8205},
abstract = {Trachoma, a chronic ocular disease caused by Chlamydia trachomatis (Ct), is the leading infectious cause of blindness worldwide. Despite WHO's SAFE (Surgery, Antibiotics, Facial cleanliness, Environmental improvement) strategy, ~100M are at risk of blindness. Using metagenomic shotgun sequencing, we characterized the ocular microbiome of 680 villagers in Amhara Ethiopia, identifying 10 Community State Types (CSTs) associated with different population characteristics. Children with the highest prevalence of inflammatory trachoma and Ct were in CST10, dominated by Haemophilus influenzae and four other Haemophilus spp. Adults with the highest prevalence of scarring trachoma were in CST3 and CST6, dominated by Corynebacterium macginleyi. CST5, dominated by Mesomycoplasma hyorhinis and Staphylococcus aureus, had the lowest prevalence of Ct and trachoma, and was the only CST without zoonotic Chlamydia spp. Both M. hyorhinis, a zoonotic porcine bacterium, and S. aureus are capable of forming biofilms, which may competitively prevent/down-regulate chlamydial infections. Other CSTs were dominated by environmental species like Vibrio. This is the first microbiome study to develop CSTs for trachoma. Pathogenic and potentially protective microbes showed distinct associations with demographic, clinical, and chlamydial characteristics, which will guide the design of microbial therapeutics as alternatives to antibiotics and strategies for WHO's global elimination of blinding trachoma.},
}

@article {pmid42523378,
year = {2026},
author = {Baskin, BM and Easton, A and Tschang, M and Lee, SJ and Skillen, E and Wong, K and Schuessler, B and Meabon, J and Wolden-Hanson, T and Cook, DG and Gibbons, SM and Schindler, AG},
title = {Non-invasive Vagal Nerve Stimulation as a Potential Treatment for Repetitive Blast Trauma.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.13.737563},
pmid = {42523378},
issn = {2692-8205},
abstract = {BACKGROUND: Polytrauma caused by exposure to high explosives (blast) is increasingly common among military personnel and civilians yet treatment for related post-concussive symptoms and chronic behavioral dysfunction is limited. Therapeutic targets following these injuries are typically focused on the central nervous system, with less attention placed on potentially more accessible peripheral targets. Vagus nerve stimulation (VNS) has recently gained traction as a potential therapeutic modality but has yet to be examined in a blast trauma setting.

METHODS: Our well-established blast overpressure model was utilized to induce repetitive (3x) blast trauma, followed by treatment with non-invasive transcutaneous VNS one hour following each blast exposure in male mice. Acutely following repetitive blast exposure, we measured serum and brain cytokine levels, fecal microbial abundance, and locomotion and anxiety-like behavior in the open field assay. Chronically (1-3 months post blast), mice were assessed for behavioral outcomes related to mild traumatic brain injury (mTBI) and posttraumatic stress disorder (PTSD), including acoustic startle (hyperreactivity), probabilistic discounting (risky decision making), and two-bottle choice test (voluntary alcohol consumption).

RESULTS: VNS treatment following blast exposure decreased acute blast-induced inflammatory response in the blood and brain, especially serum IL-9 and IP-10, and brain MPC-1. Chronic behavior tests demonstrated a VNS-dependent reduction in blast-induced risky decision-making and a decreased intake and preference for ethanol. Conversely, VNS was not effective in preventing acute blast effects on the microbiome or chronic hyperreactivity behaviors measured with acoustic startle.

DISCUSSION: This study identifies the vagus nerve as a novel peripheral target for treating acute and chronic blast-induced dysfunction.},
}

@article {pmid42523540,
year = {2026},
author = {Danner, R and Cho, J and Detwiler, Z and Williams, J and Han, JA and Yang, C and Diebold, X and Maeder, K and Van Vranken, JG and Walker, AS and Lesser, C and Chaudhari, SN},
title = {Gut microbiome derived folate metabolite suppresses colorectal cancer progression.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.14.738490},
pmid = {42523540},
issn = {2692-8205},
abstract = {The gut microbiota influences colorectal cancer (CRC) progression, primarily through the secretion of small molecule metabolites. While numerous microbial products are known to drive CRC, endogenous protective mechanisms remain largely uncharacterized. Utilizing a folate metabolomics platform, we demonstrate that the healthy gut microbiota produces folinic acid (FA), a known chemotherapeutic adjuvant also known as leucovorin. This microbially derived folinic acid is progressively depleted in mouse models of colitis-associated CRC and in human clinical metagenomic cohorts with advancing disease severity. Mechanistically, folinic acid acts as a signaling molecule that directly binds and inhibits the intracellular protease calpain-2. This interaction stabilizes epithelial E-cadherin protein expression and suppresses CRC epithelial-to-mesenchymal transition driving metastasis. Genetically manipulating gut microbial production of FA is sufficient to modulate CRC in vivo , even in the presence of chronic inflammation. This study reframes folinic acid from a chemotherapeutic enhancer to an endogenous microbial metabolite that actively suppresses CRC progression.},
}

@article {pmid42523620,
year = {2026},
author = {Al-Ali, N and Al-Awadhi, H and Hassane, M and Al-Salam, S and Al-Marzooq, F},
title = {Optimized protocol for profiling mucosa-associated microbiota from formalin-fixed paraffin-embedded gut tissues from treatment-naïve pediatric patients with Crohn's disease.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1885816},
pmid = {42523620},
issn = {2235-2988},
mesh = {Humans ; *Crohn Disease/microbiology/pathology ; Paraffin Embedding ; RNA, Ribosomal, 16S/genetics ; Child ; Formaldehyde ; *Intestinal Mucosa/microbiology ; DNA, Bacterial/genetics ; *Gastrointestinal Microbiome/genetics ; Female ; Tissue Fixation ; Sequence Analysis, DNA ; Polymerase Chain Reaction ; Bacteria/classification/genetics/isolation & purification ; Male ; Adolescent ; Biopsy ; },
abstract = {BACKGROUND: Formalin-fixed, paraffin-embedded (FFPE) tissues are yet underutilized resources for microbiome studies. Data on the mucosa-associated microbiota (MAM) of patients with Crohn's disease (CD) are scarce, due to several methodological limitations. In this study, we aimed to develop and validate a new optimized amplicon-based workflow to profile MAM from FFPE gut biopsies of pediatric CD patients.

METHODS: We examined 68 FFPE samples, including 34 biopsies from treatment-naïve patients with CD and 34 from healthy controls (HC). V3-V7 regions of the 16S rRNA gene were amplified and sequenced on the Oxford Nanopore platform. Two protocols were tested: Protocol 1 (P1), consisting of a single PCR amplification and purification step, and Protocol 2 (P2), including two sequential PCR amplifications with purification after each round. The second amplification and purification steps were introduced to increase sequencing yield and improve microbiota detection.

RESULTS: P2 consistently outperformed P1, yielding significantly higher DNA concentration and purity, reducing human DNA contamination and sustaining pore performance. P2 also generated more microbial reads and recovered a richer, more taxonomically diverse community, including increased detection of species with low abundance. More taxa were enriched in P2 across all levels, enhancing species-level resolution. P2 enabled comprehensive detection of pathogenic genera, such as Escherichia, Mycobacterium, and Klebsiella, which were significantly enriched in the P2 samples compared to the P1 samples. Alpha diversity analysis showed increased richness and reduced evenness in P2 compared to P1, with a significant difference in beta diversity, while maintaining community structure in both CD and HC.

CONCLUSIONS: The optimized workflow with a two-step strategy improved sequencing performance and enhanced microbiota detection in FFPE tissues. This approach enabled successful profiling of MAM, providing a novel method for retrospective characterization of the microbiome from archival tissues and providing a scalable platform for clinical biomarker discovery.},
}

Humans
*Crohn Disease/microbiology/pathology
Paraffin Embedding
RNA, Ribosomal, 16S/genetics
Child
Formaldehyde
*Intestinal Mucosa/microbiology
DNA, Bacterial/genetics
*Gastrointestinal Microbiome/genetics
Female
Tissue Fixation
Sequence Analysis, DNA
Polymerase Chain Reaction
Bacteria/classification/genetics/isolation & purification
Male
Adolescent
Biopsy

@article {pmid42523711,
year = {2026},
author = {Glazunova, E and Kurnosov, A and Bogacheva, A and Makarov, V and Zlobovskaya, O},
title = {Virulome over taxonomy: refining the driver-passenger model in colorectal carcinogenesis.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1858868},
pmid = {42523711},
issn = {2235-2988},
mesh = {*Colorectal Neoplasms/microbiology/pathology/diagnosis ; Humans ; *Carcinogenesis ; *Gastrointestinal Microbiome ; *Virulence Factors ; Microbiota ; Animals ; },
abstract = {Colorectal carcinogenesis is increasingly viewed as a predominantly microbiome-driven process, yet it extends well beyond simple taxonomic associations. The taxon-based classical driver-passenger model, while conceptually useful, may benefit from incorporating the underlying mechanisms of microbial participation and the functional complexity of taxa contributions across CRC stages. In particular, the same taxa may exert distinct effects across carcinogenesis, and individual metabolic pathways frequently mediate multiple and divergent host responses. To address these limitations, we re-examine the roles of CRC-associated microbiota through the lens of individual virulence factor effects on the host, demonstrating their functional pleiotropy, and propose an expanded driver-passenger model. This approach highlights the central role of the virulome in CRC initiation, promotion and progression. By shifting the analytical focus from taxonomy to function, the proposed framework enables improved causality assessment and supports the development of stage-specific diagnostic and prognostic markers, as well as more targeted microbiome-directed therapeutic strategies.},
}

*Colorectal Neoplasms/microbiology/pathology/diagnosis
Humans
*Carcinogenesis
*Gastrointestinal Microbiome
*Virulence Factors
Microbiota
Animals

@article {pmid42523736,
year = {2026},
author = {Togaev, U and Mathur, V and Rakhmonkulova, A and Agarwal, S and Mathur, A and Turageldiyev, S and Ruzmetov, R and Turaev, AS and Tillyabaev, Z and Matchanov, A and Sillam-Dussès, D},
title = {Comparative metagenomic analysis of gut microbiota in Anacanthotermes turkestanicus and A. ahngerianus reveals diet- and habitat-driven functional divergence.},
journal = {Frontiers in insect science},
volume = {6},
number = {},
pages = {1807673},
pmid = {42523736},
issn = {2673-8600},
abstract = {The gut microbiome of termites plays a crucial role in lignocellulose degradation and nutrient recycling. This study presents the first metagenomic characterization of the gut microbiota in two lower termite species, Anacanthotermes ahngerianus and Anacanthotermes turkestanicus, collected from distinct ecological habitats. In Uzbekistan, the first lives in building a mound in nature in the West part while the second mainly lives in contact with human constructions in the East part without building a proper mound. Both species showed similar bacterial dominance (~53%) in their guts but A. ahngerianus exhibited higher overall microbial diversity (Shannon index: 4.046 vs. 3.363; Simpson's index: 0.927 vs. 0.776). Moreover, both termite species showed differences in microbial profiles, including bacterial taxa and eukaryotic groups relevant to lower-termite gut symbiosis. Protist-associated eukaryotic reads were retained because flagellated protists are essential symbionts of lower termites, whereas unexpected non-protist eukaryotic assignments were interpreted cautiously and were not used as evidence of functional gut symbionts or host adaptation. Functional profiling revealed enrichment of pathways related to carbohydrate metabolism, amino acid transport, and energy production in both species. However, A. turkestanicus exhibited stronger bacterial dominance associated with lignocellulose degradation and nitrogen cycling, while A. ahngerianus maintained a more balanced representation of bacteria, fungi, and viruses. These findings suggest that species identity and ecological habits may be associated with differences in gut microbiome structure and predicted functional potential.},
}

@article {pmid42523806,
year = {2026},
author = {Zafar, M and Wang, Y and Wajid, K and Zhao, B and Cao, Y and Hu, S and Xu, G},
title = {Tri-kingdom interactions in bamboo microbiomes: mechanisms of pathogen cooperation and implications for disease management.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1865230},
pmid = {42523806},
issn = {1664-302X},
abstract = {Multi-kingdom disease complexes, where fungi, bacteria, and viruses interact synergistically, are increasingly recognized as a threat to bamboo, a fast-growing Poaceae lineage of high ecological and economic value. However, the mechanisms regulating tri-kingdom disease synergy in bamboo remain poorly understood. This review addresses a central question: Through which molecular and ecological pathways do pathogens from three kingdoms cooperatively enhance bamboo disease severity? We synthesize four key synergy mechanisms: (1) Facilitation of infection: Fusarium proliferatum hyphae build physical entry points as well as transport channels that assist Erwinia sp. to colonize vascular tissues. (2) Immunosuppression: Bamboo mosaic virus (BaMV; genus Potexvirus, family Alphaflexiviridae) inhibits host RNA silencing through viral-encoded proteins TGBp1 and CP, which bind small RNA's and inhibit amplification by RDR6, thereby establishing a permissive environment for secondary invaders, a mechanism inferred from other Potexvirus systems, as direct co-infection evidence in bamboo is currently unavailable. (3) Metabolic cross-feeding: fungal virulence enhanced by bacterial metabolites (e.g., lipopeptides, siderophores), although metabolic synergy in bamboo has not been demonstrated. (4) Biofilm protection: scanning electron microscopy reveals bacterial biofilm on the fungal hyphae surfaces that protect pathogens against host defenses. Quantitatively, the Fusarium-Erwinia co-infection synergy coefficient of bamboo culm rot is S ≈ 1.8, indicating approximately 80% disease severity. Assuming multiplicative independence among mechanisms, tri-kingdom synergy could exceed S > 3.0, a testable hypothesis. This review identifies the following knowledge gaps: (1) no mycovirus isolated from a bamboo-infecting fungus; (2) no bacteriophage characterized against bamboo bacterial pathogen; (3) no quantified studies involving BaMV; and (4) no genome-wide association studies identifying genetic determinants of synergy. This review proposes that effective biocontrol means disrupting the interfaces of pathogen cooperation - disrupting infection courts, interfering with immunosuppression, chelating iron, and degrading biofilm-rather than introducing beneficial microbes. This review proposes a conceptual framework for cross-kingdom microbial interactions in bamboo-associated microbiomes.},
}

@article {pmid42523840,
year = {2026},
author = {Bankar, VR and Chapadgaonkar, SS and Bhattacharyya, K and K, P},
title = {From diversity to function: microbiome-mediated plant growth promotion, secondary metabolism, and antimicrobial resistance in Rauwolfia serpentina.},
journal = {Frontiers in bioinformatics},
volume = {6},
number = {},
pages = {1796770},
pmid = {42523840},
issn = {2673-7647},
abstract = {INTRODUCTION: This study presents the first metagenomic analysis of the root and rhizosphere microbiomes of Rauvolfia serpentina, an endangered medicinal plant. Metagenomic sequencing and bioinformatics analysis were used to characterize the diverse microbial communities and their functional attributes to assess the ecological and biotechnological potential of this plant-associated microbiome.

METHODS: High-throughput Illumina sequencing and bioinformatics analysis were used to profile the microbial communities. Functional annotation was performed to identify plant growth-promoting traits using PLABASE, to predict pathways for the biosynthesis of novel bioactive compounds using antiSMASH, and to identify antimicrobial resistance genes using ResFinder.

RESULTS: The analysis revealed highly diverse microbial communities in both habitats, predominantly composed of Pseudomonadota, Bacillota, and Actinomycetota, with minor but consistent contributions from archaea and eukaryotes. Functional annotation identified extensive PGPTs, including genes associated with phosphate solubilization, nitrogen fixation, siderophore-mediated iron acquisition, and stress tolerance. The rhizosphere microbiome exhibited greater metabolic versatility and stress tolerance, characterized by a higher copy number of heavy metal efflux pumps, whereas the root microbiome was enriched in genes involved in plant hormone regulation and plant-microbe interactions. A diverse array of non-ribosomal peptide synthase, polyketide synthase, and lasso peptide pathways were predicted, underscoring the potential to produce novel bioactive compounds. These distinct functional profiles demonstrates that the protected root endomicrobiome specializes in plant signalling and nutrient assimilation, while the rhizosphere microbiome, facing higher competition, specializes in nutrient acquisition and stress resilience.

CONCLUSION: These findings provide novel insights into the ecological specialization and biotechnological potential of the R. serpentina microbiome, offering significant implications for the sustainable utilization and conservation of this endangered medicinal plant.},
}

@article {pmid42523841,
year = {2026},
author = {Hu, B and Du, L and Chu, D and Kou, E and Zhao, H and Dong, B and Wang, B and Zhu, Y},
title = {Gut microbial metabolites in cutaneous inflammation: shared mechanisms and therapeutic opportunities.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1850282},
pmid = {42523841},
issn = {1664-3224},
mesh = {Humans ; Animals ; *Gastrointestinal Microbiome/immunology ; *Skin/metabolism/immunology ; *Dermatitis, Atopic/metabolism/therapy ; Inflammation/metabolism ; },
abstract = {Cutaneous inflammation is influenced by systemic signals beyond the skin, and gut microbial metabolites contribute to skin homeostasis and inflammatory responses. Major classes of gut-derived metabolites, including short-chain fatty acids, tryptophan-derived compounds, and secondary bile acids, may shape cutaneous inflammation through immune, neural, and endocrine pathways. However, current research remains fragmented across metabolite classes and pathways, and cross-pathway interactions remain unclear. As a result, the relationship between metabolite disturbances and distinct inflammatory phenotypes remains incompletely understood. Atopic dermatitis and chronic spontaneous urticaria are used as representative examples of this variability. This review summarizes major metabolite classes, the pathways linking them to cutaneous inflammation, and current therapeutic strategies targeting these pathways. Therapeutic strategies targeting gut microbial metabolites include direct metabolite supplementation, microbiome-targeted strategies that modify metabolite output, and indirect host-directed interventions. Available evidence suggests that gut microbial metabolites may serve as potential therapeutic targets in cutaneous inflammation. However, current limitations include context-dependent effects, limited causal evidence, variable treatment response, and unresolved issues in delivery and tissue specificity.},
}

Humans
Animals
*Gastrointestinal Microbiome/immunology
*Skin/metabolism/immunology
*Dermatitis, Atopic/metabolism/therapy
Inflammation/metabolism

@article {pmid42523904,
year = {2026},
author = {Labiner, A and Spoiala, EL and Apetrei, C and Trandafir, LM and Pandrea, I},
title = {Gut feelings and sweet teeth: nutritional solutions to the gut damage in inflammatory bowel disease and HIV infection.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1878885},
pmid = {42523904},
issn = {2296-861X},
abstract = {Damage to the mucosal layer of the gut is a central feature of chronic inflammatory diseases, often resulting in gut dysbiosis, microbial imbalances, and dysregulated immunometabolism. Gut dysfunction significantly impacts human health, disrupting metabolic, cardiovascular, and neurological systems, and leading to metabolic syndrome. Here, we discuss two clinical entities that are apparently unrelated but actually share similar alterations to gut mucosal barrier integrity: inflammatory bowel disease (IBD) and human immunodeficiency virus (HIV). We use the particular cases of pediatric IBD and nonhuman primate models of HIV infection to compare and contrast the impact of these diseases on gut integrity and microbiome composition. We also explore potential therapies, focusing on dietary interventions. Both HIV infection and IBD cause gut barrier disruption, but via different mechanisms. HIV rapidly depletes mucosal CD4[+] T cells (especially Th17 cells), weakening epithelial defenses, leading to a loss of tight junctions ("leaky gut"), microbial translocation, and systemic inflammation. In IBD (Crohn's disease and ulcerative colitis), chronic immune attacks on the gut lining produce ulcers and tight-junction defects. These ulcerations trigger immune-cell infiltration and markedly increase permeability. In both conditions, impaired mucus and epithelial integrity result in higher circulating lipopolysaccharides (LPS), macrophage activation, and systemic inflammation. HIV and IBD also induce distinct yet overlapping dysbioses. HIV infection is associated with markedly reduced bacterial diversity and an overgrowth of potentially inflammatory taxa (e.g., Proteobacteria, Prevotella). Similarly, IBD patients have low diversity and loss of beneficial Firmicutes (notably Faecalibacterium prausnitzii) with relative Proteobacteria overabundance. In both diseases, the gut flora shifts away from fiber-fermenting commensals to "pathobionts," fueling local inflammation. While the therapeutic potential of targeting metabolic products is widely explored, there is also a push towards discovering nondrug solutions, particularly through diet and nutrition. We present the effects of micronutrient intake, feeding mechanisms (exclusive enteral nutrition), and different diets (high fiber, Mediterranean, high fat) on disease progression and cellular metabolism. As a low-intervention approach, nutrition has enormous potential to improve human health by reducing inflammation and associated metabolic disturbances. Finally, we emphasize the capabilities of using animal models to elucidate the complexities of disease mechanics in IBD and HIV.},
}

