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RJR: Recommended Bibliography 29 Sep 2026 at 01:54 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2026-09-26
Developmental Origins of Health and Disease: The role of Clostridioides difficile Colonization of Gut Microbiota During Infancy.
Archives of medical research, 58(1):103526 pii:S0188-4409(26)00148-7 [Epub ahead of print].
The DOHaD theory was originally proposed to explain the link between fetal development and risk for non-communicable disease - NCD. With advancements in human microbiome research, this theory has been extended to consider postnatal development of the infant gut microbiome and how this contributes to NCD trajectories. C. difficile transiently colonizes the gut microbiota of up to 50% of infants without causing symptoms, but has been associated with disease in the longterm. We reviewed and summarized the current literature to identify prenatal, birth and postnatal factors contributing to C. difficile colonization, and subsequent changes in host biology and NCD outcomes. Many early-life factors promote C. difficile colonization, including prenatal overweight, cesarean birth, hospitalization, antibiotic exposure, formula feeding, histamine-2 receptor antagonist treatment, household pets and smoking, and daycare attendance. Whereas, prenatal milk consumption and having siblings seem to protect against colonization. When C. difficile is present in the gut, associated changes to gut microbiota and metabolites are reported in observational studies. Clinical trial evidence suggests that preceding changes like a reduction in Bifidobacterium species, could promote C. difficile colonization. C. difficile colonization during infancy increases the risk for NCD, including obesity and many atopic diseases (asthma, eczema, food and peanut sensitization). Furthermore, its colonization and abundance was found to be a statistical mediator of these health outcomes, pointing to a potential mediating role for C. difficile in NCD onset. Evidence from the current literature supports the inclusion of C. difficile colonization during infancy as an important biomarker in the developmental origins of disease.
Additional Links: PMID-42800207
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PubMed:
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@article {pmid42800207,
year = {2026},
author = {Challa, S and Kudo, N and Bashar, S and Amjad, S and Kozyrskyj, AL},
title = {Developmental Origins of Health and Disease: The role of Clostridioides difficile Colonization of Gut Microbiota During Infancy.},
journal = {Archives of medical research},
volume = {58},
number = {1},
pages = {103526},
doi = {10.1016/j.arcmed.2026.103526},
pmid = {42800207},
issn = {1873-5487},
abstract = {The DOHaD theory was originally proposed to explain the link between fetal development and risk for non-communicable disease - NCD. With advancements in human microbiome research, this theory has been extended to consider postnatal development of the infant gut microbiome and how this contributes to NCD trajectories. C. difficile transiently colonizes the gut microbiota of up to 50% of infants without causing symptoms, but has been associated with disease in the longterm. We reviewed and summarized the current literature to identify prenatal, birth and postnatal factors contributing to C. difficile colonization, and subsequent changes in host biology and NCD outcomes. Many early-life factors promote C. difficile colonization, including prenatal overweight, cesarean birth, hospitalization, antibiotic exposure, formula feeding, histamine-2 receptor antagonist treatment, household pets and smoking, and daycare attendance. Whereas, prenatal milk consumption and having siblings seem to protect against colonization. When C. difficile is present in the gut, associated changes to gut microbiota and metabolites are reported in observational studies. Clinical trial evidence suggests that preceding changes like a reduction in Bifidobacterium species, could promote C. difficile colonization. C. difficile colonization during infancy increases the risk for NCD, including obesity and many atopic diseases (asthma, eczema, food and peanut sensitization). Furthermore, its colonization and abundance was found to be a statistical mediator of these health outcomes, pointing to a potential mediating role for C. difficile in NCD onset. Evidence from the current literature supports the inclusion of C. difficile colonization during infancy as an important biomarker in the developmental origins of disease.},
}
RevDate: 2026-09-26
Phylogenomic analysis of Rhizobiaceae strains from the Cerrado biome, Brazil, reveals a novel genus, Brasilibacterium gen. nov., and three novel species: Brasilibacterium cachoeirinhense sp. nov., Brasilibacterium lagoinhense sp. nov., and Martinezella lalimensis sp. nov.
Systematic and applied microbiology, 49(6):126772 pii:S0723-2020(26)00080-9 [Epub ahead of print].
Rhizobiaceae is one of the most representative families, encompassing rhizobial species, valuable allies in the sustainable production of legumes such as cowpea (Vigna unguiculata). Interestingly, beyond rhizobia, studies have increasingly reported the presence of a wide diversity of non-symbiotic bacteria that compose the microbiome of cowpea nodules. In this study, we performed a systematic analysis, with an emphasis on phylogenomic aspects, of 12 strains trapped from cowpea in soils of indigenous lands in Mato Grosso do Sul, Central-Western Brazil (Cerrado biome), which had been preliminarily characterized. The results highlighted the rich and little-explored Rhizobiaceae biodiversity, revealing a novel genus, Brasilibacterium gen. nov., and three novel species: Brasilibacterium cachoeirinhense sp. nov. (CNPSo 3794[T] = BR 15710[T] = LMG 34800[T]), Brasilibacterium lagoinhense sp. nov. (CNPSo 3920[T] = BR 15708[T] = 34801[T]), and Martinezella lalimensis sp. nov. (CNPSo 3959[T] = BR 15709[T] = LMG 34802[T]). However, none of the strains belonging to these novel species was able to re-nodulate cowpea or the promiscuous legumes Phaseolus vulgaris and Macroptilium atropurpureum, suggesting either the loss of symbiotic genes or their endophytic nature. In addition to the novel species accessed, "Rhizobium atlanticum", "Martinezella aureum", "Martinezella centroccidentale", "Martinezella hainanensis", and "Martinezella dioscoreae" were also identified based on genomic sequences, with the latter two reported for the first time in Brazil.
Additional Links: PMID-42800287
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PubMed:
Citation:
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@article {pmid42800287,
year = {2026},
author = {Delai, CV and Moura, FT and Klepa, MS and Assunção, MC and Kitagawa, HY and Ercole, TG and Ribeiro, RA and Nogueira, MA and Hungria, M},
title = {Phylogenomic analysis of Rhizobiaceae strains from the Cerrado biome, Brazil, reveals a novel genus, Brasilibacterium gen. nov., and three novel species: Brasilibacterium cachoeirinhense sp. nov., Brasilibacterium lagoinhense sp. nov., and Martinezella lalimensis sp. nov.},
journal = {Systematic and applied microbiology},
volume = {49},
number = {6},
pages = {126772},
doi = {10.1016/j.syapm.2026.126772},
pmid = {42800287},
issn = {1618-0984},
abstract = {Rhizobiaceae is one of the most representative families, encompassing rhizobial species, valuable allies in the sustainable production of legumes such as cowpea (Vigna unguiculata). Interestingly, beyond rhizobia, studies have increasingly reported the presence of a wide diversity of non-symbiotic bacteria that compose the microbiome of cowpea nodules. In this study, we performed a systematic analysis, with an emphasis on phylogenomic aspects, of 12 strains trapped from cowpea in soils of indigenous lands in Mato Grosso do Sul, Central-Western Brazil (Cerrado biome), which had been preliminarily characterized. The results highlighted the rich and little-explored Rhizobiaceae biodiversity, revealing a novel genus, Brasilibacterium gen. nov., and three novel species: Brasilibacterium cachoeirinhense sp. nov. (CNPSo 3794[T] = BR 15710[T] = LMG 34800[T]), Brasilibacterium lagoinhense sp. nov. (CNPSo 3920[T] = BR 15708[T] = 34801[T]), and Martinezella lalimensis sp. nov. (CNPSo 3959[T] = BR 15709[T] = LMG 34802[T]). However, none of the strains belonging to these novel species was able to re-nodulate cowpea or the promiscuous legumes Phaseolus vulgaris and Macroptilium atropurpureum, suggesting either the loss of symbiotic genes or their endophytic nature. In addition to the novel species accessed, "Rhizobium atlanticum", "Martinezella aureum", "Martinezella centroccidentale", "Martinezella hainanensis", and "Martinezella dioscoreae" were also identified based on genomic sequences, with the latter two reported for the first time in Brazil.},
}
RevDate: 2026-09-26
Effects of biogas slurry-borne antibiotics and polypropylene microplastics on the rhizosphere microbiome and metabolome of Hybrid Pennisetum.
Ecotoxicology and environmental safety, 324:120843 pii:S0147-6513(26)01173-5 [Epub ahead of print].
Antibiotic residues in biogas slurry and microplastic contamination are increasingly occurring in agricultural soils. However, their combined effects on rhizosphere ecological processes remain poorly understood. In this study, the individual and combined effects of polypropylene microplastics (PP-MPs, 1% w/w) and biogas slurry (BS, 0.5% w/w) on the rhizosphere soil of Hybrid Pennisetum were investigated by conducting an integrated analysis of 16S rRNA gene sequencing and untargeted metabolomics. The results revealed that PP-MPs alone significantly reduced soil bacterial α-diversity and inhibited urease, sucrase, and alkaline phosphatase activities while significantly increasing catalase and fluorescein diacetate hydrolase activities. BS amendment increased nutrient availability and microbial diversity. Notably, compared with BS alone, the coapplication of PP-MPs and BS induced significant soil acidification and increased the retention of multiple antibiotics, including tetracyclines, fluoroquinolones, and macrolides, in the rhizosphere. The combined treatment generated a unique bacterial community assemblage with increased Pseudomonadota and Bacteroidota abundances, restored microbial co-occurrence network complexity, and uniquely enriched pathways related to secondary metabolite biosynthesis and microbial metabolism in diverse environments. Procrustes analysis confirmed the tight coupling between shifts in the microbial community and metabolic reprogramming. Key hub metabolites, including prostaglandin derivatives and hydroxylated fatty acids, exhibited strong connectivity with genera frequently associated with antibiotic resistance potential, such as Pseudomonas, Bacillus, and Streptomyces. Overall, PP-MPs altered the ecological outcome of biogas slurry application by enhancing antibiotic persistence and coupling nutrient enrichment with contaminant-driven microbial and metabolic reprogramming. These results highlight the need to consider microplastic contamination when evaluating the agricultural safety of biogas slurry application in forage production systems.
Additional Links: PMID-42800336
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PubMed:
Citation:
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@article {pmid42800336,
year = {2026},
author = {Song, X and Teng, L and Jiang, H and Sun, X and Jiang, J and Zheng, X},
title = {Effects of biogas slurry-borne antibiotics and polypropylene microplastics on the rhizosphere microbiome and metabolome of Hybrid Pennisetum.},
journal = {Ecotoxicology and environmental safety},
volume = {324},
number = {},
pages = {120843},
doi = {10.1016/j.ecoenv.2026.120843},
pmid = {42800336},
issn = {1090-2414},
abstract = {Antibiotic residues in biogas slurry and microplastic contamination are increasingly occurring in agricultural soils. However, their combined effects on rhizosphere ecological processes remain poorly understood. In this study, the individual and combined effects of polypropylene microplastics (PP-MPs, 1% w/w) and biogas slurry (BS, 0.5% w/w) on the rhizosphere soil of Hybrid Pennisetum were investigated by conducting an integrated analysis of 16S rRNA gene sequencing and untargeted metabolomics. The results revealed that PP-MPs alone significantly reduced soil bacterial α-diversity and inhibited urease, sucrase, and alkaline phosphatase activities while significantly increasing catalase and fluorescein diacetate hydrolase activities. BS amendment increased nutrient availability and microbial diversity. Notably, compared with BS alone, the coapplication of PP-MPs and BS induced significant soil acidification and increased the retention of multiple antibiotics, including tetracyclines, fluoroquinolones, and macrolides, in the rhizosphere. The combined treatment generated a unique bacterial community assemblage with increased Pseudomonadota and Bacteroidota abundances, restored microbial co-occurrence network complexity, and uniquely enriched pathways related to secondary metabolite biosynthesis and microbial metabolism in diverse environments. Procrustes analysis confirmed the tight coupling between shifts in the microbial community and metabolic reprogramming. Key hub metabolites, including prostaglandin derivatives and hydroxylated fatty acids, exhibited strong connectivity with genera frequently associated with antibiotic resistance potential, such as Pseudomonas, Bacillus, and Streptomyces. Overall, PP-MPs altered the ecological outcome of biogas slurry application by enhancing antibiotic persistence and coupling nutrient enrichment with contaminant-driven microbial and metabolic reprogramming. These results highlight the need to consider microplastic contamination when evaluating the agricultural safety of biogas slurry application in forage production systems.},
}
RevDate: 2026-09-26
Microbial filtering and functional reprogramming in soil exposed to spent NCM battery black powder.
Ecotoxicology and environmental safety, 324:120847 pii:S0147-6513(26)01177-2 [Epub ahead of print].
Spent lithium-ion battery black powder is an emerging complex contaminant, which contains transition metals, residual electrolyte salts, and compounds derived from organic electrolytes or binders. Its ecological effects on soil microbiomes remain poorly understood. Here, we designed a soil microcosm experiment with using red soil exposed to a concentration gradient of black powder derived from nickel-cobalt-manganese (NCM) lithium-ion batteries. Samples were collected at two incubation time points and analyzed by shotgun metagenomic sequencing. Black powder exposure produced a nonlinear taxonomic response, with species-level alpha diversity increasing under intermediate exposure, while rare-taxon abundance distributions shifted markedly under medium and high exposure. The LEfSe and PLS-DA analyses identified concentration- and time-dependent indicator taxa, including enrichment of Actinomycetota-related taxa and depletion of Nitrospira and Candidatus Methylomirabilis under high exposure. Community structure diverged significantly along the concentration gradient, and PERMANOVA attributed 23.2% of taxonomic variation to treatment. Structural equation modeling showed no significant direct path from black powder concentration to functional potential; instead, the model was consistent with a possible indirect association through community restructuring. Functional alpha diversity generally declined with increasing black powder concentration. High concentration exposure was associated with reduced relative abundance of KEGG Orthology entries (KOs) related to nitrogen cycling and increased stress-response and organic-matter-decomposition signatures. Overall, these results suggest that NCM-derived black powder can alter soil microbial functional profiles by reshaping community composition.
Additional Links: PMID-42800338
Publisher:
PubMed:
Citation:
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@article {pmid42800338,
year = {2026},
author = {Gui, Y and Yu, W and Shi, Y and Li, Y and Yang, X and Zhang, H and Yan, W and Liu, Q and Jiang, G},
title = {Microbial filtering and functional reprogramming in soil exposed to spent NCM battery black powder.},
journal = {Ecotoxicology and environmental safety},
volume = {324},
number = {},
pages = {120847},
doi = {10.1016/j.ecoenv.2026.120847},
pmid = {42800338},
issn = {1090-2414},
abstract = {Spent lithium-ion battery black powder is an emerging complex contaminant, which contains transition metals, residual electrolyte salts, and compounds derived from organic electrolytes or binders. Its ecological effects on soil microbiomes remain poorly understood. Here, we designed a soil microcosm experiment with using red soil exposed to a concentration gradient of black powder derived from nickel-cobalt-manganese (NCM) lithium-ion batteries. Samples were collected at two incubation time points and analyzed by shotgun metagenomic sequencing. Black powder exposure produced a nonlinear taxonomic response, with species-level alpha diversity increasing under intermediate exposure, while rare-taxon abundance distributions shifted markedly under medium and high exposure. The LEfSe and PLS-DA analyses identified concentration- and time-dependent indicator taxa, including enrichment of Actinomycetota-related taxa and depletion of Nitrospira and Candidatus Methylomirabilis under high exposure. Community structure diverged significantly along the concentration gradient, and PERMANOVA attributed 23.2% of taxonomic variation to treatment. Structural equation modeling showed no significant direct path from black powder concentration to functional potential; instead, the model was consistent with a possible indirect association through community restructuring. Functional alpha diversity generally declined with increasing black powder concentration. High concentration exposure was associated with reduced relative abundance of KEGG Orthology entries (KOs) related to nitrogen cycling and increased stress-response and organic-matter-decomposition signatures. Overall, these results suggest that NCM-derived black powder can alter soil microbial functional profiles by reshaping community composition.},
}
RevDate: 2026-09-26
Integrated multi-omics reveals persistent extracellular matrix remodeling in chronic duck footpad dermatitis.
Poultry science, 105(12):107830 pii:S0032-5791(26)01462-8 [Epub ahead of print].
Footpad dermatitis (FPD) is a common welfare and production problem in intensively reared poultry, yet the mechanisms responsible for its chronic progression remain poorly understood. To investigate the biological changes associated with chronic FPD, healthy and FPD-affected ducks (Health and FPD groups) were compared using histopathology, transcriptomics, proteomics, microbiome profiling, and metabolomics, with 3-8 biological replicates per group depending on the analytical platform. Histological examination demonstrated marked extracellular matrix (ECM) remodeling, characterized by collagen disorganization, an altered type I/type III collagen ratio, and disrupted matrix organization. Transcriptomic and proteomic analyses consistently identified alterations in ECM-receptor interaction, focal adhesion, and integrin β1/TGF-β-related signaling pathways, showing host molecular alterations associated with persistent ECM remodeling. FPD was also accompanied by marked alterations in both skin and gut microbial communities together with widespread metabolic alterations. Correlation analysis further identified associations among differential microbial taxa, metabolites, and ECM-related genes and proteins. Collectively, these findings indicate that chronic FPD is characterized by persistent extracellular matrix remodeling accompanied by extensive host molecular, microbial, and metabolic alterations. This study extends the current understanding of chronic FPD and provides a foundation for future studies aimed at improving footpad health, animal welfare, and production sustainability in poultry.
Additional Links: PMID-42800451
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PubMed:
Citation:
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@article {pmid42800451,
year = {2026},
author = {Ma, C and Zong, Y and Zhang, H and Liang, Z and Pan, A and Pi, J and Wu, Y},
title = {Integrated multi-omics reveals persistent extracellular matrix remodeling in chronic duck footpad dermatitis.},
journal = {Poultry science},
volume = {105},
number = {12},
pages = {107830},
doi = {10.1016/j.psj.2026.107830},
pmid = {42800451},
issn = {1525-3171},
abstract = {Footpad dermatitis (FPD) is a common welfare and production problem in intensively reared poultry, yet the mechanisms responsible for its chronic progression remain poorly understood. To investigate the biological changes associated with chronic FPD, healthy and FPD-affected ducks (Health and FPD groups) were compared using histopathology, transcriptomics, proteomics, microbiome profiling, and metabolomics, with 3-8 biological replicates per group depending on the analytical platform. Histological examination demonstrated marked extracellular matrix (ECM) remodeling, characterized by collagen disorganization, an altered type I/type III collagen ratio, and disrupted matrix organization. Transcriptomic and proteomic analyses consistently identified alterations in ECM-receptor interaction, focal adhesion, and integrin β1/TGF-β-related signaling pathways, showing host molecular alterations associated with persistent ECM remodeling. FPD was also accompanied by marked alterations in both skin and gut microbial communities together with widespread metabolic alterations. Correlation analysis further identified associations among differential microbial taxa, metabolites, and ECM-related genes and proteins. Collectively, these findings indicate that chronic FPD is characterized by persistent extracellular matrix remodeling accompanied by extensive host molecular, microbial, and metabolic alterations. This study extends the current understanding of chronic FPD and provides a foundation for future studies aimed at improving footpad health, animal welfare, and production sustainability in poultry.},
}
RevDate: 2026-09-26
Metabolomic signatures associated with probiotic use in atopic dermatitis: An exploratory study.
Journal of pharmaceutical and biomedical analysis, 283:117744 pii:S0731-7085(26)00412-7 [Epub ahead of print].
Atopic dermatitis (AD) is a chronic inflammatory skin disorder modulated by complex interactions between immune dysregulation and compromised skin-barrier integrity, in which the gut microbiome may play a role in the natural course of the disease. Therefore, by influencing the composition of the gut microbiome, one of the effective therapeutic options for AD treatment may include probiotics. To extend our knowledge of probiotics and how gut microbiome may affect disease evolution, this exploratory study assessed the systemic effects of a 90-day probiotic supplementation in AD patients, integrating clinical assessment, serum cytokine profile, and GC-MS-based metabolomics. Clinical improvement was observed following probiotic supplementation, with reductions in treated patients of the main clinical indices to assess the AD severity (i.e., SCORAD, EASI, and DLQI). These patients also showed reduced serum levels of pro-inflammatory cytokines (i.e., IL-1β, IL-6, and IL-8), indicating attenuation of systemic inflammation. Moreover, metabolomic analysis revealed a marked change between baseline (T0) and post-treatment (T1) serum profiles of AD patients, consistent with a reduction in inflammatory signalling and improved clinical status. These findings highlight meaningful metabolic remodelling associated with probiotic supplementation and support further investigation of probiotics as a potential adjunctive strategy in AD.
Additional Links: PMID-42800464
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PubMed:
Citation:
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@article {pmid42800464,
year = {2026},
author = {Salvatore, MM and Maione, A and Di Brizzi, EV and Fedi, L and de Alteriis, E and Andolfi, A and Salvatore, F and Argenziano, G and Guida, M and Brancaccio, G and Galdiero, E},
title = {Metabolomic signatures associated with probiotic use in atopic dermatitis: An exploratory study.},
journal = {Journal of pharmaceutical and biomedical analysis},
volume = {283},
number = {},
pages = {117744},
doi = {10.1016/j.jpba.2026.117744},
pmid = {42800464},
issn = {1873-264X},
abstract = {Atopic dermatitis (AD) is a chronic inflammatory skin disorder modulated by complex interactions between immune dysregulation and compromised skin-barrier integrity, in which the gut microbiome may play a role in the natural course of the disease. Therefore, by influencing the composition of the gut microbiome, one of the effective therapeutic options for AD treatment may include probiotics. To extend our knowledge of probiotics and how gut microbiome may affect disease evolution, this exploratory study assessed the systemic effects of a 90-day probiotic supplementation in AD patients, integrating clinical assessment, serum cytokine profile, and GC-MS-based metabolomics. Clinical improvement was observed following probiotic supplementation, with reductions in treated patients of the main clinical indices to assess the AD severity (i.e., SCORAD, EASI, and DLQI). These patients also showed reduced serum levels of pro-inflammatory cytokines (i.e., IL-1β, IL-6, and IL-8), indicating attenuation of systemic inflammation. Moreover, metabolomic analysis revealed a marked change between baseline (T0) and post-treatment (T1) serum profiles of AD patients, consistent with a reduction in inflammatory signalling and improved clinical status. These findings highlight meaningful metabolic remodelling associated with probiotic supplementation and support further investigation of probiotics as a potential adjunctive strategy in AD.},
}
RevDate: 2026-09-28
CmpDate: 2026-09-27
Microbial community coalescence restructures co-occurrence architecture and generates regime-specific patterns of network complexity and stability.
ISME communications, 6(1):ycag260.
Microbial community coalescence (MCC), the mixing of distinct microbiomes, is increasingly recognized as an important process in natural and managed microbial systems. However, how MCC reorganizes species association architecture and whether this restructuring alters community stability remain poorly understood. Here, we investigated how MCC modifies microbial co-occurrence networks and whether resulting architectures deviate from expectations based on stochastic reshuffling or direct compositional mixing of donor communities. Using controlled soil microcosms, we manipulated pairwise coalescence scenarios across a gradient of biotic dilution and tracked community reassembly over 30 days. Empirical association networks were then compared to two reference frameworks: a stochastic balanced-averaging null model and a donor-preserving compositional mixing model. Across treatments, MCC produced extensive restructuring of species association architecture, with empirical networks exhibiting substantially higher node turnover and a predominance of novel correlations relative to both reference expectations. Higher-order network properties also frequently diverged from expected simulated outcomes, indicating that coalescence reshapes correlation architecture beyond stochastic or additive donor mixing. The consequences of this restructuring for network stability were strongly context-dependent. In one coalescence regime, reductions in biotic complexity led to coordinated declines in network complexity and robustness, accompanied by increased fragmentation and vulnerability, whereas other regimes remained insensitive to the biotic dilution gradient. Moreover, community diversity predicted network architecture only under specific coalescence contexts, revealing regime-specific relationships between community diversity, network complexity, and network stability. Together, these results demonstrate that MCC reorganizes microbial association networks in patterns consistent with context-dependent ecological processes that generate distinct complexity and stability patterns.
Additional Links: PMID-42801049
PubMed:
Citation:
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@article {pmid42801049,
year = {2026},
author = {Bresciani, L and Custer, GF and Dini-Andreote, F},
title = {Microbial community coalescence restructures co-occurrence architecture and generates regime-specific patterns of network complexity and stability.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag260},
pmid = {42801049},
issn = {2730-6151},
abstract = {Microbial community coalescence (MCC), the mixing of distinct microbiomes, is increasingly recognized as an important process in natural and managed microbial systems. However, how MCC reorganizes species association architecture and whether this restructuring alters community stability remain poorly understood. Here, we investigated how MCC modifies microbial co-occurrence networks and whether resulting architectures deviate from expectations based on stochastic reshuffling or direct compositional mixing of donor communities. Using controlled soil microcosms, we manipulated pairwise coalescence scenarios across a gradient of biotic dilution and tracked community reassembly over 30 days. Empirical association networks were then compared to two reference frameworks: a stochastic balanced-averaging null model and a donor-preserving compositional mixing model. Across treatments, MCC produced extensive restructuring of species association architecture, with empirical networks exhibiting substantially higher node turnover and a predominance of novel correlations relative to both reference expectations. Higher-order network properties also frequently diverged from expected simulated outcomes, indicating that coalescence reshapes correlation architecture beyond stochastic or additive donor mixing. The consequences of this restructuring for network stability were strongly context-dependent. In one coalescence regime, reductions in biotic complexity led to coordinated declines in network complexity and robustness, accompanied by increased fragmentation and vulnerability, whereas other regimes remained insensitive to the biotic dilution gradient. Moreover, community diversity predicted network architecture only under specific coalescence contexts, revealing regime-specific relationships between community diversity, network complexity, and network stability. Together, these results demonstrate that MCC reorganizes microbial association networks in patterns consistent with context-dependent ecological processes that generate distinct complexity and stability patterns.},
}
RevDate: 2026-09-28
CmpDate: 2026-09-27
Vaginal Microbiome Profiles and Reproductive Outcomes: Implications for Natural Conception and Assisted Reproduction.
Cureus, 18(8):e115276.
The vaginal microbiome is increasingly recognized as an important determinant of female reproductive health, with emerging evidence linking its composition and function to fertility, implantation, and pregnancy outcomes. This narrative review synthesizes current evidence on the role of the vaginal microbiome in natural conception and assisted reproductive technology (ART), with emphasis on underlying mechanisms, clinical implications, and emerging therapeutic applications. Contemporary literature examining vaginal microbiome composition, community state types (CSTs), host-microbiome interactions, and reproductive outcomes was qualitatively synthesized alongside evidence from mechanistic studies and emerging multi-omics and artificial intelligence (AI)-based approaches. Lactobacillus-dominant profiles, particularly those enriched in Lactobacillus crispatus, are often associated with more favorable reproductive outcomes, whereas Lactobacillus iners-dominant communities may show more variable associations; dysbiotic, highly diverse microbial profiles have been associated with adverse outcomes including infertility, implantation failure, and pregnancy loss, although these relationships vary according to the Lactobacillus species involved, sampling compartment, population studied, and reproductive endpoint. The vaginal microbiome may influence reproductive success through effects on epithelial barrier integrity, immune regulation, inflammatory signaling, microbial metabolite production, sperm function, and endometrial receptivity. Emerging evidence also supports functional interplay between the vaginal and endometrial microbial environments. In natural conception, microbial composition may affect sperm viability, fertilization, and early pregnancy maintenance, whereas in ART, it has been associated with implantation, clinical pregnancy, and live birth outcomes. Multi-omics and AI-based approaches may improve risk stratification and predictive modeling, while microbiome-directed interventions, including probiotics and vaginal microbiota transplantation, remain promising but investigational. The vaginal microbiome therefore represents a potential biomarker and investigational therapeutic target in reproductive medicine; however, routine clinical application remains limited by methodological heterogeneity, inconsistent definitions of dysbiosis, and insufficient interventional evidence. Standardized sampling and analytical methods, together with well-designed prospective and interventional studies, are needed before microbiome profiling and targeted modulation can be integrated into routine fertility care.
Additional Links: PMID-42801055
PubMed:
Citation:
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@article {pmid42801055,
year = {2026},
author = {Prakash, V and Galiotte, S and Mhatre, U and John, AC and Ahmadi, H and Manah, YM and Ahmed Ali Elgasim, D and Nair, AS and Rai, M},
title = {Vaginal Microbiome Profiles and Reproductive Outcomes: Implications for Natural Conception and Assisted Reproduction.},
journal = {Cureus},
volume = {18},
number = {8},
pages = {e115276},
pmid = {42801055},
issn = {2168-8184},
abstract = {The vaginal microbiome is increasingly recognized as an important determinant of female reproductive health, with emerging evidence linking its composition and function to fertility, implantation, and pregnancy outcomes. This narrative review synthesizes current evidence on the role of the vaginal microbiome in natural conception and assisted reproductive technology (ART), with emphasis on underlying mechanisms, clinical implications, and emerging therapeutic applications. Contemporary literature examining vaginal microbiome composition, community state types (CSTs), host-microbiome interactions, and reproductive outcomes was qualitatively synthesized alongside evidence from mechanistic studies and emerging multi-omics and artificial intelligence (AI)-based approaches. Lactobacillus-dominant profiles, particularly those enriched in Lactobacillus crispatus, are often associated with more favorable reproductive outcomes, whereas Lactobacillus iners-dominant communities may show more variable associations; dysbiotic, highly diverse microbial profiles have been associated with adverse outcomes including infertility, implantation failure, and pregnancy loss, although these relationships vary according to the Lactobacillus species involved, sampling compartment, population studied, and reproductive endpoint. The vaginal microbiome may influence reproductive success through effects on epithelial barrier integrity, immune regulation, inflammatory signaling, microbial metabolite production, sperm function, and endometrial receptivity. Emerging evidence also supports functional interplay between the vaginal and endometrial microbial environments. In natural conception, microbial composition may affect sperm viability, fertilization, and early pregnancy maintenance, whereas in ART, it has been associated with implantation, clinical pregnancy, and live birth outcomes. Multi-omics and AI-based approaches may improve risk stratification and predictive modeling, while microbiome-directed interventions, including probiotics and vaginal microbiota transplantation, remain promising but investigational. The vaginal microbiome therefore represents a potential biomarker and investigational therapeutic target in reproductive medicine; however, routine clinical application remains limited by methodological heterogeneity, inconsistent definitions of dysbiosis, and insufficient interventional evidence. Standardized sampling and analytical methods, together with well-designed prospective and interventional studies, are needed before microbiome profiling and targeted modulation can be integrated into routine fertility care.},
}
RevDate: 2026-09-28
CmpDate: 2026-09-27
Nutrition and Endometriosis: Current Evidence on Dietary Risk Factors and Clinical Impact - A Narrative Review.
Journal of inflammation research, 19:612344.