@article {pmid42524136,
year = {2026},
author = {Alanazi, YN},
title = {Functional convergence amid taxonomic variability in gut microbiome-immune checkpoint inhibitor research: a bibliometric and mechanistic synthesis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1883259},
pmid = {42524136},
issn = {1664-3224},
mesh = {Humans ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; *Gastrointestinal Microbiome/immunology/drug effects ; Bibliometrics ; Animals ; Tumor Microenvironment/immunology/drug effects ; *Neoplasms/immunology/drug therapy/microbiology ; },
abstract = {Immune checkpoint inhibitors (ICIs) have transformed cancer therapy, yet clinical responses remain highly variable, and microbiome-associated findings lack reproducibility across studies. Increasing evidence implicates the gut microbiome in modulating ICI efficacy; however, findings remain inconsistent at the taxonomic level, raising the possibility that functionally convergent immunological mechanisms may underlie this apparent variability. To address this, a critical synthesis was conducted, integrating bibliometric mapping of publications indexed in the Web of Science Core Collection (2013-2025; n = 2,195) with a secondary analysis of ClinicalTrials.gov to evaluate interventional activity. Bibliometric approaches assessed scientific production, thematic evolution, and co-citation structure, complemented by a cross-cohort functional integration of representative clinical and preclinical studies to evaluate whether microbiome-ICI interactions converge on shared immunological pathways despite divergent taxonomic signatures. Publication output increased steadily, with a marked translational surge following landmark clinical studies in 2018 and a peak in trial initiation in 2021. Thematic analyses revealed a shift from mechanistic and tumor-centered research toward clinically oriented and intervention-driven themes, including microbiome modulation, microbial metabolites, and the tumor microenvironment. Although individual response-associated taxa differed substantially across independent cohorts, qualitative functional integration supported a model of convergence in immunomodulatory pathways involving short-chain fatty acid production, dendritic cell activation, and CD8[+] T-cell priming. Collectively, these findings suggest that apparent taxonomic inconsistencies across microbiome-ICI studies may reflect underlying functional convergence rather than biological contradiction, supporting a shift toward function-based frameworks for biomarker discovery and microbiome-directed immunomodulation.},
}

Humans
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
*Gastrointestinal Microbiome/immunology/drug effects
Bibliometrics
Animals
Tumor Microenvironment/immunology/drug effects
*Neoplasms/immunology/drug therapy/microbiology

@article {pmid42524160,
year = {2026},
author = {Kumar, A and Dahal, N and Lamichhaney, S and Kumar, R},
title = {Melting Mountains, Shifting Microbiomes: Reconsidering Microbial Roles in Post-Glacial Ecosystem Services.},
journal = {Current opinion in environmental sustainability},
volume = {83},
number = {},
pages = {},
pmid = {42524160},
issn = {1877-3435},
abstract = {The coldest biomes on Earth are mountains with permanent glaciers and permafrost, vulnerable to climate change. These biomes have experienced marked changes and are projected to undergo accelerated transformation due to elevation-dependent warming. While the physical and vegetative responses to glacial retreat are well documented, associated microbial and biochemical shifts remain poorly understood. During deglaciation, newly exposed forefields undergo rapid physical, chemical, and ecological transitions, selecting for specialised microbial communities that mediate ecosystem development through nutrient cycling, soil formation, carbon storage, and early plant establishment. These early-stage microbiomes should not be viewed as passive responders but as active ecosystem engineers shaping post-glacial landscapes and influencing water quality, biodiversity, and downstream ecosystem services. Ignoring microbial contributions in climate assessments risks underestimating ecosystem trajectories and weakening adaptation strategies. This review highlights the need to integrate microbial processes into mountain sustainability frameworks to support informed management, conservation, and long-term ecosystem resilience.},
}

@article {pmid42524177,
year = {2026},
author = {Homayouni-Rad, A and Houshyar, J and Alikhah, H and Kamalledin Moghadam, S and Osouli, Z and Asgharzadeh, A and Sarabi-Aghdam, V and Asghari, A},
title = {Psychobiotic Effects of Postbiotics in Depression, Psychosis and Mania.},
journal = {Health promotion perspectives},
volume = {16},
number = {1},
pages = {27-47},
pmid = {42524177},
issn = {2228-6497},
abstract = {BACKGROUND: The gut microbiota significantly influences mental health through the gut-brain axis, modulating mood, cognition, and emotional regulation. While probiotics and prebiotics have been widely studied for their psychobiotic effects, postbiotics-metabolic byproducts of probiotics-represent an underexplored area with potential therapeutic applications. Understanding the role of postbiotics in mental health disorders, such as depression, psychosis, and mania, could lead to novel treatment strategies. This review examines the psychobiotic potential of postbiotics and their mechanisms of action.

METHODS: A systematic literature review was conducted to evaluate the effects of postbiotics on mental health conditions. We searched PubMed, Medline, EMBASE, and the Cochrane Library for English-language articles published between January 1, 2015, and January 1, 2025, using keywords such as "postbiotic," "paraprobiotic," "depression," "anxiety," and "psychosis." A manual search supplemented the electronic search to ensure comprehensive coverage. Studies focusing on postbiotic effects on mood regulation, neuroinflammation, and neurotransmitter modulation were included.

RESULTS: Postbiotics demonstrate promising psychobiotic effects in depression, psychosis, and mania. They modulate neurotransmitter levels, including serotonin and gamma-aminobutyric acid (GABA), and reduce neuroinflammation, contributing to improved mood and cognitive function. Additionally, postbiotics influence the hypothalamic-pituitary-adrenal (HPA) axis, enhancing stress response and emotional regulation. These findings suggest that postbiotics may serve as effective therapeutic agents for mental health disorders.

CONCLUSION: Postbiotics offer significant potential as novel interventions for mental health conditions, with mechanisms involving neurotransmitter modulation and neuroinflammation reduction. Further empirical research is needed to elucidate their clinical applications and optimize therapeutic protocols. This review highlights the importance of postbiotics in advancing innovative strategies to improve mental health outcomes and well-being.},
}

@article {pmid42524374,
year = {2026},
author = {Oneda, E and Noventa, S and Libertini, M and Cherri, S and Manno, A and Meriggi, F and Petrelli, F and Zaniboni, A},
title = {Post-diagnostic ultra-processed food exposure in gastrointestinal cancers: scoping review with narrative synthesis and clinical implications.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1884359},
pmid = {42524374},
issn = {2296-861X},
abstract = {BACKGROUND: Modifiable lifestyle factors, including diet quality, are strongly associated with the incidence of gastrointestinal cancers. However, the impact of ultra-processed food (UPF) consumption after cancer diagnosis remains poorly understood, with scarce and fragmented evidence. In particular, the role of post-diagnostic UPF exposure in shaping survival outcomes and disease progression has not been systematically explored.

METHODS: We conducted a scoping review with narrative synthesis of the available literature on post-diagnostic UPF consumption and clinical outcomes in gastrointestinal cancers. Eligible studies included adult patients with gastrointestinal malignancies, assessment of dietary exposure after diagnosis, and outcomes such as overall survival, cancer-specific mortality, recurrence, progression, and treatment-related outcomes.

RESULTS: Direct evidence was extremely limited. The only available prospective study in colorectal cancer survivors showed that higher post-diagnostic UPF intake was not associated with overall or cancer-specific mortality but was associated with increased cardiovascular mortality, highlighting the relevance of competing risks in cancer survivorship. Furthermore, specific UPF subgroups showed adverse associations with colorectal cancer-specific mortality. Supportive studies suggested that dietary quality may deteriorate after treatment, with increasing UPF consumption over time. Mechanistic evidence supports a biologically plausible link between UPF exposure, metabolic dysfunction, chronic inflammation, microbiota alterations, and survivorship outcomes.

CONCLUSIONS: Despite the increasing burden of gastrointestinal cancers and the widespread consumption of ultra-processed foods, post-diagnostic UPF exposure remains largely overlooked in oncologic research. Direct evidence is currently limited and mainly restricted to colorectal cancer survivors, where higher UPF intake has been associated with cardiovascular mortality but not consistently with cancer-specific outcomes. These findings, together with biological plausibility from mechanistic studies, support the need for prospective post-diagnostic cohorts and intervention trials integrating standardized dietary assessment into gastrointestinal cancer survivorship research.},
}

@article {pmid42524477,
year = {2026},
author = {Zhuang, J and Zhong, Y and Lin, Z and Lu, Y and Wang, H and Chen, L and Yang, K and Tan, D and Qiu, Y and Zhang, Y and Wang, H and Ge, Z},
title = {From Host-Microbiome Symbiosis to Clinical Translation: A Gut Microbiome Perspective on Radiation Enteritis.},
journal = {International journal of biological sciences},
volume = {22},
number = {12},
pages = {6709-6734},
pmid = {42524477},
issn = {1449-2288},
mesh = {Humans ; *Enteritis/microbiology/etiology ; *Gastrointestinal Microbiome/physiology/radiation effects ; *Symbiosis ; *Radiation Injuries/microbiology ; Animals ; },
abstract = {Radiotherapy is an essential component of multimodal treatment for solid tumors, and more than half of patients with cancer receive radiation during their disease course. Because of the unique anatomical and physiological features of the intestine, radiation enteritis (RE) remains a common and clinically challenging complication of abdominal and pelvic irradiation, with limited effective treatment options. In this review, we re-examine RE from a host-microbiome perspective. We summarize classical pathophysiological mechanisms and discuss how radiotherapy reshapes gut microbial composition and metabolism. We also highlight the roles of microbial metabolites, including short-chain fatty acids, bile acids and tryptophan derivatives, in barrier repair, immune homeostasis and stem-cell regeneration. Finally, we discuss microbiome heterogeneity across disease phases, tumor types and host factors, as well as microbiota-mediated gut-brain, gut-cardiopulmonary, gut-skin and gut-bone-marrow axes involved in systemic radiation injury. We further outline microbiome-based strategies for individualized risk stratification and early prediction, and recent advances and limitations of probiotics and synbiotics, fecal microbiota transplantation, dietary and lifestyle interventions, drugs and natural products, engineered microbes and novel delivery systems, highlighting the gut microbiome as a promising entry point to improve prevention and treatment of RE and systemic radiation toxicity.},
}

Humans
*Enteritis/microbiology/etiology
*Gastrointestinal Microbiome/physiology/radiation effects
*Symbiosis
*Radiation Injuries/microbiology
Animals

@article {pmid42524481,
year = {2026},
author = {Kosaruk, W and Towiboon, P and Klinhom, S},
title = {Faecal immunoglobulin A as a non-invasive biomarker of mucosal immunity and health in zoo and wild mammals.},
journal = {Conservation physiology},
volume = {14},
number = {1},
pages = {coag054},
pmid = {42524481},
issn = {2051-1434},
abstract = {Non-invasive biomarkers of immune function are increasingly important for assessing health, welfare and disease risk in zoo and wild mammals, particularly because they support repeated monitoring while minimizing handling-related disturbance. Secretory immunoglobulin A (IgA), a key component of mucosal immunity, can be quantified from faecal samples and provides a practical measure of gut-associated immune activity without invasive sampling. We conducted a systematic literature review of 21 peer-reviewed studies that quantified faecal IgA across diverse mammalian taxa and ecological contexts. Across species, faecal IgA was technically measurable and biologically responsive, but its interpretation was strongly context dependent. Reported patterns reflected interactions among pathogen exposure, physiological stress, nutritional state, life-history stage and management conditions. In captive settings, faecal IgA frequently varied with individual heterogeneity and management factors and showed inconsistent alignment with endocrine stress markers. In free-ranging populations, faecal IgA more commonly tracked parasite burden, reproductive investment, seasonal variation and host-microbiome dynamics. However, most ecological and welfare-associated patterns were derived from observational designs, which limit causal inference. Additionally, methodological heterogeneity in assay validation, sample processing and preservation limited direct quantitative comparison among studies. Overall, faecal IgA does not function as a unidimensional indicator of stress or welfare, but rather as a context-sensitive marker of mucosal immune allocation. We integrate these findings into a conceptual framework linking external pressures, mucosal immune dynamics, complementary biomarkers and health-related outcomes to guide interpretation across zoo and wild settings. When embedded within longitudinal and multi-marker approaches supported by species-specific validation, faecal IgA has potential to contribute meaningfully to non-invasive health assessment in conservation physiology.},
}

@article {pmid42524566,
year = {2026},
author = {Tsai, HL and Chen, YP and Tsai, JY and Yep, CY and Tan, CW and Lee, CP and Wu, CY and Tsai, TH},
title = {Progressive Shifts in Oral Plaque Microbiota From Health to Coronary Artery Disease and Acute Myocardial Infarction.},
journal = {Cardiology research},
volume = {17},
number = {4},
pages = {288-299},
pmid = {42524566},
issn = {1923-2829},
abstract = {BACKGROUND: Growing evidence links oral microbial dysbiosis to atherosclerotic cardiovascular disease (ASCVD), yet its role in acute myocardial infarction (AMI) and the transition from stable coronary artery disease (CAD) to acute events remains unclear. We aimed to characterize taxonomic and functional alterations of the oral plaque microbiome across cardiovascular health states and explore their clinical relevance.

METHODS: We enrolled 60 age- and sex-matched adults, 20 in each group. Supragingival plaque underwent 16S rRNA sequencing and functional inference. Alpha and beta diversity were assessed, and differential features were identified by Linear Discriminant Analysis Effect Size (LEfSe). The metabolic pathway predictions were using Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway.

RESULTS: Alpha and beta diversity showed no significant differences in overall microbial richness, evenness, or global community structure among groups. However, marked taxonomic shifts were observed. AMI patients exhibited enrichment of pro-inflammatory genera (Veillonella, Porphyromonas, Dialister, Megasphaera, and Acidaminococcus) and depletion of commensal taxa (Haemophilus and Lautropia). LEfSe identified disease-specific microbial signatures distinguishing healthy control, CAD, and AMI. Functional prediction revealed enrichment of arachidonic acid, pyrimidine, and D-glutamine/D-glutamate metabolism in CAD, with further increases in necroptosis-, proteasome-, and inflammation-related pathways in AMI, whereas two-component signaling systems were enriched in healthy controls.

CONCLUSIONS: The oral microbiome exhibits progressive taxonomic and functional shifts from health to CAD and AMI, supporting an oral-cardiovascular axis and highlighting oral microbial profiles as potential noninvasive biomarkers for ASCVD risk stratification.},
}

@article {pmid42524765,
year = {2026},
author = {Littlejohn, C and Chang, YC and Teles, F and Korostoff, JM and Redding, LE},
title = {Evolution of the fecal and oral microbiota after prophylactic antibiotics administered for dental surgeries.},
journal = {Journal of the American Dental Association (1939)},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.adaj.2026.04.020},
pmid = {42524765},
issn = {1943-4723},
abstract = {BACKGROUND: The human oral and gut microbiomes play critical roles in maintaining overall health. Although systemic antibiotics are frequently prescribed perioperatively in dental procedures, their impact on microbiota composition and diversity remains inadequately understood. The authors' objective was to characterize the evolution of the gut and oral microbiomes after a course of antibiotics administered for dental surgeries. The authors hypothesized that the microbiome would experience disruption but eventually recover to baseline levels and that patient-related factors would influence the extent of disruption and recovery.

METHODS: Saliva and stool samples were collected from patients undergoing dental surgeries and receiving prophylactic antibiotics (n = 64) at baseline and then at 3, 10, 30, and 90 days after surgery. Microbial diversity and composition were assessed using 16S ribosomal RNA sequencing. Shotgun metagenomics sequencing was applied to a subset of samples to evaluate changes in antimicrobial resistance genes.

RESULTS: Significant (P < .01) declines in alpha diversity were observed in both oral and fecal microbiomes, most notably at days 3 and 10, with near recovery at day 90. The oral microbiome exhibited greater disruption than the gut microbiome, suggesting higher susceptibility to postoperative disturbance. Patient-level factors including sex, race, gastroesophageal reflux disease, and antibiotic type influenced baseline diversity, disruption, and recovery. Results of taxonomic analyses revealed that key health-associated genera were substantially altered postsurgery. Some antimicrobial resistance genes increased in relative abundance over time, consistent with potential long-term ecological consequences of antibiotic use.

CONCLUSIONS: The findings highlight the dynamic response of the human microbiome to antibiotic exposure and oral surgery and underscore the importance of antibiotic stewardship in practice. Further research on functional outcomes and host-microbiome interactions is warranted to optimize perioperative care in dentistry.

PRACTICAL IMPLICATIONS: Consideration of patient factors is essential to minimize unnecessary disruption of the microbiome and mitigate the risk of developing resistance.},
}

@article {pmid42524911,
year = {2026},
author = {Mattos, AA and Alves, CA and Acuña, J and Mattos, AZ},
title = {DYSBIOSIS IN ACUTE-ON-CHRONIC LIVER FAILURE - FROM A PATHOPHYSIOLOGICAL COMPONENT TO A THERAPEUTIC TARGET.},
journal = {Arquivos de gastroenterologia},
volume = {63},
number = {},
pages = {e25141},
doi = {10.1590/S0004-2803.24612025-141},
pmid = {42524911},
issn = {1678-4219},
mesh = {Humans ; *Acute-On-Chronic Liver Failure/microbiology/physiopathology/therapy/etiology ; *Dysbiosis/complications/physiopathology/therapy/microbiology ; Gastrointestinal Microbiome/physiology ; Liver Cirrhosis/complications/microbiology ; Bacterial Translocation ; },
abstract = {BACKGROUND: Acute-on-chronic liver failure (ACLF) affects approximately one-third of patients hospitalized for acute decompensation of cirrhosis. These patients exhibit an extremely high degree of systemic inflammation, and infections as well as severe alcohol-related hepatitis are the most common precipitating factors of ACLF.

OBJECTIVE: This paper aims to discuss the most relevant aspects of ACLF emphasizing the role of gut dysbiosis.

METHODS: This review includes clinical and epidemiological studies, meta-analyses, and other articles published in English and indexed in the following databases: PubMed, Scopus, and Embase. Only full-text articles were selected.

RESULTS: ACLF is the most severe complication in patients with cirrhosis and is associated with high mortality rates. Bacterial translocation is considered responsible for the systemic inflammation leading to acute decompensation of cirrhosis when other precipitating events are not identified. Different microbiome profiles may influence the incidence of decompensation and thus the clinical course of the disease. Dysbiosis causes intestinal inflammation, which contributes to gut barrier dysfunction and pathological bacterial translocation, the main triggering factor of the cascade leading to acute decompensation of cirrhosis and multiple organ failure. Since dysbiosis plays a central role in the pathophysiology of acute decompensation of cirrhosis and ACLF, it is expected that treatments targeting the microbiome could modify the course of the disease. Despite current limitations, the role of probiotics, prebiotics, postbiotics, rifaximin, bacteriophages, and fecal microbiota transplantation is discussed in the present review.

CONCLUSION: ACLF is a highly significant complication of liver disease. Dysbiosis and the gut-liver axis play key roles in its pathophysiology. This knowledge supports the idea that manipulation of the microbiome may be a potential therapeutic strategy.},
}

Humans
*Acute-On-Chronic Liver Failure/microbiology/physiopathology/therapy/etiology
*Dysbiosis/complications/physiopathology/therapy/microbiology
Gastrointestinal Microbiome/physiology
Liver Cirrhosis/complications/microbiology
Bacterial Translocation

@article {pmid42524914,
year = {2026},
author = {Calixto, SL and Macedo, ACLP and Aguiar, JAK},
title = {GUT MICROBIOTA ALTERATIONS IN RODENT MODELS OF CHOLESTASIS INDUCED BY BILE DUCT LIGATION: A SYSTEMATIC REVIEW.},
journal = {Arquivos de gastroenterologia},
volume = {63},
number = {},
pages = {e25159},
doi = {10.1590/S0004-2803.24612025-159},
pmid = {42524914},
issn = {1678-4219},
mesh = {Animals ; *Cholestasis/microbiology ; *Gastrointestinal Microbiome/physiology ; Disease Models, Animal ; Ligation ; Bile Ducts/surgery ; Mice ; *Dysbiosis/microbiology ; Rats ; },
abstract = {BACKGROUND AND OBJECTIVE: Cholestatic liver diseases are a major public health issue, marked by impaired bile flow and significant disruptions in liver and systemic physiology. Growing evidence points to the gut microbiota as a key player in cholestasis pathogenesis through gut-liver axis interactions. This systematic review aimed to synthesize and evaluate current findings on intestinal microbiota changes in rodents (rats and mice) subjected to bile duct ligation (BDL)-induced cholestasis, focusing on microbial diversity, taxonomic shifts, and potential pathophysiological implications.