Endometriosis (EM) is a severe chronic inflammatory disease characterized by the presence of endometrium-like tissue outside the uterine cavity, causing pain and significantly reducing quality of life. Worldwide, around 10% of women of reproductive age are affected and there is no cure as of now. The limited treatment options focus on hormone therapy, surgery and pain management--without satisfactory long-term effects. Nutritional strategies might support the prevention and treatment of EM-associated pain as nutrients and phytochemicals exert anti-inflammatory and antioxidant effects, modulate the immune system and hormonal balance. In addition, diet is a key determinant of the composition, health, and function of the gut microbiome. To identify the multitude of potential nutrition-related factors that influence the clinical picture of EM, we conducted a targeted literature search in PubMed, Web of Science, and Google Scholar in 2025. This narrative review examines the association of thirteen areas-including macro- and micronutrients, dietary patterns, contaminants, allergens, and food intolerances-with the risk of EM and therapeutic options. At present, there is only limited scientific evidence regarding the therapeutic benefits of dietary strategies. There are promising indications for the supportive potential of an anti-inflammatory diet, based on elements of the MedD resulting in a regular intake of long-chain n-3 polyunsaturated fatty acids, secondary plant compounds, dietary fibers, vitamins, minerals and trace elements. Certain foods (or food groups) may contribute to a worsening of symptoms in individual patients with EM (eg, cruciferous vegetables, foods containing histamine, gluten, FODMAPs). Since these foods usually provide important nutrients, avoiding them as a preventive measure can lead to nutrient deficiencies. Therefore, individual assessment is required to determine the extent to which these foods are tolerated by women diagnosed with EM. To clarify the supportive role of personalized nutritional concepts to support therapy of EM, there is an urgent need for further high-quality studies.
Additional Links: PMID-42801160
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@article {pmid42801160,
year = {2026},
author = {Dawczynski, C and Raschke, J and Klein, L and Schmidt, I and Eichler, S and Förster, M and Velho, RV and Knappe-Drzikova, B and Mechsner, S and Maier, D and Haange, SB and Rolle-Kampczyk, UE and Von Bergen, M and Held, M and Varadarajan, S and Hitzler, M and Kolassa, I},
title = {Nutrition and Endometriosis: Current Evidence on Dietary Risk Factors and Clinical Impact - A Narrative Review.},
journal = {Journal of inflammation research},
volume = {19},
number = {},
pages = {612344},
pmid = {42801160},
issn = {1178-7031},
abstract = {Endometriosis (EM) is a severe chronic inflammatory disease characterized by the presence of endometrium-like tissue outside the uterine cavity, causing pain and significantly reducing quality of life. Worldwide, around 10% of women of reproductive age are affected and there is no cure as of now. The limited treatment options focus on hormone therapy, surgery and pain management--without satisfactory long-term effects. Nutritional strategies might support the prevention and treatment of EM-associated pain as nutrients and phytochemicals exert anti-inflammatory and antioxidant effects, modulate the immune system and hormonal balance. In addition, diet is a key determinant of the composition, health, and function of the gut microbiome. To identify the multitude of potential nutrition-related factors that influence the clinical picture of EM, we conducted a targeted literature search in PubMed, Web of Science, and Google Scholar in 2025. This narrative review examines the association of thirteen areas-including macro- and micronutrients, dietary patterns, contaminants, allergens, and food intolerances-with the risk of EM and therapeutic options. At present, there is only limited scientific evidence regarding the therapeutic benefits of dietary strategies. There are promising indications for the supportive potential of an anti-inflammatory diet, based on elements of the MedD resulting in a regular intake of long-chain n-3 polyunsaturated fatty acids, secondary plant compounds, dietary fibers, vitamins, minerals and trace elements. Certain foods (or food groups) may contribute to a worsening of symptoms in individual patients with EM (eg, cruciferous vegetables, foods containing histamine, gluten, FODMAPs). Since these foods usually provide important nutrients, avoiding them as a preventive measure can lead to nutrient deficiencies. Therefore, individual assessment is required to determine the extent to which these foods are tolerated by women diagnosed with EM. To clarify the supportive role of personalized nutritional concepts to support therapy of EM, there is an urgent need for further high-quality studies.},
}
RevDate: 2026-09-28
CmpDate: 2026-09-27
Gut Microbiota in Hepatocellular Carcinoma: Etiology-Specific Evidence, Mechanisms, and Translational Challenges.
Journal of hepatocellular carcinoma, 13:636365.
Hepatocellular carcinoma (HCC) usually develops in patients with chronic liver disease and remains a major cause of cancer-related death worldwide. Increasing evidence suggests that dysbiosis of the gut microbiota is related to hepatocarcinogenesis through the gut-liver axis. Patients with HCC often show enrichment of pro-inflammatory or endotoxin-producing bacteria and loss of short-chain fatty acid-producing and barrier-protective taxa. These changes may increase intestinal permeability and microbial translocation and may contribute to chronic hepatic inflammation, immune disturbance, and metabolic changes. Lipopolysaccharide, secondary bile acids, and trimethylamine-N-oxide are among the microbial products that may connect intestinal dysbiosis with liver fibrosis and tumor progression. Clinical studies have also examined microbial signatures for early HCC detection, risk stratification, recurrence, and response to immune checkpoint inhibitors. However, most cohorts are small and differ in etiology, region, medication exposure, and sequencing method. Animal studies indicate that antibiotics, probiotics, fecal microbiota transplantation, and diet can change tumor development or treatment response, but direct clinical evidence in HCC remains limited. This review summarizes the compositional, mechanistic, and clinical evidence and discusses the present status of microbiota-targeted strategies in HCC.
Additional Links: PMID-42801214
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@article {pmid42801214,
year = {2026},
author = {Guan, X},
title = {Gut Microbiota in Hepatocellular Carcinoma: Etiology-Specific Evidence, Mechanisms, and Translational Challenges.},
journal = {Journal of hepatocellular carcinoma},
volume = {13},
number = {},
pages = {636365},
pmid = {42801214},
issn = {2253-5969},
abstract = {Hepatocellular carcinoma (HCC) usually develops in patients with chronic liver disease and remains a major cause of cancer-related death worldwide. Increasing evidence suggests that dysbiosis of the gut microbiota is related to hepatocarcinogenesis through the gut-liver axis. Patients with HCC often show enrichment of pro-inflammatory or endotoxin-producing bacteria and loss of short-chain fatty acid-producing and barrier-protective taxa. These changes may increase intestinal permeability and microbial translocation and may contribute to chronic hepatic inflammation, immune disturbance, and metabolic changes. Lipopolysaccharide, secondary bile acids, and trimethylamine-N-oxide are among the microbial products that may connect intestinal dysbiosis with liver fibrosis and tumor progression. Clinical studies have also examined microbial signatures for early HCC detection, risk stratification, recurrence, and response to immune checkpoint inhibitors. However, most cohorts are small and differ in etiology, region, medication exposure, and sequencing method. Animal studies indicate that antibiotics, probiotics, fecal microbiota transplantation, and diet can change tumor development or treatment response, but direct clinical evidence in HCC remains limited. This review summarizes the compositional, mechanistic, and clinical evidence and discusses the present status of microbiota-targeted strategies in HCC.},
}
RevDate: 2026-09-28
CmpDate: 2026-09-27
Effect of low dose azithromycin on the fecal microbiome and fecal bile acids in healthy dogs.
Journal of veterinary internal medicine, 40(5):.
BACKGROUND: Azithromycin has prokinetic effects at low doses in people, cats, and anecdotally, in dogs; however, antibiotics alter the fecal microbiome and metabolome.
HYPOTHESIS/OBJECTIVES: To prospectively evaluate the effects of low-dose azithromycin, hypothesizing that it would alter the fecal microbiome and fecal bile acids in healthy dogs.
ANIMALS: Eleven healthy research dogs.
METHODS: Prospective study. Dogs received azithromycin (2 mg/kg PO q8h) for 8 days. Fecal samples were collected before (day 1), during (day 6), and after azithromycin administration (days 11, 26, 36, 45). Fecal consistency was assessed daily. Microbiome analysis included qPCR quantification of 16 core bacterial taxa and the Dysbiosis Index. Fecal concentrations of conjugated and unconjugated bile acids (UBAs) were measured on days 1, 11, and 45.
RESULTS: Fecal scores increased during azithromycin administration (P = .009). Abundance of 7 of 16 taxa decreased significantly on day 6, including Peptacetobacter hiranonis (P. hiranonis; P < .001), Faecalibacterium (P < .001), and Fusobacterium (P = .031). Abundance of Streptococcus significantly decreased on day 11 (P = .003). Percentage of primary UBAs increased (P = .017; median, 94.06%; range, 0.73%-96.08%), returned to baseline by day 45, and negatively correlated with abundance of P. hiranonis (r = -0.936 [95% CI, -0.973, -0.852], P < .001). Abundance of 8 of 9 significantly altered taxa recovered, with abundance of Streptococcus remaining decreased.
Low-dose azithromycin induces a mostly reversible dysbiosis and reversible decrease in secondary fecal UBAs. Atypical decreases in Streptococcus abundance can also occur.
Additional Links: PMID-42801332
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@article {pmid42801332,
year = {2026},
author = {Smith, C and Husnik, R and Gaschen, F and Kirk, C and Zhu, X and Suchodolski, J},
title = {Effect of low dose azithromycin on the fecal microbiome and fecal bile acids in healthy dogs.},
journal = {Journal of veterinary internal medicine},
volume = {40},
number = {5},
pages = {},
pmid = {42801332},
issn = {1939-1676},
support = {//Department of Small Animal Clinical Sciences of the University of Tennessee/ ; },
mesh = {Animals ; Dogs/microbiology ; *Feces/microbiology/chemistry ; *Azithromycin/pharmacology/administration & dosage ; *Anti-Bacterial Agents/pharmacology/administration & dosage ; Female ; Male ; *Bile Acids and Salts/analysis ; *Microbiota/drug effects ; *Gastrointestinal Microbiome/drug effects ; Prospective Studies ; },
abstract = {BACKGROUND: Azithromycin has prokinetic effects at low doses in people, cats, and anecdotally, in dogs; however, antibiotics alter the fecal microbiome and metabolome.
HYPOTHESIS/OBJECTIVES: To prospectively evaluate the effects of low-dose azithromycin, hypothesizing that it would alter the fecal microbiome and fecal bile acids in healthy dogs.
ANIMALS: Eleven healthy research dogs.
METHODS: Prospective study. Dogs received azithromycin (2 mg/kg PO q8h) for 8 days. Fecal samples were collected before (day 1), during (day 6), and after azithromycin administration (days 11, 26, 36, 45). Fecal consistency was assessed daily. Microbiome analysis included qPCR quantification of 16 core bacterial taxa and the Dysbiosis Index. Fecal concentrations of conjugated and unconjugated bile acids (UBAs) were measured on days 1, 11, and 45.
RESULTS: Fecal scores increased during azithromycin administration (P = .009). Abundance of 7 of 16 taxa decreased significantly on day 6, including Peptacetobacter hiranonis (P. hiranonis; P < .001), Faecalibacterium (P < .001), and Fusobacterium (P = .031). Abundance of Streptococcus significantly decreased on day 11 (P = .003). Percentage of primary UBAs increased (P = .017; median, 94.06%; range, 0.73%-96.08%), returned to baseline by day 45, and negatively correlated with abundance of P. hiranonis (r = -0.936 [95% CI, -0.973, -0.852], P < .001). Abundance of 8 of 9 significantly altered taxa recovered, with abundance of Streptococcus remaining decreased.
Low-dose azithromycin induces a mostly reversible dysbiosis and reversible decrease in secondary fecal UBAs. Atypical decreases in Streptococcus abundance can also occur.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Dogs/microbiology
*Feces/microbiology/chemistry
*Azithromycin/pharmacology/administration & dosage
*Anti-Bacterial Agents/pharmacology/administration & dosage
Female
Male
*Bile Acids and Salts/analysis
*Microbiota/drug effects
*Gastrointestinal Microbiome/drug effects
Prospective Studies
RevDate: 2026-09-27
CmpDate: 2026-09-27
Exploratory integrative analysis of infant gut microbiome and metabolome suggests diet- and microbiome-derived metabolites associated with childhood asthma.
Metabolomics : Official journal of the Metabolomic Society, 22(5):.
BACKGROUND: Early-life gut microbiome composition has been linked to childhood asthma risk, but the metabolic pathways underlying this association remain unclear.
OBJECTIVE: To integrate infant gut microbiome and metabolome data to identify pathways associated with asthma risk.
METHODS: Participants were from the INSPIRE birth cohort with early infancy 16S rRNA microbiome data (n=402), urinary metabolomics (n=199), and stool metabolomics (n=58). Overlapping datasets included 89 (urine) and 58 (stool) infants. Current asthma at age 6 was assessed by validated questionnaires. Nested sparse partial least squares discriminant analysis prioritized metabolites and amplicon sequence variants (ASVs) feature selection, followed by Spearman rank correlations to evaluate metabolite-microbiome associations with Bonferroni correction.
RESULTS: Several significant correlations were identified in associations between the stool microbiome and metabolites, primarily involving lipid-related metabolites and microbiome taxa such as Staphylococcus sp. (unclassified), Enterobacteriaceae sp. (unclassified), Veillonella sp. (unclassified), Thomasclavelia ramosa, Bacteroides sp.(unclassified), and Clostridium innocuum group. The correlations between stool microbiome and urine metabolites were weak. Many associated metabolites are likely diet-derived, with microbiome co-metabolising.
CONCLUSION: Exploratory microbiome-metabolite correlations suggest diet-related metabolites may link the infant gut environment to later asthma risk.
Additional Links: PMID-42801402
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Citation:
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@article {pmid42801402,
year = {2026},
author = {Turi, KN and Wu, X and Li, Y and Rosas-Salazar, C and Gebretsadik, T and Shilts, MH and Das, SR and Gern, J and Xu, Y and Hartert, TV},
title = {Exploratory integrative analysis of infant gut microbiome and metabolome suggests diet- and microbiome-derived metabolites associated with childhood asthma.},
journal = {Metabolomics : Official journal of the Metabolomic Society},
volume = {22},
number = {5},
pages = {},
pmid = {42801402},
issn = {1573-3890},
support = {K01HL149989//National Institute of Health (NIH)/ ; K23HL148638//National Institute of Health (NIH)/ ; UG3/UH3 OD023282//National Institute of Health (NIH)/ ; U19 AI 095227//National Institute of Health (NIH)/ ; },
mesh = {Humans ; *Asthma/metabolism/microbiology ; *Metabolome/physiology ; Infant ; *Gastrointestinal Microbiome/physiology ; Feces/microbiology ; *Diet ; Metabolomics/methods ; RNA, Ribosomal, 16S/genetics ; Male ; Female ; Child ; },
abstract = {BACKGROUND: Early-life gut microbiome composition has been linked to childhood asthma risk, but the metabolic pathways underlying this association remain unclear.
OBJECTIVE: To integrate infant gut microbiome and metabolome data to identify pathways associated with asthma risk.
METHODS: Participants were from the INSPIRE birth cohort with early infancy 16S rRNA microbiome data (n=402), urinary metabolomics (n=199), and stool metabolomics (n=58). Overlapping datasets included 89 (urine) and 58 (stool) infants. Current asthma at age 6 was assessed by validated questionnaires. Nested sparse partial least squares discriminant analysis prioritized metabolites and amplicon sequence variants (ASVs) feature selection, followed by Spearman rank correlations to evaluate metabolite-microbiome associations with Bonferroni correction.
RESULTS: Several significant correlations were identified in associations between the stool microbiome and metabolites, primarily involving lipid-related metabolites and microbiome taxa such as Staphylococcus sp. (unclassified), Enterobacteriaceae sp. (unclassified), Veillonella sp. (unclassified), Thomasclavelia ramosa, Bacteroides sp.(unclassified), and Clostridium innocuum group. The correlations between stool microbiome and urine metabolites were weak. Many associated metabolites are likely diet-derived, with microbiome co-metabolising.
CONCLUSION: Exploratory microbiome-metabolite correlations suggest diet-related metabolites may link the infant gut environment to later asthma risk.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Asthma/metabolism/microbiology
*Metabolome/physiology
Infant
*Gastrointestinal Microbiome/physiology
Feces/microbiology
*Diet
Metabolomics/methods
RNA, Ribosomal, 16S/genetics
Male
Female
Child
RevDate: 2026-09-27
Supramolecular Zinc-Polyphenol Coordination Assemblies Mitigate Colonic Inflammation by Regulating Mucosal Barrier and Microbiome.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
To overcome the poor bioavailability and environmental instability of physical polyphenol co-assemblies while maximizing their preventive efficacy, the authors engineered carrier-free, metal-phenolic coordination nanoparticles (ZnCA NPs) utilizing divalent zinc (Zn[2+]) to bridge curcumin and anthocyanin. This coordination chemistry transforms the binary polyphenols into a stable, quasi-amorphous state, substantially enhancing their aqueous dispersibility and gastrointestinal stability. Benefiting from this structural evolution, ZnCA NPs exhibited superior colonic accumulation and efficient reactive oxygen and nitrogen species scavenging. In zebrafish and murine colitis models, ZnCA NPs effectively reinforced the mucosal barrier and mitigated microenvironmental inflammation. Mechanistically, transcriptomic profiling revealed that ZnCA NPs modulated the colonic microenvironment by downregulating core NF-κB, MAPK, and JAK-STAT signaling cascades. Crucially, ZnCA NPs enriched beneficial commensals, most prominently Muribaculaceae, to attenuate dextran sulfate sodium-induced dysbiosis; the functional contribution of this remodeled microbiota in maintaining colonic homeostasis was microbiota transplantation. This study transitions polyphenol nanomedicine from fragile physical self-assembly to robust metal-phenolic coordination for enhanced prevention of intestinal inflammation.
Additional Links: PMID-42801677
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Citation:
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@article {pmid42801677,
year = {2026},
author = {Xie, Q and Ye, M and Liu, X and Wang, J and Chen, Y and Tan, L and Fu, J and Huang, X},
title = {Supramolecular Zinc-Polyphenol Coordination Assemblies Mitigate Colonic Inflammation by Regulating Mucosal Barrier and Microbiome.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e77647},
pmid = {42801677},
issn = {2198-3844},
abstract = {To overcome the poor bioavailability and environmental instability of physical polyphenol co-assemblies while maximizing their preventive efficacy, the authors engineered carrier-free, metal-phenolic coordination nanoparticles (ZnCA NPs) utilizing divalent zinc (Zn[2+]) to bridge curcumin and anthocyanin. This coordination chemistry transforms the binary polyphenols into a stable, quasi-amorphous state, substantially enhancing their aqueous dispersibility and gastrointestinal stability. Benefiting from this structural evolution, ZnCA NPs exhibited superior colonic accumulation and efficient reactive oxygen and nitrogen species scavenging. In zebrafish and murine colitis models, ZnCA NPs effectively reinforced the mucosal barrier and mitigated microenvironmental inflammation. Mechanistically, transcriptomic profiling revealed that ZnCA NPs modulated the colonic microenvironment by downregulating core NF-κB, MAPK, and JAK-STAT signaling cascades. Crucially, ZnCA NPs enriched beneficial commensals, most prominently Muribaculaceae, to attenuate dextran sulfate sodium-induced dysbiosis; the functional contribution of this remodeled microbiota in maintaining colonic homeostasis was microbiota transplantation. This study transitions polyphenol nanomedicine from fragile physical self-assembly to robust metal-phenolic coordination for enhanced prevention of intestinal inflammation.},
}
RevDate: 2026-09-27
CmpDate: 2026-09-27
Immunological Mechanisms of the Gut-brain-cardiovascular Axis in Coronary Heart Disease with Comorbid Anxiety and Depression.
Iranian journal of allergy, asthma, and immunology, 25(5):623-631.
Coronary heart disease (CHD) is frequently accompanied by anxiety and depression, conditions that markedly worsen cardiovascular outcomes. Increasing evidence indicates that immune dysregulation, driven by gut microbiota alterations, plays a central role in linking psychological disorders with cardiovascular pathology through the gut-brain-cardiovascular axis. This narrative review systematically summarizes recent advances in the immunological mechanisms underlying CHD complicated by anxiety and depression. We focus on gut microbiota-immune interactions, inflammatory signaling pathways, immune-related microbial metabolites, and neuroimmune communication that collectively shape cardiovascular and mental health. Relevant studies addressing immune biomarkers, cytokine profiles, intestinal barrier dysfunction, and immune-modulating therapeutic strategies were critically analyzed. Gut microbiota dysbiosis contributes to intestinal barrier impairment and translocation of microbial products, leading to activation of innate and adaptive immune responses. Elevated pro-inflammatory cytokines, including interleukin 6 and tumor necrosis factor α, serve as key mediators linking systemic inflammation with atherosclerosis and neuropsychiatric symptoms. Microbial metabolites, such as trimethylamine N-oxide, exacerbate immune-driven vascular inflammation, whereas short-chain fatty acids exert immunoregulatory and anti-inflammatory effects. Neuroimmune mechanisms, including hypothalamic-pituitary-adrenal (HPA) axis activation and immune modulation of autonomic function, further integrate psychological stress with cardiovascular immune injury. Immune dysregulation represents a unifying mechanism connecting gut microbiota imbalance, neuropsychiatric disorders, and coronary heart disease. Targeting immune-microbiota interactions within the gut-brain-cardiovascular axis may offer novel diagnostic biomarkers and immunomodulatory therapeutic strategies for CHD patients with comorbid anxiety and depression. This immunological perspective provides a translational framework for future research and integrated clinical management.
Additional Links: PMID-42801774
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PubMed:
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@article {pmid42801774,
year = {2026},
author = {Xu, Y and Chen, X},
title = {Immunological Mechanisms of the Gut-brain-cardiovascular Axis in Coronary Heart Disease with Comorbid Anxiety and Depression.},
journal = {Iranian journal of allergy, asthma, and immunology},
volume = {25},
number = {5},
pages = {623-631},
doi = {10.18502/ijaai.v25i5.22253},
pmid = {42801774},
issn = {1735-5249},
mesh = {Humans ; *Depression/immunology/epidemiology ; *Coronary Disease/immunology/epidemiology ; *Anxiety/immunology/epidemiology ; Animals ; *Gastrointestinal Microbiome/immunology ; *Brain/immunology ; Comorbidity ; *Brain-Gut Axis/immunology ; *Cardiovascular System/immunology ; Intestinal Barrier Function ; },
abstract = {Coronary heart disease (CHD) is frequently accompanied by anxiety and depression, conditions that markedly worsen cardiovascular outcomes. Increasing evidence indicates that immune dysregulation, driven by gut microbiota alterations, plays a central role in linking psychological disorders with cardiovascular pathology through the gut-brain-cardiovascular axis. This narrative review systematically summarizes recent advances in the immunological mechanisms underlying CHD complicated by anxiety and depression. We focus on gut microbiota-immune interactions, inflammatory signaling pathways, immune-related microbial metabolites, and neuroimmune communication that collectively shape cardiovascular and mental health. Relevant studies addressing immune biomarkers, cytokine profiles, intestinal barrier dysfunction, and immune-modulating therapeutic strategies were critically analyzed. Gut microbiota dysbiosis contributes to intestinal barrier impairment and translocation of microbial products, leading to activation of innate and adaptive immune responses. Elevated pro-inflammatory cytokines, including interleukin 6 and tumor necrosis factor α, serve as key mediators linking systemic inflammation with atherosclerosis and neuropsychiatric symptoms. Microbial metabolites, such as trimethylamine N-oxide, exacerbate immune-driven vascular inflammation, whereas short-chain fatty acids exert immunoregulatory and anti-inflammatory effects. Neuroimmune mechanisms, including hypothalamic-pituitary-adrenal (HPA) axis activation and immune modulation of autonomic function, further integrate psychological stress with cardiovascular immune injury. Immune dysregulation represents a unifying mechanism connecting gut microbiota imbalance, neuropsychiatric disorders, and coronary heart disease. Targeting immune-microbiota interactions within the gut-brain-cardiovascular axis may offer novel diagnostic biomarkers and immunomodulatory therapeutic strategies for CHD patients with comorbid anxiety and depression. This immunological perspective provides a translational framework for future research and integrated clinical management.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Depression/immunology/epidemiology
*Coronary Disease/immunology/epidemiology
*Anxiety/immunology/epidemiology
Animals
*Gastrointestinal Microbiome/immunology
*Brain/immunology
Comorbidity
*Brain-Gut Axis/immunology
*Cardiovascular System/immunology
Intestinal Barrier Function
RevDate: 2026-09-27
CmpDate: 2026-09-27
Postpartum vulvar biology beyond atrophy: a 5-axis mechanistic review of genitourinary syndrome of lactation.
Sexual medicine reviews, 14(3):.
INTRODUCTION: The 2024 introduction of genitourinary syndrome of lactation (GSL) established the syndromic and epidemiological foundation for postpartum genitourinary care, naming a distinct clinical entity and documenting its prevalence. This narrative mechanistic review asks a complementary question: what biological systems translate the postpartum hormonal environment and parturition exposure into the observed spectrum of postpartum lower-genital-tract vulnerability, vulvar and vestibular symptom variability, and recovery? From this synthesis, the Postpartum Vulvar Tissue-State Model is derived as a multi-axis mechanistic framework beneath the GSL syndromic construct, characterizing 5 biological axes whose postpartum trajectories diverge in timing and reversibility. This review synthesizes evidence on postpartum vulvar tissue biology across 5 partially independent systems-epithelial/stromal, vascular, intracrine, neurological/sensory, and microbial-and to derive a multi-axis mechanistic framework explaining symptom variability, recovery trajectories, and persistent postpartum dyspareunia.
METHODS: Narrative mechanistic review integrating peer-reviewed literature from reproductive endocrinology, lower genital tract tissue biology, vulvovaginal and vestibular tissue biology, sensory neuroscience, pelvic pain biology, and microbiome science. Literature was identified through PubMed and Google Scholar searches without date restriction. This narrative synthesis was not designed as a systematic review and does not follow PRISMA reporting guidelines. Findings are presented with explicit labeling of empirically established mechanisms, cross-domain extrapolations from adjacent literatures, and novel framework-generating hypotheses.
RESULTS: The synthesis identifies 5 biological axes that shape postpartum vulvar tissue state: (I) epithelial and stromal remodeling driven primarily by estrogen receptor alpha withdrawal, altered matrix metalloproteinase activity, and parturition-related wound biology; (II) vascular and nitric oxide signaling disruption affecting arousal-linked lubrication; (III) intracrine steroidogenesis, a tissue-level compensatory system whose postpartum function remains uncharacterized; (IV) neurological and sensory sensitization plausibly initiated by parturition-associated inflammation, nociceptor activation, and mast cell/NGF signaling; and (V) microbial ecosystem disruption mediated by glycogen depletion and Lactobacillus decline. These axes interact in a cascade architecture in which early endocrine and mechanical disruption may propagate through microbial, barrier, and neuroinflammatory pathways, potentially establishing persistent sensitization independent of hormonal recovery.
DISCUSSION: This review derives the Postpartum Vulvar Tissue-State Model as a mechanistic framework beneath GSL as a syndromic construct. The model distinguishes 3 temporal phases of tissue-state evolution, identifies persistent postpartum dyspareunia as a potential neuroinflammatory sequela in a subset of women, and provides a biological rationale for axis-differentiated clinical assessment and earlier intervention.
Additional Links: PMID-42801791
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PubMed:
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@article {pmid42801791,
year = {2026},
author = {Kelly, L},
title = {Postpartum vulvar biology beyond atrophy: a 5-axis mechanistic review of genitourinary syndrome of lactation.},
journal = {Sexual medicine reviews},
volume = {14},
number = {3},
pages = {},
doi = {10.1093/sxmrev/qeag076},
pmid = {42801791},
issn = {2050-0521},
mesh = {Humans ; Female ; *Postpartum Period/physiology ; *Lactation/physiology ; *Vulva/pathology/physiopathology ; Syndrome ; Atrophy ; },
abstract = {INTRODUCTION: The 2024 introduction of genitourinary syndrome of lactation (GSL) established the syndromic and epidemiological foundation for postpartum genitourinary care, naming a distinct clinical entity and documenting its prevalence. This narrative mechanistic review asks a complementary question: what biological systems translate the postpartum hormonal environment and parturition exposure into the observed spectrum of postpartum lower-genital-tract vulnerability, vulvar and vestibular symptom variability, and recovery? From this synthesis, the Postpartum Vulvar Tissue-State Model is derived as a multi-axis mechanistic framework beneath the GSL syndromic construct, characterizing 5 biological axes whose postpartum trajectories diverge in timing and reversibility. This review synthesizes evidence on postpartum vulvar tissue biology across 5 partially independent systems-epithelial/stromal, vascular, intracrine, neurological/sensory, and microbial-and to derive a multi-axis mechanistic framework explaining symptom variability, recovery trajectories, and persistent postpartum dyspareunia.
METHODS: Narrative mechanistic review integrating peer-reviewed literature from reproductive endocrinology, lower genital tract tissue biology, vulvovaginal and vestibular tissue biology, sensory neuroscience, pelvic pain biology, and microbiome science. Literature was identified through PubMed and Google Scholar searches without date restriction. This narrative synthesis was not designed as a systematic review and does not follow PRISMA reporting guidelines. Findings are presented with explicit labeling of empirically established mechanisms, cross-domain extrapolations from adjacent literatures, and novel framework-generating hypotheses.
RESULTS: The synthesis identifies 5 biological axes that shape postpartum vulvar tissue state: (I) epithelial and stromal remodeling driven primarily by estrogen receptor alpha withdrawal, altered matrix metalloproteinase activity, and parturition-related wound biology; (II) vascular and nitric oxide signaling disruption affecting arousal-linked lubrication; (III) intracrine steroidogenesis, a tissue-level compensatory system whose postpartum function remains uncharacterized; (IV) neurological and sensory sensitization plausibly initiated by parturition-associated inflammation, nociceptor activation, and mast cell/NGF signaling; and (V) microbial ecosystem disruption mediated by glycogen depletion and Lactobacillus decline. These axes interact in a cascade architecture in which early endocrine and mechanical disruption may propagate through microbial, barrier, and neuroinflammatory pathways, potentially establishing persistent sensitization independent of hormonal recovery.
DISCUSSION: This review derives the Postpartum Vulvar Tissue-State Model as a mechanistic framework beneath GSL as a syndromic construct. The model distinguishes 3 temporal phases of tissue-state evolution, identifies persistent postpartum dyspareunia as a potential neuroinflammatory sequela in a subset of women, and provides a biological rationale for axis-differentiated clinical assessment and earlier intervention.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
*Postpartum Period/physiology
*Lactation/physiology
*Vulva/pathology/physiopathology
Syndrome
Atrophy
RevDate: 2026-09-27
Combined imidacloprid and chlorpyrifos disrupt gut microbiota-host interactions and reduced performance and survival in honey bees.
Journal of insect physiology pii:S0022-1910(26)00143-5 [Epub ahead of print].