METHODS: A comprehensive literature search was conducted in PubMed, Scopus, and Embase for studies published from January 2020 to February 2025, following PRISMA guidelines. Eligible studies included original research using BDL in rodents without therapeutic intervention and reporting gut microbiota profiles. Data were qualitatively analyzed, emphasizing experimental conditions and microbiome outcomes.

RESULTS: Twenty-two studies met inclusion criteria. Most used 16S rRNA sequencing; two used shotgun metagenomics. BDL consistently induced gut dysbiosis, with reductions in alpha diversity (in most studies), altered beta diversity, and shifts in dominant phyla such as Firmicutes, Bacteroidetes, Proteobacteria, Actinobacteria, and Verrucomicrobiota. At finer taxonomic levels, increases in Prevotella, Enterococcus, Escherichia coli, and Alistipes were common, while Lactobacillus and Ruminococcus often decreased. Elevated levels of Akkermansia muciniphila and Bifidobacterium pseudolongum may represent compensatory microbial responses.

CONCLUSION: Bile duct ligation (BDL)-induced cholestasis leads to complex changes in the microbiota that can worsen intestinal barrier integrity, increase bacterial translocation, and intensify liver inflammation. These findings reinforce the central role of the gut-liver axis and corroborate the potential of microbiota-targeted therapies in the management of cholestatic liver diseases. However, as most of the available evidence derives from experimental models, further well-designed clinical studies are needed to validate the safety, efficacy, and translational applicability of these strategies in human diseases.},
}

Animals
*Cholestasis/microbiology
*Gastrointestinal Microbiome/physiology
Disease Models, Animal
Ligation
Bile Ducts/surgery
Mice
*Dysbiosis/microbiology
Rats

@article {pmid42524945,
year = {2026},
author = {Theocharidou, CC and Tsinaris, Z and Peristeri, AM and Akritidou, O and Nikopoulou, A},
title = {Gut microbiome changes in critically ill adults: a systematic review of longitudinal sequencing studies.},
journal = {Critical care science},
volume = {38},
number = {},
pages = {e20260392},
doi = {10.62675/2965-2774.20260392},
pmid = {42524945},
issn = {2965-2774},
mesh = {Humans ; *Critical Illness ; *Gastrointestinal Microbiome/physiology ; Longitudinal Studies ; RNA, Ribosomal, 16S ; Adult ; },
abstract = {OBJECTIVE: Critical illness profoundly alters the gut microbiome, yet its temporal evolution and clinical relevance remain unclear. This systematic review aimed to synthesize evidence from longitudinal sequencing studies describing gut microbiome changes in critically ill adults and their association with clinical outcomes.

METHODS: We systematically searched MEDLINE®, Scopus, and Cochrane CENTRAL from inception to May 2025 for longitudinal observational studies analyzing gastrointestinal samples by sequencing in adult critically ill patients at ≥ 2 times points. Extracted data included study and patient characteristics, as well as microbiome outcomes, including alpha and beta diversity metrics and taxonomic abundance profiles. Due to heterogeneity, we undertook a structured descriptive synthesis: alpha diversity results were grouped by trajectory and compared across intensive care unit populations; beta diversity findings were tabulated and narratively synthesized; and reported associations with mortality and multidrug-resistant organism colonization were summarized narratively. Risk of bias was assessed with RoBANS 2, and certainty of evidence with GRADE.

RESULTS: Thirty-six studies comprising 2,067 critically ill adults were included. Most used 16S rRNA sequencing targeting the V4 region. A decline in alpha diversity was reported in 18 out of 31 studies, while 8 found no change and 4 mixed patterns. Beta diversity shifts over time were reported in 11 studies. Taxonomic analyses consistently revealed the expansion of opportunistic taxa such as Enterococcus, Klebsiella, and other Enterobacteriaceae, alongside the depletion of obligate anaerobes, including Blautia, Coprococcus, and Faecalibacterium. Early low diversity and pathogen-dominated microbiomes were associated with increased mortality. Associations with multidrug-resistant organism colonization were inconsistent. Certainty of evidence (GRADE) for all outcomes was rated very low due to heterogeneity and imprecision.

CONCLUSION: Longitudinal sequencing studies demonstrate progressive loss of microbial diversity and enrichment of pathogenic taxa during critical illness. These shifts, particularly Enterococcus and Klebsiella overgrowth, correlate with adverse outcomes and may reflect the combined effects of antibiotics, disease severity, and critical care interventions. Standardized sampling, sequencing, and reporting protocols are needed to enable meta-analytic synthesis and guide microbiome-targeted interventions in the intensive care unit.},
}

Humans
*Critical Illness
*Gastrointestinal Microbiome/physiology
Longitudinal Studies
RNA, Ribosomal, 16S
Adult

@article {pmid42525211,
year = {2026},
author = {Louie, JCY},
title = {The Gut-brain-adipose Axis in Ultra-processed Food and Obesity: A Mechanistic Synthesis and Its Implications for Food Classification.},
journal = {Current obesity reports},
volume = {15},
number = {1},
pages = {},
pmid = {42525211},
issn = {2162-4968},
mesh = {Humans ; *Obesity/etiology/physiopathology/metabolism ; Animals ; *Fast Foods/adverse effects/classification ; *Gastrointestinal Microbiome/physiology ; *Brain/metabolism ; *Adipose Tissue/metabolism/physiopathology ; Inflammation ; },
abstract = {PURPOSE OF REVIEW: Consumption of ultra-processed food (UPF) tracks closely with obesity across populations, and the Nova classification has become the dominant tool for capturing that exposure. Why UPF promotes weight gain is a separate question, and the biological answer has accumulated in fragments. I draw those strands together and ask whether three mechanisms usually studied in isolation: gut microbial disruption, hypothalamic inflammation, and adipose tissue dysfunction, are better understood as one connected system, and what that would mean for how UPF is classified.

RECENT FINDINGS: Three experimental literatures have converged on a shared pathway. Dietary emulsifiers and non-sugar sweeteners alter microbial composition and weaken the intestinal barrier, raising circulating lipopolysaccharide. In animal models this signal reaches the hypothalamus, where it activates inflammatory pathways, recruits glia, and blunts the leptin response that normally limits intake; though whether the same sequence operates in humans remains unestablished. Visceral fat that expands under this regime secretes its own inflammatory load, which feeds back onto both the gut and the brain. A 2025 UK Biobank analysis added a human imaging dimension, reporting structural differences in feeding-related brain regions that scaled with UPF intake and were only partly explained by adiposity. The evidence coheres best when the three arms are read as a single self-reinforcing loop in which each influences the others. Within that frame, the limitation of the Nova classification becomes specific and tractable: Group 4 mixes products that engage the loop strongly with products that barely touch it. This review sets out where the mechanistic evidence is firm, where it remains thin, and how an attribute-aware refinement of Group 4 might be tested.},
}

Humans
*Obesity/etiology/physiopathology/metabolism
Animals
*Fast Foods/adverse effects/classification
*Gastrointestinal Microbiome/physiology
*Brain/metabolism
*Adipose Tissue/metabolism/physiopathology
Inflammation

@article {pmid42525291,
year = {2026},
author = {Gutiérrez-Ávila, JL and Gutiérrez-Rebolledo, GA and Avila-Bonilla, RG and Pardo, MES},
title = {Functional Equivalence and Conserved Sexual Dimorphism in the Gut Microbiome: A Cross-Species Meta-analysis.},
journal = {Journal of molecular evolution},
volume = {},
number = {},
pages = {},
pmid = {42525291},
issn = {1432-1432},
abstract = {The murine model is a standard system in translational microbiome research, yet its functional equivalence to the human microbiome remains debated. To evaluate its translational validity, we conducted a comparative whole-genome shotgun (WGS) metagenomic meta-analysis, integrating an initial retrieval of 520 datasets from 5 independent cohorts (BioProjects) across Homo sapiens (n = 202), Mus musculus (n = 75), and Drosophila melanogaster (n = 243) samples. Taxonomic and functional profiles were evaluated using strict bioinformatic quality control and batch-effect mitigation. Taxonomic profiling revealed pronounced divergence driven by host-specific ecological constraints and filtering. However, metabolic reconstruction demonstrated substantial functional equivalence, supporting the functional redundancy hypothesis for core mammalian metabolic circuits. We also noted a methodological vulnerability in our dataset: a low-depth murine sample clustered with invertebrate profiles, suggesting that technical noise or insufficient depth might artificially compress mammalian functional diversity. Comparative analysis identified sex-biased metabolic pathways conserved across mammalian hosts. Specifically, we observed a consistent enrichment of steroid metabolism in females and mineralocorticoid regulation in males. These findings indicate that functional conservation between humans and mice is modular rather than global. Consequently, the translational value of the murine model lies in domain-specific functional equivalence rather than taxonomic imitation. Moreover, the conservation of sex-specific metabolic signatures suggests that biological sex is a fundamental organising principle of microbiome function. This study highlights the necessity of mapping conserved metabolic modules and rigorously controlling inter-study variance to effectively deploy murine models in biomedical research.},
}

@article {pmid42525313,
year = {2026},
author = {Naqvi, SAH and Rehman, AU and Umar, UUD},
title = {Host-recruited Bacillus and Pseudomonas strains provide potential biocontrol and yield protection against rice bacterial leaf blight.},
journal = {World journal of microbiology & biotechnology},
volume = {42},
number = {8},
pages = {},
pmid = {42525313},
issn = {1573-0972},
mesh = {*Oryza/microbiology/growth & development ; *Plant Diseases/microbiology/prevention & control ; *Bacillus/isolation & purification/physiology/genetics/classification ; Rhizosphere ; *Biological Control Agents ; *Xanthomonas/pathogenicity ; Soil Microbiology ; *Pseudomonas/isolation & purification/physiology/genetics/classification ; RNA, Ribosomal, 16S/genetics ; Pakistan ; Plant Leaves/microbiology ; Indoleacetic Acids/metabolism ; Antibiosis ; },
abstract = {Bacterial leaf blight (BLB), caused by Xanthomonas oryzae pv. oryzae (Xoo), threatens global rice production while growing bactericide resistance and environmental concerns necessitate sustainable disease management alternatives. We employed a microbiome-guided, habitat-specific isolation strategy targeting naturally recovered plants from BLB-endemic hotspots across ten districts of Punjab, Pakistan operating on the ecological premise that plants under pathogen pressure selectively enrich protective microbial taxa, making disease-affected hosts the most coherent source of adapted biocontrol agents. Screening of 1,036 bacterial isolates from rice rhizosphere and phyllosphere using dual-culture antagonism assays yielded six elite strains: Bacillus velezensis, B. amyloliquefaciens, B. subtilis, Pseudomonas fluorescens, and two P. aeruginosa isolates, confirmed by 16 S rRNA and rpoD gene sequencing (> 99% sequence identity). Biochemical profiling revealed multifunctional plant growth-promoting traits including siderophore production, biological nitrogen fixation, indole-3-acetic acid biosynthesis, phosphate solubilization, and hydrogen cyanide production, indicating the potential capacity of selected strains for integrated disease suppression and plant growth promotion. Greenhouse trials across six rice varieties with contrasting genetic resistance backgrounds demonstrated significant reductions in BLB incidence (25-67%) and severity (31-55%) relative to uninoculated controls. Field validation under natural pathogen pressure across two consecutive growing seasons confirmed robust performance, with incidence suppression of 33-65% and severity reduction of 46-67% compared to controls. B. velezensis fsdls3 emerged as the most effective individual agent, achieving 114.5% mean yield protection relative to diseased controls and approaching streptomycin sulfate performance with no statistically significant overall yield difference while outperforming the chemical standard on specific variety-strain combinations. Five of six PGPR agents exceeded the 100% yield protection threshold, delivering agronomic co-benefits including enhanced tillering, increased productive panicles, and elevated total biomass unavailable from chemical bactericide treatment alone. Pronounced cultivar × treatment interactions confirmed that PGPR efficacy is modulated by host genetic background, with resistant varieties carrying pyramided Xa resistance genes showing additive responses to biological treatment. These results establish habitat-adapted, host-recruited PGPR as scientifically credible and ecologically coherent alternatives to chemical bactericides for integrated BLB management in rice.},
}

*Oryza/microbiology/growth & development
*Plant Diseases/microbiology/prevention & control
*Bacillus/isolation & purification/physiology/genetics/classification
Rhizosphere
*Biological Control Agents
*Xanthomonas/pathogenicity
Soil Microbiology
*Pseudomonas/isolation & purification/physiology/genetics/classification
RNA, Ribosomal, 16S/genetics
Pakistan
Plant Leaves/microbiology
Indoleacetic Acids/metabolism
Antibiosis

@article {pmid42525325,
year = {2026},
author = {Mohan, VK and Joshi, SR},
title = {Single spore propagation of native arbuscular mycorrhizal fungi associated with Khasi mandarin and their symbiotic efficacy in maize.},
journal = {Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]},
volume = {57},
number = {1},
pages = {},
pmid = {42525325},
issn = {1678-4405},
support = {(BT/PR40089/NER/951663/2020)//Department of Biotechnology, Ministry of Science and Technology, India/ ; },
mesh = {*Mycorrhizae/physiology/classification/genetics/isolation & purification/growth & development ; *Zea mays/microbiology/growth & development ; *Symbiosis ; *Spores, Fungal/genetics/growth & development/isolation & purification/classification/physiology ; *Citrus/microbiology ; Plant Roots/microbiology/growth & development ; Soil Microbiology ; Phylogeny ; Rhizosphere ; DNA, Fungal/genetics ; },
abstract = {Arbuscular Mycorrhizal Fungi (AMF) are important members of the soil microbiome that form symbiotic relationships with plant roots, improving nutrient uptake and stress resilience. In the present study, native AMF associated with the rhizosphere of Khasi Mandarin (Citrus reticulata Blanco) were isolated using the wet sieving and decanting method. Trap culture was used to increase the number of native AMF spores. Healthy spores were identified and used for single-spore inoculation to establish single-spore-derived cultures. Molecular identification of the AMF isolates was performed by amplification of the 18 S rDNA region. A controlled pot experiment was conducted to assess the effects of the obtained pure cultures on plant growth. Inoculated maize plants showed significant improvement in root and shoot biomass. This study focuses on evaluating the potential of native AMF isolates associated with Khasi mandarin and their use as cross-inoculants to develop biofertilizer that promote the growth of non-host plants.},
}

*Mycorrhizae/physiology/classification/genetics/isolation & purification/growth & development
*Zea mays/microbiology/growth & development
*Symbiosis
*Spores, Fungal/genetics/growth & development/isolation & purification/classification/physiology
*Citrus/microbiology
Plant Roots/microbiology/growth & development
Soil Microbiology
Phylogeny
Rhizosphere
DNA, Fungal/genetics

@article {pmid42525349,
year = {2026},
author = {Dos Reis, JBA},
title = {Functional diversity and ecological consequences of endophytic Bacillus-plant interactions.},
journal = {Folia microbiologica},
volume = {},
number = {},
pages = {},
pmid = {42525349},
issn = {1874-9356},
abstract = {The genus Bacillus, particularly endophytic species, has been widely studied as a source of plant growth-promoting bacteria in agricultural systems. These microorganisms contribute to plant performance through nutrient acquisition, phytohormone production, pathogen suppression, microbiome modulation, and enhanced tolerance to biotic and abiotic stresses. However, their ecological roles, functional plasticity, and genomic diversity remain poorly integrated into conceptual frameworks that extend beyond crop-based applications. Functional plasticity is reflected in their ability to colonize diverse plant hosts and tissues and to promote similar plant responses through distinct molecular mechanisms. Likewise, genomic diversity is evidenced by variation in accessory genomes, biosynthetic gene clusters, and regulatory networks that shape ecological functions and metabolite production. This review examines endophytic Bacillus as a model for understanding how metabolically versatile and genomically plastic bacteria establish functional, but context-dependent, associations with plants. Drawing on evidence from functional genomics, pangenomics, metabolomics, and microbial ecology, we discuss mechanisms associated with plant growth promotion and emphasize their dependence on host identity, environmental conditions, and microbial interactions. We address functional convergence arising from distinct genetic and metabolic routes, the contribution of accessory genomes and regulatory variation, and the ecological consequences of microbial inoculation in resident plant-associated microbiomes. We also highlight the limitations of in vitro screening approaches and the need for experimental validation across multiple biological scales to establish robust genotype-phenotype relationships. Finally, we extend the discussion beyond agricultural systems to consider the use of endophytic Bacillus in wild plant systems and ecological restoration, emphasizing the importance of evaluating both functional outcomes and ecological impacts.},
}

@article {pmid42525450,
year = {2026},
author = {Schöpf, F and Marongiu, GL and Roderer, D},
title = {The role of adhesins of Fusobacterium nucleatum in colorectal cancer - a structural perspective.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2709265},
doi = {10.1080/19490976.2026.2709265},
pmid = {42525450},
issn = {1949-0984},
mesh = {Humans ; *Fusobacterium nucleatum/metabolism/chemistry/genetics/physiology/pathogenicity ; *Colorectal Neoplasms/microbiology/pathology ; *Adhesins, Bacterial/metabolism/chemistry/genetics ; Host-Pathogen Interactions ; *Fusobacterium Infections/microbiology ; },
abstract = {Fusobacterium nucleatum is frequently found in the colon microbiome of colorectal cancer (CRC) patients. The bacterium is not only a passive bystander of CRC, but is actively involved in disease progression through mediating tumor growth stimulation, metastasis, and immune evasion. These outcomes are achieved through the action of several adhesins that are located on the outer membrane surface of F. nucleatum, which bind to different receptors on tumor or immune cells. Adhesin-receptor interaction as the initial step of host-pathogen interaction then triggers signal transduction pathways responsible for uncontrolled cell growth or downregulation of immune cells. For a number of CRC-relevant adhesins of F. nucleatum (FadA, Fap2, CbpF), the receptors have been known already for several years, but only recently mechanistic details have been elucidated through the determination of high-resolution structures of the complexes. In the case of other adhesins (RadD, Aim1), receptors have only recently been identified, or are as of yet unknown, and the mechanistic details underlying the interaction remain enigmatic. Here, we review the relevance of particular F. nucleatum adhesins in CRC progression, with a focus on recent mechanistic insights derived from structural biology.},
}

Humans
*Fusobacterium nucleatum/metabolism/chemistry/genetics/physiology/pathogenicity
*Colorectal Neoplasms/microbiology/pathology
*Adhesins, Bacterial/metabolism/chemistry/genetics
Host-Pathogen Interactions
*Fusobacterium Infections/microbiology

@article {pmid42525582,
year = {2026},
author = {Wertz, PW and Fluhr, JW},
title = {Ceramides and the Defective Barrier in Atopic Dermatitis.},
journal = {Skin pharmacology and physiology},
volume = {},
number = {},
pages = {1},
doi = {10.1159/spp/aetag001},
pmid = {42525582},
issn = {1660-5535},
abstract = {BACKGROUND: Atopic dermatitis (AD) is a common remitting-relapsing inflammatory skin disease characterized by eczematous lesions, xerosis and pruritis. It is associated with a defective permeability barrier and increased susceptibility to Staphylococcus aureus colonization. It has been demonstrated that the abrogated epidermal barrier is related to a decreased mass of ceramides and long-chain fatty acids in the stratum corneum (SC).

SUMMARY: A defective permeability barrier of the SC is the primary defect in AD. This defect reflects a reduction of ceramide and fatty acid mass in the SC due to reduced glucocerebrosidase and acid sphingomyelinase activity and a shift in fatty acid synthesis from long-chain to short-chain fatty acids and the incorporation of these shorter fatty acids into ceramides. Topically applied ceramides can restore epidermal function to a damaged barrier. Ceramide-containing moisturizers have produced partial restoration of the barrier function in AD by influencing lipid organization.

KEY MESSAGE: Correcting the barrier defect by topically supplied ceramides and long-chain fatty acids in sufficient amounts could contribute to restoration of the microbiome and decreasing irritation and pruritis.},
}

@article {pmid42525820,
year = {2026},
author = {Von, KY and Lim, L and Ab Majid, AH},
title = {Midgut microbiota profiling of Blattella germanica (Blattodea: Ectobiidae).},
journal = {Journal of insect science (Online)},
volume = {26},
number = {4},
pages = {},
doi = {10.1093/jisesa/ieag074},
pmid = {42525820},
issn = {1536-2442},
support = {R504-LR-GAL007-0000001030-E136//Industry Research/ ; },
mesh = {Animals ; RNA, Ribosomal, 16S/analysis ; *Blattellidae/microbiology/growth & development ; *Gastrointestinal Microbiome ; Bacteria/classification/genetics ; Male ; Female ; RNA, Bacterial/analysis ; },
abstract = {A detailed understanding of the core microbiome in Blattella germanica is essential for clarifying host-symbiont interactions. Although factors such as diet, developmental stage, and environmental conditions influence cockroach gut microbial communities, their combined effects remain poorly understood. Moreover, most studies rely on whole-gut homogenates, leaving the midgut microbiota largely uncharacterized. Hence, 16S rRNA gene amplicon sequencing was used to characterize and compare the midgut bacterial community structure from 28 samples (including 1 negative control), considering the factors of developmental stage, sex, physiological status, and environmental origin. Microbial community profiling revealed 923 unique genera corresponding to 505 families, 306 orders, 137 classes, and 47 phyla. Bacterial communities belonging to the families Lactobacillaceae, Desulfovibrionaceae, Lachnospiraceae, Dysgonomonadaceae, Christensenellaceae, and Rikenellaceae were consistently present across all treatment groups. Alpha diversity analysis showed significant differences in Shannon diversity, while Simpson and Chao1 diversity indices showed no significant variation. Beta diversity analysis based on UniFrac distances revealed significant differences in microbial community composition across experimental conditions, with stronger separation observed when considering taxa abundance. PERMANOVA indicated that both physiological status and environmental origin significantly shaped community structure, while host sex and developmental stage showed significant effects only in weighted UniFrac distance. Family-level and prevalence analyses consistently demonstrated greater similarity between laboratory-fed and starved groups, whereas field-collected samples exhibited a more distinct and less shared taxonomic profile. Overall, these findings advance current understanding of compartment-specific gut microbiota and underscore the ecological stability of microbiome taxa under diverse conditions.},
}

Animals
RNA, Ribosomal, 16S/analysis
*Blattellidae/microbiology/growth & development
*Gastrointestinal Microbiome
Bacteria/classification/genetics
Male
Female
RNA, Bacterial/analysis

@article {pmid42526180,
year = {2026},
author = {Serna, G and Obón-Santacana, M and Baraibar, I and Moratalla-Navarro, F and Napoli, S and Ruiz-Pace, F and Mulet, N and Guinó, E and Alonso, L and Boleda, L and Garcia, A and Vidal, J and Iglesias, M and Aguilera, L and Landolfi, S and Fernández Montes, A and Lopez Vega, ML and Cuatrecasas, M and Lopez-Prades, S and Gardeazabal, I and López López, C and Cagigal Cobo, ML and González-Flores, E and Lopez-Hidalgo, JL and García Alfonso, P and Ortega, L and Roselló, S and Tarazona, N and Comas Navarro, R and Bambaren, C and Arregui, D and Fasani, R and Gallego, P and Jimenez, J and Santiago, A and Aguilera, M and Colldeforns, B and Bayó, N and Tabernero, J and Élez, E and Moreno, V and Nuciforo, P},
title = {Intratumoral Fusobacterium species and survival in resectable colorectal cancer: a multicenter cohort study.},
journal = {ESMO open},
volume = {11},
number = {8},
pages = {108342},
doi = {10.1016/j.esmoop.2026.108342},
pmid = {42526180},
issn = {2059-7029},
abstract = {BACKGROUND: Despite standard-of-care treatment, a substantial proportion of patients with resectable colorectal cancer (CRC) relapse. We investigated the impact of surgical and postsurgical Fusobacterium spp. detection as a prognostic biomarker in stage I to III CRC from a national multicenter ambispective observational study.

PATIENTS AND METHODS: Patients with stage I to III CRC were enrolled at nine referral centers. Intratumoral Fusobacterium spp. was centrally detected using RNA in situ hybridization in surgical tumor samples. Correlations were analyzed between intratumoral Fusobacterium spp. and outcomes [recurrence-free survival (RFS), disease-free survival (DFS), CRC-specific survival (CRC-SS), and overall survival (OS)]. As an exploratory aim, Fusobacteriumnucleatum clearance in stool at follow-up using quantitative PCR was investigated.

RESULTS: Among 740 assessable patients (median age 61 years; 63% men), 21% had detectable intratumoral Fusobacterium spp. (classified as Fusobacterium-positive tumors). Fusobacterium spp. positivity was more common in right-sided, high-grade tumors with venous, lymphatic, and perineural invasion (VELIPI) and was associated with reduced immune infiltration. At a median follow-up of 48.6 months, Fusobacterium spp. positivity was independently associated with shorter RFS [hazard ratio (HR) 1.87, 95% confidence interval (CI) 1.23-2.84, P = 0.003] and DFS (HR 1.84, 95% CI 1.27-2.70, P = 0.001) but not with CRC-SS (HR 1.39, 95% CI 0.72-2.70, P = 0.321) or OS (HR 1.51, 95% CI 0.91-2.50, P = 0.113) in fully adjusted multivariate models. Adjuvant chemotherapy (ACT) significantly improved DFS in Fusobacterium-negative patients (HR 0.38, 95% CI 0.20-0.74, P = 0.004), but not in Fusobacterium-positive patients (HR 0.68, 95% CI 0.25-1.8, P = 0.44). Post-operative Fusobacteriumnucleatum positivity in stool during follow-up was detectable up to 3 years before recurrence and associated with an increased risk of relapse (odds ratio 61.0, 95% CI 2.3-1652, P = 0.01).

CONCLUSIONS: The presence of Fusobacterium spp. identifies a subset of patients with CRC with aggressive biology, immune suppression, and reduced benefit to ACT. Testing for Fusobacterium spp. in tumors and stool may support precision oncology approaches to guide treatment decision making and post-operative surveillance strategies.},
}

@article {pmid42526286,
year = {2026},
author = {Tito Tadeo, RY},
title = {Comment on: "Glucose metabolism's impact on Blastocystis presence in the human gut".},
journal = {Clinical nutrition (Edinburgh, Scotland)},
volume = {64},
number = {},
pages = {106736},
doi = {10.1016/j.clnu.2026.106736},
pmid = {42526286},
issn = {1532-1983},
}

@article {pmid42526339,
year = {2026},
author = {Teng, Y and Zhu, K and Fang, K and Verma, KK and Chang, X and Huang, Z and Liu, Y},
title = {Host genotype modulates melatonin-associated drought resilience in citrus accompanied by rhizosphere microbiome restructuring.},
journal = {Plant physiology and biochemistry : PPB},
volume = {238},
number = {},
pages = {111587},
doi = {10.1016/j.plaphy.2026.111587},
pmid = {42526339},
issn = {1873-2690},
abstract = {Exogenous melatonin (MT) has emerged as a potent biostimulant for mitigating plant drought stress; however, whether its efficacy depends on the host genetic background to orchestrate rhizosphere microbiome assembly remains unclear. Here, we integrated plant physiological traits, soil biochemical properties, and amplicon sequencing to decipher the genotype-dependent responses of drought-tolerant (DR) and drought-sensitive (DS) citrus cultivars to MT application under water deficit. While MT alleviated oxidative damage and growth inhibition in both genotypes, the DR cultivar exhibited a superior, system-level resilience characterized by a profound enhancement of rhizosphere fertility and microbial biomass. Co-occurrence network analysis showed that MT treatment was associated with marked topological reorganization in the DR rhizosphere, including increased bacterial modularity and fungal connectivity, whereas such changes were comparatively limited in the DS cultivar. Furthermore, Random Forest models and Mantel tests identified divergent patterns of candidate bacterial taxa associated with plant and soil traits. The DR genotype showed a relative enrichment of Paenibacillus and Rugosimonospora, which were strongly associated with soil nutrient-related indicators and microbial biomass. In contrast, the DS genotype showed a relative enrichment of Sphingobacterium, which was more closely associated with host antioxidant-related traits than with soil nutrient-related indicators. Collectively, our findings provide correlative evidence that melatonin-associated drought resilience co-occurs with coordinated changes in host physiological traits and rhizosphere microbiome properties, and that these associations vary with host genotype. This study provides preliminary insights into genotype-dependent plant-microbiome associations under biostimulant application and suggests that host genetic background should be considered when evaluating rhizosphere responses to exogenous agents.},
}

@article {pmid42526436,
year = {2026},
author = {Fang, Q and Schneider, KM},
title = {Bile acids in cancer: From metabolism to immunomodulation.},
journal = {Immunity},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.immuni.2026.07.003},
pmid = {42526436},
issn = {1097-4180},
abstract = {Bile acids have emerged as compartmentalized immunometabolic signals that link host metabolism, microbial ecology, and tumor immunity. Altered bile acid profiles are common across malignancies and are associated with tumor progression, immune tone, and responsiveness to immunotherapy. Bile acids shape the gut microbiota, and in turn, microbial enzymes diversify the bile acid pool, generating distinct bile acid species that can remodel the tumor immune landscape. Depending on species identity, concentration, and context, bile acids can support immune surveillance or enforce immune escape by reshaping antigen priming, lymphocyte fitness, myeloid suppression, and immune cell trafficking. Here, we synthesize emerging concepts defining a microbiome-bile acid-immune axis in cancer and highlight therapeutic opportunities to harness bile acid signaling as next-generation strategies in oncology.},
}

@article {pmid42526445,
year = {2026},
author = {Mallard de La Varende, AL and Tian, AL and Thomas, S and Lahmar, I and Messaoudene, M and Li, S and Motiño, O and Guillaume-Dit-Taunière, H and Iebba, V and Hurtado, Y and Pham, TN and Thélémaque, C and Araujo-Voces, M and Suissa, D and Ly, P and Reich, E and Vitali, G and Arlunno, BT and Durand, S and Aprahamian, F and Leduc, M and Forveille, S and Kepp, O and de la Calle-Fabregat, C and Schippers, A and Wagner, N and Fournier, PE and Honda, K and Marmorino, F and Cremolini, C and Maleki Vareki, S and Lenehan, JG and Marabelle, A and Danlos, FX and Deligne, M and Truntzer, C and Ghiringhelli, F and Ree, AH and Bousquet, PA and Meltzer, S and Ginhoux, F and Rummel, D and Fu, Y and Quinn, RA and Alves Costa Silva, C and Iacovelli, R and Ciccarese, C and Porcari, S and Elkrief, A and Routy, B and Ianiro, G and Derosa, L and Kroemer, G and Fidelle, M and Zitvogel, L},
title = {Subclinical cholestasis is a hallmark of gut dysbiosis causing resistance to cancer immunotherapy.},
journal = {Cancer cell},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ccell.2026.06.022},
pmid = {42526445},
issn = {1878-3686},
abstract = {Gut dysbiosis compromises cancer immunosurveillance by downregulating ileal mucosal addressin cell adhesion molecule 1 (MAdCAM-1), but the metabolic landscape associated with gut dysbiosis remains elusive. Here, we show that antibiotics (ABX) or ABX-associated Enterocloster species lead to the loss of secondary bile acids (BAs) including deoxycholic acid (DCA) and the accumulation of tauro-conjugated primary BAs (tauro-chenodeoxycholic acid [TCDCA] and tauro-β-muricholic acid [T-βMCA]) from the alternative pathway in the plasma of patients and mice. Fecal microbial transplantation (FMT), the ileum-specific farnesoid X receptor (FXR) agonist fexaramine, or glycodeoxycholic acid (GDCA) compensated dysbiosis-associated BA abnormalities and circumvent primary resistance to PD-1 blockade. GDCA curtailed ABX-induced MAdCAM-1 downregulation and T cell exhaustion in tumors. Subclinical cholestasis defined by elevation of γ-glutamyl transferase (γGT) correlated with increased TCDCA and decreased soluble MAdCAM-1 in plasma and predicted poor survival in multivariate analyses in six cohorts of patients who received immunotherapy. Hence, subclinical cholestasis accompanies gut dysbiosis, paving the way to immunoresistance.},
}

@article {pmid42526595,
year = {2026},
author = {Ding, X and Du, J and Wang, Z and Lu, L and Fan, S},
title = {Taurine mitigates intestinal injury and spatial memory deficits induced by high-fat diet and abdominal irradiation.},
journal = {Life sciences},
volume = {},
number = {},
pages = {124604},
doi = {10.1016/j.lfs.2026.124604},
pmid = {42526595},
issn = {1879-0631},
abstract = {Combined metabolic dysfunction and ionizing radiation produce multifactorial systemic harm, challenging organismal homeostasis and cognitive function. Here, we define a new role for dietary taurine (Tau) protection against combined high-fat diet (HFD) and whole-abdominal irradiation (WAI) stress. In a two-sex murine model, we show that Tau intervention blocks metabolic organ damage and severe structural enteropathy. Histological analyses indicate that Tau preserves the intestinal mucosal barrier, which is accompanied by the restoration of Mucin 2 (MUC2) expression. Furthermore, 16S rRNA sequencing showed that Tau reshapes gut dysbiosis, increasing the relative abundance of the mucin-degrading bacterium Akkermansia muciniphila, which may potentially contribute to mucosal homeostasis. Coincident with the stabilization of this mucin-microbiome interface, we observed that Tau attenuates systemic endotoxemia and reduces inflammatory extracellular vesicle transmission of the gut-brain axis. Consequently, this reduced peripheral inflammation preserves hippocampal dentate gyrus (DG) architecture and ameliorates spatial memory deficit. Importantly, while this microbiome-gut-brain protection is similar in both sexes, systemic immune responses are strikingly sexually dimorphic, mandating a sex-stratified therapeutic approach. Together, these studies reveal a potential microbiome-associated link in Tau-induced systemic resilience, providing a translatable nutritional strategy against combined radiotoxic and metabolic disorders.},
}

@article {pmid42526737,
year = {2026},
author = {Neves, LBM and Domingues, D and Baldessarini, BL and Laino, P and Lima, BC},
title = {Cannabinoid receptor-mediated modulation of the gut-brain axis under chronic stress: Neuroinflammatory mechanisms, microbial metabolites, and sexual dimorphism.},
journal = {Progress in neuro-psychopharmacology & biological psychiatry},
volume = {},
number = {},
pages = {111860},
doi = {10.1016/j.pnpbp.2026.111860},
pmid = {42526737},
issn = {1878-4216},
abstract = {Chronic stress disrupts the gut-brain axis (GBA) through coordinated dysfunction of the intestinal barrier and of the vascular interfaces that protect the brain, fostering a neuroinflammatory state implicated in mood disorders, neuropsychiatric conditions, and chronic pain. This narrative review synthesizes evidence across five domains. First, the inflammatory cascade by which stress-induced disruption of the epithelial and gut vascular barriers activates the NLRP3 inflammasome and sustains central neuroinflammation. Second, microbial metabolites, namely short-chain fatty acids (SCFAs), tryptophan-kynurenine products, and indole derivatives, as modulators of gut-brain homeostasis. Third, the gut microbiome-endocannabinoidome axis, including the capacity of commensal bacteria to generate endocannabinoid-like N-acyl amides that engage host receptors. Fourth, the receptor-specific pharmacology of phytocannabinoids, distinguishing Δ9-tetrahydrocannabinol (THC), which acts principally at CB1 and CB2 with comparable affinity, from cannabidiol (CBD), which has low affinity for these receptors and signals mainly through TRPV1, TRPA1, GPR55, PPARs, and 5-HT1A. Fifth, sexual dimorphism in barrier vulnerability and treatment response. In rodent models, chronic stress reduces intestinal and blood-brain barrier tight junction expression, elevates circulating lipopolysaccharide, and activates the NLRP3 inflammasome, while tryptophan metabolism shifts toward neurotoxic kynurenine products. Cannabinoid modulation of the kynurenine pathway and cannabinoid-mediated restoration of blood-brain barrier integrity remain mechanistic hypotheses extrapolated from indirect evidence rather than demonstrated mechanisms in chronic psychological stress paradigms. Human data are largely limited to small trials of microbiota-targeted interventions and of CBD in anxiety, and to observational endocannabinoidome-microbiome studies. These observations provide a preclinical rationale for GBA-targeted pharmacological strategies, with translational claims explicitly separated from mechanistic plausibility.},
}

@article {pmid42526766,
year = {2026},
author = {Wijen, A and von Wintersdorff, C and Lijnen, A and Savelkoul, P},
title = {Comparison of human DNA depletion and bacterial enrichment methods from large blood volumes to improve bloodstream infection diagnosis.},
journal = {Journal of microbiological methods},
volume = {},
number = {},
pages = {107644},
doi = {10.1016/j.mimet.2026.107644},
pmid = {42526766},
issn = {1872-8359},
abstract = {Culture-independent methods have the potential to improve diagnosis of bloodstream infections by directly identifying microorganisms from whole blood without the need for culture. However, performance is limited by abundant human DNA, inhibitory components, and low concentrations of circulating microorganisms. Human DNA depletion and bacterial enrichment methods may overcome these challenges by selectively lysing human cells or by directly isolating bacteria, enabling the use of larger blood volumes. We compared three manual methods processing up to 10 mL of whole blood: Polaris and Ultra Deep Microbiome Prep10 deplete human DNA through chemical lysis, and SwiftX Sepsis enriches bacteria through paramagnetic-base extraction. Whole blood samples were spiked with Klebsiella pneumoniae and Staphylococcus aureus at concentrations ~1000, 100, 10 and 1 CFU/mL blood. Bacterial recovery and human DNA depletion were measured by quantitative real-time PCR. Resulting Cq values were converted to genome equivalents per mL blood using a defined formula. Polaris and Ultra Deep outperformed SwiftX for recovery of S. aureus, with Polaris generally yielding better results than Ultra Deep. For K. pneumoniae, Polaris recovered the highest bacterial amounts and significantly outperformed SwiftX at the three highest concentrations, while Ultra Deep showed no significant differences compared with the other methods. Ultra Deep achieved greatest depletion of human DNA. Polaris and SwiftX had similar processing times, whereas Ultra Deep took 1.5× longer. In conclusion, Polaris demonstrated the highest overall bacterial recovery. These methods may improve culture-independent bloodstream infection diagnostics by enabling the processing of larger blood volumes, comparable to those used in routine blood cultures.},
}

@article {pmid42526964,
year = {2026},
author = {Vilhem, S},
title = {["Disorganizing" psychiatry: from the search for a target organ to welcoming the person-in-their-world].},
journal = {Soins; la revue de reference infirmiere},
volume = {71},
number = {907},
pages = {60-64},
doi = {10.1016/j.soin.2026.06.019},
pmid = {42526964},
issn = {0038-0814},
mesh = {Humans ; *Psychiatry/trends ; },
abstract = {Contemporary psychiatric research tends to center on the brain. Faced with its own dead ends, it also seeks leads in genes, the microbiome, and the search for biomarkers. This headlong rush reveals a fundamental difficulty in identifying, naming, and defining what the discipline actually treats. This article proposes to "disorganize" psychiatry-that is, to halt the search for the single organ it has never had-and to rebuild it around its true object: the person, within their environment, embedded in their history, and in the history of their environments. The aim is to promote a psychiatry that welcomes rather than one that targets.},
}

Humans
*Psychiatry/trends

@article {pmid42166402,
year = {2026},
author = {Peta Martinez, NA and Reinoso Arnaldi, M and Santiago-Rodriguez, TM and Rodriguez-Fernandez, IA},
title = {Microbiota-Based Interventions Differentially Rescue Gut and Social Behavior Phenotypes in <italic>Drosophila</italic> with Kdm5 Deficiency.},
journal = {Developmental neuroscience},
volume = {},
number = {},
pages = {1-21},
pmid = {42166402},
issn = {1421-9859},
abstract = {INTRODUCTION: Autism spectrum disorder (ASD) is a lifelong neurological and developmental disorder that is often accompanied by gastrointestinal (GI) issues. The bidirectional communication system known as the gut microbiota-brain axis may help explain how GI dysfunction contributes to neurological symptoms. Loss-of-function mutations in the histone demethylases KDM5A, KDM5B, or KDM5C are found in patients with intellectual disability and ASD. Here, we use a genetically tractable Drosophila model of loss-of-function of the ASD-associated chromatin regulator Kdm5 to investigate how host genetic disruption influences gut microbial composition and social behavior. Previous studies using a Drosophila Kdm5 loss-of-function (Kdm5LOF) revealed gut microbial dysbiosis, reduced abundance of Lactiplantibacillus plantarum, and impaired social behavior. While L. plantarum supplementation rescued intestinal abnormalities, it did not restore social behavior.

METHODS: We evaluated multiple microbiota-based interventions, including probiotic supplementation with L. plantarum, Lactobacillus helveticus, their combination, and fecal microbiota transplantation (FMT), to determine their capacity to modulate gut microbial composition and behavior in adult Kdm5LOF flies. Gut bacterial abundance was quantified using colony-forming unit assays and full-length 16S rRNA gene sequencing. Social behavior was assessed using the social distance assay, while anxiety-like behavior and locomotion were evaluated using the open field test. Gut-specific Kdm5 knockdown was used to assess tissue-specific contributions to microbiota and behavioral phenotypes.