Gut microbiota plays a central role in insect physiology and health. However, how agrochemical exposure perturbs gut microbiota of the host and its downstream functional consequences remains understudied. Here, we employed an integrative multi-omics framework combining microbiome profiling, transcriptomics, and metabolomics to investigate how field-realistic exposures to the insecticides chlorpyrifos (CPF), imidacloprid (IMD), and their combination (IC) affect gut microbial composition as well as sucrose consumption, body weight dynamics, and survival in bees. We found that sucrose consumption was significantly reduced in bees exposed to IMD and IC, but not in the CPF group. Survival probability was significantly lower only in the IC group, whereas IMD and IC treatments caused greater weight loss compared to controls. Furthermore, IC exposure induced pronounced gut dysbiosis, and severe midgut structural damage, including epithelial degeneration and disruption of gut barrier integrity. At the functional level, IC exposure suppressed key detoxification enzymes, including glutathione S-transferase (GST) and cytochrome P450, indicating impaired xenobiotic metabolism. Multi-omics integration revealed 842 differentially expressed genes and 193 metabolites under IC exposure, with alterations in key pathways associated with energy metabolism, oxidative stress response, immune regulation, and host-microbiome interactions. These findings demonstrate that combined pesticide exposure disrupts gut microbiota composition and function, leading to cascading effects on host metabolic and detoxification processes as well as the overall health, and highlights the need for careful pesticide management to mitigate adverse impacts of combined pesticides across the environment.
Additional Links: PMID-42801970
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PubMed:
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@article {pmid42801970,
year = {2026},
author = {Chen, S and Wang, J and Yang, S and Han, J and Zhou, S and Shi, X and Li-Byarlay, H and Luo, D and Ma, C},
title = {Combined imidacloprid and chlorpyrifos disrupt gut microbiota-host interactions and reduced performance and survival in honey bees.},
journal = {Journal of insect physiology},
volume = {},
number = {},
pages = {105070},
doi = {10.1016/j.jinsphys.2026.105070},
pmid = {42801970},
issn = {1879-1611},
abstract = {Gut microbiota plays a central role in insect physiology and health. However, how agrochemical exposure perturbs gut microbiota of the host and its downstream functional consequences remains understudied. Here, we employed an integrative multi-omics framework combining microbiome profiling, transcriptomics, and metabolomics to investigate how field-realistic exposures to the insecticides chlorpyrifos (CPF), imidacloprid (IMD), and their combination (IC) affect gut microbial composition as well as sucrose consumption, body weight dynamics, and survival in bees. We found that sucrose consumption was significantly reduced in bees exposed to IMD and IC, but not in the CPF group. Survival probability was significantly lower only in the IC group, whereas IMD and IC treatments caused greater weight loss compared to controls. Furthermore, IC exposure induced pronounced gut dysbiosis, and severe midgut structural damage, including epithelial degeneration and disruption of gut barrier integrity. At the functional level, IC exposure suppressed key detoxification enzymes, including glutathione S-transferase (GST) and cytochrome P450, indicating impaired xenobiotic metabolism. Multi-omics integration revealed 842 differentially expressed genes and 193 metabolites under IC exposure, with alterations in key pathways associated with energy metabolism, oxidative stress response, immune regulation, and host-microbiome interactions. These findings demonstrate that combined pesticide exposure disrupts gut microbiota composition and function, leading to cascading effects on host metabolic and detoxification processes as well as the overall health, and highlights the need for careful pesticide management to mitigate adverse impacts of combined pesticides across the environment.},
}
RevDate: 2026-09-27
CmpDate: 2026-09-27
Microbial and Metabolic Flexibility in Response to Habitat Disturbance in an Ecologically Specialist Primate.
Molecular ecology, 35(18):e70562.
In the Anthropocene, understanding what renders a species prone to extinction is critical to wildlife management. Ecological specialists are hypothesised to be at particular risk, given that morphological, physiological, and/or behavioural constraints are expected to impede their responses to rapid habitat degradation. Nevertheless, studies have found mixed support for this hypothesis, raising the question, 'how resilient are specialists to environmental change?' Here, we test the hypothesis that ecological specialists, limited by behavioural and physiological constraints, may be at an energetic disadvantage in degraded habitats. Specifically, we tested whether Critically Endangered dietary specialist primates, black-and-white ruffed lemurs (Varecia variegata), living in secondary forests suffered nutritional and energetic deficits compared to those in primary forest habitats over a 12-month period. To do this, we used mixed modelling approaches to examine relationships among behaviour, nutritional chemistry, 16S sequencing, metagenome functional predictions, metabolite profiles, and energetic outcomes. Compared to primary forest-living conspecifics, we found that animals in the degraded forest consumed slightly fewer calories from less diverse diets. These animals exhibited less diverse gut microbiota, reduced microbial functional potential, and altered metabolomic profiles. Nevertheless, despite apparent nutritional constraints, energetic outcomes were broadly similar across habitats. These findings suggest that an organism's gut microbiome may be able to regulate microbial metabolic potential to facilitate resilience under suboptimal conditions. These findings highlight host-microbiome interactions as an important component of resilience in ecological specialists, with broad implications for predicting species persistence amid ongoing environmental change.
Additional Links: PMID-42802107
Publisher:
PubMed:
Citation:
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@article {pmid42802107,
year = {2026},
author = {Beeby, N and Rasoanarimalala, C and Rasoavolandrainy, MF and Rothman, JM and Higham, JP and Sardaro, MLS and Amato, KR and Webster, TH and Baden, AL},
title = {Microbial and Metabolic Flexibility in Response to Habitat Disturbance in an Ecologically Specialist Primate.},
journal = {Molecular ecology},
volume = {35},
number = {18},
pages = {e70562},
doi = {10.1111/mec.70562},
pmid = {42802107},
issn = {1365-294X},
mesh = {Animals ; *Ecosystem ; Diet ; Forests ; *Gastrointestinal Microbiome/genetics ; *Strepsirhini/microbiology/metabolism/physiology ; RNA, Ribosomal, 16S/genetics ; Energy Metabolism ; Lemuridae ; },
abstract = {In the Anthropocene, understanding what renders a species prone to extinction is critical to wildlife management. Ecological specialists are hypothesised to be at particular risk, given that morphological, physiological, and/or behavioural constraints are expected to impede their responses to rapid habitat degradation. Nevertheless, studies have found mixed support for this hypothesis, raising the question, 'how resilient are specialists to environmental change?' Here, we test the hypothesis that ecological specialists, limited by behavioural and physiological constraints, may be at an energetic disadvantage in degraded habitats. Specifically, we tested whether Critically Endangered dietary specialist primates, black-and-white ruffed lemurs (Varecia variegata), living in secondary forests suffered nutritional and energetic deficits compared to those in primary forest habitats over a 12-month period. To do this, we used mixed modelling approaches to examine relationships among behaviour, nutritional chemistry, 16S sequencing, metagenome functional predictions, metabolite profiles, and energetic outcomes. Compared to primary forest-living conspecifics, we found that animals in the degraded forest consumed slightly fewer calories from less diverse diets. These animals exhibited less diverse gut microbiota, reduced microbial functional potential, and altered metabolomic profiles. Nevertheless, despite apparent nutritional constraints, energetic outcomes were broadly similar across habitats. These findings suggest that an organism's gut microbiome may be able to regulate microbial metabolic potential to facilitate resilience under suboptimal conditions. These findings highlight host-microbiome interactions as an important component of resilience in ecological specialists, with broad implications for predicting species persistence amid ongoing environmental change.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Ecosystem
Diet
Forests
*Gastrointestinal Microbiome/genetics
*Strepsirhini/microbiology/metabolism/physiology
RNA, Ribosomal, 16S/genetics
Energy Metabolism
Lemuridae
RevDate: 2026-09-27
Oral microbiome signatures of molar-incisor hypomineralisation: insights from a pilot study.
European archives of paediatric dentistry : official journal of the European Academy of Paediatric Dentistry [Epub ahead of print].
PURPOSE: Molar-incisor hypomineralisation (MIH) is a developmental condition that may increase plaque retention and caries risk, yet its microbial signature remains unclear. We compared plaque microbiome diversity and community composition in children with MIH and healthy controls, including tooth-level MIH severities.
METHODS: In this cross-sectional pilot study, supragingival plaque was collected from 30 children aged 7-16 years (15 MIH, 15 controls), yielding 63 samples. Controls contributed one pooled molar sample per child (n = 15), whereas MIH participants provided 48 pooled molar samples stratified by lesion severity. The V3-V4 region of the 16S rRNA gene was sequenced (via the Illumina NovaSeq platform), and reads were processed in R. Diversity and differential abundance were analysed in R using mixed-effects models, PERMANOVA, and ANCOM-BC2.
RESULTS: Children with MIH had significantly higher plaque scores (p = 0.009). Community structure remained similar between groups and across severities (PERMANOVA R[2] <0.06), with variation driven more by individual differences. The core microbiome was largely shared; however, controls retained nine additional genera (≥ 90% prevalence) not consistently present in MIH. Bacterial evenness was significantly lower in MIH (Shannon β = 0.404; 95% CI 0.10-0.71; FDR-adjusted p = 0.042), whilst community richness and phylogenetic diversity were comparable. Effect sizes suggested higher Neisseria and Abiotrophia, and lower TM7x in MIH although not statistically significant (all q ≥ 0.161).
CONCLUSIONS: MIH was associated with higher plaque accumulation and reduced microbial evenness, without a clear alteration of overall community structure. Directional trends and reduced consistency of highly prevalent core genera warrant confirmation in larger studies.
Additional Links: PMID-42802209
PubMed:
Citation:
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@article {pmid42802209,
year = {2026},
author = {Alsaid, M and Heng, NCK and Ekambaram, M and Hasmun, NN},
title = {Oral microbiome signatures of molar-incisor hypomineralisation: insights from a pilot study.},
journal = {European archives of paediatric dentistry : official journal of the European Academy of Paediatric Dentistry},
volume = {},
number = {},
pages = {},
pmid = {42802209},
issn = {1996-9805},
support = {RF0005 2025//New Zealand Dental Research Foundation (NZDRF)/ ; PhD scholarship//Applied Science Private University/ ; },
abstract = {PURPOSE: Molar-incisor hypomineralisation (MIH) is a developmental condition that may increase plaque retention and caries risk, yet its microbial signature remains unclear. We compared plaque microbiome diversity and community composition in children with MIH and healthy controls, including tooth-level MIH severities.
METHODS: In this cross-sectional pilot study, supragingival plaque was collected from 30 children aged 7-16 years (15 MIH, 15 controls), yielding 63 samples. Controls contributed one pooled molar sample per child (n = 15), whereas MIH participants provided 48 pooled molar samples stratified by lesion severity. The V3-V4 region of the 16S rRNA gene was sequenced (via the Illumina NovaSeq platform), and reads were processed in R. Diversity and differential abundance were analysed in R using mixed-effects models, PERMANOVA, and ANCOM-BC2.
RESULTS: Children with MIH had significantly higher plaque scores (p = 0.009). Community structure remained similar between groups and across severities (PERMANOVA R[2] <0.06), with variation driven more by individual differences. The core microbiome was largely shared; however, controls retained nine additional genera (≥ 90% prevalence) not consistently present in MIH. Bacterial evenness was significantly lower in MIH (Shannon β = 0.404; 95% CI 0.10-0.71; FDR-adjusted p = 0.042), whilst community richness and phylogenetic diversity were comparable. Effect sizes suggested higher Neisseria and Abiotrophia, and lower TM7x in MIH although not statistically significant (all q ≥ 0.161).
CONCLUSIONS: MIH was associated with higher plaque accumulation and reduced microbial evenness, without a clear alteration of overall community structure. Directional trends and reduced consistency of highly prevalent core genera warrant confirmation in larger studies.},
}
RevDate: 2026-09-27
CmpDate: 2026-09-27
Medicinal-plant immunity and specialized metabolism in plant-pathogen interactions: mechanisms and applications.
Planta, 264(5):.
Medicinal-plant immunity and specialized metabolism are mechanistically linked, but rigorous receptor validation, causal multi-omics, and field trials are needed for reliable translational applications. Medicinal plants combine classical immune signaling with lineage-specific specialized metabolism. This review focuses on the immune systems of medicinal plants and on how pathogen perception reshapes the biosynthesis of pharmacologically valuable secondary metabolites. We synthesize evidence for pattern-triggered immunity (PTI) and effector-triggered immunity (ETI), emphasizing pattern-recognition receptors (PRRs), nucleotide-binding leucine-rich repeat (NLR) proteins, MAP kinase (MAPK) signaling, calcium influx, reactive oxygen species (ROS), salicylic acid (SA), jasmonic acid (JA), ethylene (ET), and abscisic acid (ABA) crosstalk. Examples from Atractylodes macrocephala, Panax ginseng, Cannabis sativa, Catharanthus roseus, Artemisia annua, Hypericum perforatum, Salvia miltiorrhiza, and Withania somnifera illustrate both progress and major knowledge gaps. We distinguish well-validated medicinal-plant mechanisms from inferences based on Arabidopsis, rice, tomato, and Nicotiana reference systems. The review further evaluates elicitor treatments, microbial inoculants, genetic engineering, genome editing, integrated pest management (IPM), multi-omics, and microbiome engineering as strategies to improve both disease resistance and metabolite quality. We propose that future studies should test mechanistic links between receptor activation, transcription-factor networks, metabolite flux, and field-level medicinal quality through paired transcriptomics, proteomics, metabolomics, microbiome profiling, and targeted perturbation experiments. This synthesis provides a focused framework for translating plant-pathogen biology into resilient and chemically consistent medicinal-plant production.
Additional Links: PMID-42802241
PubMed:
Citation:
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@article {pmid42802241,
year = {2026},
author = {Khalil, AAK and Bae, H},
title = {Medicinal-plant immunity and specialized metabolism in plant-pathogen interactions: mechanisms and applications.},
journal = {Planta},
volume = {264},
number = {5},
pages = {},
pmid = {42802241},
issn = {1432-2048},
mesh = {*Plant Immunity/physiology ; *Plants, Medicinal/immunology/metabolism/microbiology ; *Host-Pathogen Interactions/immunology ; Innate Immunity Recognition ; Signal Transduction ; Multiomics ; *Plant Diseases/immunology/microbiology ; },
abstract = {Medicinal-plant immunity and specialized metabolism are mechanistically linked, but rigorous receptor validation, causal multi-omics, and field trials are needed for reliable translational applications. Medicinal plants combine classical immune signaling with lineage-specific specialized metabolism. This review focuses on the immune systems of medicinal plants and on how pathogen perception reshapes the biosynthesis of pharmacologically valuable secondary metabolites. We synthesize evidence for pattern-triggered immunity (PTI) and effector-triggered immunity (ETI), emphasizing pattern-recognition receptors (PRRs), nucleotide-binding leucine-rich repeat (NLR) proteins, MAP kinase (MAPK) signaling, calcium influx, reactive oxygen species (ROS), salicylic acid (SA), jasmonic acid (JA), ethylene (ET), and abscisic acid (ABA) crosstalk. Examples from Atractylodes macrocephala, Panax ginseng, Cannabis sativa, Catharanthus roseus, Artemisia annua, Hypericum perforatum, Salvia miltiorrhiza, and Withania somnifera illustrate both progress and major knowledge gaps. We distinguish well-validated medicinal-plant mechanisms from inferences based on Arabidopsis, rice, tomato, and Nicotiana reference systems. The review further evaluates elicitor treatments, microbial inoculants, genetic engineering, genome editing, integrated pest management (IPM), multi-omics, and microbiome engineering as strategies to improve both disease resistance and metabolite quality. We propose that future studies should test mechanistic links between receptor activation, transcription-factor networks, metabolite flux, and field-level medicinal quality through paired transcriptomics, proteomics, metabolomics, microbiome profiling, and targeted perturbation experiments. This synthesis provides a focused framework for translating plant-pathogen biology into resilient and chemically consistent medicinal-plant production.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Plant Immunity/physiology
*Plants, Medicinal/immunology/metabolism/microbiology
*Host-Pathogen Interactions/immunology
Innate Immunity Recognition
Signal Transduction
Multiomics
*Plant Diseases/immunology/microbiology
RevDate: 2026-09-28
Pseudomonadaceae Promotes Tobacco Defense Against Pathogen Invasion via Root Exudate Reprogramming.
Plant, cell & environment [Epub ahead of print].
Microbial pathogens pose a serious challenge to food security under climate change. Microbiomes can filter out incoming pathogens. However, the specific microbial taxa and mechanisms that indicate the response of the microbiome and plant health to the invasion of pathogens remain largely unknown. Here, we combine multiple field surveys and experiments with DNA and RNA sequencing using tobacco (Nicotiana tabacum) and the bacterial wilt pathogen Ralstonia solanacearum as the model system, and f ind that Pseudomonadaceae constitute an important root-associated component against pathogen invasions. Based on this finding, we develop synthetic microbial consortia, which support plant health by establishing protective microbial barriers and systemically reprogramming root immunity and metabolism. Targeted metabolite profiling further identifies vanillin as a candidate bioactive component of SynCom-induced root exudates, with its concentration increasing by approximately 240% under SynCom inoculation. Exogenous vanillin inhibits the growth and motility of R. solanacearum and also suppresses several other soilborne pathogens. Together, our work establishes the root microbiome as an important component of plant immune defense and highlights microbiome inoculation as a potential tool to enhance crop resistance against increasing pathogen pressures under climate change.
Additional Links: PMID-42802634
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PubMed:
Citation:
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@article {pmid42802634,
year = {2026},
author = {Hong, C and Sonne, C and Li, Y and Hua, Z and Yang, D and Dong, Y and Cao, F and Carrión, VJ and Delgado-Baquerizo, M and Li, X},
title = {Pseudomonadaceae Promotes Tobacco Defense Against Pathogen Invasion via Root Exudate Reprogramming.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.70900},
pmid = {42802634},
issn = {1365-3040},
support = {32430069//National Natural Science Foundation of China/ ; W2412011//National Natural Science Foundation of China/ ; BE2022420//The Jiangsu Special Fund on Technology Innovation of Carbon Dioxide Peaking and Carbon Neutrality/ ; 10.13039/501100011033//TED2021-130908B-C41/AEI/10.13039/501100011033/Unión Europea NextGenerationEU/PRTR and the Spanish Ministry of Science and Innovation for the I + D + i project PID2020-115813RA-I00/ ; },
abstract = {Microbial pathogens pose a serious challenge to food security under climate change. Microbiomes can filter out incoming pathogens. However, the specific microbial taxa and mechanisms that indicate the response of the microbiome and plant health to the invasion of pathogens remain largely unknown. Here, we combine multiple field surveys and experiments with DNA and RNA sequencing using tobacco (Nicotiana tabacum) and the bacterial wilt pathogen Ralstonia solanacearum as the model system, and f ind that Pseudomonadaceae constitute an important root-associated component against pathogen invasions. Based on this finding, we develop synthetic microbial consortia, which support plant health by establishing protective microbial barriers and systemically reprogramming root immunity and metabolism. Targeted metabolite profiling further identifies vanillin as a candidate bioactive component of SynCom-induced root exudates, with its concentration increasing by approximately 240% under SynCom inoculation. Exogenous vanillin inhibits the growth and motility of R. solanacearum and also suppresses several other soilborne pathogens. Together, our work establishes the root microbiome as an important component of plant immune defense and highlights microbiome inoculation as a potential tool to enhance crop resistance against increasing pathogen pressures under climate change.},
}
RevDate: 2026-09-28
CmpDate: 2026-09-28
The Gut-Brain Axis in Sleep Deprivation: Mechanisms, Dysbiosis, and Potential Therapeutic Avenues.
Iranian journal of medical sciences, 51(8):533-542.
Sleep is fundamental to metabolic regulation, cardiovascular health, immune balance, and cognitive performance. Emerging evidence indicates that sleep deprivation alters gut microbial communities and immune signaling, thereby influencing the gut-brain axis. This narrative review synthesized current findings on how sleep loss engages gut-brain pathways and evaluated therapeutic avenues linked to specific mechanisms, drawing on peer-reviewed human and animal studies and prioritizing sleep- and brain-relevant outcomes. Evidence converged on three mechanistic pillars: (1) circadian and microbial misalignment, which disrupts diurnal microbiome dynamics; (2) inflammatory and barrier dysfunction loops that increase permeability and immune activation; and (3) altered neurotransmitter and metabolite signaling, including shifts in tryptophan pathways and reduced short-chain fatty acid production, with downstream effects on neuroinflammation and plasticity. Human data supported associations between sleep loss, poor sleep quality, and impaired cognition. However, causal inference was limited by small sample sizes, study heterogeneity, and mixed endpoints. Interventions such as probiotics, prebiotics, postbiotics, synbiotics, diet-based short-chain fatty acid strategies, and chronobiotics are biologically plausible, yet they are supported mainly by small trials or preclinical models. Fecal microbiota transplantation shows exploratory, yet faces significant safety, standardization, and regulatory challenges. Collectively, the evidence indicated that sleep deprivation disrupts gut microbiota composition and gut-brain signaling, with consequences for neuroinflammation, neurotransmitter balance, and cognition. This review highlighted the consequent need for standardized endpoints, strain-resolved microbiome analyses, and well-powered randomized controlled trials.
Additional Links: PMID-42802736
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Citation:
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@article {pmid42802736,
year = {2026},
author = {Karami, E and Mohammadi, MT and Shirvani, H and Bazgir, B},
title = {The Gut-Brain Axis in Sleep Deprivation: Mechanisms, Dysbiosis, and Potential Therapeutic Avenues.},
journal = {Iranian journal of medical sciences},
volume = {51},
number = {8},
pages = {533-542},
pmid = {42802736},
issn = {1735-3688},
mesh = {Humans ; *Sleep Deprivation/physiopathology/complications ; Animals ; *Gastrointestinal Microbiome/physiology ; *Dysbiosis/physiopathology/etiology ; *Brain-Gut Axis/physiology ; *Brain/physiopathology ; Probiotics/therapeutic use ; },
abstract = {Sleep is fundamental to metabolic regulation, cardiovascular health, immune balance, and cognitive performance. Emerging evidence indicates that sleep deprivation alters gut microbial communities and immune signaling, thereby influencing the gut-brain axis. This narrative review synthesized current findings on how sleep loss engages gut-brain pathways and evaluated therapeutic avenues linked to specific mechanisms, drawing on peer-reviewed human and animal studies and prioritizing sleep- and brain-relevant outcomes. Evidence converged on three mechanistic pillars: (1) circadian and microbial misalignment, which disrupts diurnal microbiome dynamics; (2) inflammatory and barrier dysfunction loops that increase permeability and immune activation; and (3) altered neurotransmitter and metabolite signaling, including shifts in tryptophan pathways and reduced short-chain fatty acid production, with downstream effects on neuroinflammation and plasticity. Human data supported associations between sleep loss, poor sleep quality, and impaired cognition. However, causal inference was limited by small sample sizes, study heterogeneity, and mixed endpoints. Interventions such as probiotics, prebiotics, postbiotics, synbiotics, diet-based short-chain fatty acid strategies, and chronobiotics are biologically plausible, yet they are supported mainly by small trials or preclinical models. Fecal microbiota transplantation shows exploratory, yet faces significant safety, standardization, and regulatory challenges. Collectively, the evidence indicated that sleep deprivation disrupts gut microbiota composition and gut-brain signaling, with consequences for neuroinflammation, neurotransmitter balance, and cognition. This review highlighted the consequent need for standardized endpoints, strain-resolved microbiome analyses, and well-powered randomized controlled trials.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Sleep Deprivation/physiopathology/complications
Animals
*Gastrointestinal Microbiome/physiology
*Dysbiosis/physiopathology/etiology
*Brain-Gut Axis/physiology
*Brain/physiopathology
Probiotics/therapeutic use
RevDate: 2026-09-28
Integrative holo-omic data analysis predicts interactions across the host-microbiome axis.
Microbiology spectrum [Epub ahead of print].
Understanding the interplay between host organisms and their microbiomes is central to the development of sustainable food systems. However, high dimensionality and spurious associations remain major obstacles to extracting meaningful biological insight from multi-omic host-associated microbiome data; a challenge further exacerbated when "holo-omic" analyses across the host-microbiome boundary are considered. Here, we show that a computational method designed for multi-omic analysis in eukaryotes can be leveraged to integrate and analyze five layers of holo-omic data from porcine hosts and their gut microbiomes. We collected caecal tissue and digesta samples during a feeding trial that tested the impact of microbiota-directed fibers (acetylated galactoglucomannan) at critical developmental stages. From 800,000 features including microbial and host genes, metagenome-assembled genomes, and metabolites from caecal tissue and digesta, we used multiset correlation and factor analysis to select the most relevant features for capturing coordinated patterns across omic layers. From these features, we predicted over 2,000 putative host-microbiome interactions based on co-occurrence. Some interactions reflected previously known relationships between animal and microbiome features, such as microbial genes for carbohydrate metabolism being linked to glycoside abundances in host tissue. Other predicted co-occurrences included features that were not detected in single-omic analysis and offer new hypotheses of host-microbiome interactions that warrant future investigation. Hence, we showcase an application of holo-omic analysis that avoids common pitfalls in high-dimensional data analysis, identifies known interactions as a form of validation, and most importantly, predicts new leads for understanding host-microbiome symbiosis.IMPORTANCEWhile study systems involving mammalian hosts and their microbiomes are inherently complex, multi- and holo-omic analyses promise to provide interpretable results with translational value for the animal production industry. Unfortunately, computational methods capable of this kind of integration are currently scarce, as most existing multi-omics approaches have been developed for analysis of data layers within a single multicellular organism. We propose to adapt existing multi-omic methods for holo-omics by combining feature selection and interaction inference. This two-step analysis approach addresses common challenges in data-driven studies and can be implemented with a variety of tools for feature selection and interaction modeling. Through this holistic approach, we show that both known and novel relationships across the holobiont axis can be identified in a data-driven manner, offering new targets for the continued study and experimental validation of host-microbiome interactions and the effect of dietary interventions on production animals.
Additional Links: PMID-42803159
Publisher:
PubMed:
Citation:
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@article {pmid42803159,
year = {2026},
author = {Merkesvik, J and Langa, J and Pietroni, C and Alberdi, A and Poulsen, LL and Bojesen, AM and Meuronen, T and Turunen, S and Kärkkäinen, O and Westereng, B and Pope, PB and Hvidsten, TR},
title = {Integrative holo-omic data analysis predicts interactions across the host-microbiome axis.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0026326},
doi = {10.1128/spectrum.00263-26},
pmid = {42803159},
issn = {2165-0497},
abstract = {Understanding the interplay between host organisms and their microbiomes is central to the development of sustainable food systems. However, high dimensionality and spurious associations remain major obstacles to extracting meaningful biological insight from multi-omic host-associated microbiome data; a challenge further exacerbated when "holo-omic" analyses across the host-microbiome boundary are considered. Here, we show that a computational method designed for multi-omic analysis in eukaryotes can be leveraged to integrate and analyze five layers of holo-omic data from porcine hosts and their gut microbiomes. We collected caecal tissue and digesta samples during a feeding trial that tested the impact of microbiota-directed fibers (acetylated galactoglucomannan) at critical developmental stages. From 800,000 features including microbial and host genes, metagenome-assembled genomes, and metabolites from caecal tissue and digesta, we used multiset correlation and factor analysis to select the most relevant features for capturing coordinated patterns across omic layers. From these features, we predicted over 2,000 putative host-microbiome interactions based on co-occurrence. Some interactions reflected previously known relationships between animal and microbiome features, such as microbial genes for carbohydrate metabolism being linked to glycoside abundances in host tissue. Other predicted co-occurrences included features that were not detected in single-omic analysis and offer new hypotheses of host-microbiome interactions that warrant future investigation. Hence, we showcase an application of holo-omic analysis that avoids common pitfalls in high-dimensional data analysis, identifies known interactions as a form of validation, and most importantly, predicts new leads for understanding host-microbiome symbiosis.IMPORTANCEWhile study systems involving mammalian hosts and their microbiomes are inherently complex, multi- and holo-omic analyses promise to provide interpretable results with translational value for the animal production industry. Unfortunately, computational methods capable of this kind of integration are currently scarce, as most existing multi-omics approaches have been developed for analysis of data layers within a single multicellular organism. We propose to adapt existing multi-omic methods for holo-omics by combining feature selection and interaction inference. This two-step analysis approach addresses common challenges in data-driven studies and can be implemented with a variety of tools for feature selection and interaction modeling. Through this holistic approach, we show that both known and novel relationships across the holobiont axis can be identified in a data-driven manner, offering new targets for the continued study and experimental validation of host-microbiome interactions and the effect of dietary interventions on production animals.},
}
RevDate: 2026-09-28
Geographic Variation and Core Signatures of the Root Canal Microbiome: A Cross-Country Comparative Study.
International endodontic journal [Epub ahead of print].
AIM: Root canal infections harbour complex microbial communities that may vary across geographic populations. This study aimed to compare the root canal microbiome across Spain, Sweden, and the USA, identifying key microbial taxa, compositional and functional differences, and cohort-associated microbial signatures.
METHODS: 16S rRNA gene sequencing datasets from primary root canal infections were retrieved from three geographic cohorts (Spain n = 32, Sweden n = 14, USA n = 25). All samples targeted the V3-V4 region and were sequenced using the Illumina MiSeq platform. Alpha and beta diversity metrics were assessed to evaluate within- and between-sample variation. Taxonomic composition was characterized, followed by differential abundance analysis and identification of the core microbiome. Microbial co-occurrence networks were inferred using the SPRING method, and hub taxa were identified based on eigenvector centrality.
RESULTS: Significant differences in microbial richness between cohorts were observed based on Chao1 index and observed richness. Beta diversity analyses revealed statistically significant but modest separation of microbial communities among populations (R[2] = 6.8%), with substantial overlap between cohorts. Bacillota, Bacteroidota, Fusobacteriota, and Actinomycetota were dominant across cohorts, although their relative abundances varied. Core microbiome analysis identified both shared and cohort-associated taxa at genus and species levels. SPRING-based co-occurrence networks identified cohort-associated hub taxa, including Fretibacterium fastidiosum in the USA, Dialister pneumosintes in Spain, and Treponema denticola in Sweden. Furthermore, predictive functional profiling suggested differences in microbial functional potential among geographic cohorts.
CONCLUSION: While root canal infections share a core microbiome, subtle population-specific microbial signatures were identified. However, the modest effect size suggests that geographic variation alone explains only a limited proportion of microbial composition. Larger and more balanced studies are required to further evaluate geographic influences on the root canal microbiome and their potential clinical relevance.
Additional Links: PMID-42803208
Publisher:
PubMed:
Citation:
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@article {pmid42803208,
year = {2026},
author = {Leimarembi Devi, N and Rakhimova, O and Staley, C and Ordinola-Zapata, R and Moliz, MTA and Pérez-Carrasco, V and Vestman, NR},
title = {Geographic Variation and Core Signatures of the Root Canal Microbiome: A Cross-Country Comparative Study.},
journal = {International endodontic journal},
volume = {},
number = {},
pages = {},
doi = {10.1111/iej.70277},
pmid = {42803208},
issn = {1365-2591},
support = {977100//Region of Vasterbotten (Sweden) via TUA/ ; RV-967705//ALF/ ; JCSMK23-0158//Kempestiftelserna Kempe/ ; },
abstract = {AIM: Root canal infections harbour complex microbial communities that may vary across geographic populations. This study aimed to compare the root canal microbiome across Spain, Sweden, and the USA, identifying key microbial taxa, compositional and functional differences, and cohort-associated microbial signatures.