RESULTS: Kdm5 deficiency resulted in reduced abundance of culturable Lactobacillus, Acetobacter, and Enterobacter species, accompanied by impaired social behavior. L. plantarum supplementation restored gut microbial abundance in both whole-body Kdm5LOF and gut-specific Kdm5 knockdown models but did not significantly rescue social behavior. In contrast, L. helveticus significantly improved social interaction in Kdm5LOF flies despite minimal effects on gut bacterial abundance, revealing a dissociation between microbial restoration and behavioral outcomes. Gut-specific Kdm5 knockdown phenocopied both microbial and social defects observed in Kdm5LOF mutants. Notably, FMT from healthy donors partially restored Lactobacillus abundance, reshaped gut microbial community structure, and partially improved social behavior in Kdm5LOF recipient flies.

CONCLUSION: Together, these findings identify Kdm5 as a key regulator of gut microbial viability and social behavior and demonstrate that microbiota-based interventions exert strain- and phenotype-specific effects. Our results reveal that restoration of microbial abundance alone is insufficient to rescue social behavior and highlight the importance of functional host-microbe interactions in gut-brain communication. This work establishes Drosophila as a tractable platform for dissecting epigenetic regulation of microbiota-behavior relationships in the context of disruption of an ASD-associated gene and for studying microbiota-based modulation of host physiology and behavior. All experiments were conducted in adult flies, and thus, these findings reflect post-developmental effects of Kdm5 disruption.},
}

@article {pmid42509250,
year = {2026},
author = {Higashikawa, F and Kanno, K},
title = {Individual variability in hydrogen-producing microbes influences the response to hydrogen supplementation on sleep quality: a randomized, double-blind, placebo-controlled, parallel study.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {42509250},
issn = {2045-2322},
support = {No number//Shinryo Corporation (Fukuoka, Japan)/ ; },
abstract = {Hydrogen has been reported to exert antioxidant and anti-inflammatory effects, and its potential health benefits have been investigated. However, to our knowledge, evidence regarding its impact on sleep quality in healthy individuals remains extremely limited. In addition, the influence of inter-individual variability in the gut microbiota on hydrogen efficacy has seldom been studied. In this study, we aimed to assess the impact of hydrogen-rich jelly on sleep quality and examine the influence of gut microbiota on this effect. A total of 44 healthy adults with poor sleep quality were randomized to receive either hydrogen-rich jelly or placebo jelly. No significant differences were observed between the intervention groups in the changes in sleep-related outcomes, including OSA-MA, VAS, PSQI, and STAI scores, in the overall analysis. Notably, when participants were stratified by the mean change in the VAS score for sleep quality, gut microbiota β-diversity showed apparent clustering in the hydrogen group but not in the placebo group. This cluster was explained by the differences in the relative abundance of hydrogen-producing bacteria, such as Bacteroides. Linear mixed-effects model analyses revealed significant interaction effects in the group × H2-producers in the VAS for sleep quality and mental stress, with greater improvement in participants with a lower abundance of hydrogen-producing bacteria. In conclusion, these exploratory findings raise the hypothesis that baseline gut microbiota composition, particularly microbial hydrogen-producing capacity, may modify individual responses to hydrogen supplementation. This hypothesis warrants confirmation in larger studies to explore its implications for microbiome-informed stratification in future hydrogen intervention research.Clinical trial registration: This clinical trial was registered with the University Hospital Medical Information Network Clinical Trial Registry on 27/12/2023 (UMIN-CTR, UMIN000053237).},
}

@article {pmid42509270,
year = {2026},
author = {Chettry, V and Kumar, R and Testa, R},
title = {Biodiversity and natural capital in ecologically sensitive regions.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {42509270},
issn = {2045-2322},
abstract = {Biodiversity and natural capital support economic systems, human well-being and climate resilience. Yet conservation and planning have focused mainly on visible ecosystems such as forests, wetlands and agricultural landscapes, while overlooking belowground biodiversity and the complex interactions between rural and rapidly urbanizing regions. This Collection analyses species, community and microbiome responses to environmental gradients, management interventions and climate constraints, and the effects of these responses on productivity, habitat quality, ecosystem functioning and natural capital. Several contributions highlight that climate-adapted seed sourcing in grand fir can maintain forest growth and carbon sequestration under changing moisture regimes, and that diverse multi-crops in boreal conditions raise biomass and net energy yields while lowering environmental pressures. Other studies introduce integrated indicators such as habitat quality indices for wetland waterfowl, soil functional networks in shaded coffee systems centred on total organic carbon, and multidimensional niche assessments for zooplankton communities. Together, these papers demonstrate complementary approaches for treating biodiversity as natural capital and for sustaining the ecosystem services that support human well-being, sustainable production and informed conservation and management decisions.},
}

@article {pmid42509322,
year = {2026},
author = {Connors, BM and Thompson, J and Gangan, MS and Quinn-Bohmann, N and Gibbons, SM and Grant, J and Castellanos-Sanchez, A and McCann, JR and Rawls, JF and Venturelli, OS},
title = {Designing fiber-gut microbiome interactions with active learning.},
journal = {Nature chemical biology},
volume = {},
number = {},
pages = {},
pmid = {42509322},
issn = {1552-4469},
support = {R01EB030340//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; R01EB030340//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; R01EB030340//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; R35GM124774//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; R01DK133468//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; R01DK133468//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; R35GM124774//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; R35GM124774//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; W911NF-19-1-0269//United States Department of Defense | United States Army | U.S. Army Research, Development and Engineering Command | Army Research Office (ARO)/ ; W911NF-19-1-0269//United States Department of Defense | United States Army | U.S. Army Research, Development and Engineering Command | Army Research Office (ARO)/ ; },
abstract = {Identifying synergies between dietary fibers and beneficial bacteria holds promise for precision interventions that optimize gut health, yet these interactions remain largely unexplored. Here we integrate machine learning, Bayesian optimization and high-throughput community construction to investigate how dietary fibers shape health-relevant functions of human gut microbial communities. To efficiently navigate the landscape of fiber-microbiome interactions, we implemented a design-test-learn cycle to identify fiber-species combinations that maximize a multiobjective function capturing beneficial community properties. Our model-guided approach revealed a highly butyrogenic and robust ecological motif characterized by the copresence of inulin, Bacteroides uniformis and Anaerostipes caccae and a higher-order interaction with Prevotella copri. Human fecal communities invaded with model-designed species-fiber combinations displayed predictable gut-beneficial outputs. In sum, we demonstrate a framework for designing synthetic microbial communities with desired functions in response to key nutrients.},
}

@article {pmid42509323,
year = {2026},
author = {Spazzapan, M and Raison, N and Steves, C and Sahai, A},
title = {The urinary microbiome, overactive bladder and bladder pain syndrome/interstitial cystitis - mechanisms, diagnostics and therapeutic opportunities.},
journal = {Nature reviews. Urology},
volume = {},
number = {},
pages = {},
pmid = {42509323},
issn = {1759-4820},
abstract = {Overactive bladder and bladder pain syndrome/interstitial cystitis are prevalent, multifactorial disorders with poorly understood pathophysiology. The discovery of the urinary microbiome has overturned the sterile urine paradigm and created new opportunities for mechanistic and translational research. Increasing evidence suggests that bladder microbial communities are associated with urothelial signalling, immune tone and neural pathways that influence urgency, pain and treatment response. In overactive bladder, Lactobacillus-predominant profiles are associated with lower symptom burden and improved response to pharmacotherapy, whereas Gardnerella-enriched and Pseudomonadota-enriched communities positively correlate with refractory disease. In bladder pain syndrome/interstitial cystitis, microbial alterations are not based on a single pathogenic signature but converge on metabolic and immune dysregulation. Multi-omics studies integrating metagenomics, metabolomics and host immune data are beginning to define functional pathways linking microbial metabolites, epithelial barrier function and nociceptor sensitization. Results from emerging clinical trials suggest that urinary microbiome profiling might enable patient stratification and inform treatment selection, whereas interventions, such as probiotics, oestrogen therapy or dietary modulation, hold potential as adjunctive strategies. Together, these advances position the urinary microbiome as a promising contributor to lower urinary tract health and a potential target for precision urology, although the functional importance and causal role of the low-biomass urinary microbiome in disease remain crucial unresolved questions.},
}

@article {pmid42509522,
year = {2026},
author = {Chen, PY and Hsu, TW and Chiang, TY and Huang, CL},
title = {Comparative analysis of root microbiomes in four Swertia species from Taiwan.},
journal = {Journal of plant research},
volume = {},
number = {},
pages = {},
pmid = {42509522},
issn = {1618-0860},
support = {NSTC 103-2621-B-006-002-//National Science and Technology Council/ ; },
abstract = {Swertia (Gentianaceae) comprises four species endemic to Taiwan that possess significant medicinal potential. While root microbiomes are known to promote plant adaptation, the microbial ecology of Taiwanese Swertia remains largely unexplored. We investigated the rhizosphere and root endosphere microbiomes of these species using 16S rRNA gene sequencing and predictive functional profiling, integrated with host phylogenetic data. Our results revealed that rhizosphere bacterial communities were significantly more diverse than those in the root endosphere. PERMANOVA indicated that host species and plant compartment significantly influenced bacterial communities, but the high residual variance suggests that much of the community variation remains unexplained by the variables measured in this study. Phylogenetic analysis indicated that the root endosphere is more strongly influenced by host phylogeny, with closely related species harboring more similar communities. Functional profiling further demonstrated that the rhizosphere is predicted to be enriched in pathways related to nitrogen fixation and organic matter degradation, whereas the endosphere harbors bacterial taxa potentially associated with pathogen suppression. These findings underscore the multifaceted roles of the root microbiome in supporting the development, stress adaptation, and ecosystem sustainability of Swertia species in Taiwan's unique altitudinal gradients.},
}

@article {pmid42509593,
year = {2026},
author = {Woods, R and Jennings, EF and Smith, L and Almushri, K and Hanson, L and Gamrot, O and Adetunji, A and Oguanya, CV and Imongan, H and John, K and Omuluche, E and Harte, M and Murgatroyd, C},
title = {Effect of Prenatal and Postnatal Stress in Rats on the Gut Microbiome in Adolescence.},
journal = {Journal of neurochemistry},
volume = {170},
number = {7},
pages = {e70530},
pmid = {42509593},
issn = {1471-4159},
support = {BB/W017598/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; //Cancer Prevention Research Trust/ ; //Manchester Metropolitan University/ ; },
abstract = {Previous research suggests that early-life stress (ELS) increases the risk of mental health disorders later in life. It is hypothesised that ELS disrupts the developing gut microbiome, which in turn may alter neuroendocrine and immune system development, thereby increasing disease susceptibility. However, the specific microbial taxa and pathways mediating these effects remain poorly characterised. Here, we used rat models to investigate whether ELS leads to long-term alterations in the gut microbiome. Microbial composition was assessed using 16S rRNA Nanopore sequencing of DNA extracted from faecal pellets of adolescent male and female rats exposed to: (i) early postnatal dexamethasone (DEXA; a synthetic glucocorticoid) or saline control, (ii) prenatal stress (PRS) and controls, or (iii) postnatal stress (POS) and controls. Microbiome structure was evaluated using richness, evenness, dominance and diversity indices. We show that ELS induces model-specific and sex-dependent changes in gut microbiome composition, primarily at the level of overall community structure rather than individual taxa. DEXA exposure produced the most consistent compositional signature, particularly in males, whereas PRS showed minimal detectable effects and POS exhibited a more heterogeneous response characterised by increased dispersion and limited taxonomic shifts. More broadly, these findings demonstrate that integrating beta-diversity analyses with machine learning approaches can identify reproducible microbiome patterns associated with ELS, even in the absence of large taxonomic changes. Applying similar frameworks in larger and longitudinal cohorts will be important to determine how these subtle microbial signatures contribute to long-term physiological outcomes.},
}

@article {pmid42509729,
year = {2026},
author = {Kirillova, M and Dzhalilova, D and Zolotova, N and Kirillov, V and Ogneva, L and Kirillov, M and Portnova, T and Berlizeva, N and Fokichev, N and Makarova, O},
title = {Colon Histophysiological Features and Gut Microbiome in Tolerant and Susceptible to Oxygen Deficiency Wistar Rats After the Prolonged Intermittent Hypoxic Exposure.},
journal = {Biomolecules},
volume = {16},
number = {7},
pages = {},
doi = {10.3390/biom16070935},
pmid = {42509729},
issn = {2218-273X},
support = {25-25-00061//Russian Science Foundation/ ; },
abstract = {Systemic hypoxia influences the state of the intestinal epithelial barrier and the microbiome; however, the role of the initial tolerance of the organism to oxygen deficiency in the development of these changes remains poorly studied. The aim of the study was to evaluate the colon histophysiological features and the gut microbiome in rats that were tolerant and susceptible to hypoxia under intermittent hypoxic exposure of varying severity. In male Wistar rats, tolerance to oxygen deficiency was determined according to the Hif1a, Epas1, and Hif3a expression levels in peripheral blood leukocytes, after which they were subjected to intermittent hypoxic exposure at an "altitude" of 5000 m or 7000 m for 1 h daily for 21 days. Subsequently, the state of the intestinal epithelial barrier was assessed using histological, histochemical, and immunohistochemical methods, and the microbiota composition was analyzed by PCR. Under normoxic conditions, in comparison with rats that are tolerant to hypoxia, susceptible animals demonstrated a greater volume fraction of goblet cells and a low abundance of Parabacteroides spp. Intermittent hypoxic exposure induced multidirectional changes depending on the initial tolerance and the severity of the regimen. In tolerant-to-hypoxia animals, an increase in the goblet cells volume fraction was detected after the exposure at the 5000 m "altitude", while at an "altitude" of 7000 m, a decrease in the number of cells in the lamina propria of the mucosa and Clostridium perfringens gr. abundance, as well as a reduction in the Firmicutes/Bacteroidetes ratio, was observed. In susceptible-to-hypoxia animals, a higher abundance of Clostridium perfringens gr. in comparison with tolerant rats was revealed after the exposure at an "altitude" of 7000 m, with no structural changes in the intestinal wall. Thus, intermittent hypoxic exposure led to a rearrangement of the gut microbiome and the morphofunctional characteristics of the intestinal barrier, and the severity of these changes depended on the initial tolerance of the organism to oxygen deficiency and the severity of the hypoxic regime, which should be taken into account when conducting biomedical research.},
}

@article {pmid42509733,
year = {2026},
author = {Chou, YL and Lin, HJ and Hsu, YA and Lin, ES and Chen, CS and Tien, PT and Chen, JJ and Wu, MY and Chuang, CY and Wan, L},
title = {Vitamin D3 Reshapes Gut Microbiota and Metabolite Profiles in a Rat Model of Inflammation-Induced Myopia.},
journal = {Biomolecules},
volume = {16},
number = {7},
pages = {},
doi = {10.3390/biom16070939},
pmid = {42509733},
issn = {2218-273X},
support = {MOST107-2320-B-039-049-MY3//National Science and Technology Council, Taiwan/ ; 111-2314-B-039-054//National Science and Technology Council, Taiwan/ ; 111-2314-B-039-053-MY3//National Science and Technology Council, Taiwan/ ; NSTC-112-2314-B-039-029//National Science and Technology Council, Taiwan/ ; DMR-113-146//China Medical University Hospital, Taiwan/ ; DMR-112-223//China Medical University Hospital, Taiwan/ ; CMU112-MF-49//China Medical University, Taiwan/ ; TTCRD 111-14//Taichung Tzu Chi Hospital, Taiwan/ ; },
abstract = {Myopia is increasingly recognized as an inflammatory ocular disease. Vitamin D3 is a potential modulator of the gut-eye axis, but its role in inflammation-induced myopia remains unclear. This study investigated whether vitamin D3 supplementation attenuates myopia progression by regulating retinal inflammation, gut microbiota composition, and microbiota-derived metabolites in a TGF-β2-induced myopia model. Three-week-old Brown Norway rats received weekly periocular TGF-β2 injections with or without daily oral vitamin D3, and myopia development was evaluated on days 1 and 21 by axial length and refractive error. Cecal contents were analyzed for α- and β-diversity and taxonomic differences, and day-21 serum underwent untargeted metabolomic profiling of microbiota-derived metabolites, including bile acids and imidazole derivatives; Spearman correlation linked microbial or metabolic alterations with myopia progression. TGF-β2 induced axial elongation, myopic refractive shifts, and upregulated retinal pro-inflammatory cytokines (p-NFκB, IL-1β, TNF-α), while vitamin D3 supplementation markedly attenuated myopia progression and retinal inflammation. Cecal α-diversity did not differ among control, vitamin D3, TGF-β2, and TGF-β2+vitamin D3 groups, but vitamin D3 significantly reshaped β-diversity and reduced the Firmicutes/Bacteroidota ratio. Distinct metabolite profiles were observed, with the vitamin D3 group showing reduced hyodeoxycholic acid and elevated imidazole derivatives (imidazolepropionic and methylimidazoleacetic acids). Vitamin D3 supplementation attenuated myopia progression by reducing retinal inflammation and concurrently reshaping the gut microbiome and its metabolites compared to the control and myopic groups. These results underscore the potential of vitamin D3 to modulate the gut-retina axis as a nutritional approach for mitigating myopia development.},
}

@article {pmid42509738,
year = {2026},
author = {Wali, Z and Neha, and Shahwan, M and Dinislam, K and Shamsi, A and Anwar, S},
title = {Network Biology of Alzheimer's Disease and Related Neurodegenerative Disorders: Molecular Mechanisms and Therapeutic Strategies.},
journal = {Biomolecules},
volume = {16},
number = {7},
pages = {},
doi = {10.3390/biom16070944},
pmid = {42509738},
issn = {2218-273X},
support = {NA//Ajman University/ ; },
abstract = {The most persistent biomedical challenges of the 21st century are neurodegenerative disorders (NDs), where molecular alterations lead to devastating clinical consequences and progressive neuronal loss. The prevalence of neurodegeneration is continuously rising and becoming the main contributor to chronic disability and mortality. Despite their clinical differences, many conditions share pathogenic processes, including oxidative stress, protein misfolding and aggregation, mitochondrial dysfunction, and neuroinflammation. Instead of functioning independently, these processes cooperate to form a self-reinforcing network that gradually weakens synapses and ultimately leads to neuronal death. This study redefines neurodegeneration as a disorder of system-level failure by emphasizing poor cellular stress integration. In addition to demonstrating how gut microbiome gene networks impact inflammation and amyloid production, new research highlights the relationships between mitochondrial-lysosomal interactions, endoplasmic reticulum stress responses, and transcriptionally driven synaptic vulnerability. A key molecular topic is the interaction and pathogenic convergence of the JAK/STAT, HIF-1α, and Notch signaling pathways. Under ongoing metabolic stress, prolonged stimulation of this triad increases inflammation, hinders the regenerative processes, and maintains pseudo-hypoxic conditions, explaining why single-target treatments have mostly been unsuccessful. This review also explores progress in fluid, digital, and imaging biomarkers that facilitate early diagnosis and patient stratification, and assesses new disease-modifying approaches such as antisense oligonucleotides, immunomodulators, gene therapies, and small-molecular agents. Artificial intelligence is emphasized as an essential tool for integrating multimodal data, drug discovery and predictive modeling.},
}