METHODS: 16S rRNA gene sequencing datasets from primary root canal infections were retrieved from three geographic cohorts (Spain n = 32, Sweden n = 14, USA n = 25). All samples targeted the V3-V4 region and were sequenced using the Illumina MiSeq platform. Alpha and beta diversity metrics were assessed to evaluate within- and between-sample variation. Taxonomic composition was characterized, followed by differential abundance analysis and identification of the core microbiome. Microbial co-occurrence networks were inferred using the SPRING method, and hub taxa were identified based on eigenvector centrality.
RESULTS: Significant differences in microbial richness between cohorts were observed based on Chao1 index and observed richness. Beta diversity analyses revealed statistically significant but modest separation of microbial communities among populations (R[2] = 6.8%), with substantial overlap between cohorts. Bacillota, Bacteroidota, Fusobacteriota, and Actinomycetota were dominant across cohorts, although their relative abundances varied. Core microbiome analysis identified both shared and cohort-associated taxa at genus and species levels. SPRING-based co-occurrence networks identified cohort-associated hub taxa, including Fretibacterium fastidiosum in the USA, Dialister pneumosintes in Spain, and Treponema denticola in Sweden. Furthermore, predictive functional profiling suggested differences in microbial functional potential among geographic cohorts.
CONCLUSION: While root canal infections share a core microbiome, subtle population-specific microbial signatures were identified. However, the modest effect size suggests that geographic variation alone explains only a limited proportion of microbial composition. Larger and more balanced studies are required to further evaluate geographic influences on the root canal microbiome and their potential clinical relevance.},
}
RevDate: 2026-09-28
Gestational period as a key stage in the promotion of children's oral health. Pilot study.
European journal of paediatric dentistry [Epub ahead of print].
AIM: To assess the knowledge and attitudes of a group of pregnant women regarding the importance of maintaining a healthy lifestyle during pregnancy, to improve their oral health and that of their children.
BACKGROUND: The first thousand days of a baby's life, spanning from conception to two years of age, are marked by rapid development and the establishment of critical elements such as the gastrointestinal and oral microbiome. This period is crucial for fostering healthy habits that will positively impact the future adult's health profile.
METHODS: A cross-sectional study was conducted involving 54 pregnant women. Data were collected using a survey previously validated through expert review and pilot testing.
CONCLUSION: There appears to be a notable lack of information among pregnant women regarding both their own oral health and that of their future babies. This is partly attributed to insufficient support from healthcare professionals during pregnancy.
Additional Links: PMID-42803221
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@article {pmid42803221,
year = {2026},
author = {Pometti, AM and Palazón Radford, E and Medina-Sotomayor, P and Ribelles Llop, M and Leyda Menéndez, AM},
title = {Gestational period as a key stage in the promotion of children's oral health. Pilot study.},
journal = {European journal of paediatric dentistry},
volume = {},
number = {},
pages = {1},
doi = {10.23804/ejpd.2026.2766},
pmid = {42803221},
issn = {2035-648X},
abstract = {AIM: To assess the knowledge and attitudes of a group of pregnant women regarding the importance of maintaining a healthy lifestyle during pregnancy, to improve their oral health and that of their children.
BACKGROUND: The first thousand days of a baby's life, spanning from conception to two years of age, are marked by rapid development and the establishment of critical elements such as the gastrointestinal and oral microbiome. This period is crucial for fostering healthy habits that will positively impact the future adult's health profile.
METHODS: A cross-sectional study was conducted involving 54 pregnant women. Data were collected using a survey previously validated through expert review and pilot testing.
CONCLUSION: There appears to be a notable lack of information among pregnant women regarding both their own oral health and that of their future babies. This is partly attributed to insufficient support from healthcare professionals during pregnancy.},
}
RevDate: 2026-09-28
Rhizosphere Microbiome-Mediated Drought Resilience in Cereals: Implications for Grain Nutrition, Yield, and Tolerance.
Plant, cell & environment [Epub ahead of print].
Drought-mediated declines in grain nutritional quality and cereal yield put global food security at risk, yet the rhizosphere microbiome provides an alternative solution for improving crop tolerance. Our review synthesised existing knowledge on how soil microbiomes, particularly arbuscular mycorrhizal fungi (AMF) and plant-growth-promoting rhizobacteria (PGPR), simultaneously regulate three interlinked pillars of crop performance (stress tolerance, grain nutrient uptake, and yield) under drought. Our in-depth analysis showed that such relationships were governed by synergies (improved root architecture improves all three traits) and trade-offs (i.e., ABA-induced stomatal closure improves water efficiency but restricts carbon assimilation). Furthermore, these relationships were governed at different biological layers through multi-omics (metagenomics, transcriptomics, proteomics, and metabolomics) to identify biomarkers and pathways. With the application of an integrated framework through bioinformatics, it is now possible to reveal the hidden molecular layout between cereals and their underground partners, identify drought-responsive pathways, and discover biomarkers (nutrient transporter gene, microbial abundance, osmolyte accumulation, and root exudates). Despite advancements, critical technical gaps hinder data integration and standardised pipelines to identify complex traits through heterogeneous databases of omics. Our review proposes an integrated framework linking multi-omics tools, microbiome traits, and crop outcomes. Furthermore, we provide a research roadmap prioritising drought biofortification, synthetic communities (SynComs), microbial consortia, and spatial omics. Such research directly supports hidden hunger and food security agendas, while progressing climate-resilient agriculture.
Additional Links: PMID-42803406
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PubMed:
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@article {pmid42803406,
year = {2026},
author = {Saeed, M and Huang, X and Mustafa, G and Li, M and Yang, P},
title = {Rhizosphere Microbiome-Mediated Drought Resilience in Cereals: Implications for Grain Nutrition, Yield, and Tolerance.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.70901},
pmid = {42803406},
issn = {1365-3040},
support = {2024BBB001//Hubei Provincial Key Research and Development Projects/ ; 2023AFB614//Hubei Provincial Natural Science Foundation/ ; 2023AFA016//Hubei Provincial Natural Science Foundation/ ; },
abstract = {Drought-mediated declines in grain nutritional quality and cereal yield put global food security at risk, yet the rhizosphere microbiome provides an alternative solution for improving crop tolerance. Our review synthesised existing knowledge on how soil microbiomes, particularly arbuscular mycorrhizal fungi (AMF) and plant-growth-promoting rhizobacteria (PGPR), simultaneously regulate three interlinked pillars of crop performance (stress tolerance, grain nutrient uptake, and yield) under drought. Our in-depth analysis showed that such relationships were governed by synergies (improved root architecture improves all three traits) and trade-offs (i.e., ABA-induced stomatal closure improves water efficiency but restricts carbon assimilation). Furthermore, these relationships were governed at different biological layers through multi-omics (metagenomics, transcriptomics, proteomics, and metabolomics) to identify biomarkers and pathways. With the application of an integrated framework through bioinformatics, it is now possible to reveal the hidden molecular layout between cereals and their underground partners, identify drought-responsive pathways, and discover biomarkers (nutrient transporter gene, microbial abundance, osmolyte accumulation, and root exudates). Despite advancements, critical technical gaps hinder data integration and standardised pipelines to identify complex traits through heterogeneous databases of omics. Our review proposes an integrated framework linking multi-omics tools, microbiome traits, and crop outcomes. Furthermore, we provide a research roadmap prioritising drought biofortification, synthetic communities (SynComs), microbial consortia, and spatial omics. Such research directly supports hidden hunger and food security agendas, while progressing climate-resilient agriculture.},
}
RevDate: 2026-09-28
Synbiotic supplementation may attenuate osteoporosis following spinal cord injury in a rat model.
The journal of spinal cord medicine [Epub ahead of print].
CONTEXT: Spinal cord injury (SCI) often leads to severe bone loss and a higher risk of osteoporosis. Current treatments have not fully addressed bone deterioration, which remains a major clinical issue. New research suggests that the gut microbiota may influence bone health, and probiotics might help improve bone status. This study aimed to assess the effect of synbiotic supplementation, which combines probiotics and prebiotics, on bone health in a rat model of SCI-induced osteoporosis.
METHODS: Male Wistar rats were randomly divided into three groups: control (sham), SCI, and SCI + synbiotic. Spinal cord injury was surgically induced at the T10 level. The synbiotic group received 1 mL of Lactocare® (containing probiotics and fructooligosaccharides) orally, three times a week for four weeks after the injury. We measured bone mineral density (BMD), bone volume/total volume (BV/TV), alkaline phosphatase (ALP) levels, and bone strength (maximum breaking force).
RESULTS: Although ALP activity decreased in the treatment group, the reduction was not statistically significant and levels did not return to those of the control group, synbiotic supplementation led to a significant decrease in bone loss compared to the SCI group (P < 0.05), and bone strength parameters improved significantly in the treatment group. This indicates reduced bone turnover and better bone integrity.
CONCLUSION: Synbiotic treatment may reduce osteoporosis following SCI by influencing bone metabolism. These results lay the groundwork for future studies on gut-targeted therapies for bone loss related to SCI.
Additional Links: PMID-42803436
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@article {pmid42803436,
year = {2026},
author = {Shirazani, SMT and Golipoor, M and Ch, MH and Zaminy, A},
title = {Synbiotic supplementation may attenuate osteoporosis following spinal cord injury in a rat model.},
journal = {The journal of spinal cord medicine},
volume = {},
number = {},
pages = {1-8},
doi = {10.1080/10790268.2026.2672829},
pmid = {42803436},
issn = {2045-7723},
abstract = {CONTEXT: Spinal cord injury (SCI) often leads to severe bone loss and a higher risk of osteoporosis. Current treatments have not fully addressed bone deterioration, which remains a major clinical issue. New research suggests that the gut microbiota may influence bone health, and probiotics might help improve bone status. This study aimed to assess the effect of synbiotic supplementation, which combines probiotics and prebiotics, on bone health in a rat model of SCI-induced osteoporosis.
METHODS: Male Wistar rats were randomly divided into three groups: control (sham), SCI, and SCI + synbiotic. Spinal cord injury was surgically induced at the T10 level. The synbiotic group received 1 mL of Lactocare® (containing probiotics and fructooligosaccharides) orally, three times a week for four weeks after the injury. We measured bone mineral density (BMD), bone volume/total volume (BV/TV), alkaline phosphatase (ALP) levels, and bone strength (maximum breaking force).
RESULTS: Although ALP activity decreased in the treatment group, the reduction was not statistically significant and levels did not return to those of the control group, synbiotic supplementation led to a significant decrease in bone loss compared to the SCI group (P < 0.05), and bone strength parameters improved significantly in the treatment group. This indicates reduced bone turnover and better bone integrity.
CONCLUSION: Synbiotic treatment may reduce osteoporosis following SCI by influencing bone metabolism. These results lay the groundwork for future studies on gut-targeted therapies for bone loss related to SCI.},
}
RevDate: 2026-09-28
Vascular effects of micro- and nanoplastics in humans: Systematic review.
Kardiologia polska pii:VM/OJS/J/114989 [Epub ahead of print].
Plastics have been accumulating in the environment for over 100 years and are environmental pollutants already recognized as relevant risk factors for human health, including the cardiovascular system. Plastics break down into smaller particles called microplastics (with diameters ranging from 1 micrometer to 5 millimeters) and nanoplastics (with diameters smaller than 1 micrometer), which are resistant to natural degradation. Micro- and nanoplastics (MNPs) enter the human body through ingestion, inhalation, dermal penetration, injection, and implantation. MNPs are heterogeneous in their origins, chemical compositions, and structures. Their toxicity varies according to the type of plastic (most prevalent polymers being polyethylene, polypropylene, polystyrene, polyethylene terephthalate, and polyvinyl chloride), the plastic micro-additives like bisphenols and phthalates, the size of the particles, the other non-organic and organic substances, which they transfer (heavy metals, polycyclic aromatic hydrocarbons, bacteria, viruses, antibiotics), etc. In this review, we will focus on the known vascular effects of these particles - on the coronary arteries, visceral arteries and peripheral arteries, and the methods of MNPs detection. We will also discuss their penetration pathways, measures to reduce exposure, the role of a healthy gut microbiome in the absorption of these particles, investigational approaches to reducing damage, and new biodegradable alternatives (e.g., polyhydroxyalkanoates). Additionally, we will discuss the existing scientific evidence, particularly from the Bulgarian database. Finally, we will discuss the major knowledge gaps involving MNPs clinical research. Current evidence of vascular toxicity in humans is still with limited mechanistic validation.
Additional Links: PMID-42803455
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PubMed:
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@article {pmid42803455,
year = {2026},
author = {Koleva, K and Velikov, T and Panayotov, P and Hristova, I and Koleva, G and Rigatelli, G and Gil, RJ and Vassilev, D},
title = {Vascular effects of micro- and nanoplastics in humans: Systematic review.},
journal = {Kardiologia polska},
volume = {},
number = {},
pages = {},
doi = {10.33963/v.phj.114989},
pmid = {42803455},
issn = {1897-4279},
abstract = {Plastics have been accumulating in the environment for over 100 years and are environmental pollutants already recognized as relevant risk factors for human health, including the cardiovascular system. Plastics break down into smaller particles called microplastics (with diameters ranging from 1 micrometer to 5 millimeters) and nanoplastics (with diameters smaller than 1 micrometer), which are resistant to natural degradation. Micro- and nanoplastics (MNPs) enter the human body through ingestion, inhalation, dermal penetration, injection, and implantation. MNPs are heterogeneous in their origins, chemical compositions, and structures. Their toxicity varies according to the type of plastic (most prevalent polymers being polyethylene, polypropylene, polystyrene, polyethylene terephthalate, and polyvinyl chloride), the plastic micro-additives like bisphenols and phthalates, the size of the particles, the other non-organic and organic substances, which they transfer (heavy metals, polycyclic aromatic hydrocarbons, bacteria, viruses, antibiotics), etc. In this review, we will focus on the known vascular effects of these particles - on the coronary arteries, visceral arteries and peripheral arteries, and the methods of MNPs detection. We will also discuss their penetration pathways, measures to reduce exposure, the role of a healthy gut microbiome in the absorption of these particles, investigational approaches to reducing damage, and new biodegradable alternatives (e.g., polyhydroxyalkanoates). Additionally, we will discuss the existing scientific evidence, particularly from the Bulgarian database. Finally, we will discuss the major knowledge gaps involving MNPs clinical research. Current evidence of vascular toxicity in humans is still with limited mechanistic validation.},
}
RevDate: 2026-09-28
Resolving host-episymbiont interaction dynamics through continuous cultivation.
mSystems [Epub ahead of print].
Minisyncoccota are an elusive lineage of "microbial dark matter" predicted to compose ~25% of total bacterial diversity. Despite near ubiquity, these organisms are challenging to cultivate, resulting from their specialized episymbiotic lifestyle. All cultivated representatives, predominantly Nanosynbacteria, depend on cognate prokaryotic hosts for growth. Studying the growth dynamics of episymbiotic bacteria and their hosts in batch cultures suggests that episymbionts typically reduce host populations and that hosts eventually adapt to episymbiont stress after serial passaging. However, discontinuous batch cultures do not reflect natural interactions between these organisms due to their drastically different growth rates, which complicates the investigation of host inhibition and adaptation. To describe these dynamics, we utilized continuous culture via small-scale bioreactors. Within a bioreactor, host bacteria can be cultivated at a consistent growth rate, providing the perfect substrate for cultivation of model Nanosynbacteria. Quantification of time until host crash, crash severity, host adaptation, and stable co-culture population provides mechanistic ways to describe episymbiont-host interactions. We used these techniques to compare infection by three episymbionts, revealing distinct infection patterns ranging from mild inhibition with rapid host adaptation to rapid host collapse followed by "arms-race" oscillation dynamics. Then, bioreactors were used to quantify the episymbiotic role played by a known host-binding type 4 pili (T4P-2), demonstrating that loss of pilus-range host binding (approximately 100-800 nm) significantly delayed the host crash without altering general crash dynamics. These experiments reveal that episymbionts can have drastically different effects on bacterial communities and provide the tools necessary to describe strain/species differences and molecular interactions.IMPORTANCEEpisymbiotic Minisyncoccota represent one of the largest branches of life on Earth, as well as one of the least understood. Furthermore, because Minisyncoccota can manipulate their hosts' growth and morphology, they have immense ecological potential to shape the communities they occupy, both environmental and microbiome-associated. Our study highlights, for the first time, the potential of small-scale continuous cultivation for studying episymbiotic interactions that cannot be captured in discontinuous cultures. Herein, we used these techniques to interrogate interspecies variation in host inhibition potential and to determine how loss of a pilus-dependent binding factor mechanistically alters the cycle of episymbiont infection; however, this cultivation platform will enable researchers to answer many new questions about these ubiquitous host-episymbiont interactions.
Additional Links: PMID-42803565
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@article {pmid42803565,
year = {2026},
author = {Grossman, AS and Weng, J and Silverman, AD and Bor, B},
title = {Resolving host-episymbiont interaction dynamics through continuous cultivation.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0059226},
doi = {10.1128/msystems.00592-26},
pmid = {42803565},
issn = {2379-5077},
abstract = {Minisyncoccota are an elusive lineage of "microbial dark matter" predicted to compose ~25% of total bacterial diversity. Despite near ubiquity, these organisms are challenging to cultivate, resulting from their specialized episymbiotic lifestyle. All cultivated representatives, predominantly Nanosynbacteria, depend on cognate prokaryotic hosts for growth. Studying the growth dynamics of episymbiotic bacteria and their hosts in batch cultures suggests that episymbionts typically reduce host populations and that hosts eventually adapt to episymbiont stress after serial passaging. However, discontinuous batch cultures do not reflect natural interactions between these organisms due to their drastically different growth rates, which complicates the investigation of host inhibition and adaptation. To describe these dynamics, we utilized continuous culture via small-scale bioreactors. Within a bioreactor, host bacteria can be cultivated at a consistent growth rate, providing the perfect substrate for cultivation of model Nanosynbacteria. Quantification of time until host crash, crash severity, host adaptation, and stable co-culture population provides mechanistic ways to describe episymbiont-host interactions. We used these techniques to compare infection by three episymbionts, revealing distinct infection patterns ranging from mild inhibition with rapid host adaptation to rapid host collapse followed by "arms-race" oscillation dynamics. Then, bioreactors were used to quantify the episymbiotic role played by a known host-binding type 4 pili (T4P-2), demonstrating that loss of pilus-range host binding (approximately 100-800 nm) significantly delayed the host crash without altering general crash dynamics. These experiments reveal that episymbionts can have drastically different effects on bacterial communities and provide the tools necessary to describe strain/species differences and molecular interactions.IMPORTANCEEpisymbiotic Minisyncoccota represent one of the largest branches of life on Earth, as well as one of the least understood. Furthermore, because Minisyncoccota can manipulate their hosts' growth and morphology, they have immense ecological potential to shape the communities they occupy, both environmental and microbiome-associated. Our study highlights, for the first time, the potential of small-scale continuous cultivation for studying episymbiotic interactions that cannot be captured in discontinuous cultures. Herein, we used these techniques to interrogate interspecies variation in host inhibition potential and to determine how loss of a pilus-dependent binding factor mechanistically alters the cycle of episymbiont infection; however, this cultivation platform will enable researchers to answer many new questions about these ubiquitous host-episymbiont interactions.},
}
RevDate: 2026-09-28
Beyond the parasite: skin-intrinsic cytolytic circuits drive disease in cutaneous leishmaniasis and reveal targets for host-directed therapy.
Microbiology and molecular biology reviews : MMBR [Epub ahead of print].
SUMMARYCutaneous leishmaniasis (CL) is a globally prevalent parasitic disease in which tissue pathology often arises primarily from immune-mediated damage rather than uncontrolled parasite replication. Despite effective Th1 responses and the production of IFN-γ, lesions often fail to resolve, highlighting an uncoupling of protective immunity from disease pathogenesis. This review synthesizes evidence from experimental models and human studies demonstrating that skin-intrinsic cytolytic inflammatory circuits-rather than parasite burden-are dominant drivers of lesion persistence and treatment failure in CL. Central to this pathway is the accumulation of cytotoxic CD8[+] T cells within lesions, where perforin-dependent cell death triggers NLRP3 inflammasome activation and IL-1β production. IL-1β acts as a potent amplifier of inflammation by promoting neutrophil recruitment, tissue injury, and local hypoxia, which further programs pathogenic CD8[+] T-cell differentiation. These responses are exacerbated by alterations of the skin microbiome, particularly the dominance of Staphylococcus aureus, and are normally constrained by Foxp3[+] regulatory T cells that limit excessive IFN-γ-driven cytotoxicity. In parallel, parasite persistence within permissive macrophage subsets provides a continuous antigenic stimulus that sustains inflammation without achieving sterilizing immunity. Together, these interconnected pathways form a self-reinforcing inflammatory circuit that promotes ulceration, chronic disease, and therapeutic failure. Importantly, this pathogenic network is largely dispensable for parasite control and, therefore, provides multiple targets for host-directed therapies that could complement anti-parasitic drugs and improve clinical outcomes in CL.
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@article {pmid42803567,
year = {2026},
author = {Novais, FO and Scott, P},
title = {Beyond the parasite: skin-intrinsic cytolytic circuits drive disease in cutaneous leishmaniasis and reveal targets for host-directed therapy.},
journal = {Microbiology and molecular biology reviews : MMBR},
volume = {},
number = {},
pages = {e0005825},
doi = {10.1128/mmbr.00058-25},
pmid = {42803567},
issn = {1098-5557},
abstract = {SUMMARYCutaneous leishmaniasis (CL) is a globally prevalent parasitic disease in which tissue pathology often arises primarily from immune-mediated damage rather than uncontrolled parasite replication. Despite effective Th1 responses and the production of IFN-γ, lesions often fail to resolve, highlighting an uncoupling of protective immunity from disease pathogenesis. This review synthesizes evidence from experimental models and human studies demonstrating that skin-intrinsic cytolytic inflammatory circuits-rather than parasite burden-are dominant drivers of lesion persistence and treatment failure in CL. Central to this pathway is the accumulation of cytotoxic CD8[+] T cells within lesions, where perforin-dependent cell death triggers NLRP3 inflammasome activation and IL-1β production. IL-1β acts as a potent amplifier of inflammation by promoting neutrophil recruitment, tissue injury, and local hypoxia, which further programs pathogenic CD8[+] T-cell differentiation. These responses are exacerbated by alterations of the skin microbiome, particularly the dominance of Staphylococcus aureus, and are normally constrained by Foxp3[+] regulatory T cells that limit excessive IFN-γ-driven cytotoxicity. In parallel, parasite persistence within permissive macrophage subsets provides a continuous antigenic stimulus that sustains inflammation without achieving sterilizing immunity. Together, these interconnected pathways form a self-reinforcing inflammatory circuit that promotes ulceration, chronic disease, and therapeutic failure. Importantly, this pathogenic network is largely dispensable for parasite control and, therefore, provides multiple targets for host-directed therapies that could complement anti-parasitic drugs and improve clinical outcomes in CL.},
}
RevDate: 2026-09-28
CmpDate: 2026-09-28
From dysbiosis to disease: the role of gut microbial communities in Toxoplasma gondii pathogenesis, zoonotic transmission, diagnostic innovation, and therapeutic outcomes.
Veterinary research communications, 50(6):.
Toxoplasma gondii, an obligate intracellular protozoan infecting approximately one-third of the global human population, causes substantial morbidity in immunocompromised individuals, congenital complications, neuropsychiatric sequelae, and considerable economic losses in livestock production. Gut microbial communities critically modulate T. gondii infection susceptibility, disease progression, and clinical outcomes, positioning the microbiome as a central axis in toxoplasmosis pathogenesis. This review examines the bidirectional relationship between gut microbiota and T. gondii, wherein dysbiosis functions simultaneously as a consequence and driver of disease severity. Protective commensal taxa reinforce intestinal barrier integrity, produce short-chain fatty acids, and stimulate anti-parasitic immunity through IFN-γ, IL-12, and tryptophan-aryl hydrocarbon receptor signaling, while pathobionts exacerbate immunopathology via TLR4 and inflammasome activation. Conversely, acute infection drives rapid microbial community collapse with persistent Proteobacteria expansion, butyrate-producing taxa depletion, neuroinflammation, and cognitive impairment in chronic infection. Across the One Health spectrum, host-specific microbiome signatures in felids, livestock, wildlife, and environmental reservoirs modulate zoonotic transmission dynamics and population-level susceptibility. Diagnostically, emerging microbiome-based approaches including metagenomics and multi-omics platforms offer promising biomarker discovery opportunities, though validated clinical signatures remain absent. Microbiome-targeted therapeutic strategies including probiotics, prebiotics, fecal microbiota transplantation, and postbiotics show preclinical promise, although human clinical trial validation is critically lacking. Critical research gaps and interdisciplinary One Health priorities are identified to advance microbiome-informed surveillance, diagnosis, and treatment of toxoplasmosis.
Additional Links: PMID-42803857
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@article {pmid42803857,
year = {2026},
author = {Ali, S and Ali, B and Shaukat, A and Alghamdi, S and Kabrah, A and Ahmed, MA and Zhang, L},
title = {From dysbiosis to disease: the role of gut microbial communities in Toxoplasma gondii pathogenesis, zoonotic transmission, diagnostic innovation, and therapeutic outcomes.},
journal = {Veterinary research communications},
volume = {50},
number = {6},
pages = {},
pmid = {42803857},
issn = {1573-7446},
mesh = {Animals ; *Dysbiosis/veterinary/parasitology/microbiology ; *Gastrointestinal Microbiome ; *Toxoplasma/physiology ; *Zoonoses/transmission/parasitology/microbiology ; Humans ; *Toxoplasmosis, Animal/transmission/microbiology/diagnosis ; *Toxoplasmosis/transmission/therapy/microbiology/diagnosis/parasitology ; },
abstract = {Toxoplasma gondii, an obligate intracellular protozoan infecting approximately one-third of the global human population, causes substantial morbidity in immunocompromised individuals, congenital complications, neuropsychiatric sequelae, and considerable economic losses in livestock production. Gut microbial communities critically modulate T. gondii infection susceptibility, disease progression, and clinical outcomes, positioning the microbiome as a central axis in toxoplasmosis pathogenesis. This review examines the bidirectional relationship between gut microbiota and T. gondii, wherein dysbiosis functions simultaneously as a consequence and driver of disease severity. Protective commensal taxa reinforce intestinal barrier integrity, produce short-chain fatty acids, and stimulate anti-parasitic immunity through IFN-γ, IL-12, and tryptophan-aryl hydrocarbon receptor signaling, while pathobionts exacerbate immunopathology via TLR4 and inflammasome activation. Conversely, acute infection drives rapid microbial community collapse with persistent Proteobacteria expansion, butyrate-producing taxa depletion, neuroinflammation, and cognitive impairment in chronic infection. Across the One Health spectrum, host-specific microbiome signatures in felids, livestock, wildlife, and environmental reservoirs modulate zoonotic transmission dynamics and population-level susceptibility. Diagnostically, emerging microbiome-based approaches including metagenomics and multi-omics platforms offer promising biomarker discovery opportunities, though validated clinical signatures remain absent. Microbiome-targeted therapeutic strategies including probiotics, prebiotics, fecal microbiota transplantation, and postbiotics show preclinical promise, although human clinical trial validation is critically lacking. Critical research gaps and interdisciplinary One Health priorities are identified to advance microbiome-informed surveillance, diagnosis, and treatment of toxoplasmosis.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*Dysbiosis/veterinary/parasitology/microbiology
*Gastrointestinal Microbiome
*Toxoplasma/physiology
*Zoonoses/transmission/parasitology/microbiology
Humans
*Toxoplasmosis, Animal/transmission/microbiology/diagnosis
*Toxoplasmosis/transmission/therapy/microbiology/diagnosis/parasitology
RevDate: 2026-09-28
The effect of pectin supplementation on geriatric individuals with frailty: a randomised placebo-controlled dietary intervention study.
GeroScience [Epub ahead of print].
Frailty is associated with impaired physical function, psychological decline, and alterations in the gut microbiome, yet nutritional strategies targeting these interconnected pathways remain limited. Low-methoxy (LM) pectin, a fermentable dietary fibre derived from plant cell walls, has demonstrated immunomodulatory and microbiome-modifying effects in preclinical studies, but evidence in older adults with frailty is scarce. We conducted a 4-week double-blind, randomised, placebo-controlled trial evaluating LM pectin supplementation in older adults with frailty. Thirty-one participants were enrolled, and 29 completed the intervention. Physical performance, psychological well-being, quality of life, inflammatory biomarkers, and gut microbiome composition were assessed at baseline and follow-up. Compared with placebo, low-methoxy pectin supplementation significantly improved lower limb function measured by the 30-second sit-to-stand test (2.07 ± 1.94 vs 0.71 ± 2.27 repetitions; p = 0.038), while no significant changes were observed in Timed Up and Go performance. Supplementation also reduced anxiety and depression scores and improved several Short Form-36 domains, including physical functioning, vitality, mental health, and social functioning. No significant differences were detected in circulating inflammatory biomarkers. Gut microbiome analysis demonstrated increased relative abundance of Coprococcus comes, an acetate-producing species linked to gut-brain signalling and psychological health. These findings provide preliminary evidence that LM pectin supplementation may improve physical and psychological outcomes and alter gut microbial composition in older adults with frailty. Larger, adequately powered trials are needed to determine whether these changes are reproducible and to investigate potential microbiome-related mechanisms. Trial registration number: NCT06955975 (https://clinicaltrials.gov/study/NCT06955975 ; Clinical Trials.gov; 2025-06-22).
Additional Links: PMID-42803883
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@article {pmid42803883,
year = {2026},
author = {Al-Tameemi, NK and Kouraki, A and Kelly, T and Grove, JI and Rollins, KE and Aithal, GP and Valdes, AM},
title = {The effect of pectin supplementation on geriatric individuals with frailty: a randomised placebo-controlled dietary intervention study.},
journal = {GeroScience},
volume = {},
number = {},
pages = {},
pmid = {42803883},
issn = {2509-2723},
abstract = {Frailty is associated with impaired physical function, psychological decline, and alterations in the gut microbiome, yet nutritional strategies targeting these interconnected pathways remain limited. Low-methoxy (LM) pectin, a fermentable dietary fibre derived from plant cell walls, has demonstrated immunomodulatory and microbiome-modifying effects in preclinical studies, but evidence in older adults with frailty is scarce. We conducted a 4-week double-blind, randomised, placebo-controlled trial evaluating LM pectin supplementation in older adults with frailty. Thirty-one participants were enrolled, and 29 completed the intervention. Physical performance, psychological well-being, quality of life, inflammatory biomarkers, and gut microbiome composition were assessed at baseline and follow-up. Compared with placebo, low-methoxy pectin supplementation significantly improved lower limb function measured by the 30-second sit-to-stand test (2.07 ± 1.94 vs 0.71 ± 2.27 repetitions; p = 0.038), while no significant changes were observed in Timed Up and Go performance. Supplementation also reduced anxiety and depression scores and improved several Short Form-36 domains, including physical functioning, vitality, mental health, and social functioning. No significant differences were detected in circulating inflammatory biomarkers. Gut microbiome analysis demonstrated increased relative abundance of Coprococcus comes, an acetate-producing species linked to gut-brain signalling and psychological health. These findings provide preliminary evidence that LM pectin supplementation may improve physical and psychological outcomes and alter gut microbial composition in older adults with frailty. Larger, adequately powered trials are needed to determine whether these changes are reproducible and to investigate potential microbiome-related mechanisms. Trial registration number: NCT06955975 (https://clinicaltrials.gov/study/NCT06955975 ; Clinical Trials.gov; 2025-06-22).},
}
RevDate: 2026-09-28
An engineered probiotic Escherichia coli Nissle 1917 strain for Amuc_1100 delivery in a CT26 colorectal tumor model.
Probiotics and antimicrobial proteins [Epub ahead of print].
Engineered probiotics provide a microbial platform for the localized delivery of bioactive proteins. Escherichia coli Nissle 1917 (EcN) is an attractive bacterial chassis for this purpose because of its ability to colonize tumors and its genetic tractability. Amuc_1100, an outer membrane protein of Akkermansia muciniphila, has shown antitumor and immunomodulatory effects after oral administration. However, whether EcN-based delivery can improve the antitumor performance of microbiome-derived proteins such as Amuc_1100 remains unclear. Here, EcN was engineered with a pelB-His-Amuc_1100 expression cassette to generate EcN(pAmuc), which was evaluated in an immunocompetent CT26 colorectal tumor model. After a single intravenous administration, viable EcN(pAmuc) remained recoverable from tumors for up to 21 days, and His-tagged cargo-related protein signals were detected in tumor tissue at the study endpoint. EcN(pAmuc) reduced tumor growth and prolonged survival compared with untreated CT26-bearing mice and the oral recombinant Amuc_1100 regimen, with median survival increasing from 21 to 33 days relative to the untreated group. Treatment was accompanied by an increase in intratumoral CD3-positive cell proportion from 3.39% to 9.35% and TUNEL positivity from 5.08% to 10.41%, together with lower Ki-67 positivity and intratumoral TGF-β levels and a higher splenic CD8[+] T-cell proportion. Short-term safety-related assessments, including body weight, organ weights, peripheral white blood cell counts, serum creatinine, and major-organ histology, revealed no clear treatment-associated abnormalities under the conditions tested. These findings support EcN as a delivery chassis for Amuc_1100 and provide a basis for further optimization of this engineered probiotic platform in colorectal tumor models.
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@article {pmid42803915,
year = {2026},
author = {Wang, X and Wang, Y and Wu, D and Kang, Y and Li, R and Yang, G and Chen, G and Chen, Z and Hong, W and Cui, G},
title = {An engineered probiotic Escherichia coli Nissle 1917 strain for Amuc_1100 delivery in a CT26 colorectal tumor model.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {42803915},
issn = {1867-1314},
support = {[2022]101 and [2022]112//Excellent Young Talents Plan of Guizhou Medical University/ ; gzwkj2025-168//Guizhou Provincial Health Commission Project/ ; QKBPT GHJD[2025]006//International Science and Technology Cooperation Base of Guizhou Province/ ; ZDSYS[2023]004//Guizhou Key Laboratory/ ; KXJZ [2024]009//Science and Technology Program Project of Guizhou Province/ ; D20009//National "111" Project/ ; [2025]024//Central-Guided Local Science and Technology Projects/ ; S202310660097 and S2024106601411//Guizhou University Students Innovation Project/ ; 32460046, 32560029//National Natural Science Foundation of China/ ; },
abstract = {Engineered probiotics provide a microbial platform for the localized delivery of bioactive proteins. Escherichia coli Nissle 1917 (EcN) is an attractive bacterial chassis for this purpose because of its ability to colonize tumors and its genetic tractability. Amuc_1100, an outer membrane protein of Akkermansia muciniphila, has shown antitumor and immunomodulatory effects after oral administration. However, whether EcN-based delivery can improve the antitumor performance of microbiome-derived proteins such as Amuc_1100 remains unclear. Here, EcN was engineered with a pelB-His-Amuc_1100 expression cassette to generate EcN(pAmuc), which was evaluated in an immunocompetent CT26 colorectal tumor model. After a single intravenous administration, viable EcN(pAmuc) remained recoverable from tumors for up to 21 days, and His-tagged cargo-related protein signals were detected in tumor tissue at the study endpoint. EcN(pAmuc) reduced tumor growth and prolonged survival compared with untreated CT26-bearing mice and the oral recombinant Amuc_1100 regimen, with median survival increasing from 21 to 33 days relative to the untreated group. Treatment was accompanied by an increase in intratumoral CD3-positive cell proportion from 3.39% to 9.35% and TUNEL positivity from 5.08% to 10.41%, together with lower Ki-67 positivity and intratumoral TGF-β levels and a higher splenic CD8[+] T-cell proportion. Short-term safety-related assessments, including body weight, organ weights, peripheral white blood cell counts, serum creatinine, and major-organ histology, revealed no clear treatment-associated abnormalities under the conditions tested. These findings support EcN as a delivery chassis for Amuc_1100 and provide a basis for further optimization of this engineered probiotic platform in colorectal tumor models.},
}
RevDate: 2026-09-28
Aflatoxin-associated hepatocarcinogenesis in a changing climate: the gut microbiome as a missing link in the One Health framework.
Naunyn-Schmiedeberg's archives of pharmacology [Epub ahead of print].
Global anthropogenic climate change is restructuring the thermohygric parameters that govern Aspergillus flavus and Aspergillus parasiticus ecology, expanding the geographic range and contamination intensity of aflatoxin in staple food crops worldwide. Aflatoxin B1, a Group 1 IARC carcinogen and the most potent naturally occurring hepatocarcinogen, undergoes CYP3A4/CYP1A2-mediated bioactivation to the exo-8,9-epoxide, which alkylates N7-guanine residues in DNA, generating AFB1-N7-guanine adducts that produce G → T transversions culminating in the TP53 R249S gain-of-function mutation, a molecular fingerprint of aflatoxin-driven hepatocellular carcinoma. Beyond direct genotoxicity, AFB1 drives mitochondrial dysfunction through oxidative phosphorylation impairment, glutathione depletion, cardiolipin peroxidation, and mitochondrial membrane potential collapse. It activates NF-κB, STAT3, and TGF-β inflammatory signaling; and engages hepatic stellate cells in fibrogenesis culminating in cirrhosis. Critically, AFB1 also disrupts the gut microbiome, depleting butyrateproducing Ruminococcaceae, Faecalibacterium prausnitzii, and Akkermansia muciniphila while expanding pro-inflammatory Proteobacteria and Enterobacteriaceae. These dysbiotic changes compromise tight junction integrity, increase intestinal permeability, elevate portal LPS, and activate hepatic TLR4/MyD88/NF-κB and NLRP3 inflammasome cascades that amplify the carcinogenic consequences of direct AFB1 genotoxicity. This review integrates mechanistic evidence from molecular toxicology, microbiome biology, immunometabolism, and systems oncology to establish a unified framework positioning gut dysbiosis as a modifiable intermediate pathway in climate-sensitive aflatoxin-driven carcinogenesis.
Additional Links: PMID-42803968
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@article {pmid42803968,
year = {2026},
author = {Oyedokun, PA and Owolabi, VP and Oyedokun, MD and Ndako, JA and Adegbola, PI and Oyedokun, NA},
title = {Aflatoxin-associated hepatocarcinogenesis in a changing climate: the gut microbiome as a missing link in the One Health framework.},
journal = {Naunyn-Schmiedeberg's archives of pharmacology},
volume = {},
number = {},
pages = {},
pmid = {42803968},
issn = {1432-1912},
abstract = {Global anthropogenic climate change is restructuring the thermohygric parameters that govern Aspergillus flavus and Aspergillus parasiticus ecology, expanding the geographic range and contamination intensity of aflatoxin in staple food crops worldwide. Aflatoxin B1, a Group 1 IARC carcinogen and the most potent naturally occurring hepatocarcinogen, undergoes CYP3A4/CYP1A2-mediated bioactivation to the exo-8,9-epoxide, which alkylates N7-guanine residues in DNA, generating AFB1-N7-guanine adducts that produce G → T transversions culminating in the TP53 R249S gain-of-function mutation, a molecular fingerprint of aflatoxin-driven hepatocellular carcinoma. Beyond direct genotoxicity, AFB1 drives mitochondrial dysfunction through oxidative phosphorylation impairment, glutathione depletion, cardiolipin peroxidation, and mitochondrial membrane potential collapse. It activates NF-κB, STAT3, and TGF-β inflammatory signaling; and engages hepatic stellate cells in fibrogenesis culminating in cirrhosis. Critically, AFB1 also disrupts the gut microbiome, depleting butyrateproducing Ruminococcaceae, Faecalibacterium prausnitzii, and Akkermansia muciniphila while expanding pro-inflammatory Proteobacteria and Enterobacteriaceae. These dysbiotic changes compromise tight junction integrity, increase intestinal permeability, elevate portal LPS, and activate hepatic TLR4/MyD88/NF-κB and NLRP3 inflammasome cascades that amplify the carcinogenic consequences of direct AFB1 genotoxicity. This review integrates mechanistic evidence from molecular toxicology, microbiome biology, immunometabolism, and systems oncology to establish a unified framework positioning gut dysbiosis as a modifiable intermediate pathway in climate-sensitive aflatoxin-driven carcinogenesis.},
}
RevDate: 2026-09-25
CmpDate: 2026-09-25
From rhizosphere to gut: microbial drivers of tea flavor and bioactivity.
NPJ science of food, 10(1):.
Across cultivation, processing, and consumption, tea quality and bioactivity are shaped by plant-microbiota interactions. This review develops a field-to-gut framework centered on the tea plant holobiont and downstream microbial partners. Within that frame, rhizosphere and endophytic microbiota are examined as regulators of flavor precursors, host metabolism, and defense. Processing microbiota are considered for remodeling tea chemistry and gut microbiota for bioactivating tea compounds, with microbial transmission, ecological replacement, and metabolite carryover distinguished and translational directions identified in microbiome-guided cultivation, controlled fermentation, and metabotype-informed nutrition.
Additional Links: PMID-42791270
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@article {pmid42791270,
year = {2026},
author = {Qi, M and Xie, J and Li, S and Zeng, L and Luo, L},
title = {From rhizosphere to gut: microbial drivers of tea flavor and bioactivity.},
journal = {NPJ science of food},
volume = {10},
number = {1},
pages = {},
pmid = {42791270},
issn = {2396-8370},
support = {U25A20693//the Joint Fund Project of the National Natural Science Foundation/ ; 2022YFD1600803//the National Key Research and Development Program of China/ ; CQMAITS202508//the Chongqing Modern Agricultural Industry Technology System/ ; SWU-XDJH202316//he Fundamental Research Funds for the Central Universities/ ; },
abstract = {Across cultivation, processing, and consumption, tea quality and bioactivity are shaped by plant-microbiota interactions. This review develops a field-to-gut framework centered on the tea plant holobiont and downstream microbial partners. Within that frame, rhizosphere and endophytic microbiota are examined as regulators of flavor precursors, host metabolism, and defense. Processing microbiota are considered for remodeling tea chemistry and gut microbiota for bioactivating tea compounds, with microbial transmission, ecological replacement, and metabolite carryover distinguished and translational directions identified in microbiome-guided cultivation, controlled fermentation, and metabotype-informed nutrition.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Genetically Predicted Gut Microbial Taxa and Inflammatory Proteins Associated With Atrial Fibrillation: A Bidirectional Mendelian Randomization and Colocalization Study.
Journal of arrhythmia, 42(5):e70454.
BACKGROUND: Observational studies have linked the gut microbiota and inflammatory proteins to atrial fibrillation (AF), but confounding, reverse causation, and instrument validity remain concerns.
METHODS: We evaluated 473 microbial traits and 91 inflammatory proteins in relation to AF using two GWAS datasets. Sensitivity analyses included instruments selected at p < 5 × 10[-8], MR-RAPS, cis/trans-stratified protein MR, reverse MR, and FGF-5 colocalization. Participants were predominantly of European ancestry.
RESULTS: Under conventional IVW analysis, six associations were FDR-significant in the discovery analysis and remained FDR-significant when selectively evaluated in the second AF GWAS, with FDR correction applied across the six prioritized tests: Leptospirae (OR 0.605, 95% CI 0.457-0.800), Leptospirales (0.499, 0.371-0.673), leukemia inhibitory factor receptor (LIF-R; 0.905, 0.869-0.943), TWEAK (0.891, 0.856-0.927), FGF-5 (1.077, 1.051-1.103), and interleukin-6 (0.886, 0.834-0.942). At p < 5 × 10[-8], neither microbial trait had a harmonized instrument, whereas the protein estimates retained their directions. MR-RAPS supported LIF-R in both datasets, but support for the other signals varied. The prioritized proteins also differed in cis/trans genetic architecture. The FGF-5 cis-only estimates were based on two harmonized instruments and were therefore preliminary, while cis-region colocalization provided little evidence of a shared variant (PP.H4 = 0.0045).
CONCLUSIONS: The conventional IVW associations varied in robustness across alternative analyses. These findings prioritize hypotheses, not established causal pathways or clinical targets. Generalizability beyond predominantly European populations remains uncertain.
Additional Links: PMID-42798960
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Citation:
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@article {pmid42798960,
year = {2026},
author = {Yi, C and Zheng, W and Zhao, J and Cai, W and Wang, J and Song, L and Bai, M and Zhang, Z},
title = {Genetically Predicted Gut Microbial Taxa and Inflammatory Proteins Associated With Atrial Fibrillation: A Bidirectional Mendelian Randomization and Colocalization Study.},
journal = {Journal of arrhythmia},
volume = {42},
number = {5},
pages = {e70454},
pmid = {42798960},
issn = {1880-4276},
abstract = {BACKGROUND: Observational studies have linked the gut microbiota and inflammatory proteins to atrial fibrillation (AF), but confounding, reverse causation, and instrument validity remain concerns.
METHODS: We evaluated 473 microbial traits and 91 inflammatory proteins in relation to AF using two GWAS datasets. Sensitivity analyses included instruments selected at p < 5 × 10[-8], MR-RAPS, cis/trans-stratified protein MR, reverse MR, and FGF-5 colocalization. Participants were predominantly of European ancestry.
RESULTS: Under conventional IVW analysis, six associations were FDR-significant in the discovery analysis and remained FDR-significant when selectively evaluated in the second AF GWAS, with FDR correction applied across the six prioritized tests: Leptospirae (OR 0.605, 95% CI 0.457-0.800), Leptospirales (0.499, 0.371-0.673), leukemia inhibitory factor receptor (LIF-R; 0.905, 0.869-0.943), TWEAK (0.891, 0.856-0.927), FGF-5 (1.077, 1.051-1.103), and interleukin-6 (0.886, 0.834-0.942). At p < 5 × 10[-8], neither microbial trait had a harmonized instrument, whereas the protein estimates retained their directions. MR-RAPS supported LIF-R in both datasets, but support for the other signals varied. The prioritized proteins also differed in cis/trans genetic architecture. The FGF-5 cis-only estimates were based on two harmonized instruments and were therefore preliminary, while cis-region colocalization provided little evidence of a shared variant (PP.H4 = 0.0045).
CONCLUSIONS: The conventional IVW associations varied in robustness across alternative analyses. These findings prioritize hypotheses, not established causal pathways or clinical targets. Generalizability beyond predominantly European populations remains uncertain.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Subtype-associated gut microbial taxa and their clinical correlates in acute ischemic stroke: comparison of large-artery atherosclerosis and small-vessel occlusion.
Frontiers in microbiology, 17:1867057.
OBJECTIVE: The gut microbiome gets altered during ischemic stroke (IS); however, whether distinct microbial signatures characterize specific IS subtypes, such as large-artery atherosclerosis (LAA) and small-vessel occlusion (SVO), and their relation to subtype-specific clinical features, remains unclear. This study aimed at comparing gut microbiome profiles among patients with LAA, patients with SVO, and healthy controls (HCs); further, the associations between subtype-enriched microbial taxa and clinical parameters were examined.
METHODS: We compared gut microbiome profiles and clinical associations among patients with LAA, patients with SVO, and HCs (n = 50 per group), using 16S rRNA sequencing to analyze microbial diversity and taxonomic composition. Correlation analyses were then performed between clinical parameters and the identified differential taxa.
RESULTS: Linear discriminant analysis effect size analysis showed that, compared with HCs, patients with IS had reduced alpha diversity and distinct beta diversity. No significant differences were observed between patients with LAA and SVO in alpha diversity (all indices, p > 0.05) or beta diversity (R [2] = 0.009, p = 0.595). Taxa enriched in HCs (Agathobaculum, Holdemanella, and Prevotella) were negatively associated with age, D-dimer levels, and modified Rankin Scale scores. LAA-enriched taxa (Desulfovibrio and Eubacterium) were positively correlated with Fazekas scale scores. SVO-enriched taxa (Catenibacterium, Collinsella, Megamonas, Sellimonas, and Weissella) were positively correlated with hemoglobin A1c, body mass index, and National Institutes of Health Stroke Scale scores.
CONCLUSION: Although overall microbial diversity did not differ between patients with LAA and SVO, subtype-enriched taxa were associated with distinct clinical features. These findings support the presence of subtype-specific microbial patterns that may reflect different pathophysiological processes; however, causal relationships remain to be established.
Additional Links: PMID-42799038
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Citation:
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@article {pmid42799038,
year = {2026},
author = {Park, S and Choi, J and Sadra, A and Lee, SH and Sohn, JH},
title = {Subtype-associated gut microbial taxa and their clinical correlates in acute ischemic stroke: comparison of large-artery atherosclerosis and small-vessel occlusion.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1867057},
pmid = {42799038},
issn = {1664-302X},
abstract = {OBJECTIVE: The gut microbiome gets altered during ischemic stroke (IS); however, whether distinct microbial signatures characterize specific IS subtypes, such as large-artery atherosclerosis (LAA) and small-vessel occlusion (SVO), and their relation to subtype-specific clinical features, remains unclear. This study aimed at comparing gut microbiome profiles among patients with LAA, patients with SVO, and healthy controls (HCs); further, the associations between subtype-enriched microbial taxa and clinical parameters were examined.
METHODS: We compared gut microbiome profiles and clinical associations among patients with LAA, patients with SVO, and HCs (n = 50 per group), using 16S rRNA sequencing to analyze microbial diversity and taxonomic composition. Correlation analyses were then performed between clinical parameters and the identified differential taxa.
RESULTS: Linear discriminant analysis effect size analysis showed that, compared with HCs, patients with IS had reduced alpha diversity and distinct beta diversity. No significant differences were observed between patients with LAA and SVO in alpha diversity (all indices, p > 0.05) or beta diversity (R [2] = 0.009, p = 0.595). Taxa enriched in HCs (Agathobaculum, Holdemanella, and Prevotella) were negatively associated with age, D-dimer levels, and modified Rankin Scale scores. LAA-enriched taxa (Desulfovibrio and Eubacterium) were positively correlated with Fazekas scale scores. SVO-enriched taxa (Catenibacterium, Collinsella, Megamonas, Sellimonas, and Weissella) were positively correlated with hemoglobin A1c, body mass index, and National Institutes of Health Stroke Scale scores.
CONCLUSION: Although overall microbial diversity did not differ between patients with LAA and SVO, subtype-enriched taxa were associated with distinct clinical features. These findings support the presence of subtype-specific microbial patterns that may reflect different pathophysiological processes; however, causal relationships remain to be established.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Correction: The impact of short-term intensive fasting on physical health and gut microbiota in obese individuals.
Frontiers in nutrition, 13:1985899.
[This corrects the article DOI: 10.3389/fnut.2026.1873000.].
Additional Links: PMID-42799088
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@article {pmid42799088,
year = {2026},
author = {Ji, F and Wang, S and Wang, L and Zhao, Y and Zhong, J and Wang, R and Qu, J and Lu, Y and Yuan, N and Zhang, Q},
title = {Correction: The impact of short-term intensive fasting on physical health and gut microbiota in obese individuals.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1985899},
doi = {10.3389/fnut.2026.1985899},
pmid = {42799088},
issn = {2296-861X},
abstract = {[This corrects the article DOI: 10.3389/fnut.2026.1873000.].},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Microbial inoculants for soil restoration: a risk-proportional stewardship framework integrating strain-resolved genomics and adaptive governance.
Sustainable microbiology, 3(3):qvag036.
Global soil degradation and increasing reliance on chemical inputs threaten agricultural sustainability, driving interest in microbial inoculants as tools for soil restoration. These biological products have the potential to enhance nutrient cycling, improve soil structure, and support plant resilience, but their environmental release raises important safety and stewardship considerations. Here, we propose a risk-proportional framework for the responsible deployment of microbial inoculants grounded in release-based stewardship. The framework integrates genome-resolved strain identification, exclusionary hazard screening, bioassay-based risk triage, ecological testing under realistic conditions, and monitored field deployment. Drawing on evidence from microbial ecology and invasion biology, we highlight how inoculants can alter resident microbial communities, influence ecosystem function, and, in some cases, facilitate gene flow, underscoring the need for risk assessment. We further outline a federated, genome-informed data infrastructure to support traceability, cross-jurisdiction learning, and adaptive management. Together, this approach provides a scalable and scientifically grounded pathway to balance innovation and safety, enabling microbial technologies to contribute to soil restoration and climate-resilient agriculture.
Additional Links: PMID-42799157
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@article {pmid42799157,
year = {2026},
author = {Edlund, A and Beattie, GA and Salles, JF and Gilbert, JA and Jansson, JK and Lennon, JT and Martiny, JBH and Sanders, IR and Schadt, CW and Jacobsen, CS and Sullivan, MB},
title = {Microbial inoculants for soil restoration: a risk-proportional stewardship framework integrating strain-resolved genomics and adaptive governance.},
journal = {Sustainable microbiology},
volume = {3},
number = {3},
pages = {qvag036},
pmid = {42799157},
issn = {2755-1970},
abstract = {Global soil degradation and increasing reliance on chemical inputs threaten agricultural sustainability, driving interest in microbial inoculants as tools for soil restoration. These biological products have the potential to enhance nutrient cycling, improve soil structure, and support plant resilience, but their environmental release raises important safety and stewardship considerations. Here, we propose a risk-proportional framework for the responsible deployment of microbial inoculants grounded in release-based stewardship. The framework integrates genome-resolved strain identification, exclusionary hazard screening, bioassay-based risk triage, ecological testing under realistic conditions, and monitored field deployment. Drawing on evidence from microbial ecology and invasion biology, we highlight how inoculants can alter resident microbial communities, influence ecosystem function, and, in some cases, facilitate gene flow, underscoring the need for risk assessment. We further outline a federated, genome-informed data infrastructure to support traceability, cross-jurisdiction learning, and adaptive management. Together, this approach provides a scalable and scientifically grounded pathway to balance innovation and safety, enabling microbial technologies to contribute to soil restoration and climate-resilient agriculture.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Crossroads of well-being: oral health, neurology, neuronutrition and healthy aging.
Open medicine (Warsaw, Poland), 21(1):20261515.
Oral health is increasingly recognized as a critical component of systemic and neurological resilience during aging. In particular, the oral microbiome may represent a modifiable interface linking periodontal inflammation, neuroimmune activation, and the risk of neurodegenerative disorders.Emerging evidence increasingly supports a link between oral microbiome dysbiosis and the pathogenesis of neurodegenerative disorders. Chronic inflammatory conditions, such as periodontitis, are associated with systemic inflammation, which may contribute to neuroinflammation. Key oral pathogens can translocate into the systemic circulation, compromise the integrity of the blood-brain barrier, and activate microglia. Mechanisms linking oral microbiome dysbiosis to neurodegeneration include systemic inflammation mediated by pro-inflammatory cytokines, direct bacterial invasion of the central nervous system, and modulation of the oral-gut-brain axis through alterations in the gut microbiota and neuroimmune interactions. Personalized neuronutritional strategies, including dietary intake and supplementation with polyphenols, may improve oral health and reduce systemic inflammation. The interdisciplinary integration of neurology, dentistry, and neuronutrition offers new opportunities for the prevention and management of neurodegenerative disorders. Promising approaches include the development of early diagnostic biomarkers of oral dysbiosis and targeted interventions aimed at restoring microbial homeostasis. Further research is needed to clarify causal relationships and optimize strategies for modulating the oral microbiome to preserve cognitive function.
Additional Links: PMID-42799301
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@article {pmid42799301,
year = {2026},
author = {Popovskaya, K and Badaeva, A and Kosareva, A and Novikov, V and Danilov, A and Danilov, A and Calabrese, V and Rashan, L and Isola, G and Sobin, A and Rasamatov, B and Kotenev, V and Gosteeva, E and Archakova, D and Vitish, E and Zacharyan, A and Sachkova, M and Popova, A and Korlykhanova, V and Rudenok, V},
title = {Crossroads of well-being: oral health, neurology, neuronutrition and healthy aging.},
journal = {Open medicine (Warsaw, Poland)},
volume = {21},
number = {1},
pages = {20261515},
pmid = {42799301},
issn = {2391-5463},
abstract = {Oral health is increasingly recognized as a critical component of systemic and neurological resilience during aging. In particular, the oral microbiome may represent a modifiable interface linking periodontal inflammation, neuroimmune activation, and the risk of neurodegenerative disorders.Emerging evidence increasingly supports a link between oral microbiome dysbiosis and the pathogenesis of neurodegenerative disorders. Chronic inflammatory conditions, such as periodontitis, are associated with systemic inflammation, which may contribute to neuroinflammation. Key oral pathogens can translocate into the systemic circulation, compromise the integrity of the blood-brain barrier, and activate microglia. Mechanisms linking oral microbiome dysbiosis to neurodegeneration include systemic inflammation mediated by pro-inflammatory cytokines, direct bacterial invasion of the central nervous system, and modulation of the oral-gut-brain axis through alterations in the gut microbiota and neuroimmune interactions. Personalized neuronutritional strategies, including dietary intake and supplementation with polyphenols, may improve oral health and reduce systemic inflammation. The interdisciplinary integration of neurology, dentistry, and neuronutrition offers new opportunities for the prevention and management of neurodegenerative disorders. Promising approaches include the development of early diagnostic biomarkers of oral dysbiosis and targeted interventions aimed at restoring microbial homeostasis. Further research is needed to clarify causal relationships and optimize strategies for modulating the oral microbiome to preserve cognitive function.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Gut dysbiosis induced by sunflower oil-based sucrose-free high-fat diet leads to steatohepatitis.
Frontiers in nutrition, 13:1831803.
High-fat diets (HFDs) are known to disrupt gut microbiota, contributing to obesity, inflammation, and metabolic disorders. Although sucrose is a known driver of gut dysbiosis, the microbiome alterations caused by sucrose-free fish oil and sunflower oil-based HFDs remain unclear. To investigate how sucrose-free sunflower oil-based (S-HFD) and fish oil-based (F-HFD) high-fat diets influence gut microbiota composition, metabolic health, and liver inflammation in mice. C57BL/6 mice were fed either S-HFD or F-HFD for 24 weeks. Body weight, insulin sensitivity, liver inflammation, and gene expression were assessed. Gut microbiota composition was analyzed using 16S rRNA sequencing, followed by diversity analysis and taxonomic profiling with Microbiome Analyst and MIAOME tools. Despite similar body weights between groups, the gut microbiota composition differed significantly. The S-HFD group showed a higher abundance of Firmicutes (40%) compared to the F-HFD group (3%), while Verrucomicrobia were dominant in F-HFD (26%) and nearly absent in S-HFD. Taxa such as RF39, Christensenellaceae, Mogibacteriaceae, and Yaniella were enriched in S-HFD mice and associated with metabolic and immune dysregulation. S-HFD mice also had elevated fasting glucose, increased hepatic monocyte/macrophage (F4/80+) infiltration, macrovesicular steatosis, lobular inflammation, and upregulation of genes related to fatty acid oxidation (Cpt1a), monocyte chemotaxis (Ccl2), lipogenesis (Scd1, Fasn, Acaca), and glycolysis (Pklr). Conversely, F-HFD mice showed increased expression of the insulin-sensitive gene FATP1. Sucrose-free sunflower oil- and fish oil-based high-fat diets induce distinct gut microbiota changes and metabolic responses. S-HFD is associated with gut dysbiosis and steatohepatitis-like features, highlighting the importance of fat sources in shaping microbiome-host interactions in metabolic disease.
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@article {pmid42799394,
year = {2026},
author = {Bahman, F and Malik, MZ and Kochumon, S and Nazim, R and Al Madhoun, A and Sindhu, S and Tuomilehto, J and Al-Mulla, F and Ahmad, R},
title = {Gut dysbiosis induced by sunflower oil-based sucrose-free high-fat diet leads to steatohepatitis.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1831803},
pmid = {42799394},
issn = {2296-861X},
abstract = {High-fat diets (HFDs) are known to disrupt gut microbiota, contributing to obesity, inflammation, and metabolic disorders. Although sucrose is a known driver of gut dysbiosis, the microbiome alterations caused by sucrose-free fish oil and sunflower oil-based HFDs remain unclear. To investigate how sucrose-free sunflower oil-based (S-HFD) and fish oil-based (F-HFD) high-fat diets influence gut microbiota composition, metabolic health, and liver inflammation in mice. C57BL/6 mice were fed either S-HFD or F-HFD for 24 weeks. Body weight, insulin sensitivity, liver inflammation, and gene expression were assessed. Gut microbiota composition was analyzed using 16S rRNA sequencing, followed by diversity analysis and taxonomic profiling with Microbiome Analyst and MIAOME tools. Despite similar body weights between groups, the gut microbiota composition differed significantly. The S-HFD group showed a higher abundance of Firmicutes (40%) compared to the F-HFD group (3%), while Verrucomicrobia were dominant in F-HFD (26%) and nearly absent in S-HFD. Taxa such as RF39, Christensenellaceae, Mogibacteriaceae, and Yaniella were enriched in S-HFD mice and associated with metabolic and immune dysregulation. S-HFD mice also had elevated fasting glucose, increased hepatic monocyte/macrophage (F4/80+) infiltration, macrovesicular steatosis, lobular inflammation, and upregulation of genes related to fatty acid oxidation (Cpt1a), monocyte chemotaxis (Ccl2), lipogenesis (Scd1, Fasn, Acaca), and glycolysis (Pklr). Conversely, F-HFD mice showed increased expression of the insulin-sensitive gene FATP1. Sucrose-free sunflower oil- and fish oil-based high-fat diets induce distinct gut microbiota changes and metabolic responses. S-HFD is associated with gut dysbiosis and steatohepatitis-like features, highlighting the importance of fat sources in shaping microbiome-host interactions in metabolic disease.},
}
RevDate: 2026-09-26
Reframing the Gut-Brain Axis: The Gut Wall as a Neural Immune Interface in Multiple Sclerosis and Autoimmune Neurological Diseases.