@article {pmid42509759,
year = {2026},
author = {Miszczak, MM and Kłosowska-Buryło, K and Pieczyńska, JM and Bielecka, M and Prescha, A},
title = {Mulberry, Gut Microbiota and Gut Functionality: Effects Shaped by Raw Material and Processing Methods.},
journal = {Biomolecules},
volume = {16},
number = {7},
pages = {},
doi = {10.3390/biom16070965},
pmid = {42509759},
issn = {2218-273X},
abstract = {Mulberry species (Morus spp.) provide phytochemically distinct plant materials in which leaves are typically characterized by high levels of iminosugars (notably 1-deoxynojirimycin), flavonols/flavones, and polysaccharides, whereas fruits-especially Morus nigra-contain substantial amounts of anthocyanins alongside other phenolic compounds and polysaccharides. Importantly, the composition and biological properties of mulberry-derived products depend not only on species and plant part (leaf vs. fruit), but also on preparation and processing variables, including drying, maceration, fermentation, and extraction, or fractionation strategy (e.g., aqueous vs. hydroalcoholic extracts or enriched fractions). Such technological factors may substantially influence the chemical composition, bioavailability, and functionality of mulberry-derived preparations and thereby modify their interactions with gut microbiota and host metabolic processes. Available preclinical studies indicate that mulberry leaf- and fruit-derived preparations can affect gut microbial composition or activity in experimental models of metabolic dysfunction. Reported findings frequently include enrichment of microbial taxa commonly regarded as beneficial, such as Bifidobacterium, Lactobacillus, and Akkermansia, normalization of dysbiosis-associated microbial patterns, and increased production of short-chain fatty acids, particularly acetate, propionate, and butyrate. These microbial changes are sometimes observed alongside improvements in metabolic parameters such as glucose regulation, lipid profile, adiposity, or inflammatory markers. However, reported responses differ across plant parts, species, and preparation approaches, indicating that phytochemical composition and processing strategy are likely to influence biological outcomes. Interpretation of the current evidence is limited by the predominance of non-human studies and by incomplete or inconsistent reporting of extract composition, processing conditions, and standardization procedures. These factors reduce comparability between studies and complicate mechanistic interpretation of microbiome-related effects. Overall, existing preclinical data support the possibility that mulberry-derived preparations may influence metabolic health through microbiota-associated pathways shaped by both botanical origin and preparative technology. Well-designed human intervention studies using chemically characterized and standardized preparations, together with comprehensive gut microbiome analyses, are needed to determine the translational relevance of these observations and to identify which mulberry-derived preparations offer the greatest potential for supporting gut and metabolic health.},
}

@article {pmid42510534,
year = {2026},
author = {Chen, Y and Zhu, J and Gui, H and Liu, M and Zhang, Y and Wu, Z and Liu, C and Wang, M},
title = {Linking Gut Microbiota, Mitochondrial Redox Dysfunction, and Ferroptosis in Cardiometabolic Diseases: A Narrative Review of Mechanistic Evidence and Redox-Targeted Interventions.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {15},
number = {7},
pages = {},
doi = {10.3390/antiox15070803},
pmid = {42510534},
issn = {2076-3921},
abstract = {Cardiometabolic diseases are increasingly understood as disorders involving compartment-specific redox disruption rather than a uniform excess of reactive oxygen species. This narrative review synthesizes evidence for a proposed gut microbiota-mitochondria ferroptosis framework in which dysbiosis-derived lipopolysaccharide, trimethylamine N-oxide, short-chain fatty acids, bile acids, and tryptophan metabolites may modulate mitochondrial reactive species production, antioxidant defenses, iron handling, lipid peroxide detoxification, and inflammatory signaling. The reference set was assembled through searches of PubMed and Web of Science Core Collection, supplemented by targeted Google Scholar searches and citation chaining during manuscript preparation and revision through June 2026 and was organized around microbial metabolites, mitochondrial redox biology, ferroptosis pathways, disease-specific evidence, and redox-targeted interventions. Because this is a narrative synthesis rather than a systematic review, the framework should be interpreted as hypothesis-generating rather than as a systematically validated pathological model. Across atherosclerosis, diabetic cardiomyopathy, metabolic dysfunction-associated steatotic liver disease, obesity-associated insulin resistance, chronic kidney disease, and cardiorenal metabolic injury, the most consistent mechanistic links involve mtROS, impaired mitophagy, glutathione/GPX4 and SLC7A11 dysfunction, ACSL4-dependent lipid peroxidation, Nrf2 signaling, NLRP3 activation, and cGAS-STING-associated inflammation, although human causal evidence remains uneven. Importantly, much of the current literature supports local links within this sequence rather than a fully verified dysbiosis-metabolite-mitochondria ferroptosis-organ dysfunction chain in the same study. We therefore emphasize evidence tiers, terminology discipline, and biomarker requirements when interpreting ferroptosis-sensitive injury. Polyphenols, flavonoids, probiotics, postbiotics, melatonin, CoQ10-related strategies, mitochondria-targeted antioxidants, and ferroptosis-sensitive approaches may be most translatable when paired with microbiome, metabolomic, lipidomic, pharmacokinetic, and redox biomarkers.},
}

@article {pmid42510544,
year = {2026},
author = {Song, J and Kong, G and Wang, X and Zhai, Y and Wang, J and Xu, J and Li, C and Liu, W and Han, Y and Han, Z},
title = {Dietary Hydroxy-Selenomethionine Improves Antioxidant Status and Reduces Somatic Cell Count in Dairy Cows: Multi-Omics Insights into Rumen Microbiota and Metabolic Profiles.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {15},
number = {7},
pages = {},
doi = {10.3390/antiox15070813},
pmid = {42510544},
issn = {2076-3921},
abstract = {High-yielding dairy cows are highly susceptible to lactational oxidative stress, which compromises mammary barrier integrity and elevates mastitis risk. This study investigated the potential biological mechanisms by which dietary hydroxy-selenomethionine (HMSeBA) alleviates oxidative stress and improves health in dairy cows. Forty Holstein cows were assigned to a basal control group (0.32 mg Se/kg DM) or an HMSeBA-supplemented group (0.64 mg Se/kg DM) for 105 days. HMSeBA significantly enhanced selenium bioavailability in both milk and blood, comprehensively strengthening antioxidant defenses (increased glutathione peroxidase activity, decreased malondialdehyde) and elevated serum immunoglobulins (IgA, IgM, IgG), accompanied by a reduction in milk somatic cell count, without significantly affecting milk yield, feed intake, or milk production efficiency. Multi-omics analysis revealed that HMSeBA supplementation altered the rumen microenvironment by enriching fiber-degrading genera (Prevotellaceae_Ga6A1_group, Xylanibacter, Segatella) and shifting metabolites, including feed flavonoids, peptides, 1-deoxy-D-xylulose-5-phosphate, and 3-OH-C6-HSL. The positive correlation of ruminal 3-OH-C6-HSL with both blood selenium and these enriched taxa suggests a potential link between microbial activity and host selenium status. These findings indicate that HMSeBA supplementation improves the antioxidant and immune status of dairy cows, accompanied by exploratory, hypothesis-generating shifts in the ruminal microbiome and metabolome. Collectively, these findings highlight HMSeBA as a promising nutritional strategy to produce selenium-enriched milk while safeguarding udder health.},
}

@article {pmid42510625,
year = {2026},
author = {Maiese, K},
title = {Chasing the FoxO in Metabolic Disorders: Novel Considerations for Oxidative Stress, Programmed Cell Death, Wnt, and the Gut Microbiome.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {15},
number = {7},
pages = {},
doi = {10.3390/antiox15070895},
pmid = {42510625},
issn = {2076-3921},
abstract = {Lifespan is increasing throughout the world leading to a rise in non-communicable diseases in the global population that impacts over 800 million individuals with metabolic disorders, such as diabetes mellitus. Metabolic disease presents a significant challenge for clinical care since multi-organ disease progression ensues despite a broad array of treatment protocols. The pursuit of innovative strategies with mammalian forkhead transcription factors of the "O" class (FoxOs) and intimately related pathways of aging, cellular senescence, telomere integrity, oxidative stress, programmed cell death with apoptosis, autophagy, ferroptosis, pyroptosis, and cuproptosis, Wnt/β-catenin signaling, Wnt1 inducible signaling pathway protein 1, and the gut microbiome becomes vital to address the clinical hurdles of metabolic disorders. Platforms incorporating novel diagnostics with artificial intelligence and machine learning can further address the underlying mechanisms tied to FoxOs that include the mechanistic target of rapamycin, AMP activated protein kinase, silent mating type information regulation 2 homolog 1 (S. cerevisiae), and glucagon-like peptide-1 receptor agonists that can markedly influence biological outcomes. Given the premise that it is essential to comprehend the intimate relationship that FoxO signaling pathways hold, FoxOs offer an exciting and promising approach to address the clinical aspects of disease onset, progression, and treatment with metabolic disorders.},
}

@article {pmid42510626,
year = {2026},
author = {Mederle, AL and Lascu, A and Manzur, AR and Caraba, A and Staicu, RE and Noveanu, L and Aburel, OM},
title = {Oxidative Stress in Inflammatory Bowel Disease: From Redox Dysregulation to Translational Targeting.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {15},
number = {7},
pages = {},
doi = {10.3390/antiox15070894},
pmid = {42510626},
issn = {2076-3921},
abstract = {Oxidative stress has emerged as an important component of the complex pathophysiology of inflammatory bowel disease (IBD), where increasing evidence suggests an interaction between redox imbalance, immune activation, epithelial dysfunction, and chronic intestinal inflammation. This structured narrative review critically synthesizes current evidence regarding the biological basis of oxidative stress in IBD, with emphasis on cellular and molecular mechanisms, oxidative biomarkers, therapeutic modulation of redox pathways, and their translational relevance. Current evidence indicates that oxidative stress is associated with immune-cell activation, mitochondrial dysfunction, impairment of epithelial homeostasis, and dysregulation of redox-sensitive signaling pathways. Biomarkers including nitric oxide metabolites, malondialdehyde, myeloperoxidase, total antioxidant capacity, serum thiols, and antioxidant enzymes have demonstrated associations with inflammatory activity, while anti-inflammatory, antioxidant, and dietary interventions have been reported to modulate oxidative biomarkers in selected clinical studies. However, substantial methodological heterogeneity, variability in analytical techniques, and limited prospective validation currently restrict their routine clinical application. Moreover, many mechanistic pathways have been characterized predominantly in experimental models, highlighting the need to distinguish biological plausibility from evidence supporting clinical implementation. Overall, oxidative stress represents a promising area of investigation that may contribute to a better understanding of IBD biology and support future biomarker-guided and precision medicine approaches. Nevertheless, further standardized translational and longitudinal clinical studies are required before oxidative biomarkers and redox-targeted strategies can be integrated into routine patient care.},
}

@article {pmid42510634,
year = {2026},
author = {Hwang, JH and Choi, YK},
title = {Protective Effects of Natural Products, Functional Foods, and Probiotics on NSAID-Induced Small Intestinal Injury: A Systematic Review with Mechanistic Considerations of Oxidative Stress and Microbiome Modulation.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {15},
number = {7},
pages = {},
doi = {10.3390/antiox15070903},
pmid = {42510634},
issn = {2076-3921},
support = {NRF-2022R1A2C1013518//National Research Foundation of Korea/ ; },
abstract = {NSAID-induced small intestinal injury is a clinically significant complication among chronic NSAID and aspirin users, yet effective treatment options remain limited. This systematic review evaluated natural products, functional foods, and probiotics for preventing or treating NSAID-induced small intestinal injury. PubMed, Embase, CENTRAL, and CNKI were searched from inception to January 2026 for randomized studies involving adults with NSAID- or aspirin-induced enteropathy assessed using capsule endoscopy or intestinal permeability testing. Risk of bias was assessed using RoB 2 and ROBINS-I. Due to substantial clinical and methodological heterogeneity, meta-analysis was not performed, and findings were synthesized narratively. Twenty-two studies were included: 21 randomized controlled trials and one quasi-randomized study. Geranylgeranylacetone demonstrated protective effects in three of four capsule endoscopy studies. Lactoferrin, zinc carnosine, and fish protein hydrolysate reduced indomethacin-induced intestinal hyperpermeability. Probiotic effects appeared outcome-dependent, with more consistent benefits observed for capsule endoscopy-based mucosal injury outcomes than for intestinal permeability outcomes. Among randomized trials, three were rated as having low risk of bias, 15 had some concerns, and three had high risk. Overall, preliminary evidence suggests that selected natural-origin interventions may protect against NSAID/aspirin-induced small intestinal injury. However, because the certainty of evidence was generally low or very low, these findings should be interpreted as hypothesis-generating and require confirmation in larger, methodologically rigorous trials.},
}

@article {pmid42510673,
year = {2026},
author = {Dlamini, NH and Kameni, SL and Fan, P and Park, S and Liao, SF and Feugang, JM},
title = {Seminal Plasma Microbiome Composition and Its Association with Sperm Morphology in Breeding Boars.},
journal = {Biology},
volume = {15},
number = {14},
pages = {},
doi = {10.3390/biology15141126},
pmid = {42510673},
issn = {2079-7737},
support = {6066-31000-015-00D//USDA-ARS/ ; },
abstract = {Semen quality is a key determinant of reproductive performance in breeding boars, and emerging evidence suggests the seminal microbiome may influence sperm function. However, the composition of the seminal plasma microbiome and its relationship to sperm quality remain poorly characterized. This study aimed to investigate the microbial composition of boar seminal plasma and its association with sperm quality. Semen ejaculates collected from Duroc boars were analyzed and classified as Passed (≥70% normal morphology) or Failed (<70% normal morphology). Seminal plasma was isolated by centrifugation and analyzed using 16S/ITS rRNA gene sequencing. The dominant bacterial phyla were Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria. The most abundant genera included Porphyromonas, Bacteroides, and Cladosporium. Only the Shannon diversity index was significantly higher in Failed samples for the bacterial microbiome (p = 0.038). Furthermore, correlation analysis showed a negative association between Tenericutes and sperm concentration (r = -0.90; p = 0.014). Linear discriminant analysis identified microbial biomarkers associated with sperm quality, including Rhodococcus, Sphingomonas, Lactobacillus, Streptococcus, and Empedobacter. The increased abundance of these genera in Failed samples suggests disruption of the normal seminal microbial community. In conclusion, boar seminal plasma harbors a distinct bacterial and fungal microbiome that is associated with sperm morphology.},
}

@article {pmid42510732,
year = {2026},
author = {Cembalo, G and Turrini, M and Baldi, S and Amedei, A},
title = {Beyond the Human Binary: Decoding Hormone-Immune Plasticity in Transgender Health.},
journal = {Biology},
volume = {15},
number = {14},
pages = {},
doi = {10.3390/biology15141187},
pmid = {42510732},
issn = {2079-7737},
abstract = {Sex- and gender-based immune differences have often been interpreted through a male-female biological binary, overlooking how endocrine signaling dynamically shapes immune function. Gender-affirming hormone therapy (GAHT) offers a unique physiological model to disentangle the effects of sex steroids from chromosomal background and examine immune plasticity in contexts relevant to reproductive health. This hormone-informed framework proposes that estradiol and testosterone regulate immune set-points across innate, adaptive, metabolic, and mucosal compartments. Through genomic and non-genomic signaling via androgen and estrogen receptors (AR, ERα/β), these hormones drive distinct immune outcomes: testosterone dampens type I interferon responses in plasmacytoid dendritic cells and reshapes monocyte inflammatory profiles, while estradiol promotes macrophage polarization and enhances T helper1 (Th1) responses. Hormonal effects are closely coupled to cellular metabolism: androgen signaling acts as a "metabolic brake" on Th17 cells by limiting glutaminolysis, a process reinforced by epigenetic remodeling, and is reflected in shifts in the circulating metabolome, positioning metabolomics as a sensitive tool for monitoring hormone-driven immune adaptation. Regardless, hormones also reshape mucosal barriers and reproductive microbiome composition. GAHT alters vaginal and gut microbial communities and their metabolism, influencing mucosal immunity, local inflammation, and reproductive tract homeostasis, with potential implications for fertility preservation, susceptibility to reproductive tract infections, and long-term genital mucosal health. Collectively, this evidence underscores that human immunity is highly responsive to endocrine context. This review synthesizes evidence linking endocrine trajectories, tissue microenvironments, reproductive biology, and social determinants of health, aiming to advance understanding of immune plasticity and contribute to a more inclusive framework of human immune diversity.},
}

@article {pmid42510739,
year = {2026},
author = {Liu, X and Zhao, X and Li, H and Wu, Y and Yao, Y and Wang, Z},
title = {Comparative Study on Blood Gas Indicators, Antioxidant Capacity, Intestinal Metabolome, and Microbiome in High- and Low-Performance Tumbler Pigeons.},
journal = {Biology},
volume = {15},
number = {14},
pages = {},
doi = {10.3390/biology15141193},
pmid = {42510739},
issn = {2079-7737},
support = {2023B02036//The Xinjiang Uygur Autonomous Region Key Research and Development Project/ ; },
abstract = {The purpose of this experiment is to investigate the differences in blood gas indicators, antioxidant indicators, and lactate content between high- and low-performance tumbler pigeons after exercise, and to use metabolomics and metagenomics techniques to screen for differential metabolites and bacteria related to tumbler pigeon exercise. This experiment selected 12 high-performing (HP) and 12 low-performing (LP) tumbler pigeons, half male and half female, and all pigeons were raised under the same conditions. Three experimental pigeons were grouped for exercise training, with a 20 min training session. The results showed significant differences (p < 0.05) in multiple blood gas parameters related to acid-base balance and gas exchange between the HP and LP groups after tumbler pigeon exercise. In addition, the content of glutathione peroxidase (GSH Px), superoxide dismutase (SOD), and catalase (CAT) in the liver of the HP group of tumbler pigeons was significantly lower than that of the LP group (p < 0.05). In comparison, the content of malondialdehyde (MDA) was significantly higher than that of the LP group (p < 0.05). The content of lactate (Lac) was significantly higher than that of the LP group (p < 0.05). Non-targeted metabolomics analysis revealed that differential metabolites were mainly enriched in pathways such as biosynthesis of unsaturated fatty acids, starch and sucrose metabolism, and fatty acid synthesis. Intestinal metagenomics analysis revealed that the Corynebacteriaceae, Bacillus, Pseudomonad phylum and Corynebacterium were significant biomarkers with significant differences in the gut microbiota of the HP group of tumbler pigeons (p < 0.05). In summary, there are significant differences in blood physiological parameters, antioxidant capacity, lactate content, intestinal metabolites, and gut microbiota between high- and low-performance tumbler pigeons after exercise. This result provides theoretical guidance and data support for cultivating high-performance tumbler pigeons.},
}

@article {pmid42510753,
year = {2026},
author = {Zhang, X and Li, Y and Zhang, X and Shi, W and Deng, H and Yi, L and Zhou, S and Yu, D},
title = {Maternal Polystyrene Nanoplastic Exposure Impairs Cardiac Development in Mouse Offspring and Identifies Lactation as a Sensitive Window in Males.},
journal = {Biology},
volume = {15},
number = {14},
pages = {},
doi = {10.3390/biology15141207},
pmid = {42510753},
issn = {2079-7737},
abstract = {Maternal exposure to nanoplastics is a growing concern, but its effects on offspring cardiac development and the relative importance of prenatal and lactational exposure remain unclear. Pregnant C57BL/6J mice were orally exposed to 50 nm polystyrene nanoplastics at 3, 15, or 75 μg/g body weight from gestational day 1 to postnatal day 21. A cross-fostering design was used to distinguish gestational exposure from lactational exposure. Maternal polystyrene nanoplastic exposure caused dose-dependent cardiac dysfunction in offspring, including reduced ejection fraction and fractional shortening, increased myocardial injury markers, cardiomyocyte hypertrophy, and fibrosis. Cross-fostering showed that lactationally exposed offspring exhibited more severe cardiac abnormalities than offspring exposed only during gestation, indicating that the nursing period may represent a more vulnerable window. In male offspring, polystyrene nanoplastic exposure was also associated with gut microbiota dysbiosis and cardiac transcriptomic changes. Enrichment analysis identified downregulation of genes related to AMP-activated protein kinase signalling, and integrated microbiome-transcriptome analysis suggested associations between altered gut taxa and cardiac differentially expressed genes. These findings indicate that maternal polystyrene nanoplastic exposure induces offspring cardiac developmental toxicity, with stronger effects during lactation, and suggest the involvement of gut microbial and cardiac molecular remodelling.},
}

@article {pmid42510952,
year = {2026},
author = {H Navia, S and Illescas, O and Silva-Magaña, MA and Juárez-Avelar, I and Terrazas-Rodriguez, M and Vaca-Paniagua, F and Díaz Velásquez, CE and Vega, L and Terrazas, LI and Rodríguez-Sosa, M},
title = {MIF Deficiency Modulates Gut Microbiota Composition and Promotes Colitis-Associated Colorectal Cancer in a Murine Model.},
journal = {Current issues in molecular biology},
volume = {48},
number = {7},
pages = {},
doi = {10.3390/cimb48070712},
pmid = {42510952},
issn = {1467-3045},
support = {CIKAS-FICDTEM25-019//Mexico State Council for Science and Technology (COMECyT)/ ; IN208126//Programa Académico de Investigación e Innovación Tecnológica (PAPIIT)-UNAM/ ; IV200425//Programa Académico de Investigación e Innovación Tecnológica (PAPIIT)-UNAM/ ; },
abstract = {Intestinal dysbiosis is a hallmark of both inflammatory bowel conditions and colorectal cancer, yet the mechanisms by which inflammatory mediators alter microbial communities and may contribute to tumor development remain poorly understood. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine involved in innate immunity and the progression of inflammatory and neoplastic disorders. In this study, sequencing of the microbial 16S rRNA gene was performed to characterize the fecal microbiota profiles of wild-type (WT) and MIF-knockout (MIF-KO) BALB/c mice subjected to AOM/DSS-induced colitis-associated colorectal cancer (CAC). CAC induction resulted in marked microbial shifts, including increases in Muribaculaceae and Bacteroidota, in both WT and MIF-KO mice. Notably, MIF-KO CAC mice developed more severe disease compared with WT CAC mice. Furthermore, FMT experiments revealed that the fecal microbiota from MIF-KO donors was associated with increased tumor burden in WT recipients under CAC-inducing conditions compared with that in recipients colonized with WT-derived microbiota. Together, these findings suggest that MIF deficiency is associated with gut microbiota remodeling during CAC and support a potential relationship between the MIF-dependent host context, microbial composition and colorectal cancer severity.},
}