Annals of neurology [Epub ahead of print].
Gut wall physiology in multiple sclerosis (MS) and autoimmune neurologic diseases remains underexplored. This review examines gut wall dysfunctions' contribution to MS and autoimmune neurological disorder pathogenesis and progression. We discuss 3 inter-related aspects of gut physiology: intestinal barrier, enteric nervous system (ENS), and mucosal immunity. We highlight the ENS as a putative target of immune injury in selected antibody-mediated and T cell-associated neurologic diseases. Finally, we propose a unifying framework in which the gut functions as a site of immune priming and target of autoimmune injury, bridging microbiome-driven mechanisms in MS with ENS-directed autoimmunity across neurologic diseases. ANN NEUROL 2026.
Additional Links: PMID-42799661
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@article {pmid42799661,
year = {2026},
author = {Montini, F and Pittock, SJ and Cacciaguerra, L and Weiner, HL and Schwerdtfeger, LA},
title = {Reframing the Gut-Brain Axis: The Gut Wall as a Neural Immune Interface in Multiple Sclerosis and Autoimmune Neurological Diseases.},
journal = {Annals of neurology},
volume = {},
number = {},
pages = {},
doi = {10.1002/ana.78380},
pmid = {42799661},
issn = {1531-8249},
abstract = {Gut wall physiology in multiple sclerosis (MS) and autoimmune neurologic diseases remains underexplored. This review examines gut wall dysfunctions' contribution to MS and autoimmune neurological disorder pathogenesis and progression. We discuss 3 inter-related aspects of gut physiology: intestinal barrier, enteric nervous system (ENS), and mucosal immunity. We highlight the ENS as a putative target of immune injury in selected antibody-mediated and T cell-associated neurologic diseases. Finally, we propose a unifying framework in which the gut functions as a site of immune priming and target of autoimmune injury, bridging microbiome-driven mechanisms in MS with ENS-directed autoimmunity across neurologic diseases. ANN NEUROL 2026.},
}
RevDate: 2026-09-26
Effects of a Mushroom-Based β-Glucan and Bovine Colostrum Blend on the Gastrointestinal Health and Immune Function of Healthy Adult Dogs.
Journal of animal science pii:8836608 [Epub ahead of print].
Mushroom-derived β-glucans and bovine colostrum have potential roles in modulating gut health and immune function, but limited data are available regarding their effects on the gut microbiome, microbial metabolites, and immune responsiveness in adult dogs. Twenty healthy adult beagle dogs (8 females, 12 males; age: 5.6±2.5 yr old; body weight: 9.55±0.92 kg; body condition score: 5.7±0.5) were used in a randomized, blinded, placebo-controlled study using a completely randomized design. After a 3-wk wash-in phase, dogs were assigned to one of two treatment groups (n = 10/group) and fed for 12 wk: placebo consisting of cellulose, rice bran, liver, and natural food coloring or a mushroom complex consisting of mushroom complex consisting of mushroom (turkey tail mushroom, red reishi, and lion's mane) water extracts and bovine colostrum (MC). Each treatment (1.8 g/d) was top dressed on the diet. Fecal samples (characteristics, microbial fermentation metabolites, immunoglobulin A, microbiota) and blood samples (serum chemistry, hematology, immunoglobulins, oxidative stress markers) were collected after the wash-in phase (wk 0) and after 6 and 12 wk. Immune function was evaluated ex vivo by stimulating whole blood cells with toll-like receptor agonists and measuring tumor necrosis factor-alpha production. Data were analyzed using Mixed Models, using baseline data used as a covariate. Statistical significance was set at P < 0.05 and trends were considered at P < 0.10. All dogs remained healthy throughout the study, with fecal characteristics, serum chemistry, hematology, and serum immunoglobulins and oxidative stress markers being unchanged. Dogs fed MC had greater fecal acetate, propionate, and total short-chain fatty acid concentrations than controls. Fecal bacterial alpha and beta diversity metrics remained stable over time. Significant treatment*time interactions were observed for 5 fecal bacterial genera (Atopobiaceae unclassified, Prevotella_9, Lactobacillus, Megamonas, Phascolarctobacterium). Relative abundances of fecal Candidatus_Stoquefichus, Epulopiscium, and Negativibacillus tended to be increased by MC (P < 0.10). The relative abundances of several genera were affected by time. In summary, the mushroom complex was well tolerated and did not adversely affect gut health, immune status, or microbial diversity in healthy dogs. Our results suggest that it may slightly alter gut microbiota populations and microbial fermentation metabolites.
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@article {pmid42799681,
year = {2026},
author = {Wang, TL and Oba, PM and Mioto, JC and Bauer, LL and Koziol, SA and Panda, C and Pourafshar, S and Dilger, RN and Loman, BR and Swanson, KS},
title = {Effects of a Mushroom-Based β-Glucan and Bovine Colostrum Blend on the Gastrointestinal Health and Immune Function of Healthy Adult Dogs.},
journal = {Journal of animal science},
volume = {},
number = {},
pages = {},
doi = {10.1093/jas/skag312},
pmid = {42799681},
issn = {1525-3163},
abstract = {Mushroom-derived β-glucans and bovine colostrum have potential roles in modulating gut health and immune function, but limited data are available regarding their effects on the gut microbiome, microbial metabolites, and immune responsiveness in adult dogs. Twenty healthy adult beagle dogs (8 females, 12 males; age: 5.6±2.5 yr old; body weight: 9.55±0.92 kg; body condition score: 5.7±0.5) were used in a randomized, blinded, placebo-controlled study using a completely randomized design. After a 3-wk wash-in phase, dogs were assigned to one of two treatment groups (n = 10/group) and fed for 12 wk: placebo consisting of cellulose, rice bran, liver, and natural food coloring or a mushroom complex consisting of mushroom complex consisting of mushroom (turkey tail mushroom, red reishi, and lion's mane) water extracts and bovine colostrum (MC). Each treatment (1.8 g/d) was top dressed on the diet. Fecal samples (characteristics, microbial fermentation metabolites, immunoglobulin A, microbiota) and blood samples (serum chemistry, hematology, immunoglobulins, oxidative stress markers) were collected after the wash-in phase (wk 0) and after 6 and 12 wk. Immune function was evaluated ex vivo by stimulating whole blood cells with toll-like receptor agonists and measuring tumor necrosis factor-alpha production. Data were analyzed using Mixed Models, using baseline data used as a covariate. Statistical significance was set at P < 0.05 and trends were considered at P < 0.10. All dogs remained healthy throughout the study, with fecal characteristics, serum chemistry, hematology, and serum immunoglobulins and oxidative stress markers being unchanged. Dogs fed MC had greater fecal acetate, propionate, and total short-chain fatty acid concentrations than controls. Fecal bacterial alpha and beta diversity metrics remained stable over time. Significant treatment*time interactions were observed for 5 fecal bacterial genera (Atopobiaceae unclassified, Prevotella_9, Lactobacillus, Megamonas, Phascolarctobacterium). Relative abundances of fecal Candidatus_Stoquefichus, Epulopiscium, and Negativibacillus tended to be increased by MC (P < 0.10). The relative abundances of several genera were affected by time. In summary, the mushroom complex was well tolerated and did not adversely affect gut health, immune status, or microbial diversity in healthy dogs. Our results suggest that it may slightly alter gut microbiota populations and microbial fermentation metabolites.},
}
RevDate: 2026-09-26
Supplementation of a Bacillus-based DFM mixture on growth performance, methane emissions, microbiome, and metabolome in backgrounding beef heifers.
Journal of animal science pii:8836610 [Epub ahead of print].
Direct-fed microbials (DFM) have been used to improve livestock production efficiency and reduce environmental impact. Spore-forming bacteria such as Bacillus spp. present handling and processing advantages for use as a DFM; however, more information is needed about their effects in beef cattle. The objective of this study was to evaluate the effect of a DFM composed of a mixture of B. subtilis and B. licheniformis on growth performance, nutrient utilization, enteric methane (CH4) emissions, microbiome of ruminal fluid and feces, and metabolome of plasma and ruminal fluid. Angus crossbred heifers (n = 108; 318 ± 40 kg of body weight) were used in a generalized randomized block design. Heifers were fed a sorghum silage-based diet containing the following treatments: 1) control (CTL, no additive), or 2) Bacillus-based DFM [BOV, 310 mg/kg of diet dry matter (DM)], to provide an average of 3 g/animal/d. No effect of treatment (P > 0.05) was observed for DM intake, average daily gain, or gain-to-feed ratio. The DFM inclusion did not affect (P > 0.05) apparent total tract digestibility of nutrients or CH4 emissions. Alpha and beta diversity of fecal and ruminal microbiome did not differ with supplementation (P > 0.05). Multivariate analysis indicated minimal impact of the DFM on ruminal and plasma metabolomes. In ruminal fluid, supplementation with the DFM reduced the abundance of three metabolites after false discovery rate (FDR) correction (FDR < 0.05), and pathway analysis indicated that the ubiquinone biosynthesis pathway was enriched by DFM supplementation (P ≤ 0.05). In plasma, two metabolites were differentially abundant between treatments, with proline being more abundant and serine less abundant in heifers supplemented with the DFM than in control heifers (P ≤ 0.05). In summary, supplementation with a Bacillus-based DFM did not affect growth performance, efficiency of feed utilization, nutrient digestibility, or CH4 emissions in beef heifers under the experimental conditions of this trial. Minimal changes were observed in the ruminal and fecal microbiomes and the ruminal and plasma metabolomes, suggesting a limited microbial or systemic impact. Further research is needed to clarify the conditions and mechanisms by which Bacillus-based DFM may exert beneficial effects in beef cattle.
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@article {pmid42799682,
year = {2026},
author = {Maderal, A and Fernandez-Marenchino, I and Tarnonsky, F and Vargas, J and Podversich, F and Cuervo, W and Ramirez-Sepulveda, V and Blanchard, H and Gomez-Lopez, C and Gomez-Salmoral, M and Schulmeister, TM and Queiroz, OCM and Cappellozza, BI and Ogunade, I and DiLorenzo, N},
title = {Supplementation of a Bacillus-based DFM mixture on growth performance, methane emissions, microbiome, and metabolome in backgrounding beef heifers.},
journal = {Journal of animal science},
volume = {},
number = {},
pages = {},
doi = {10.1093/jas/skag304},
pmid = {42799682},
issn = {1525-3163},
abstract = {Direct-fed microbials (DFM) have been used to improve livestock production efficiency and reduce environmental impact. Spore-forming bacteria such as Bacillus spp. present handling and processing advantages for use as a DFM; however, more information is needed about their effects in beef cattle. The objective of this study was to evaluate the effect of a DFM composed of a mixture of B. subtilis and B. licheniformis on growth performance, nutrient utilization, enteric methane (CH4) emissions, microbiome of ruminal fluid and feces, and metabolome of plasma and ruminal fluid. Angus crossbred heifers (n = 108; 318 ± 40 kg of body weight) were used in a generalized randomized block design. Heifers were fed a sorghum silage-based diet containing the following treatments: 1) control (CTL, no additive), or 2) Bacillus-based DFM [BOV, 310 mg/kg of diet dry matter (DM)], to provide an average of 3 g/animal/d. No effect of treatment (P > 0.05) was observed for DM intake, average daily gain, or gain-to-feed ratio. The DFM inclusion did not affect (P > 0.05) apparent total tract digestibility of nutrients or CH4 emissions. Alpha and beta diversity of fecal and ruminal microbiome did not differ with supplementation (P > 0.05). Multivariate analysis indicated minimal impact of the DFM on ruminal and plasma metabolomes. In ruminal fluid, supplementation with the DFM reduced the abundance of three metabolites after false discovery rate (FDR) correction (FDR < 0.05), and pathway analysis indicated that the ubiquinone biosynthesis pathway was enriched by DFM supplementation (P ≤ 0.05). In plasma, two metabolites were differentially abundant between treatments, with proline being more abundant and serine less abundant in heifers supplemented with the DFM than in control heifers (P ≤ 0.05). In summary, supplementation with a Bacillus-based DFM did not affect growth performance, efficiency of feed utilization, nutrient digestibility, or CH4 emissions in beef heifers under the experimental conditions of this trial. Minimal changes were observed in the ruminal and fecal microbiomes and the ruminal and plasma metabolomes, suggesting a limited microbial or systemic impact. Further research is needed to clarify the conditions and mechanisms by which Bacillus-based DFM may exert beneficial effects in beef cattle.},
}
RevDate: 2026-09-26
Supplementation with Bacillus-based direct-fed microbials for developing beef heifers: impacts on fecal and vaginal microbiome, growth, and reproductive performance.
Journal of animal science pii:8836607 [Epub ahead of print].
This 2-year study evaluated the effects of Bacillus-based direct-fed microbial (DFM) supplementation on fecal and vaginal microbiomes, growth, and reproduction of beef heifers. On day 0 (30 days after weaning), Brangus crossbred beef heifers (n = 64 per year) were stratified by body weight (BW; 261 ± 29 kg) and age (286 ± 11 days) and randomly allocated into 1 of 16 bahiagrass pastures (1 ha and 4 heifers per pasture). Treatments (8 pastures per treatment) consisted of daily concentrate supplementation at 1.50% of BW (dry matter basis), with (BAC) or without (CON) a DFM supplement containing Bacillus subtilis 810 and B. licheniformis 809 (3 g per heifer; 6.6 × 109 CFU per day) from day 0 to 244. Heifers were estrus-synchronized from day 98 to 112, artificially inseminated (AI) on days 109 to 112, and exposed to Angus bulls from day 120 to 210 (1 bull per pasture). Fecal and vaginal swab samples were collected on days 0, 112 (timed-AI), and 210 (end of the breeding season). Effects of treatment × year were not detected (P ≥ 0.18) for any variable. Treatments did not affect herbage utilization, heifer BW, or plasma concentrations of glucose and insulin-like growth factor 1 (IGF-1). Percentage of pubertal heifers and reproductive tract scores were greater on day 60 (P = 0.05), but not on day 90 (P ≥ 0.22), for BAC vs. CON heifers. Pregnancy per AI tended (P = 0.10) to be greater for BAC vs. CON heifers. Final pregnancy percentage did not differ (P = 0.65) between treatments, whereas a greater (P ≤ 0.05) proportion of BAC heifers calved within the first 28 days of the calving season. Effects of treatment × day were detected for fecal Firmicutes, Bacteroidetes, and Clostridium, Butyrivibrio, and Blautia, which were greater in BAC vs. CON heifers on day 112 (P ≤ 0.02). Fecal Shannon and Simpson diversity indexes on day 112 were lower (P < 0.01) for BAC vs. CON heifers. Effects of treatment were detected (P ≤ 0.04) for vaginal Methanobrevibacter and Euryarchaeota, both of which were lower overall in BAC vs. CON heifers. These findings indicate that Bacillus-based DFM supplementation modulated fecal and vaginal microbial communities and improved reproductive outcomes in developing beef heifers, suggesting that reproductive benefits may be partly mediated through microbiome-host interactions.
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@article {pmid42799686,
year = {2026},
author = {Sousa, LM and Moriel, P and Izquierdo, VS and Crawford, CA and Brauner, CC and Bittar, JHJ and Monteiro, P and Binelli, M and Lazarin, JV and Vendramini, JMB and Cappellozza, BI},
title = {Supplementation with Bacillus-based direct-fed microbials for developing beef heifers: impacts on fecal and vaginal microbiome, growth, and reproductive performance.},
journal = {Journal of animal science},
volume = {},
number = {},
pages = {},
doi = {10.1093/jas/skag313},
pmid = {42799686},
issn = {1525-3163},
abstract = {This 2-year study evaluated the effects of Bacillus-based direct-fed microbial (DFM) supplementation on fecal and vaginal microbiomes, growth, and reproduction of beef heifers. On day 0 (30 days after weaning), Brangus crossbred beef heifers (n = 64 per year) were stratified by body weight (BW; 261 ± 29 kg) and age (286 ± 11 days) and randomly allocated into 1 of 16 bahiagrass pastures (1 ha and 4 heifers per pasture). Treatments (8 pastures per treatment) consisted of daily concentrate supplementation at 1.50% of BW (dry matter basis), with (BAC) or without (CON) a DFM supplement containing Bacillus subtilis 810 and B. licheniformis 809 (3 g per heifer; 6.6 × 109 CFU per day) from day 0 to 244. Heifers were estrus-synchronized from day 98 to 112, artificially inseminated (AI) on days 109 to 112, and exposed to Angus bulls from day 120 to 210 (1 bull per pasture). Fecal and vaginal swab samples were collected on days 0, 112 (timed-AI), and 210 (end of the breeding season). Effects of treatment × year were not detected (P ≥ 0.18) for any variable. Treatments did not affect herbage utilization, heifer BW, or plasma concentrations of glucose and insulin-like growth factor 1 (IGF-1). Percentage of pubertal heifers and reproductive tract scores were greater on day 60 (P = 0.05), but not on day 90 (P ≥ 0.22), for BAC vs. CON heifers. Pregnancy per AI tended (P = 0.10) to be greater for BAC vs. CON heifers. Final pregnancy percentage did not differ (P = 0.65) between treatments, whereas a greater (P ≤ 0.05) proportion of BAC heifers calved within the first 28 days of the calving season. Effects of treatment × day were detected for fecal Firmicutes, Bacteroidetes, and Clostridium, Butyrivibrio, and Blautia, which were greater in BAC vs. CON heifers on day 112 (P ≤ 0.02). Fecal Shannon and Simpson diversity indexes on day 112 were lower (P < 0.01) for BAC vs. CON heifers. Effects of treatment were detected (P ≤ 0.04) for vaginal Methanobrevibacter and Euryarchaeota, both of which were lower overall in BAC vs. CON heifers. These findings indicate that Bacillus-based DFM supplementation modulated fecal and vaginal microbial communities and improved reproductive outcomes in developing beef heifers, suggesting that reproductive benefits may be partly mediated through microbiome-host interactions.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Exogenous regulators that alleviate waterlogging stress in plants: mechanisms, integration, and translational strategies.
Planta, 264(5):.
Exogenous regulators mitigate waterlogging stress via a three-tier framework; integrated strategies boost field waterlogging resilience effectively. Waterlogging, an increasingly critical constraint on crop productivity with climate change amplifying extreme precipitation, limits rhizospheric O2 diffusion to induce hypoxia. This rapidly impairs mitochondrial respiration, forces a shift to low-efficiency glycolysis and fermentation, and accumulates potentially toxic by-products. Upon postanoxic stress, plants face an oxidative burst that compromises membrane integrity, suppresses photosynthesis, and destabilizes yield. Despite inherent adaptive programs (e.g., aerenchyma formation, adventitious rooting), most crops remain vulnerable to prolonged/recurrent waterlogging, necessitating practical interventions complementing genetic improvement. Here, we synthesize evidence that exogenous inputs-including phytohormones, osmoprotectants, antioxidants, gaseous signaling molecules, mineral nutrients, and beneficial microorganisms-mitigate injury by coordinating early signaling, metabolic maintenance, and rhizosphere stabilization. We integrate these effects into a three-tier framework: (i) resetting hypoxia perception/response thresholds, (ii) sustaining energy/redox homeostasis via balanced mitochondrial function and fermentation, and (iii) converting short-term tolerance to sustained recovery through morphological remodeling and rhizosphere improvement. Finally, we outline a translational strategy coupling exogenous regulation with functional microbiomes, targeted genetic improvement, and agronomic management to enhance field robustness and reduce environment-driven "effect drift". Highlights Exogenous regulators improve plant-waterlogging tolerance via a three-layer regulatory framework. A combined application of exogenous substances, microbiome, genetics, and agronomy enhances field waterlogging resistance. Hypoxia response, energy metabolism, and ROS homeostasis are core regulatory targets for stress alleviation.
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@article {pmid42799908,
year = {2026},
author = {Sha, S and Zeng, C and Shang, X and Zou, B and Yang, Y},
title = {Exogenous regulators that alleviate waterlogging stress in plants: mechanisms, integration, and translational strategies.},
journal = {Planta},
volume = {264},
number = {5},
pages = {},
pmid = {42799908},
issn = {1432-2048},
support = {HUDF202503//Harbin University Young Doctoral Research Initiation Foundation/ ; LH2023C067//Natural Science Foundation of Heilongjiang Province/ ; GJD1526082//Heilongjiang Province Education Science Planning Project/ ; },
mesh = {*Stress, Physiological/drug effects ; *Plant Growth Regulators/pharmacology/metabolism ; *Crops, Agricultural/physiology ; Signal Transduction ; Rhizosphere ; },
abstract = {Exogenous regulators mitigate waterlogging stress via a three-tier framework; integrated strategies boost field waterlogging resilience effectively. Waterlogging, an increasingly critical constraint on crop productivity with climate change amplifying extreme precipitation, limits rhizospheric O2 diffusion to induce hypoxia. This rapidly impairs mitochondrial respiration, forces a shift to low-efficiency glycolysis and fermentation, and accumulates potentially toxic by-products. Upon postanoxic stress, plants face an oxidative burst that compromises membrane integrity, suppresses photosynthesis, and destabilizes yield. Despite inherent adaptive programs (e.g., aerenchyma formation, adventitious rooting), most crops remain vulnerable to prolonged/recurrent waterlogging, necessitating practical interventions complementing genetic improvement. Here, we synthesize evidence that exogenous inputs-including phytohormones, osmoprotectants, antioxidants, gaseous signaling molecules, mineral nutrients, and beneficial microorganisms-mitigate injury by coordinating early signaling, metabolic maintenance, and rhizosphere stabilization. We integrate these effects into a three-tier framework: (i) resetting hypoxia perception/response thresholds, (ii) sustaining energy/redox homeostasis via balanced mitochondrial function and fermentation, and (iii) converting short-term tolerance to sustained recovery through morphological remodeling and rhizosphere improvement. Finally, we outline a translational strategy coupling exogenous regulation with functional microbiomes, targeted genetic improvement, and agronomic management to enhance field robustness and reduce environment-driven "effect drift". Highlights Exogenous regulators improve plant-waterlogging tolerance via a three-layer regulatory framework. A combined application of exogenous substances, microbiome, genetics, and agronomy enhances field waterlogging resistance. Hypoxia response, energy metabolism, and ROS homeostasis are core regulatory targets for stress alleviation.},
}
MeSH Terms:
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*Stress, Physiological/drug effects
*Plant Growth Regulators/pharmacology/metabolism
*Crops, Agricultural/physiology
Signal Transduction
Rhizosphere
RevDate: 2026-09-25
Clinical severity score-guided metagenomic analysis identifying gut microbial taxonomic and functional markers for severe hepatitis E progression.
mSystems [Epub ahead of print].
Although gut microbiome alterations have been reported in hepatitis E (HE), the taxonomic and functional determinants of disease severity remain poorly defined. Here, we performed shotgun metagenomic sequencing of fecal samples from 125 individuals spanning acute non-icteric hepatitis (ANIH), acute icteric hepatitis (AIH), acute liver failure (ALF), and healthy controls. We constructed a surrogate clinical severity index from routine blood parameters and developed an integrative analytical framework that combined XGBoost-based taxonomic modeling with LASSO-driven functional feature selection to explore microbiome-severity associations. The taxonomic model discriminated patients from controls (area under the curve [AUC] = 0.944) and identified nine bacterial species significantly associated with severity, independent of age, sex, and body mass index (BMI) (permutation test, P < 0.05), with Veillonella atypica emerging as the most robust candidate biomarker. The signature featured enrichment of lactate-utilizing Veillonella spp. and Ligilactobacillus salivarius, alongside depletion of beneficial commensals (Dorea longicatena, Ruminococcus timonensis, Eubacterium ramulus), collectively suggesting a pathogenic "lactate axis." The HE-enriched lactate utilizers were positively associated with 13 core severity-increasing KOs involved in oxidative stress adaptation (npr, hemQ, NUDT1, nfr1) and secretion/biofilm formation (gspD, fhaC, vpr, sinR) and negatively with three severity-decreasing KOs, including the butyrate fermentation gene (K14534). Strikingly, the stringent 16-KO core (intersection of four methods) explained more variance in disease severity than the broader set identified by at least three methods (R[2] = 0.61 vs. 0.47). Collectively, these findings reveal a strong link between microbiome-derived lactate metabolism and HE severity, highlighting its potential as a basis for microbiome-based severity stratification and motivating further mechanistic exploration.IMPORTANCEHepatitis E virus (HEV) infection ranges from ANIH to ALF, yet the role of the gut microbiome remains poorly understood across the severity spectrum. By performing shotgun metagenomic sequencing on fecal samples from 125 individuals and applying an integrative framework combining XGBoost-based taxonomic modeling with LASSO-driven functional selection, we identified robust microbiome-severity associations as quantified by a surrogate clinical severity index derived from routine blood parameters. These associations were characterized by enrichment of lactate-utilizing Veillonella species (notably Veillonella atypica), depletion of beneficial butyrate-producing commensals, and severity-linked shifts in microbial functional gene profiles. Such patterns are consistent with a perturbed microbial "lactate axis" in gut-liver crosstalk, although all associations remain correlational. Our findings nominate candidate microbial markers for severity stratification in hepatitis E and provide a hypothesis-generating framework to guide future mechanistic studies and microbiome-based therapeutic strategies.
Additional Links: PMID-42788735
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PubMed:
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@article {pmid42788735,
year = {2026},
author = {Shi, H and Chen, Y and Liu, X and Yang, J and Yan, D and Zhang, H and Chen, J and Wu, Z and Yuan, D and Lu, H and Li, L},
title = {Clinical severity score-guided metagenomic analysis identifying gut microbial taxonomic and functional markers for severe hepatitis E progression.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0095626},
doi = {10.1128/msystems.00956-26},
pmid = {42788735},
issn = {2379-5077},
abstract = {Although gut microbiome alterations have been reported in hepatitis E (HE), the taxonomic and functional determinants of disease severity remain poorly defined. Here, we performed shotgun metagenomic sequencing of fecal samples from 125 individuals spanning acute non-icteric hepatitis (ANIH), acute icteric hepatitis (AIH), acute liver failure (ALF), and healthy controls. We constructed a surrogate clinical severity index from routine blood parameters and developed an integrative analytical framework that combined XGBoost-based taxonomic modeling with LASSO-driven functional feature selection to explore microbiome-severity associations. The taxonomic model discriminated patients from controls (area under the curve [AUC] = 0.944) and identified nine bacterial species significantly associated with severity, independent of age, sex, and body mass index (BMI) (permutation test, P < 0.05), with Veillonella atypica emerging as the most robust candidate biomarker. The signature featured enrichment of lactate-utilizing Veillonella spp. and Ligilactobacillus salivarius, alongside depletion of beneficial commensals (Dorea longicatena, Ruminococcus timonensis, Eubacterium ramulus), collectively suggesting a pathogenic "lactate axis." The HE-enriched lactate utilizers were positively associated with 13 core severity-increasing KOs involved in oxidative stress adaptation (npr, hemQ, NUDT1, nfr1) and secretion/biofilm formation (gspD, fhaC, vpr, sinR) and negatively with three severity-decreasing KOs, including the butyrate fermentation gene (K14534). Strikingly, the stringent 16-KO core (intersection of four methods) explained more variance in disease severity than the broader set identified by at least three methods (R[2] = 0.61 vs. 0.47). Collectively, these findings reveal a strong link between microbiome-derived lactate metabolism and HE severity, highlighting its potential as a basis for microbiome-based severity stratification and motivating further mechanistic exploration.IMPORTANCEHepatitis E virus (HEV) infection ranges from ANIH to ALF, yet the role of the gut microbiome remains poorly understood across the severity spectrum. By performing shotgun metagenomic sequencing on fecal samples from 125 individuals and applying an integrative framework combining XGBoost-based taxonomic modeling with LASSO-driven functional selection, we identified robust microbiome-severity associations as quantified by a surrogate clinical severity index derived from routine blood parameters. These associations were characterized by enrichment of lactate-utilizing Veillonella species (notably Veillonella atypica), depletion of beneficial butyrate-producing commensals, and severity-linked shifts in microbial functional gene profiles. Such patterns are consistent with a perturbed microbial "lactate axis" in gut-liver crosstalk, although all associations remain correlational. Our findings nominate candidate microbial markers for severity stratification in hepatitis E and provide a hypothesis-generating framework to guide future mechanistic studies and microbiome-based therapeutic strategies.},
}
RevDate: 2026-09-25
Non-antibiotic therapeutic approaches for antimicrobial resistance: current evidence and future directions.
Expert review of clinical pharmacology [Epub ahead of print].
INTRODUCTION: Antimicrobial resistance (AMR) is a global health challenge that reduces the effectiveness of existing antibiotics, leading to increased morbidity, mortality and healthcare costs worldwide. The lack of the development of novel classes of antibiotics has led to an increased interest in non-antibiotic therapeutic approaches that focus on bacterial virulence, host-pathogen interactions, microbial ecology, and resistance mechanisms.
AREAS COVERED: This review summarizes the current evidence on non-antibiotic therapeutics including bacteriophages, antimicrobial peptides, anti-virulence agents, monoclonal antibodies, microbiome-based therapies, CRISPR-Cas systems, nanoparticles, photodynamic therapy, repurposed non-antibiotic drugs and combination strategies. We performed a literature search on PubMed, Embase, Scopus, Web of Science, and Google Scholar until May 2026. Though several approaches have demonstrated promising biological activity and favorable safety profiles, clinical evidence remains limited and heterogeneous.
EXPERT OPINION: Non-antibiotic therapeutics are vital adjunctive, salvage and precision approaches to the challenge of AMR. However, most strategies are still at an early translational stage with a paucity of high-quality randomized clinical evidence. Barriers include delivery, manufacturing complexity, regulatory uncertainty, cost, and lack of long-term safety data. Further progress will depend on standardization of production, better delivery platforms, well-designed multicentric clinical trials, and incorporation into antimicrobial stewardship and precision medicine frameworks.
Additional Links: PMID-42788817
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@article {pmid42788817,
year = {2026},
author = {Ganesan, BK and Mishra, A and Hota, D and Maiti, R},
title = {Non-antibiotic therapeutic approaches for antimicrobial resistance: current evidence and future directions.},
journal = {Expert review of clinical pharmacology},
volume = {},
number = {},
pages = {},
doi = {10.1080/17512433.2026.2739560},
pmid = {42788817},
issn = {1751-2441},
abstract = {INTRODUCTION: Antimicrobial resistance (AMR) is a global health challenge that reduces the effectiveness of existing antibiotics, leading to increased morbidity, mortality and healthcare costs worldwide. The lack of the development of novel classes of antibiotics has led to an increased interest in non-antibiotic therapeutic approaches that focus on bacterial virulence, host-pathogen interactions, microbial ecology, and resistance mechanisms.
AREAS COVERED: This review summarizes the current evidence on non-antibiotic therapeutics including bacteriophages, antimicrobial peptides, anti-virulence agents, monoclonal antibodies, microbiome-based therapies, CRISPR-Cas systems, nanoparticles, photodynamic therapy, repurposed non-antibiotic drugs and combination strategies. We performed a literature search on PubMed, Embase, Scopus, Web of Science, and Google Scholar until May 2026. Though several approaches have demonstrated promising biological activity and favorable safety profiles, clinical evidence remains limited and heterogeneous.
EXPERT OPINION: Non-antibiotic therapeutics are vital adjunctive, salvage and precision approaches to the challenge of AMR. However, most strategies are still at an early translational stage with a paucity of high-quality randomized clinical evidence. Barriers include delivery, manufacturing complexity, regulatory uncertainty, cost, and lack of long-term safety data. Further progress will depend on standardization of production, better delivery platforms, well-designed multicentric clinical trials, and incorporation into antimicrobial stewardship and precision medicine frameworks.},
}
RevDate: 2026-09-25
CmpDate: 2026-09-25
Ketogenic diet as a systems-level immunometabolic sensitization strategy in cancer therapy: integrating metabolism, immune reprogramming, microbiome dynamics, and epigenetic regulation.
Medical oncology (Northwood, London, England), 43(11):.
The ketogenic diet (KD) is increasingly being recognized as more than a simple metabolic intervention in cancer therapy. Emerging evidence suggests that KD may function as a systems-level immunometabolic sensitization strategy capable of enhancing therapeutic responsiveness through interconnected biologic mechanisms. Modern cancer therapies, including chemotherapy, targeted therapy, radiotherapy, and immunotherapy, are often limited by tumor adaptability and immune suppression. Tumors shift metabolism via the Warburg effect and fuel switching, promoting resistance under hypoxic and nutrient stress. KD is a high-fat and low-carb eating plan that increases ketone bodies such as β-hydroxybutyrate while lowering glucose availability. Under ketogenic conditions, cancer cells reduce glycolytic flux, while immune cells can oxidise ketones to sustain mitochondrial function and effector activity. KD also remodels the gut microbiome and induces epigenetic regulation through histone deacetylase inhibition. These combined effects may enhance chemotherapy, radiotherapy, targeted therapy, and immunotherapy by inducing metabolic stress, improving immune cell fitness, and altering tumour microenvironment signaling. Importantly, KD may function not as a standalone treatment but as a therapy-sensitization platform. However, current evidence remains preliminary and heterogeneous, and further mechanistic investigations and well-designed prospective clinical trials are necessary to determine optimal patient selection and long-term safety.
Additional Links: PMID-42789141
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@article {pmid42789141,
year = {2026},
author = {Mannan, MS and Khan, MW and Haseeb Khan, MA and Javed, A and Hussain, SM and Adil, H},
title = {Ketogenic diet as a systems-level immunometabolic sensitization strategy in cancer therapy: integrating metabolism, immune reprogramming, microbiome dynamics, and epigenetic regulation.},
journal = {Medical oncology (Northwood, London, England)},
volume = {43},
number = {11},
pages = {},
pmid = {42789141},
issn = {1559-131X},
mesh = {Humans ; *Diet, Ketogenic/methods ; *Neoplasms/immunology/diet therapy/metabolism/therapy/genetics ; *Epigenesis, Genetic ; Metabolic Reprogramming ; Animals ; Tumor Microenvironment/immunology ; *Gastrointestinal Microbiome ; Immunotherapy/methods ; },
abstract = {The ketogenic diet (KD) is increasingly being recognized as more than a simple metabolic intervention in cancer therapy. Emerging evidence suggests that KD may function as a systems-level immunometabolic sensitization strategy capable of enhancing therapeutic responsiveness through interconnected biologic mechanisms. Modern cancer therapies, including chemotherapy, targeted therapy, radiotherapy, and immunotherapy, are often limited by tumor adaptability and immune suppression. Tumors shift metabolism via the Warburg effect and fuel switching, promoting resistance under hypoxic and nutrient stress. KD is a high-fat and low-carb eating plan that increases ketone bodies such as β-hydroxybutyrate while lowering glucose availability. Under ketogenic conditions, cancer cells reduce glycolytic flux, while immune cells can oxidise ketones to sustain mitochondrial function and effector activity. KD also remodels the gut microbiome and induces epigenetic regulation through histone deacetylase inhibition. These combined effects may enhance chemotherapy, radiotherapy, targeted therapy, and immunotherapy by inducing metabolic stress, improving immune cell fitness, and altering tumour microenvironment signaling. Importantly, KD may function not as a standalone treatment but as a therapy-sensitization platform. However, current evidence remains preliminary and heterogeneous, and further mechanistic investigations and well-designed prospective clinical trials are necessary to determine optimal patient selection and long-term safety.},
}
MeSH Terms:
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Humans
*Diet, Ketogenic/methods
*Neoplasms/immunology/diet therapy/metabolism/therapy/genetics
*Epigenesis, Genetic
Metabolic Reprogramming
Animals
Tumor Microenvironment/immunology
*Gastrointestinal Microbiome
Immunotherapy/methods
RevDate: 2026-09-25
CmpDate: 2026-09-25
Tumor microbial biodiversity and microsatellite instability in colorectal cancer.
PloS one, 21(9):e0359555 pii:PONE-D-26-16915.
BACKGROUND: Growing evidence links the gut microbiome to colorectal cancer (CRC) progression, with certain bacterial species enriched in specific molecular tumor subtypes. DNA mismatch repair deficiency in CRC, evidenced by the presence of microsatellite instability (MSI), has been consistently associated with a favorable prognosis, and may be related to certain aspects of the microbiome. Here, we examined the relationship between tumor microbial biodiversity and MSI status.
METHODS: Diagnostic tumor tissue samples were obtained from the Seattle site of the Colon Cancer Family Registry (SCCFR) and a companion study; both recruited patients diagnosed with incident CRC from 1998 to 2007. MSI status assessment and prokaryotic 16S rRNA gene sequencing was performed on the tumor tissue samples. We used an adaptive test of alpha-diversity (aMiAD) to estimate the association between microbial biodiversity and MSI status. We performed differential abundance analysis with ANCOM-BC to identify enriched genera in tumor tissue, based on dichotomized MSI status. Analyses were adjusted for age, sex, smoking history, and tumor location (N = 632).
RESULTS: The adaptive aMiAD effect estimate was -1.08 (p = 0.29), suggesting that MSI-high tumors had lower estimated alpha-diversity, though this difference was not statistically significant. We identified 20 differentially abundant genera in CRC tumors according to MSI status, with 8 enriched genera and 12 depleted genera in MSI-high tumors. The most strongly enriched genera in MSI-high tumors were Gemella and Lawsonella, while Sporolactobacillaceae and Cloacibacterium were the most strongly depleted. Fusobacterium was enriched in MSI-high tumors only after subsetting the genus to Fusobacterium nucleatum specific sequences.
CONCLUSIONS: We did not detect a statistically significant association between the adaptive alpha-diversity measure and MSI status, though individual measures concordantly estimated a depletion of alpha-diversity in the MSI-high tumors. We found evidence of differential abundance of certain genera dependent on MSI status, including several novel associations.
Additional Links: PMID-42789554
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PubMed:
Citation:
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@article {pmid42789554,
year = {2026},
author = {Mendall, C and Hullar, MAJ and Curtis, KR and Hill, CM and Thomas, CE and Ma, N and Randolph, TW and Malen, RC and Reedy, AM and LaBrie, S and Potter, JD and Ogino, S and Newcomb, PA and Phipps, AI},
title = {Tumor microbial biodiversity and microsatellite instability in colorectal cancer.},
journal = {PloS one},
volume = {21},
number = {9},
pages = {e0359555},
doi = {10.1371/journal.pone.0359555},
pmid = {42789554},
issn = {1932-6203},
mesh = {*Microsatellite Instability ; *Colorectal Neoplasms/microbiology/genetics/pathology ; Humans ; *Biodiversity ; RNA, Ribosomal, 16S/genetics ; Female ; Male ; Aged ; Middle Aged ; },
abstract = {BACKGROUND: Growing evidence links the gut microbiome to colorectal cancer (CRC) progression, with certain bacterial species enriched in specific molecular tumor subtypes. DNA mismatch repair deficiency in CRC, evidenced by the presence of microsatellite instability (MSI), has been consistently associated with a favorable prognosis, and may be related to certain aspects of the microbiome. Here, we examined the relationship between tumor microbial biodiversity and MSI status.
METHODS: Diagnostic tumor tissue samples were obtained from the Seattle site of the Colon Cancer Family Registry (SCCFR) and a companion study; both recruited patients diagnosed with incident CRC from 1998 to 2007. MSI status assessment and prokaryotic 16S rRNA gene sequencing was performed on the tumor tissue samples. We used an adaptive test of alpha-diversity (aMiAD) to estimate the association between microbial biodiversity and MSI status. We performed differential abundance analysis with ANCOM-BC to identify enriched genera in tumor tissue, based on dichotomized MSI status. Analyses were adjusted for age, sex, smoking history, and tumor location (N = 632).
RESULTS: The adaptive aMiAD effect estimate was -1.08 (p = 0.29), suggesting that MSI-high tumors had lower estimated alpha-diversity, though this difference was not statistically significant. We identified 20 differentially abundant genera in CRC tumors according to MSI status, with 8 enriched genera and 12 depleted genera in MSI-high tumors. The most strongly enriched genera in MSI-high tumors were Gemella and Lawsonella, while Sporolactobacillaceae and Cloacibacterium were the most strongly depleted. Fusobacterium was enriched in MSI-high tumors only after subsetting the genus to Fusobacterium nucleatum specific sequences.
CONCLUSIONS: We did not detect a statistically significant association between the adaptive alpha-diversity measure and MSI status, though individual measures concordantly estimated a depletion of alpha-diversity in the MSI-high tumors. We found evidence of differential abundance of certain genera dependent on MSI status, including several novel associations.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Microsatellite Instability
*Colorectal Neoplasms/microbiology/genetics/pathology
Humans
*Biodiversity
RNA, Ribosomal, 16S/genetics
Female
Male
Aged
Middle Aged
RevDate: 2026-09-25
Stage-specific remodeling of the pulmonary microenvironment during Paragonimus proliferus infection in a rat model.
PLoS neglected tropical diseases, 20(9):e0014760 pii:PNTD-D-26-00661 [Epub ahead of print].
Paragonimiasis, a food-borne zoonosis caused by Paragonimus spp., can cause severe pulmonary inflammation and fibrosis. However, relationships among the host, parasite and lung microbiome at defined infection stages remain poorly understood. We compared independent groups of rats sampled at 14, 28 and 42 days post-infection (dpi), together with a separate group sampled after triclabendazole (TCBZ) treatment. Histopathological and molecular analyses were combined with multi-region (5R) 16S rRNA gene sequencing and fluorescence in situ hybridization (FISH). Groups sampled at later post-infection time points showed greater pulmonary inflammation and collagen deposition, with the highest values in Pp-42d; both outcomes were lower in Pp-TCBZ than in Pp-42d. Th1-, eosinophil-, Th2- and Treg- associated markers differed among experimental groups. TLR4/NF-κB -related protein expression and pulmonary microbial profiles also differed among groups including enrichment of taxa such as Lactobacillus in infected animals. FISH detected bacterial signals within inflammatory lesions and Lactobacillus-associated signals spatially associated with parasite eggs. These repeated cross-sectional findings identify stage-associated differences in pulmonary pathology, immune markers and microbiota during P. proliferus infection, together with lower pathological measures in the Pp-TCBZ group than in the untreated Pp-42d group. The egg-associated bacterial signals warrant further investigation but do not establish a functional host-parasite-microbiome mechanism.
Additional Links: PMID-42789671
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PubMed:
Citation:
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@article {pmid42789671,
year = {2026},
author = {Cheng, D and Zhang, L and Sun, L and Yin, M and Wang, Y and Yang, S and Yan, X and Zhu, X and Li, C and Chunyu, W},
title = {Stage-specific remodeling of the pulmonary microenvironment during Paragonimus proliferus infection in a rat model.},
journal = {PLoS neglected tropical diseases},
volume = {20},
number = {9},
pages = {e0014760},
doi = {10.1371/journal.pntd.0014760},
pmid = {42789671},
issn = {1935-2735},
abstract = {Paragonimiasis, a food-borne zoonosis caused by Paragonimus spp., can cause severe pulmonary inflammation and fibrosis. However, relationships among the host, parasite and lung microbiome at defined infection stages remain poorly understood. We compared independent groups of rats sampled at 14, 28 and 42 days post-infection (dpi), together with a separate group sampled after triclabendazole (TCBZ) treatment. Histopathological and molecular analyses were combined with multi-region (5R) 16S rRNA gene sequencing and fluorescence in situ hybridization (FISH). Groups sampled at later post-infection time points showed greater pulmonary inflammation and collagen deposition, with the highest values in Pp-42d; both outcomes were lower in Pp-TCBZ than in Pp-42d. Th1-, eosinophil-, Th2- and Treg- associated markers differed among experimental groups. TLR4/NF-κB -related protein expression and pulmonary microbial profiles also differed among groups including enrichment of taxa such as Lactobacillus in infected animals. FISH detected bacterial signals within inflammatory lesions and Lactobacillus-associated signals spatially associated with parasite eggs. These repeated cross-sectional findings identify stage-associated differences in pulmonary pathology, immune markers and microbiota during P. proliferus infection, together with lower pathological measures in the Pp-TCBZ group than in the untreated Pp-42d group. The egg-associated bacterial signals warrant further investigation but do not establish a functional host-parasite-microbiome mechanism.},
}
RevDate: 2026-09-25
Microbial community structure and antibiotic resistance genes in Dinaric karst groundwater under contrasting hydrological conditions.
Journal of hazardous materials, 517:143725 pii:S0304-3894(26)02706-8 [Epub ahead of print].
Karst aquifers are vulnerable drinking water resources, yet microbiome-resistome studies remain scarce. We investigated microbial community composition and antibiotic resistance gene (ARG) profiles in five karst groundwater sources along an anthropogenic gradient in coastal Croatia under contrasting hydrological conditions. 16S rRNA amplicon sequencing showed that hydrological conditions were associated with community composition. Distance-based redundancy analysis identified total organic carbon as the variable associated with community structure, while ammonium and Escherichia coli were associated with dry hydrological conditions. High-throughput qPCR (96 gene targets) revealed distinct resistome profiles across sites and conditions. Sites with greater anthropogenic influence showed higher ARG abundances than the reference site, particularly under wet hydrological conditions. Efflux pump genes were prevalent across sites and conditions, while aminoglycoside and trimethoprim ARGs were particularly prominent at the most impacted site under dry conditions. Escherichia/Shigella and Klebsiella showed the broadest ranges of significant ARG correlations under wet and dry hydrological conditions, respectively, although several associations were sensitive to individual sampling locations. Clinically relevant ARGs, including vancomycin and colistin resistance genes, were detected at low relative abundances. These findings demonstrate associations between hydrological conditions, anthropogenic influence, and karst groundwater microbiomes and resistomes, highlighting the potential of molecular AMR surveillance in drinking water sources.
Additional Links: PMID-42790045
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PubMed:
Citation:
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@article {pmid42790045,
year = {2026},
author = {Puljko, A and Weisse, L and Bošnjak, MU and Štiglić, J and Maravić, A and Udiković-Kolić, N},
title = {Microbial community structure and antibiotic resistance genes in Dinaric karst groundwater under contrasting hydrological conditions.},
journal = {Journal of hazardous materials},
volume = {517},
number = {},
pages = {143725},
doi = {10.1016/j.jhazmat.2026.143725},
pmid = {42790045},
issn = {1873-3336},
abstract = {Karst aquifers are vulnerable drinking water resources, yet microbiome-resistome studies remain scarce. We investigated microbial community composition and antibiotic resistance gene (ARG) profiles in five karst groundwater sources along an anthropogenic gradient in coastal Croatia under contrasting hydrological conditions. 16S rRNA amplicon sequencing showed that hydrological conditions were associated with community composition. Distance-based redundancy analysis identified total organic carbon as the variable associated with community structure, while ammonium and Escherichia coli were associated with dry hydrological conditions. High-throughput qPCR (96 gene targets) revealed distinct resistome profiles across sites and conditions. Sites with greater anthropogenic influence showed higher ARG abundances than the reference site, particularly under wet hydrological conditions. Efflux pump genes were prevalent across sites and conditions, while aminoglycoside and trimethoprim ARGs were particularly prominent at the most impacted site under dry conditions. Escherichia/Shigella and Klebsiella showed the broadest ranges of significant ARG correlations under wet and dry hydrological conditions, respectively, although several associations were sensitive to individual sampling locations. Clinically relevant ARGs, including vancomycin and colistin resistance genes, were detected at low relative abundances. These findings demonstrate associations between hydrological conditions, anthropogenic influence, and karst groundwater microbiomes and resistomes, highlighting the potential of molecular AMR surveillance in drinking water sources.},
}
RevDate: 2026-09-25
Multi-trophic interactions determine the impact of distinct microplastic types on soil bacteria.
Environment international, 216:110537 pii:S0160-4120(26)00495-2 [Epub ahead of print].
Microplastics are an emerging environmental problem with profound impacts on global biodiversity, as evidenced mostly in marine systems. However, the impacts of microplastics on the hotspot of biodiversity - soil - remain largely unexplored. Studies examining the influence of microplastics on a broader range of soil biodiversity, including trophic interactions between organisms, such as bacteria and nematodes, are rare. In a greenhouse experiment, we tested the impact of three different microplastics (MPs; low-density polyethylene (LDPE), polybutylene adipate terephthalate (PBAT), and a starch-based microplastic), both with and without nematode addition, on soil bacterial communities. The addition of MPs had limited effects on bacterial diversity. Bacterial alpha diversity was slightly increased by MPs (driven by LDPE and PBAT) and decreased by nematode addition. Nematode presence increased the effects of MP addition on bacterial beta diversity, with bacterial communities differing in all MP types from the control, whereas only PBAT affected the bacterial beta diversity without nematodes. We conclude that the effects of MPs on soil bacteria are MP-type-specific and elevated under more complex and thus realistic conditions found in soils, such as multitrophic conditions with nematodes. Therefore, we urge future studies on microplastics and other emerging pollutants to be conducted under conditions more representative of natural conditions, including the presence of microbiome predators.
Additional Links: PMID-42790239
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PubMed:
Citation:
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@article {pmid42790239,
year = {2026},
author = {Racicot, E and Teunissen, J and Li, G and Wang, Y and Geisen, S},
title = {Multi-trophic interactions determine the impact of distinct microplastic types on soil bacteria.},
journal = {Environment international},
volume = {216},
number = {},
pages = {110537},
doi = {10.1016/j.envint.2026.110537},
pmid = {42790239},
issn = {1873-6750},
abstract = {Microplastics are an emerging environmental problem with profound impacts on global biodiversity, as evidenced mostly in marine systems. However, the impacts of microplastics on the hotspot of biodiversity - soil - remain largely unexplored. Studies examining the influence of microplastics on a broader range of soil biodiversity, including trophic interactions between organisms, such as bacteria and nematodes, are rare. In a greenhouse experiment, we tested the impact of three different microplastics (MPs; low-density polyethylene (LDPE), polybutylene adipate terephthalate (PBAT), and a starch-based microplastic), both with and without nematode addition, on soil bacterial communities. The addition of MPs had limited effects on bacterial diversity. Bacterial alpha diversity was slightly increased by MPs (driven by LDPE and PBAT) and decreased by nematode addition. Nematode presence increased the effects of MP addition on bacterial beta diversity, with bacterial communities differing in all MP types from the control, whereas only PBAT affected the bacterial beta diversity without nematodes. We conclude that the effects of MPs on soil bacteria are MP-type-specific and elevated under more complex and thus realistic conditions found in soils, such as multitrophic conditions with nematodes. Therefore, we urge future studies on microplastics and other emerging pollutants to be conducted under conditions more representative of natural conditions, including the presence of microbiome predators.},
}
RevDate: 2026-09-25
Next-generation fermented foods from non-conventional proteins: Linking fermentation dynamics, flavor chemistry, and gut microbiome modulation.
International journal of food microbiology, 462:112076 pii:S0168-1605(26)00457-5 [Epub ahead of print].
The urgent need to diversify protein sources beyond animal agriculture has propelled non-conventional proteins (e.g., insects, microalgae, single-cell organisms, novel plants) to the forefront of food innovation. However, their adoption is limited by off-flavors, anti-nutritional factors, and low digestibility. Fermentation can address these drawbacks and may impart health-relevant benefits, though human evidence remains limited. This review defines next-generation fermented foods (NGFFs) as rationally fermented non-conventional protein substrates achieving superior sensory, nutritional, and gut health outcomes and possessing the potential to replace existing food products. We synthesize the cascading effects of controlled fermentation on these matrices, connecting fermentation dynamics with flavor chemistry and gut microbiome modulation. We dissect substrate compositional peculiarities, proteolysis kinetics, metabolic fluxes, and microbial ecology under tailored conditions, showing how process parameters steer formation of desirable volatiles and elimination of off-note compounds. We explore the prebiotic and probiotic potential of the resulting ferments, with preliminary evidence for gut microbial restructuring, short-chain fatty acid enhancement, and intestinal barrier reinforcement. From these interdependencies, we propose an integrated process-property-health (PPH) nexus to rationalize NGFF design. Finally, we discuss how artificial intelligence, synthetic biology, and life-cycle assessment can accelerate translation to sustainable, consumer-accepted food systems, providing a holistic framework for harnessing fermentation to unlock alternative proteins' full potential. Critically, we identify persistent knowledge gaps, unresolved conflicts in literature, and methodological limitations that constrain current understanding, and we propose prioritized research directions to advance the field from descriptive case studies toward predictive, mechanistic design of next-generation fermented foods.
Additional Links: PMID-42790302
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PubMed:
Citation:
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@article {pmid42790302,
year = {2026},
author = {Zhao, J and Duan, M and Cui, P and Xiong, X and Miao, P and Wang, D and Yan, X and Yu, P and Zeng, Z and Lin, Y and Masuda, Y and Honjoh, KI and Miyamoto, T and Xiao, F},
title = {Next-generation fermented foods from non-conventional proteins: Linking fermentation dynamics, flavor chemistry, and gut microbiome modulation.},
journal = {International journal of food microbiology},
volume = {462},
number = {},
pages = {112076},
doi = {10.1016/j.ijfoodmicro.2026.112076},
pmid = {42790302},
issn = {1879-3460},
abstract = {The urgent need to diversify protein sources beyond animal agriculture has propelled non-conventional proteins (e.g., insects, microalgae, single-cell organisms, novel plants) to the forefront of food innovation. However, their adoption is limited by off-flavors, anti-nutritional factors, and low digestibility. Fermentation can address these drawbacks and may impart health-relevant benefits, though human evidence remains limited. This review defines next-generation fermented foods (NGFFs) as rationally fermented non-conventional protein substrates achieving superior sensory, nutritional, and gut health outcomes and possessing the potential to replace existing food products. We synthesize the cascading effects of controlled fermentation on these matrices, connecting fermentation dynamics with flavor chemistry and gut microbiome modulation. We dissect substrate compositional peculiarities, proteolysis kinetics, metabolic fluxes, and microbial ecology under tailored conditions, showing how process parameters steer formation of desirable volatiles and elimination of off-note compounds. We explore the prebiotic and probiotic potential of the resulting ferments, with preliminary evidence for gut microbial restructuring, short-chain fatty acid enhancement, and intestinal barrier reinforcement. From these interdependencies, we propose an integrated process-property-health (PPH) nexus to rationalize NGFF design. Finally, we discuss how artificial intelligence, synthetic biology, and life-cycle assessment can accelerate translation to sustainable, consumer-accepted food systems, providing a holistic framework for harnessing fermentation to unlock alternative proteins' full potential. Critically, we identify persistent knowledge gaps, unresolved conflicts in literature, and methodological limitations that constrain current understanding, and we propose prioritized research directions to advance the field from descriptive case studies toward predictive, mechanistic design of next-generation fermented foods.},
}
RevDate: 2026-09-25
Climate-induced metabolic rewiring in plants: Impact on plant secondary metabolism and microbiome interactions.
Plant physiology and biochemistry : PPB, 239:111750 pii:S0981-9428(26)00736-9 [Epub ahead of print].
Fluctuating climate is an important factor that affects plant secondary metabolism and the plant microbiome. Environmental conditions, such as fluctuating CO2 levels, temperature and precipitation patterns, forced plants to adapt, leading to altered metabolic pathways. Simultaneously, climate-induced stress can reshape the plant microbiome, which disturbs plant growth, resilience, and even the efficacy of SMs. The interplay between climate change, plant metabolism, and the microbiome is complex, yet this relationship remains largely underexplored. Understanding how these factors co-evolve under shifting environmental conditions could unveil novel strategies for improving crop resilience, optimizing the production of bioactive compounds, and enhancing sustainable agricultural practices in the face of global climate challenges. This review explains how climate change influences the synthesis of secondary metabolism and the microbiome of the plant through transcriptional regulation networks and mechanisms underlying these responses. Moreover, the paper addresses different climate change mitigation strategies.
Additional Links: PMID-42790334
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PubMed:
Citation:
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@article {pmid42790334,
year = {2026},
author = {Rawat, B and Sharma, A and Joshi, N and Rathi, N and Sharma, A and Gururani, P and Rawat, JM},
title = {Climate-induced metabolic rewiring in plants: Impact on plant secondary metabolism and microbiome interactions.},
journal = {Plant physiology and biochemistry : PPB},
volume = {239},
number = {},
pages = {111750},
doi = {10.1016/j.plaphy.2026.111750},
pmid = {42790334},
issn = {1873-2690},
abstract = {Fluctuating climate is an important factor that affects plant secondary metabolism and the plant microbiome. Environmental conditions, such as fluctuating CO2 levels, temperature and precipitation patterns, forced plants to adapt, leading to altered metabolic pathways. Simultaneously, climate-induced stress can reshape the plant microbiome, which disturbs plant growth, resilience, and even the efficacy of SMs. The interplay between climate change, plant metabolism, and the microbiome is complex, yet this relationship remains largely underexplored. Understanding how these factors co-evolve under shifting environmental conditions could unveil novel strategies for improving crop resilience, optimizing the production of bioactive compounds, and enhancing sustainable agricultural practices in the face of global climate challenges. This review explains how climate change influences the synthesis of secondary metabolism and the microbiome of the plant through transcriptional regulation networks and mechanisms underlying these responses. Moreover, the paper addresses different climate change mitigation strategies.},
}
RevDate: 2026-09-25
The Gut-Liver Axis in Metabolic Dysfunction-Associated Steatotic Liver Disease and Associated Hepatocellular Carcinoma: Pathogenesis and Therapeutic Interventions.
The American journal of pathology pii:S0002-9440(26)00282-8 [Epub ahead of print].
Metabolic dysfunction-associated steatotic liver disease (MASLD) comprises a spectrum of liver diseases from simple steatosis to metabolic dysfunction-associated steatohepatitis and its associated fibrosis, cirrhosis, and MASLD-associated hepatocellular carcinoma (MASLD-HCC). MASLD affects over one-third of the global adult population and is closely associated with insulin resistance, obesity, genetic factors, and increasingly recognized, gut microbiome dysbiosis. The gut-liver axis, referring to the communication network between the intestinal microbiota and liver, is critical to the progression of MASLD. The gut microbiota composition and/or functions are disrupted, leading to intestinal barrier destruction, systemic inflammation and modulation of hepatic metabolism and immune responses. The review aims to summarize the effects of gut microbiota on MASLD and its malignant transition to associated HCC based on their roles of microbial metabolites, immune regulation and their associated genetic factors, and to discuss the potential application of microbiome-targeted therapeutic strategies, including probiotics and prebiotics, synbiotics and postbiotics, fecal microbiota transplantation, engineered bacteria and bacteriophage therapy, small molecule inhibitors, microbiota-derived metabolites, with the aim of providing a new vision in the treatment of MASLD and MASLD-HCC. Finally, we discuss current challenges in basic and clinical research of the role of microbiome in MASLD and propose future directions to drive progress in this field.
Additional Links: PMID-42790639
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PubMed:
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@article {pmid42790639,
year = {2026},
author = {Huai, Q and Li, X and Wang, H and Yin, S},
title = {The Gut-Liver Axis in Metabolic Dysfunction-Associated Steatotic Liver Disease and Associated Hepatocellular Carcinoma: Pathogenesis and Therapeutic Interventions.},
journal = {The American journal of pathology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ajpath.2026.09.004},
pmid = {42790639},
issn = {1525-2191},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) comprises a spectrum of liver diseases from simple steatosis to metabolic dysfunction-associated steatohepatitis and its associated fibrosis, cirrhosis, and MASLD-associated hepatocellular carcinoma (MASLD-HCC). MASLD affects over one-third of the global adult population and is closely associated with insulin resistance, obesity, genetic factors, and increasingly recognized, gut microbiome dysbiosis. The gut-liver axis, referring to the communication network between the intestinal microbiota and liver, is critical to the progression of MASLD. The gut microbiota composition and/or functions are disrupted, leading to intestinal barrier destruction, systemic inflammation and modulation of hepatic metabolism and immune responses. The review aims to summarize the effects of gut microbiota on MASLD and its malignant transition to associated HCC based on their roles of microbial metabolites, immune regulation and their associated genetic factors, and to discuss the potential application of microbiome-targeted therapeutic strategies, including probiotics and prebiotics, synbiotics and postbiotics, fecal microbiota transplantation, engineered bacteria and bacteriophage therapy, small molecule inhibitors, microbiota-derived metabolites, with the aim of providing a new vision in the treatment of MASLD and MASLD-HCC. Finally, we discuss current challenges in basic and clinical research of the role of microbiome in MASLD and propose future directions to drive progress in this field.},
}
RevDate: 2026-09-25
The Vagus Nerve in Alcohol Use Disorder: Gut-Brain Mechanisms Linking Interoception, Neuroinflammation, and Reward.
Alcohol (Fayetteville, N.Y.) pii:S0741-8329(26)00249-1 [Epub ahead of print].
Alcohol use disorder (AUD) is a leading contributor to global morbidity and mortality, yet current treatments remain underutilized and only partially effective. Although AUD has traditionally been conceptualized as a brain-centered disorder, emerging evidence supports an integrative framework in which peripheral physiological signals influence central neural circuits that regulate motivation, affect, and reinforcement. This review examines the effects of alcohol on the gut-vagal-brain axis and evaluates the role of vagal signaling in the development and maintenance of AUD. Chronic alcohol exposure disrupts intestinal barrier integrity, alters microbiome composition, and promotes systemic inflammation, generating inflammatory and metabolic signals that can engage vagal sensory pathways. However, the direct effects of these alcohol-associated peripheral adaptations on vagal signaling and downstream CNS circuits in AUD remain incompletely defined. Preclinical studies demonstrate that surgical and pharmacological manipulation of vagal signaling alters alcohol intake, relapse-like behavior, and stress responsivity, supporting a functional role for vagal pathways in alcohol-related behaviors. Clinical studies similarly report reduced vagal tone and autonomic imbalance in individuals with AUD, suggesting translational relevance. Emerging neuromodulatory approaches, including invasive and transcutaneous vagus nerve stimulation (VNS), show promise for reducing craving and improving affective symptoms; however, current evidence remains limited. In this review, we synthesize current evidence examining how chronic alcohol exposure may disrupt gut-vagal-brain communication and discuss the potential contribution of these changes to alcohol use disorder. We identify potential mechanistic pathways and knowledge gaps, and highlight the need for more circuit-specific and longitudinal studies to evaluate vagal pathways as therapeutic targets for AUD.