@article {pmid42510968,
year = {2026},
author = {Dyachenko, EI and Bel'skaya, LV},
title = {The Mechanism and Pathways of Formation and Modification of Salivary Metabolic Profile in Cancer.},
journal = {Current issues in molecular biology},
volume = {48},
number = {7},
pages = {},
pmid = {42510968},
issn = {1467-3045},
support = {23-15-00188-П//Russian Science Foundation/ ; },
abstract = {Saliva is a promising diagnostic fluid for studying diseases, including cancer. Saliva composition can reflect both local processes occurring in the oral cavity and systemic changes associated with distant tumors. This review examines changes in salivary electrolyte, amino acid, lipid, and cytokine profiles, tumor markers, and the oral microbiome in cancer. Collectively, these aspects reflect metabolic, inflammatory, immune, secretory, and tumor-associated processes. Metabolites can enter saliva via the salivary glands, systemic circulation, gingival fluid, extracellular vesicles, and oral cells, as well as directly from the site of disease during localized pathological processes. In tumors not localized in the oral cavity, changes in saliva composition are more often associated with systemic inflammation, altered oral microbiome, metabolic reprogramming, oxidative stress, and tumor-associated exosomes. Individual metabolites have limited specificity and cannot be used as independent diagnostic indicators. A comprehensive multimarker analysis of saliva is of greatest value. This approach can facilitate early diagnosis, identify the risk of disease development and progression, monitor therapy, and understand the biological changes associated with the pathological process, including tumors.},
}

@article {pmid42511027,
year = {2026},
author = {Dong, J and Li, S and Song, J and Ma, Y and Xin, H and Zhang, Y and Zhang, G},
title = {Dietary Laminaria japonica Polysaccharide Alleviates Aged-Maize-Associated Intestinal Oxidative Stress and Systemic Inflammation in Hu Sheep: Associations with Cecal Microbiome-Metabolome Remodeling.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {14},
pages = {},
doi = {10.3390/ani16142146},
pmid = {42511027},
issn = {2076-2615},
support = {ZL2024C016//Heilongjiang Provincial Science and Technology Department/ ; },
abstract = {Long-term maize storage causes oxidative deterioration, but its effects on intestinal redox status, systemic inflammation, and liver-related responses in ruminants remain unclear. Laminaria japonica polysaccharide (LJP) has antioxidant, immunomodulatory, and microbiota-regulating properties, but its efficacy during aged-maize feeding is unknown. This study evaluated whether LJP mitigates oxidative and inflammatory responses in Hu sheep fed aged maize and characterized cecal microbiome and metabolome alterations. Twenty-one Hu sheep (39.05 ± 3.55 kg) were assigned to three diets (n = 7) and fed for 10 weeks (a 14-day adaptation period followed by 8 weeks of treatment): normal maize (CK), aged maize (AM), or aged maize with 0.5% LJP (AML). Compared with CK, AM increased plasma lipopolysaccharide (0.428 vs. 0.379 EU/mL), TNF-α, and IL-1β, and raised ileal reactive oxygen species (248.79 vs. 166.23 fluorescence intensity/mg; p < 0.001) and malondialdehyde (1.87 vs. 1.63 nmol/L; p = 0.006), consistent with systemic inflammation and intestinal oxidative stress. AML lowered these inflammatory and oxidative indices and increased hepatic T-AOC (p = 0.009) and catalase activity (p = 0.013). Integrated 16S rRNA and untargeted metabolomic analysis revealed treatment-associated cecal microbe-metabolite associations. These findings indicate that aged-maize feeding was associated with intestinal and systemic redox-inflammatory changes in Hu sheep, whereas dietary LJP was associated with partial mitigation, potentially involving microbial and metabolic remodeling.},
}

@article {pmid42511028,
year = {2026},
author = {Li, L and Shi, H and Wang, S and Dou, X and Wang, P and Fan, H and Liu, X and Zhang, X and Quan, K and Wang, Y},
title = {Characterization of Fecal Microbiota and Serum Metabolome Variations Across Different Gestational Stages in Hu Sheep.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {14},
pages = {},
doi = {10.3390/ani16142149},
pmid = {42511028},
issn = {2076-2615},
support = {CARS-37//China Agriculture Research System/ ; HARS-22-15-S//Henan Agricultural Research System/ ; },
abstract = {This study investigated the variations in the fecal microbiota and serum metabolome of prolific Hu sheep across different gestational stages to understand their physiological relationships. Fecal and blood samples were collected from 24 multiparous ewes across four stages: non-pregnant and gestational days 55, 85, and 110. Fecal microbial communities were analyzed via 16S rRNA gene sequencing, and serum metabolic profiles were assessed using liquid chromatography-tandem mass spectrometry (LC-MS)-based untargeted metabolomics. Serum biochemical analysis showed that pregnant ewes had decreased urea concentrations (p < 0.05), an early-gestation peak in total cholesterol, and a mid-gestation peak in triglycerides (p < 0.05). Fecal microbiota analysis indicated higher alpha diversity during gestation than in the non-pregnant stage (p < 0.05), with Firmicutes as the dominant phylum and stage-specific variations in genera such as Negativibacillus and Monoglobus. Metabolomics analysis identified 68 differential metabolites primarily assigned to lipid, amino acid, and steroid hormone pathways. Procrustes and Spearman correlation analyses showed statistical concordance between the fecal microbial community structure and the serum metabolome. Specific genera, including UCG-005, Alistipes, and unclassified Lachnospiraceae, correlated positively with metabolites such as pregnanediol 3-O-glucuronide and specific sphingomyelins. In conclusion, the progression of pregnancy in Hu sheep is characterized by concurrent shifts in the fecal microbiota and serum metabolites. These concurrent variations correlate with host nitrogen reallocation and lipid parameters, providing baseline reference data for the nutritional management of gestating ewes. These results provide a useful reference for future studies investigating maternal physiology, nutrition, and microbiome dynamics in prolific sheep breeds.},
}

@article {pmid42511119,
year = {2026},
author = {Zhang, B and Ma, X and He, Z and Liu, J and Chen, P and Wang, F and Xie, J and Lv, C and Pan, F},
title = {Effects of Perilla Seed Extract Dietary Supplementation on Meat Quality, Rumen Fermentation, and Rumen Microbiome-Metabolome of Tan Lambs.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {14},
pages = {},
doi = {10.3390/ani16142242},
pmid = {42511119},
issn = {2076-2615},
support = {2023GAAS42//Gansu Academy of Agricultural Sciences/ ; },
abstract = {Perilla seed extract (PSE), a natural resource rich in α-linolenic acid and flavonoids, represents a promising dietary strategy to sustainably optimize rumen fermentation and improve the nutritional profile of ruminant meat. This study evaluated the effects of dietary PSE supplementation on rumen fermentation, microbiome-metabolome profiles, and subsequent meat quality in Tan lambs. Sixty 3-month-old male Tan lambs were randomly assigned to four dietary treatments (n = 15 per treatment) containing 0% (CON), 0.01% (LPSE), 0.03% (MPSE), or 0.05% (HPSE) PSE on a dry matter (DM) basis. In the rumen, the 0.03% PSE inclusion increased the propionate proportion from 20.50% to 23.80% (P-linear = 0.004) and carboxymethyl cellulase activity from 12.45 to 14.85 U/mL (P-linear = 0.007; P-quadratic = 0.045). Exploratory metagenomics showed that 0.03% PSE enriched Prevotella (18.67% to 21.06%) and Ruminococcus_E (1.20% to 2.13%), while decreasing the biohydrogenating genus Butyrivibrio compared with CON (LDA > 2, p < 0.05). These microbial shifts were accompanied by the accumulation of beneficial metabolites (e.g., small peptides and itaconic acid) and up-regulation of the pantothenate and CoA biosynthesis pathway. Consequently, the 0.03% PSE diet optimized meat quality, decreasing shear force by 12.7% (from 45.65 to 39.85 N; P-linear = 0.005, P-quadratic = 0.018) and drip loss (from 4.82% to 3.85%; P-linear = 0.022, P-quadratic = 0.015), while increasing redness (P-linear = 0.012, P-quadratic = 0.045). Furthermore, it increased meat C18:3n-3 (from 0.62% to 0.91%) and total n-3 PUFA (from 1.12% to 1.52%), while decreasing the n-6/n-3 ratio from 6.76 to 5.13 (P-linear ≤ 0.005 for all). Flavor amino acids also increased (P-linear = 0.008). These findings suggest that 0.03% PSE supplementation potentially improves lamb meat quality by favorably modulating rumen fermentation and microbe-metabolite interactions, highlighting its promise as a natural feed additive, though further validation is warranted.},
}

@article {pmid42511216,
year = {2026},
author = {Ren, T and Li, W and Wen, X and Hu, B and Fang, Z and Hu, B and Wu, W and Zeng, Z and Liu, Y},
title = {Tibetan Tea Drives Baijiu Flavor Formation via Microbial Niche Modulation in Daqu: A Multi-Omics Study.},
journal = {Foods (Basel, Switzerland)},
volume = {15},
number = {14},
pages = {},
pmid = {42511216},
issn = {2304-8158},
support = {2024NSFSC2059//Sichuan Provincial Natural Science Foundation Project Agreement/ ; S202610626104//Provincial Undergraduate Training Program on Innovation and Entrepreneurship/ ; },
abstract = {Interest in using Tibetan tea for fermented food production has increased due to its bioactive components and distinctive flavor characteristics. However, its application in Daqu prepared with Tibetan tea remains limited. This study investigated the effects of Tibetan tea addition on Daqu fermentation and Baijiu flavor formation using integrated microbiome and metabolome approaches. High-throughput sequencing, GC-MS, free amino acid analysis, electronic sensory analysis, and correlation network analysis were performed to characterize microbial and metabolic changes. Compared with wheat Daqu (WD), Tibetan tea Daqu (TD) showed higher microbial richness and enhanced fermentation performance (p < 0.05), with enrichment of functional microorganisms including Sphingobium, Komagataella, and Cyberlindnera, which were associated with enzyme activities and flavor precursor formation. Tibetan tea Daqu Baijiu (TDB) exhibited distinct metabolic profiles, with increased levels of esters, acids, terpenes, and free amino acids, contributing to a flavor profile characterized by ester aroma with sweet, umami, woody, and tea aroma characteristics. Correlation analysis revealed that Tibetan tea-driven microbial restructuring was linked to phenylalanine metabolism, esterification, and phenolic transformation pathways. These findings link raw materials, microbiota, and flavor formation, providing a basis for targeted Baijiu design.},
}

@article {pmid42511468,
year = {2026},
author = {Semlali, A and Al-Zharani, M and Dahdah, M and Chandad, F},
title = {Candida albicans in Oral Squamous Cell Carcinoma: From Microbial Dysbiosis to Tumor-Promoting Mechanisms and Translational Opportunities.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511468},
issn = {1422-0067},
support = {DDRSP2601//Imam Mohammad ibn Saud Islamic University/ ; },
abstract = {Oral squamous cell carcinoma (OSCC) remains a major global health burden with limited improvement in survival rates. While traditional risk factors such as tobacco and alcohol are well established, increasing evidence highlights the role of the oral microbiome in carcinogenesis. Among microbial species, Candida albicans (C. albicans) has emerged as a potential contributor to tumor-promoting processes. Clinical studies consistently report increased fungal colonization in oral potentially malignant disorders and OSCC, with associations to disease severity and recurrence. Mechanistically, C. albicans contributes to carcinogenesis through acetaldehyde production, chronic inflammation, oxidative stress, epithelial signaling modulation, and extracellular vesicle (EV)-mediated communication. These pathways promote tumor microenvironment remodeling and epithelial transformation. However, conflicting evidence exists regarding causality, suggesting that fungal colonization may also result from tumor-associated ecological changes. From a translational perspective, C. albicans and EV-associated signatures may represent promising biomarkers and therapeutic targets, although further validation is required. This review highlights the emerging role of fungal-host interactions in OSCC and underscores their potential in microbiome-informed precision oncology.},
}

@article {pmid42511476,
year = {2026},
author = {Cannon, M and Peldyak, J},
title = {Xylitol, Mitochondrial Plasticity, the Warburg Effect, and Oral Pathobiont-Associated Immune Evasion in Cancer Hypothesis.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511476},
issn = {1422-0067},
abstract = {The Warburg effect is better understood as regulated metabolic plasticity rather than mitochondrial failure. Many malignant cells retain functional mitochondria while increasing aerobic glycolysis, lactate production, and redox remodeling to support growth, immune escape, and adaptation to microenvironmental stress. Within the context of the cancer microenvironment, this review examines xylitol as a hypothetical metabolic modifier within a broader host-microbe-mitochondria framework. Xylitol, a five-carbon sugar alcohol, is derived endogenously through the pentose phosphate pathway (PPP) and the glucuronate-xylulose pathway, and is metabolized efficiently in humans, rats, and pigs through xylitol dehydrogenase (XDH) in hepatic mitochondria and the cytosol; whereas, it is less tolerated by obligate carnivores who lack this enzyme. Preclinical studies show that partial substitution of glucose with xylitol can reduce proliferation and glycolytic markers in oral squamous carcinoma models, and preliminary studies link xylitol to glutathione depletion, endoplasmic reticulum (ER) stress, autophagy-associated death, and altered tumor metabolomics. On the other hand, oral pathogens such as Fusobacterium nucleatum and Porphyromonas gingivalis promote tumor stemness, extracellular vesicle signaling, metastasis, and immune evasion. In addition, Streptococcus mutans, the primary cariogenic pathogen, contributes to systemic bacteremia and epithelial-mesenchymal transition. Oral and gut microbiomes modulate macrophage polarization, T cell activity, and the senescence-associated secretory phenotype (SASP), possibly promoting cancer immune evasion. The anti-adhesive properties of xylitol may limit pathogen attachment to immune cell receptors, reducing the generation of pro-tumorigenic senescent immune cells. Xylitol also offers metabolic benefits, a low glycemic index, partial insulin-independent metabolism, and potential diabetes-prevention activity that are relevant, considering the established link between metabolic disease and cancer risk. A recent study reported that higher levels of endogenous xylitol were associated with adverse cardiovascular events, but confirmation of this requires large scale prospective studies. The evolutionary dietary context of MIS 6, during which hominin populations in sub-Saharan Africa depended on polyol-rich underground storage organs, provides a biological basis for human tolerance of xylitol. As a result, we hypothesize that xylitol may be a context-dependent metabolic modifier within an integrated host-microbe-mitochondria-cancer stem cell network.},
}

@article {pmid42511508,
year = {2026},
author = {David, DE and Dramba, T and Chiriac, SA and Paraschiv, CM and Grigorasi, G and David, AG and Lupu, VV and Lupu, A and Păduraru, G and Pertea, LI and Temneanu, OR and Esanu, IM},
title = {The Gut-Heart Axis: A Microbiome-Centered Perspective on Heart Failure.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511508},
issn = {1422-0067},
abstract = {In recent years, gut microbiota has emerged as a central modulator of cardiovascular health and disease. This has led to a transition from the old understanding of cardiovascular pathology as a largely cardiac-centric problem to a systemic, multi-organ process. A growing body of evidence demonstrates that changes in the makeup of gut microbes, generally called dysbiosis, are significant in the development and progression of cardiovascular illnesses, including heart failure. Moreover, there are bidirectional interactions between the failing heart and the gut. In heart failure, impaired hemodynamics and venous congestion further worsen intestinal hypoperfusion and barrier dysfunction in a self-perpetuating cycle that exacerbates dysbiosis and systemic inflammation. The gut-heart axis offers a fresh paradigm for illness progression beyond classical neurohormonal and hemodynamic processes. The gut microbiota acts as an endocrine organ by producing bioactive metabolites such as TMAO (trimethylamine N-oxide), SCFA (short-chain fatty acids) and bile acids, which, via several routes, have a serious impact on host health and disease. This narrative review aims to summarize the current evidence for the gut microbiota as a new cardiovascular risk factor, focusing on biological mechanisms and clinical and epidemiological evidence.},
}

@article {pmid42511525,
year = {2026},
author = {Ma, C and Wang, Y and Liu, Y},
title = {GutMGene-Guided Peripheral Blood Transcriptomics Identifies an FLNA-Associated Host-Gene Signal in Diabetic Retinopathy.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511525},
issn = {1422-0067},
support = {BE2023665//Jiangsu Province Science and Technology Department/ ; },
abstract = {Diabetic retinopathy (DR) reflects retinal microvascular injury and systemic immune-metabolic stress, and most public DR transcriptomic datasets lack paired microbiome/metabolomic profiles. We used gutMGene v2.0 as a curated microbe/metabolite-host gene prior and integrated it with peripheral blood transcriptomics from GSE221521. Candidate genes were refined by weighted gene co-expression network analysis (WGCNA), repeated resampling, cross-dataset assessment, mechanism scoring, peripheral blood mononuclear cell (PBMC) single-cell localization and filamin A (FLNA)-centered single-cell gene regulatory network (GRN) virtual knockout. The gutMGene prior contained 238 host genes; 15 DR-associated genes overlapped this prior, and WGCNA retained ten candidate gut microbe and microbial metabolite-related genes (GMMRGs): FLNA, AKT1, IRAK1, BCL10, CDK6, CTSD, JUP, CXCL1, CXCR2 and IL4R. Resampling prioritized FLNA as the most consistent candidate. Cross-dataset assessment localized the strongest signal to type 2 diabetes (T2D) PBMCs, retinal endothelial cells and advanced proliferative diabetic retinopathy with diabetic macular edema (PDR + DME) retinal tissue, with weaker separation in whole blood, broad retinal tissue and six-donor type 1 diabetes (T1D) PBMCs. FLNA virtual knockout predicted cell-context-dependent perturbation of immune-related transcriptional programs, including IL4R in DR B cells and CTSD in DR monocytes/NK cells. This prior-guided study identifies FLNA within a ten-gene GMMRG set as a circulating host-response signal that links curated microbe/metabolite-host records to immune-vascular and cytoskeletal remodeling in DR.},
}

@article {pmid42511589,
year = {2026},
author = {Ciaușu-Sliwa, D and Capotă, R and Bostănaru-Iliescu, AC and Năstasă, V and Mareș, M},
title = {Molecular Mechanisms of Gut Microbiota-Immune System Crosstalk: From Mucosal Architecture to Adaptive Immunity Programming.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511589},
issn = {1422-0067},
abstract = {The mammalian gut microbiome functions as a metabolically active immunological organ and has co-evolved with its host to maintain systemic homeostasis. This review integrates current evidence on the molecular mechanisms governing bidirectional microbiota-immune communication, emphasizing evolutionary conservation, receptor-mediated signaling, and translational implications. Microbial structural ligands and metabolites-including short-chain fatty acids, bile-acid derivatives, and tryptophan catabolites-engage host receptors such as G-protein-coupled receptors, FXR/TGR5, and the aryl hydrocarbon receptor (AhR), thereby regulating epithelial barrier integrity, regulatory T-cell differentiation, Th17 polarization, mucosal IgA production, and systemic immune tone. Riboflavin-derived metabolites presented via major histocompatibility complex class-I-related molecule (MR1) further shape mucosal-associated invariant T-cell development (MAIT), illustrating metabolite-driven immune system programming. Dysbiosis induced by antibiotics, dietary perturbation, or aging disrupts these molecular networks, promoting chronic inflammatory, metabolic, autoimmune, and neuroimmune disorders. Comparative analyses across mammalian systems underscore conserved pathways of host-microbe coadaptation and immune education. Therapeutically, microbiota-modulating strategies-including probiotics, prebiotics, synbiotics, fecal microbiota transplantation (FMT), postbiotics, and IgY-based passive immunotherapy-aim to restore immunometabolic signaling. Emerging in vitro and in silico platforms further provide mechanistic precision while supporting ethically aligned translational research. Collectively, these insights position microbiota-derived molecular signaling as a central determinant of adaptive immune architecture and a targetable axis in precision immunotherapy.},
}

@article {pmid42511590,
year = {2026},
author = {Tankiewicz, M and Niciejewski, K and Dydecka, A and Topka-Bielecka, G},
title = {The Fruit Biome: Biofilm Dynamics and Consumer Health Risks with Focus on the Apple (Malus domestica) as a Model System.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511590},
issn = {1422-0067},
support = {01-30026/0010494/01/322/322/0/2026//Ministry of Science and Higher Education/ ; },
abstract = {Fruit surfaces serve as ecological interfaces that support diverse microbial communities, where biofilm formation by spoilage organisms and human pathogens contributes to postharvest safety concerns. Although fruit-associated microbiota and chemical residues have been widely investigated, the interactions between surface microstructure, residue dynamics, and microbial persistence remain insufficiently integrated. This review synthesizes current knowledge by considering three key processes: temporal succession of microbial communities, structural vulnerability of the fruit surface, and chemically mediated selective pressures. Using apple (Malus domestica) as a model system, we examine how structural features such as lenticels and cuticular microdamage interact with pesticide residues to facilitate microbial retention, sequestration, and internalization. Evidence indicates that pesticide residues may act as selective stressors and, in some cases, potential metabolic substrates, thereby enhancing microbial persistence and tolerance to sanitization. These combined factors contribute to the formation of a high-persistence surface environment. Integrating microbiological, chemical, and plant structural perspectives, this review provides a mechanistic basis for the limited effectiveness of conventional decontamination approaches and highlights the need for multidisciplinary postharvest strategies to improve produce safety and shelf life.},
}

@article {pmid42511630,
year = {2026},
author = {Yoon, Y and Hwang, J and Yang, CM and Moon, M and Lee, JJ and Lam, KHS and Castro, JC and Suryadi, T and Suhaimi, A and Lee, J},
title = {Psyllium and Glucomannan as Viscous Fiber Modulators of the Gut-Microbiome-Incretin Axis: Molecular Links to Metabolic Inflammation, Barrier Function, and GLP-1 Receptor Agonist Therapy.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511630},
issn = {1422-0067},
abstract = {Dietary fiber is an under-consumed nutritional substrate that supports gut microbial metabolism, intestinal barrier integrity, enteroendocrine signaling, and cardiometabolic regulation. Among dietary fibers, psyllium and glucomannan are clinically accessible viscous, gel-forming soluble fibers with distinct but complementary physicochemical profiles. This narrative review examines how these fibers act through luminal viscosity, nutrient diffusion, bile acid and cholesterol handling, short-chain fatty acid production, epithelial barrier support, enteroendocrine L-cell signaling, and low-grade metabolic inflammation. Psyllium has the strongest clinical support for stool normalization, glycemic modulation, and LDL cholesterol reduction, whereas glucomannan provides marked viscosity and water-holding capacity that may support satiety, lipid modulation, and weight-management strategies when appropriately hydrated and tolerated. We also discuss the emerging nutritional context of glucagon-like peptide-1 receptor agonist therapy, in which appetite suppression, reduced meal volume, delayed gastrointestinal transit, and constipation may reduce dietary fiber intake and fermentable substrate delivery to the colon. The pain- and mood-related implications are framed as hypothesis-generating extensions, because direct clinical evidence that psyllium or glucomannan improves these outcomes remains limited. A psyllium-centered, selectively glucomannan-supported strategy may help close the fiber gap and support bowel function, microbial metabolite signaling, and cardiometabolic stability during modern metabolic and weight-loss therapies.},
}

@article {pmid42511698,
year = {2026},
author = {Biasin, A and Sarro, G and Confalonieri, P and Salton, F and Confalonieri, M and Abriani, A and Campisciano, G and Comar, M and Tierno, D and Tonon, F and Adrover, A and Venditti, C and Grassi, G and Grassi, M and Abrami, M},
title = {Pilot Study on the Use of Low-Field Nuclear Magnetic Resonance as a Noninvasive Tool for Monitoring Mucus in Obstructive Lung Diseases.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511698},
issn = {1422-0067},
support = {CUP J53D23002200006//Ministry of Education, Universities and Research/ ; CUP J93C24002040002//Regione Autonoma Friuli Venezia Giulia/ ; },
abstract = {Patients with muco-obstructive lung disease (MOLD) exhibit chronic bronchitis and inflammation, along with a progressive decline in lung function. Lung monitoring is typically performed using spirometry, especially by measuring the forced expired volume in the first second (FEV1). However, the limitations of spirometry motivated the exploration of alternative approaches. The spin-spin relaxation time (T2m) and the spin-lattice relaxation time (T1m) of sputum water hydrogens were measured using low-field nuclear magnetic resonance (LF-NMR) in 38 MOLD patients and 16 controls. The levels of TNFα/IL-6, the sputum microbiome composition/amount/indices and FEV1 were determined in parallel. We also investigated the correlation between T2m/T1m and the disease index (ID); ID, calculated relying on patient FEV1/TNFα/IL-6/bacteria concentration Cb values, is a measure of the patient's distance from the average healthy control. We observed the following significant correlations: T2m/T1m with ID, T2m with Cb, a potential correlation of T2m with the bacteria genera Streptococcus and Staphylococcus, T2m with the Shannon index, which reflects the broadness of the bacterial community in the sputum, and T2m with TNFα. FEV1 did not show any correlation. Our noninvasive/radiation-free/portable method of T2m/T1m measurement shows potential value in monitoring lung conditions in MOLD patients and may contribute to improved clinical decision-making.},
}

@article {pmid42511708,
year = {2026},
author = {Green, RS and Diaz-Infante Morales, D and Schott, EM and Charbonneau, MR and Ballok, AE},
title = {A Defined Synbiotic Produces Immunomodulatory Metabolites, Engages Gut-Immune Pathways Relevant to Inflammaging, and Supports Healthy Aging in a Nematode Model.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511708},
issn = {1422-0067},
mesh = {Animals ; *Synbiotics/administration & dosage ; Humans ; *Caenorhabditis elegans/immunology ; *Healthy Aging/drug effects/immunology ; *Inflammation/immunology ; *Gastrointestinal Microbiome/drug effects/immunology ; Longevity/drug effects ; Immunomodulation ; Aging ; Intestinal Barrier Function ; },
abstract = {Chronic low-grade aging-associated inflammation, or inflammaging, is a central pillar of age-related decline in quality of life. Inflammaging is partially mediated by impaired intestinal, immune, and microbiome function, and it has been hypothesized that probiotics could be used to promote healthy aging. SBD121, a defined synbiotic containing food-derived microbial strains and prebiotic fibers, has previously been shown to improve grip strength in male rats, an important indicator of healthspan, and is under evaluation in a clinical trial of 143 newly diagnosed rheumatoid arthritis patients (NCT06005220). However, the mechanisms underlying its potential benefits have not been determined. Here, we examined the function of SBD121 in microbial, cellular, and animal models relevant to inflammaging. SBD121 inhibited the growth of potential microbial pathogens, produced immunomodulatory metabolites in vitro, and improved human intestinal cell barrier function under both basal and challenge conditions, while reducing inflammatory chemokine secretion following inflammatory challenge. SBD121 also reduced the secretion of multiple chemokines in lipopolysaccharide-stimulated human intestinal and immune cells. Finally, SBD121 improved survival and locomotor activity in a C. elegans longevity model, providing evidence of benefits to lifespan and healthspan. Together, these data demonstrate that SBD121 exhibits beneficial microbial, epithelial, immune, and longevity effects and support continued investigation of SBD121 as a candidate intervention for healthy aging.},
}

Animals
*Synbiotics/administration & dosage
Humans
*Caenorhabditis elegans/immunology
*Healthy Aging/drug effects/immunology
*Inflammation/immunology
*Gastrointestinal Microbiome/drug effects/immunology
Longevity/drug effects
Immunomodulation
Aging
Intestinal Barrier Function

@article {pmid42511743,
year = {2026},
author = {Tanaka, M and Detregiachi, CRP and Catharin, VCS and Mazuqueli, ESB and Galhardi, CM and Zutin, TLM and Hirata, M and Quesada, K and Catharin, VMCS and Haber, RSA and Miola, VFB and Barbalho, SM},
title = {Mechanism-First Psychobiotics: Fermented Vegetables, Dairy, and Soy for Depression and Anxiety.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511743},
issn = {1422-0067},
abstract = {Depression and anxiety are increasingly understood to involve systemic biological processes, where chronic stress, immune dysregulation, and vascular dysfunction converge on brain-relevant symptoms. Fermented foods are widely studied as psychobiotic candidates, yet results remain inconsistent because products vary in chemistry, viability, sodium, and biogenic amines, and trials often rely on broad symptom outcomes without exposure verification. A major gap is the lack of a reusable, mechanism-first framework that links what a product delivers to barrier, endothelial, and neurovascular target engagement. As a narrative and conceptual review rather than a systematic review, the article integrates mechanistic evidence into a conceptual framework rather than undertaking quantitative evidence synthesis. It addresses that gap by treating fermented vegetables, dairy, soy, and selected Brazilian cassava ferments and artisanal cheeses as metabolite-engineering platforms mapped onto a tri-barrier remodeling axis from gut epithelium to endothelium and platelets to the blood-brain barrier. We synthesize dosing-resolved metabolite modules, including short-chain fatty acids, tryptophan-derived indoles, bile acids, neuroactive small molecules, and peptide and exopolysaccharide fingerprints, and align them with interpretable readouts for permeability, endotoxemia proxies, endothelial activation, immunothrombosis, and epigenetic aging pace. Here we highlight how this modular framework converts heterogeneous food studies into testable exposure hypotheses, guides comparator design and phenotype stratification, and clarifies why null results can be informative. To maintain a focused scope, the review uses selected fermented-food families as representative test platforms rather than attempting a complete survey of global fermented foods. The emphasis is therefore placed on mechanisms, exposure verification, and trial-design principles that can be transferred to other products.},
}

@article {pmid42511801,
year = {2026},
author = {Cheng, A and Ee, KP},
title = {Deciphering Stress Resilience in Black Pepper (Piper nigrum L.): From Current Advances to Emerging Opportunities.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511801},
issn = {1422-0067},
support = {FRGS/1/2024/STG01/UM/02/1//Ministry of Higher Education/ ; },
abstract = {Black pepper (Piper nigrum Linn.), one of the world's most economically important spice crops, is increasingly challenged by climate-related stresses, emerging pests and diseases, and declining soil health, all of which threaten its productivity and sustainability. While previous reviews have predominantly focused on black pepper genomic resources, breeding strategies, and disease management, the integration of multi-omics technologies, microbiome science, and artificial intelligence (AI) to enhance its stress resilience has received comparatively limited attention. This review synthesizes recent advances in the molecular mechanisms underlying black pepper responses to biotic and abiotic stresses, with emphasis on omics approaches (such as genomics and transcriptomics), as well as the roles of beneficial microbial communities in enhancing stress tolerance, nutrient acquisition, and disease suppression. We further discuss emerging microbiome-assisted strategies, including the development of beneficial microbial consortia and targeted manipulation of microbial functions, for enhancing black pepper resilience under changing environmental conditions. In addition, we explore how AI-driven analytical approaches can integrate complex multi-omics and microbiome datasets to unravel the complex molecular networks governing black pepper-microbe interactions under stress conditions and accelerate precision breeding. By integrating genomics, microbial ecology, and AI, this review presents a systems-level framework for understanding and improving stress resilience in black pepper. This interdisciplinary perspective highlights new opportunities to accelerate the development of climate-resilient cultivars and advance sustainable black pepper production.},
}

@article {pmid42511815,
year = {2026},
author = {Nardelli, C and Nunziato, M and Di Maggio, F and Gelzo, M and Boccia, G and Maione, F and Peltrini, R and Carbone, F and Caldora, F and Corcione, F and De Palma, GD and Pilone, V and Castaldo, G and Matarese, G and Salvatore, F and Bruzzese, D and Sacchetti, L},
title = {CCL2: A Pro-Inflammatory Driver and Candidate Diagnostic Biomarker in Colorectal Cancer Patients.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511815},
issn = {1422-0067},
support = {RF-2010-23183729//Ministero della Salute/ ; CIRO project//Regione Campania/ ; DD 366/2018//Regione Campania/ ; 63/2024 and 32/2025//Regione Campania/ ; },
abstract = {Chronic inflammation and immune remodeling are key features of colorectal cancer (CRC) development and progression, particularly because of the high level of microbiome presence. Among inflammatory mediators, CCL2 has been implicated in the recruitment of monocytes and tumor-associated macrophages, supporting its potential role as a marker of CRC-associated inflammatory remodeling. Therefore, we evaluated nine circulating inflammatory mediators, including CCL2, to assess their potential diagnostic value in patients with CRC. The study included 96 individuals, comprising 52 CRC patients and 44 healthy controls. Plasma cytokine levels were measured using the ProteinSimple Ella microfluidic immunoassay platform, and analyses were also stratified according to sex and BMI category (BMI < 25 vs. ≥25 kg/m[2]). Patients with CRC had significantly higher levels of CCL2 and IL-6 than healthy controls (p-value < 0.001), regardless of gender or overweight or obesity, confirming a chronic pro-tumor inflammatory profile. Among all markers, CCL2 showed strong exploratory diagnostic performance with an AUC of 0.918, 90.4% sensitivity, and 90.9% specificity (cut-off 436.5 pg/mL). This study highlights the central role of CCL2 as a candidate marker of systemic chronic inflammation associated with colorectal cancer.},
}

@article {pmid42511820,
year = {2026},
author = {Jakoniuk, M and Kler, K and Kler, A and Rak, K and Ponikowska, M},
title = {NK Cell Disfunction in Atopic Dermatitis: A Missing Link Between Type 2 Inflammation, Microbial Dysbiosis and Antiviral Immunity.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511820},
issn = {1422-0067},
abstract = {Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disorder driven by epidermal barrier defects and dysregulated Th2 cell responses. While therapies primarily address adaptive immunity, the role of Natural Killer (NK) cells remains underappreciated. This review analyzes NK cell dysfunctions in AD pathogenesis, evaluating their contributions to compromised skin immunity, microbial dysbiosis, and secondary infections. Accumulating evidence reveals a systemic deficiency of mature, cytotoxic CD56[dim] and NKp80+ NK cell subsets in peripheral blood, correlating with disease severity. Within the cutaneous microenvironment, Staphylococcus aureus subverts defenses by utilizing leukocidins to lyse mature NK cells, while superantigens drive an aberrant, pro-inflammatory CD57[-]NKG2+ phenotype, exacerbating inflammation. Furthermore, localized exhaustion of functional NK cells and failure to produce interferon-gamma directly explains AD patients' unique susceptibility to severe viral complications like eczema herpeticum. Importantly, treatments such as dupilumab and gut microbiota transplantations demonstrate that these NK cell aberrations are reversible, shifting immunity toward a normalized regulatory state. In conclusion, the NK cell compartment represents a vital regulatory axis bridging innate and adaptive immunity. Targeting this axis, particularly through IL-15 superagonists, offers a promising therapeutic frontier to suppress type 2 inflammation and restore antimicrobial defenses.},
}

@article {pmid42511831,
year = {2026},
author = {Küçükkasap, T and Yavuz, A and Kuran, Ö},
title = {Fermented Foods, Functional Nutrition, and Maternal Gut Microbiota During Pregnancy: Molecular Mechanisms and the Maternal-Infant Microbiome Axis.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511831},
issn = {1422-0067},
abstract = {Pregnancy is associated with profound metabolic, hormonal, and immunological adaptations accompanied by dynamic alterations in maternal gut microbiota composition and function. Emerging evidence suggests that maternal diet is a major regulator of these microbiota-related changes and may influence maternal-fetal health through microbial metabolites and host signaling pathways. Fermented foods and functional dietary components, including prebiotics, probiotics, synbiotics, and polyphenols, have gained increasing attention because of their potential to modulate gut microbial diversity, intestinal barrier integrity, inflammatory responses, and metabolic homeostasis. Mechanistically, these effects are mediated through pathways involving short-chain fatty acids, G protein-coupled receptors, nuclear factor kappa B signaling, histone deacetylase inhibition, and immune cell regulation. Altered microbiota-associated signaling has been linked to gestational metabolic disorders such as obesity, gestational diabetes mellitus, and preeclampsia, as well as fetal immune and metabolic programming. Particular emphasis is placed on the maternal-infant microbiome axis, highlighting how maternal nutrition and microbiota-mediated signaling may influence microbial transmission, fetal programming, and early-life microbiome development. This review summarizes current evidence regarding pregnancy-associated gut microbiota alterations and discusses the molecular mechanisms through which fermented foods and functional nutrition may influence maternal and fetal health outcomes.},
}

@article {pmid42511834,
year = {2026},
author = {Khalil, M and Mahdi, L and Madani, A and Arzouni, A and Lanza, E and Piazzai, C and Marino, M and Portincasa, P},
title = {Neuroglobin: A New Player in the Gut-Brain Axis.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511834},
issn = {1422-0067},
support = {PNRR-MAD-2022-12375639//PNRR-MAD-2022-12375639 - Missione 6/Componente 2/Investimento 2.1 'Rafforzamento e po-tenziamento della ricerca biomedica del SSN' EU - Next Generation EU CUP B93C22001860007 and EU CUP J83C220020300007./ ; },
abstract = {Neuroglobin (NGB), initially identified for its oxygen-binding capacity in neuronal tissues, has emerged as a multifunctional protein involved in neuroprotection, oxidative stress regulation, and mitochondrial homeostasis. Although its functions have been extensively studied in the central nervous system (CNS), its potential role in the gut-brain axis (GBA) remains largely unexplored. The GBA integrates neural, endocrine, immune, and metabolic signaling between the gastrointestinal tract and the brain, and growing evidence from microbiome, neurobiology, endocrinology, and nutrition research suggests that several pathways involved in GBA signaling may also influence NGB expression or activity. However, direct experimental evidence, particularly from in vivo studies, remains limited. This hypothesis-driven review integrates evidence from diverse fields to explore the possibility that NGB may represent a molecular link between gut-derived signals and neuroprotective mechanisms. We summarize current knowledge of NGB biology and discuss indirect evidence indicating that microbial metabolites, dietary phytochemicals, and hormonal mediators, including estradiol, may converge on pathways associated with NGB regulation. Based on these observations, we propose a conceptual framework in which NGB could participate in gut-brain communication while emphasizing that this hypothesis requires experimental validation. By bringing together findings that have not previously been considered within a unified context, this review highlights key knowledge gaps, opens new perspectives on the potential involvement of NGB in the GBA, and provides a foundation for future mechanistic studies in neurodegenerative and neuroinflammatory disorders.},
}

@article {pmid42511843,
year = {2026},
author = {Rajarathinam, B and Nair, PV and Murali, N and Lekshmi, G and Sajeev, AK and Pillai, AB and Thomas, A and Hely, S and Arun, K and Prakash, V and Nair, BG and Venugopal, P and Aradhya, R},
title = {Antibiotic Class-Specific Effects on Inflammatory Bowel Disease: Microbiome Disruption, Risk, and Recovery.},
journal = {International journal of molecular sciences},
volume = {27},
number = {14},
pages = {},
pmid = {42511843},
issn = {1422-0067},
abstract = {Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are chronic inflammatory diseases resulting from complex interactions between host genetics, environmental factors, immune dysregulation, and the gut microbiome. Among environmental exposures, antibiotics have emerged as important factors of IBD risk and disease course because of their profound effects on intestinal microbial communities. This review synthesizes current evidence on the class-specific effects of antibiotics on IBD, integrating epidemiological, mechanistic, and clinical studies to examine how different antibiotic classes influence disease susceptibility, progression, and microbiome recovery. Current evidence indicates that antibiotic-associated IBD risk varies according to antibiotic class, cumulative exposure, age at exposure, and antimicrobial spectrum, with broad-spectrum and anti-anaerobic agents showing the strongest associations. Mechanistically, antibiotics promote dysbiosis by depleting beneficial commensal bacteria, disrupting microbial metabolite production, expanding pathobionts and the intestinal resistome, and impairing epithelial barrier integrity and immune homeostasis. The review also discusses microbiome-preserving and microbiome-restorative approaches, including antimicrobial stewardship, fecal microbiota transplantation, prebiotics, probiotics, synbiotics, postbiotics, and dietary interventions, as potential strategies to mitigate antibiotic-associated dysbiosis. Overall, the evidence highlights the class-specific effects of antibiotics in IBD and underscores the importance of microbiome-informed antimicrobial stewardship and precision therapeutic strategies to optimize patient outcomes while minimizing long-term disruptions of host-microbiome homeostasis.},
}