Additional Links: PMID-42790684
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PubMed:
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@article {pmid42790684,
year = {2026},
author = {Lehner, T and Sandoval, DA and McCullough, RL},
title = {The Vagus Nerve in Alcohol Use Disorder: Gut-Brain Mechanisms Linking Interoception, Neuroinflammation, and Reward.},
journal = {Alcohol (Fayetteville, N.Y.)},
volume = {},
number = {},
pages = {107460},
doi = {10.1016/j.alcohol.2026.107460},
pmid = {42790684},
issn = {1873-6823},
abstract = {Alcohol use disorder (AUD) is a leading contributor to global morbidity and mortality, yet current treatments remain underutilized and only partially effective. Although AUD has traditionally been conceptualized as a brain-centered disorder, emerging evidence supports an integrative framework in which peripheral physiological signals influence central neural circuits that regulate motivation, affect, and reinforcement. This review examines the effects of alcohol on the gut-vagal-brain axis and evaluates the role of vagal signaling in the development and maintenance of AUD. Chronic alcohol exposure disrupts intestinal barrier integrity, alters microbiome composition, and promotes systemic inflammation, generating inflammatory and metabolic signals that can engage vagal sensory pathways. However, the direct effects of these alcohol-associated peripheral adaptations on vagal signaling and downstream CNS circuits in AUD remain incompletely defined. Preclinical studies demonstrate that surgical and pharmacological manipulation of vagal signaling alters alcohol intake, relapse-like behavior, and stress responsivity, supporting a functional role for vagal pathways in alcohol-related behaviors. Clinical studies similarly report reduced vagal tone and autonomic imbalance in individuals with AUD, suggesting translational relevance. Emerging neuromodulatory approaches, including invasive and transcutaneous vagus nerve stimulation (VNS), show promise for reducing craving and improving affective symptoms; however, current evidence remains limited. In this review, we synthesize current evidence examining how chronic alcohol exposure may disrupt gut-vagal-brain communication and discuss the potential contribution of these changes to alcohol use disorder. We identify potential mechanistic pathways and knowledge gaps, and highlight the need for more circuit-specific and longitudinal studies to evaluate vagal pathways as therapeutic targets for AUD.},
}
RevDate: 2026-09-25
ERJ Podcast September 2026: The airway microbiome and targeted therapy in bronchiectasis.
The European respiratory journal, 68(3): pii:68/3/26E6803.
Additional Links: PMID-42790892
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Citation:
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@article {pmid42790892,
year = {2026},
author = {},
title = {ERJ Podcast September 2026: The airway microbiome and targeted therapy in bronchiectasis.},
journal = {The European respiratory journal},
volume = {68},
number = {3},
pages = {},
doi = {10.1183/13993003.E6803-2026},
pmid = {42790892},
issn = {1399-3003},
}
RevDate: 2026-09-25
CmpDate: 2026-09-25
Periodontitis and Oral Cancer Risk.
Oral and maxillofacial surgery clinics of North America, 38(4):507-513.
An association between periodontitis and oral cancer risk and progression has been suggested. It seems most likely that periodontitis plays an indirect role in oral cancer risk and progression in which its contribution to a chronic inflammatory state characterized by the persistent release of pro-inflammatory cytokines contributes to oxidative stress and DNA damage, potentially favoring carcinogenic processes. Periodontal health status of an individual may serve as a surrogate for general health as those factors which contribute to good general health, environment, lifestyle, and access to care are also determinants of oral health and impact cancer risk.
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@article {pmid42791002,
year = {2026},
author = {Mehrnia, N and Sonis, S},
title = {Periodontitis and Oral Cancer Risk.},
journal = {Oral and maxillofacial surgery clinics of North America},
volume = {38},
number = {4},
pages = {507-513},
doi = {10.1016/j.coms.2026.07.002},
pmid = {42791002},
issn = {1558-1365},
mesh = {Humans ; *Periodontitis/complications ; *Mouth Neoplasms/etiology ; Risk Factors ; Disease Progression ; },
abstract = {An association between periodontitis and oral cancer risk and progression has been suggested. It seems most likely that periodontitis plays an indirect role in oral cancer risk and progression in which its contribution to a chronic inflammatory state characterized by the persistent release of pro-inflammatory cytokines contributes to oxidative stress and DNA damage, potentially favoring carcinogenic processes. Periodontal health status of an individual may serve as a surrogate for general health as those factors which contribute to good general health, environment, lifestyle, and access to care are also determinants of oral health and impact cancer risk.},
}
MeSH Terms:
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Humans
*Periodontitis/complications
*Mouth Neoplasms/etiology
Risk Factors
Disease Progression
RevDate: 2026-09-25
CmpDate: 2026-09-25
Diagnostic Adjuncts and Biopsy Techniques for Oral Potentially Malignant Disorders and Oral Cavity Squamous Cell Carcinoma.
Oral and maxillofacial surgery clinics of North America, 38(4):515-530.
Diagnostic adjuncts for oral potentially malignant disorders such as leukoplakia or erythroplakia can aid the clinician in triaging abnormal lesions and facilitate both biopsy site selection and surgical management. No adjuncts replace gold standard biopsy and histopathological examination, and their optimal use requires training and experience. This article covers the potential applications, both in primary and expert settings, of adjuncts, such as tissue autofluorescence, toluidine blues staining, and cytopathology. It covers new and emerging adjuncts such as confocal microscopy, liquid biopsy, oral microbiome testing, and the role of artificial intelligence. Incisional biopsy site selection and techniques will also be discussed.
Additional Links: PMID-42791003
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@article {pmid42791003,
year = {2026},
author = {Wolk, R and Kerr, AR},
title = {Diagnostic Adjuncts and Biopsy Techniques for Oral Potentially Malignant Disorders and Oral Cavity Squamous Cell Carcinoma.},
journal = {Oral and maxillofacial surgery clinics of North America},
volume = {38},
number = {4},
pages = {515-530},
doi = {10.1016/j.coms.2026.07.007},
pmid = {42791003},
issn = {1558-1365},
mesh = {Humans ; *Mouth Neoplasms/pathology/diagnosis ; *Carcinoma, Squamous Cell/pathology/diagnosis ; Biopsy/methods ; Microscopy, Confocal ; *Precancerous Conditions/pathology ; },
abstract = {Diagnostic adjuncts for oral potentially malignant disorders such as leukoplakia or erythroplakia can aid the clinician in triaging abnormal lesions and facilitate both biopsy site selection and surgical management. No adjuncts replace gold standard biopsy and histopathological examination, and their optimal use requires training and experience. This article covers the potential applications, both in primary and expert settings, of adjuncts, such as tissue autofluorescence, toluidine blues staining, and cytopathology. It covers new and emerging adjuncts such as confocal microscopy, liquid biopsy, oral microbiome testing, and the role of artificial intelligence. Incisional biopsy site selection and techniques will also be discussed.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Mouth Neoplasms/pathology/diagnosis
*Carcinoma, Squamous Cell/pathology/diagnosis
Biopsy/methods
Microscopy, Confocal
*Precancerous Conditions/pathology
RevDate: 2026-09-25
Synthesis of Microbial-Derived Octadecanoids.
Lipids [Epub ahead of print].
Gut bacteria can convert dietary fatty acids into oxygenated metabolites called oxylipins, which can exert potent lipid mediator functions. The oxylipins derived from C-18 fatty acids are termed octadecanoids and associate with multiple disorders including allergy and metabolic dysregulation. This study presents the synthesis of 17 octadecanoids possessing a hydroxy group (n = 9) or a ketone (n = 8) on the 10- or 13-positions. The products of these two series were prepared for the linoleic acid (LA), α-linolenic acid (ALA) and γ-linolenic acid (GLA) pathways. The synthetic strategies provided 17 putative microbial metabolites of C-18 polyunsaturated fatty acids (PUFAs) with high purities, in 5-13 steps and overall yields from 1.5%-37%. To study the biological formation of these compounds, the parent PUFAs (LA, ALA, GLA) were fed to cultures of Enterococcus faecalis U150 and Lactobacillus acidophilus CCUG 5917, and the octadecanoid products were measured by chiral supercritical fluid chromatography coupled to tandem mass spectrometry (SFC-MS/MS). The compounds containing a hydroxy group on the 10- or 13-position are racemic, forming 9 enantiomeric pairs. Accordingly, of the 17 compounds synthesized, 9 were chiral and 8 were achiral resulting in 26 compounds. An additional 7 commercial bacteria-derived octadecanoids were measured to provide a screen of 33 compounds. Generally, PUFA supplementation resulted in selective formation of the associated octadecanoids. Of the 33 studied compounds, 16 were observed to be formed by E. faecalis and 13 by L. acidophilus. These findings demonstrate the bacteria species-specific formation of octadecanoids, which may have ramifications for associated biological response in the host.
Additional Links: PMID-42791036
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@article {pmid42791036,
year = {2026},
author = {Revol-Cavalier, J and Bankóová, K and Salamin, O and Quaranta, A and Du, J and Hamberg, M and Wheelock, CE},
title = {Synthesis of Microbial-Derived Octadecanoids.},
journal = {Lipids},
volume = {},
number = {},
pages = {},
doi = {10.1002/lipd.70067},
pmid = {42791036},
issn = {1558-9307},
support = {HLF 20230463//Hjärt-Lungfonden/ ; HLF 20210519//Hjärt-Lungfonden/ ; 2022-00796//Swedish Research Council/ ; //Larodan AB/ ; //Cayman Biomedical Research Institute (CABRI)/ ; },
abstract = {Gut bacteria can convert dietary fatty acids into oxygenated metabolites called oxylipins, which can exert potent lipid mediator functions. The oxylipins derived from C-18 fatty acids are termed octadecanoids and associate with multiple disorders including allergy and metabolic dysregulation. This study presents the synthesis of 17 octadecanoids possessing a hydroxy group (n = 9) or a ketone (n = 8) on the 10- or 13-positions. The products of these two series were prepared for the linoleic acid (LA), α-linolenic acid (ALA) and γ-linolenic acid (GLA) pathways. The synthetic strategies provided 17 putative microbial metabolites of C-18 polyunsaturated fatty acids (PUFAs) with high purities, in 5-13 steps and overall yields from 1.5%-37%. To study the biological formation of these compounds, the parent PUFAs (LA, ALA, GLA) were fed to cultures of Enterococcus faecalis U150 and Lactobacillus acidophilus CCUG 5917, and the octadecanoid products were measured by chiral supercritical fluid chromatography coupled to tandem mass spectrometry (SFC-MS/MS). The compounds containing a hydroxy group on the 10- or 13-position are racemic, forming 9 enantiomeric pairs. Accordingly, of the 17 compounds synthesized, 9 were chiral and 8 were achiral resulting in 26 compounds. An additional 7 commercial bacteria-derived octadecanoids were measured to provide a screen of 33 compounds. Generally, PUFA supplementation resulted in selective formation of the associated octadecanoids. Of the 33 studied compounds, 16 were observed to be formed by E. faecalis and 13 by L. acidophilus. These findings demonstrate the bacteria species-specific formation of octadecanoids, which may have ramifications for associated biological response in the host.},
}
RevDate: 2026-09-25
Studying the microbiome-gut-brain axis in early life: how, why, the challenges and clinical implications.
Archives of disease in childhood. Education and practice edition pii:archdischild-2025-330117 [Epub ahead of print].
Additional Links: PMID-42791066
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@article {pmid42791066,
year = {2026},
author = {Kenny, A and Vaher, K},
title = {Studying the microbiome-gut-brain axis in early life: how, why, the challenges and clinical implications.},
journal = {Archives of disease in childhood. Education and practice edition},
volume = {},
number = {},
pages = {},
doi = {10.1136/archdischild-2025-330117},
pmid = {42791066},
issn = {1743-0593},
}
RevDate: 2026-09-25
CmpDate: 2026-09-25
Scaling Phage-Bacteria Interaction Contexts: From Pairwise Mechanisms to Community Dynamics.
Annual review of virology, 13(1):223-248.
Bacteriophages (phages), viruses that parasitize bacteria, hold tremendous potential as antimicrobial agents, microbiome modulators, and industrial biocontrol tools; yet clinical and environmental applications remain frustratingly inconsistent. Decades of research on isolated phage-bacteria pairs have revealed fundamental mechanisms governing infection specificity, coevolutionary arms races, and resistance trade-offs. These foundational studies, however, do not help predict outcomes when phages encounter multi-species assemblages characteristic of natural ecosystems. In this review, we integrate recent advances examining how interaction complexity shapes phage efficacy across four scales, gradually from simple phage-bacteria pairs to phage-bacterial communities. At every scale, emergent properties arise from complex interactions. Dissecting these dynamics requires technologies that can track multiple lineages simultaneously. DNA barcoding, which inserts unique genetic identifiers into bacterial and phage genomes, offers a promising solution. While barcoding all members in a synthetic community is unrealistic, we propose that even foundational reference sets of barcoded phage-bacteria pairs would enable systematic investigation of resistance evolution, competitive interactions, and functional outcomes in realistic contexts. Bridging laboratory insights and field performance demands integrating genetic engineering, high-throughput tracking, functional profiling, and predictive modeling into a coordinated research framework.
Additional Links: PMID-42791216
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@article {pmid42791216,
year = {2026},
author = {Selvakumar, H and Koderi Valappil, S and Piya, D and Mutalik, VK},
title = {Scaling Phage-Bacteria Interaction Contexts: From Pairwise Mechanisms to Community Dynamics.},
journal = {Annual review of virology},
volume = {13},
number = {1},
pages = {223-248},
doi = {10.1146/annurev-virology-100424-123645},
pmid = {42791216},
issn = {2327-0578},
mesh = {*Bacteriophages/genetics/physiology ; *Bacteria/virology/genetics ; Host-Pathogen Interactions ; DNA Barcoding, Taxonomic ; Microbiota ; Genome, Viral ; Host Specificity ; },
abstract = {Bacteriophages (phages), viruses that parasitize bacteria, hold tremendous potential as antimicrobial agents, microbiome modulators, and industrial biocontrol tools; yet clinical and environmental applications remain frustratingly inconsistent. Decades of research on isolated phage-bacteria pairs have revealed fundamental mechanisms governing infection specificity, coevolutionary arms races, and resistance trade-offs. These foundational studies, however, do not help predict outcomes when phages encounter multi-species assemblages characteristic of natural ecosystems. In this review, we integrate recent advances examining how interaction complexity shapes phage efficacy across four scales, gradually from simple phage-bacteria pairs to phage-bacterial communities. At every scale, emergent properties arise from complex interactions. Dissecting these dynamics requires technologies that can track multiple lineages simultaneously. DNA barcoding, which inserts unique genetic identifiers into bacterial and phage genomes, offers a promising solution. While barcoding all members in a synthetic community is unrealistic, we propose that even foundational reference sets of barcoded phage-bacteria pairs would enable systematic investigation of resistance evolution, competitive interactions, and functional outcomes in realistic contexts. Bridging laboratory insights and field performance demands integrating genetic engineering, high-throughput tracking, functional profiling, and predictive modeling into a coordinated research framework.},
}
MeSH Terms:
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hide MeSH Terms
*Bacteriophages/genetics/physiology
*Bacteria/virology/genetics
Host-Pathogen Interactions
DNA Barcoding, Taxonomic
Microbiota
Genome, Viral
Host Specificity
RevDate: 2026-09-25
CmpDate: 2026-09-25
Difficult relationships between humans and bacteria: associations between multiple sclerosis and the human microbiome.
Antonie van Leeuwenhoek, 119(10):.
Multiple sclerosis (MS) is a chronic immune-mediated disease of the central nervous system, the pathogenesis of which involves complex interactions between genetic predisposition, environmental factors, and dysregulation of immune responses. This review critically synthesizes available evidence from studies demonstrating significant alterations in the composition of the human microbiome in individuals with MS. The work summarizes the current state of knowledge regarding the composition, diversity, and dysbiosis of the gut microbiome in MS, highlighting the heterogeneity of observed microbial changes depending on clinical disease phenotype, inflammatory activity, therapeutic interventions, and methodological across studies. Data from other microbial niches are also considered, including the oral and skin microbiome, as well as mucosal-associated intestinal microbiota, which may contribute to local and peripheral modulation of immune responses. The gut mycobiome is presented as a complementary component whose potential immunological relevance is currently under investigation. Observational and experimental evidence suggest that alterations in microbiota composition correlate with immune gene expression and with the differentiation of effector T cell populations, particularly along the Th17/IL-17 axis, although the casual significance of these associations in human MS remains unclear. Host genetic factors, particularly HLA class II gene polymorphisms, may also influence microbiota composition and susceptibility to autoimmunity. Furthermore, microbiome-derived metabolites detected in plasma and cerebrospinal fluid may mediate communication between the gut and the central nervous system. Overall, the available evidence points to multilevel interactions between the microbiome, host genetics, metabolism, and the immune system in MS. However, substantial methodological heterogeneity, predominantly cross-sectional study designs, treatment-related confounding, and limited reproducibility of taxon-specific findings currently restrict causal interpretation. Further longitudinal studies in patients with MS are therefore needed to determine whether microbiome alterations contribute to MS development and progression or occur as consequence of the disease and its treatment.
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@article {pmid42791381,
year = {2026},
author = {Dulębska, J and Sabat, Z and Kukla, I and Szcześniak, A and Jasińska, E and Adamus-Białek, W},
title = {Difficult relationships between humans and bacteria: associations between multiple sclerosis and the human microbiome.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {10},
pages = {},
pmid = {42791381},
issn = {1572-9699},
support = {SUPB.RN.26.006//Uniwersytet Jana Kochanowskiego w Kielcach/ ; },
mesh = {Humans ; *Multiple Sclerosis/microbiology/immunology/genetics ; *Microbiota ; Dysbiosis/microbiology ; Gastrointestinal Microbiome ; *Bacteria/classification/genetics ; Skin Microbiome ; },
abstract = {Multiple sclerosis (MS) is a chronic immune-mediated disease of the central nervous system, the pathogenesis of which involves complex interactions between genetic predisposition, environmental factors, and dysregulation of immune responses. This review critically synthesizes available evidence from studies demonstrating significant alterations in the composition of the human microbiome in individuals with MS. The work summarizes the current state of knowledge regarding the composition, diversity, and dysbiosis of the gut microbiome in MS, highlighting the heterogeneity of observed microbial changes depending on clinical disease phenotype, inflammatory activity, therapeutic interventions, and methodological across studies. Data from other microbial niches are also considered, including the oral and skin microbiome, as well as mucosal-associated intestinal microbiota, which may contribute to local and peripheral modulation of immune responses. The gut mycobiome is presented as a complementary component whose potential immunological relevance is currently under investigation. Observational and experimental evidence suggest that alterations in microbiota composition correlate with immune gene expression and with the differentiation of effector T cell populations, particularly along the Th17/IL-17 axis, although the casual significance of these associations in human MS remains unclear. Host genetic factors, particularly HLA class II gene polymorphisms, may also influence microbiota composition and susceptibility to autoimmunity. Furthermore, microbiome-derived metabolites detected in plasma and cerebrospinal fluid may mediate communication between the gut and the central nervous system. Overall, the available evidence points to multilevel interactions between the microbiome, host genetics, metabolism, and the immune system in MS. However, substantial methodological heterogeneity, predominantly cross-sectional study designs, treatment-related confounding, and limited reproducibility of taxon-specific findings currently restrict causal interpretation. Further longitudinal studies in patients with MS are therefore needed to determine whether microbiome alterations contribute to MS development and progression or occur as consequence of the disease and its treatment.},
}
MeSH Terms:
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Humans
*Multiple Sclerosis/microbiology/immunology/genetics
*Microbiota
Dysbiosis/microbiology
Gastrointestinal Microbiome
*Bacteria/classification/genetics
Skin Microbiome
RevDate: 2026-09-25
Humanizing Zophobas morio larvae microbiota for rapid screening of emerging decolonization strategies against multidrug-resistant bacteria.
European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology [Epub ahead of print].
PURPOSE: Designing efficient strategies against the gut colonization due to multidrug-resistant (MDR) bacteria is an important task. However, scalable and reliable in vivo models that possess a human-like gut microbiota are not yet available. Here, we tested whether Zophobas morio larvae (ZmL) could be used as a humanized microbiota model.
METHODS: A pooled fecal transplant material from 7 human donors was administered via contaminated food to a group of ZmL every 48-h for 28 days (T28), followed by a 28-day washout phase. A control group received the standard diet. Gut microbiota composition was assessed at 9 timepoints (from T0 to T56) by 16S rRNA gene amplicon sequencing across 3 independent runs.
RESULTS: Fecal microbiota transplants (FMTs) increased the richness of the larval gut bacterial population, with 8 of 10 top human-associated genera increasing during this phase. The experimental group exhibited higher observed richness than the control across T7-T56 (median 116 vs. 62 amplicon sequence variants; p < 0.001). A humanization score, calculated as the sum of the 10 top human genera detected in the transplanted ZmL, peaked at T14, and declined to near zero by the end of the washout phase (T56). Community composition differed significantly between groups, with the variable diet accounting for more variation than the run (PERMANOVA, R2 = 13.3%; p = 0.001).
CONCLUSIONS: Under repeated FMTs, ZmL underwent a humanization of their microbiota making this model a promising tool to study novel decolonization strategies against MDR bacteria. Future efforts should focus on the stabilization of the human-like microbiota without repeated FMTs.
Additional Links: PMID-42791458
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@article {pmid42791458,
year = {2026},
author = {Belhout, C and Freire, S and Aldeia, C and Endimiani, A},
title = {Humanizing Zophobas morio larvae microbiota for rapid screening of emerging decolonization strategies against multidrug-resistant bacteria.},
journal = {European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology},
volume = {},
number = {},
pages = {},
pmid = {42791458},
issn = {1435-4373},
abstract = {PURPOSE: Designing efficient strategies against the gut colonization due to multidrug-resistant (MDR) bacteria is an important task. However, scalable and reliable in vivo models that possess a human-like gut microbiota are not yet available. Here, we tested whether Zophobas morio larvae (ZmL) could be used as a humanized microbiota model.
METHODS: A pooled fecal transplant material from 7 human donors was administered via contaminated food to a group of ZmL every 48-h for 28 days (T28), followed by a 28-day washout phase. A control group received the standard diet. Gut microbiota composition was assessed at 9 timepoints (from T0 to T56) by 16S rRNA gene amplicon sequencing across 3 independent runs.
RESULTS: Fecal microbiota transplants (FMTs) increased the richness of the larval gut bacterial population, with 8 of 10 top human-associated genera increasing during this phase. The experimental group exhibited higher observed richness than the control across T7-T56 (median 116 vs. 62 amplicon sequence variants; p < 0.001). A humanization score, calculated as the sum of the 10 top human genera detected in the transplanted ZmL, peaked at T14, and declined to near zero by the end of the washout phase (T56). Community composition differed significantly between groups, with the variable diet accounting for more variation than the run (PERMANOVA, R2 = 13.3%; p = 0.001).
CONCLUSIONS: Under repeated FMTs, ZmL underwent a humanization of their microbiota making this model a promising tool to study novel decolonization strategies against MDR bacteria. Future efforts should focus on the stabilization of the human-like microbiota without repeated FMTs.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Effects of Aged Polymethylmethacrylate Microplastics on Physiological Biochemistry and Intestinal-Sediment Microbial Communities of Urechis unicinctus (von Drasche, 1881).
Animals : an open access journal from MDPI, 16(18): pii:ani16182829.
Microplastics (MPs) widely distribute in marine environments and generate severe hazards to marine biota, yet little is known regarding the toxic impacts of aged MPs on benthic invertebrates and their surrounding sediment microbiota. This work aimed to fill this research gap by exploring the comprehensive toxicity of aged polymethylmethacrylate microplastics (PMMA-MPs) toward Urechis unicinctus and its sediment habitat. A 21-day laboratory exposure trial was performed with two PMMA-MP treatments: environmentally realistic low concentration (10 μg/L) and extreme high concentration (1000 μg/L). Aged PMMA-MPs accumulated in the body wall and intestine of U. unicinctus, with markedly higher body wall MPs loads in the high-dose group (p < 0.05). High-concentration PMMA-MPs significantly raised intestinal total protein and triggered intense oxidative stress (p < 0.01), and the Integrated Biomarker Response value rose dose-dependently. Sediment microbial β-diversity was obviously reshaped (p < 0.05), with enriched pathogens including Klebsiella and Enterobacteriaceae under high MP exposure, while the worm's intestinal α-diversity and core microbiome remained stable, showing host adaptability. This study reveals multi-level toxic outcomes of aged PMMA-MPs on benthic worms and their sediment microhabitat, offering fundamental data to evaluate the ecological risks of weathered MPs in marine benthic systems.
Additional Links: PMID-42791686
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@article {pmid42791686,
year = {2026},
author = {Huang, Y and Guo, Y and Feng, W and Gao, L and Fu, Y and Bai, J and Liu, F},
title = {Effects of Aged Polymethylmethacrylate Microplastics on Physiological Biochemistry and Intestinal-Sediment Microbial Communities of Urechis unicinctus (von Drasche, 1881).},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {18},
pages = {},
doi = {10.3390/ani16182829},
pmid = {42791686},
issn = {2076-2615},
support = {2024XDRHXMPT11//Yantai City School-Local Integration Development Project/ ; },
abstract = {Microplastics (MPs) widely distribute in marine environments and generate severe hazards to marine biota, yet little is known regarding the toxic impacts of aged MPs on benthic invertebrates and their surrounding sediment microbiota. This work aimed to fill this research gap by exploring the comprehensive toxicity of aged polymethylmethacrylate microplastics (PMMA-MPs) toward Urechis unicinctus and its sediment habitat. A 21-day laboratory exposure trial was performed with two PMMA-MP treatments: environmentally realistic low concentration (10 μg/L) and extreme high concentration (1000 μg/L). Aged PMMA-MPs accumulated in the body wall and intestine of U. unicinctus, with markedly higher body wall MPs loads in the high-dose group (p < 0.05). High-concentration PMMA-MPs significantly raised intestinal total protein and triggered intense oxidative stress (p < 0.01), and the Integrated Biomarker Response value rose dose-dependently. Sediment microbial β-diversity was obviously reshaped (p < 0.05), with enriched pathogens including Klebsiella and Enterobacteriaceae under high MP exposure, while the worm's intestinal α-diversity and core microbiome remained stable, showing host adaptability. This study reveals multi-level toxic outcomes of aged PMMA-MPs on benthic worms and their sediment microhabitat, offering fundamental data to evaluate the ecological risks of weathered MPs in marine benthic systems.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Foie Gras Production: A Literature Review on the Welfare Implications of Force-Feeding of Ducks.
Animals : an open access journal from MDPI, 16(18): pii:ani16182838.
Foie gras production is based on the force-feeding (gavage) of waterfowl to induce hepatic steatosis and subsequent liver enlargement. This practice has been widely debated due to concerns regarding animal welfare. This review provides a comprehensive overview of foie gras production, with a primary focus on the welfare implications of force-feeding in ducks, while contextualising historical and alternative practices involving geese. Evidence was evaluated across behavioural, physiological, pathological and health-related outcomes, together with procedural, housing and environmental factors. Endocrine findings are mixed, but repeated restraint and tube insertion can cause injuries to the upper digestive tract, while progressive feed administration produces marked liver enlargement, altered hepatic function and increased metabolic heat load. Reduced activity, locomotor impairment, lesions and elevated mortality have also been reported, although study designs and production methods and conditions vary. Alternatives under investigation include spontaneous fattening, microbiome-based interventions, cultivated-cell products and plant-based or processed analogues. Evidence concerning their welfare benefits, product quality, scalability and economic feasibility remains limited. Overall, the accumulated scientific evidence raises significant concerns regarding the welfare of force-fed birds and underscores the need for continued exploration of viable alternative production strategies.
Additional Links: PMID-42791694
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PubMed:
Citation:
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@article {pmid42791694,
year = {2026},
author = {Driessen, B and Pellens, L and Nivelle, B and Van Rossem, K and Buyse, J},
title = {Foie Gras Production: A Literature Review on the Welfare Implications of Force-Feeding of Ducks.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {18},
pages = {},
doi = {10.3390/ani16182838},
pmid = {42791694},
issn = {2076-2615},
support = {LNE/STG/DWZ/16/04.//Flemish Government/ ; },
abstract = {Foie gras production is based on the force-feeding (gavage) of waterfowl to induce hepatic steatosis and subsequent liver enlargement. This practice has been widely debated due to concerns regarding animal welfare. This review provides a comprehensive overview of foie gras production, with a primary focus on the welfare implications of force-feeding in ducks, while contextualising historical and alternative practices involving geese. Evidence was evaluated across behavioural, physiological, pathological and health-related outcomes, together with procedural, housing and environmental factors. Endocrine findings are mixed, but repeated restraint and tube insertion can cause injuries to the upper digestive tract, while progressive feed administration produces marked liver enlargement, altered hepatic function and increased metabolic heat load. Reduced activity, locomotor impairment, lesions and elevated mortality have also been reported, although study designs and production methods and conditions vary. Alternatives under investigation include spontaneous fattening, microbiome-based interventions, cultivated-cell products and plant-based or processed analogues. Evidence concerning their welfare benefits, product quality, scalability and economic feasibility remains limited. Overall, the accumulated scientific evidence raises significant concerns regarding the welfare of force-fed birds and underscores the need for continued exploration of viable alternative production strategies.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Transcriptomic Landscape of Gut Microbiota-Host Interactions Reveals Domestication-Related Changes in the Pearl Oyster Pinctada maxima.
Animals : an open access journal from MDPI, 16(18): pii:ani16182849.
The offspring of domesticated Pinctada maxima exhibited various physiological and microbial adjustments to the complex and dynamic conditions of coastal environments. To support the restoration of P. maxima genetic resources and explore the molecular mechanisms underlying these phenotypic responses, we conducted a comparative analysis of the intestinal transcriptome and microbiota of wild parental and domesticated generations. Each sample generated an average of 43,600,525 clean reads, which were mapped to the P. maxima reference genome with mapping rates ranging from 63.91% to 79.48%, and a total of 3007 differentially expressed genes (DEGs) were subsequently identified. Gene Ontology analysis revealed that the DEGs were enriched in organic acid metabolism, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that the DEGs were enriched in glycosphingolipid biosynthesis and xenobiotic metabolism via cytochrome P450. Microbiota profiling revealed significant compositional shifts at phylum and genus levels, with increased alpha diversity in F1; dominant phyla transitioned towards Spirochaetota and Bacteroidota, and functional predictions pointed to enhanced metabolic and immune capacities. Quantitative validated the up-regulation of immune genes (PmHR96h, PmIAP) and down-regulation of calcium-signaling genes (PmCaM, PmHSP90), consistent with RNA-seq data. Collectively, these coordinated transcriptomic and microbial alterations reflect a multifaceted host-microbiome adaptive response to nearshore conditions. Our findings provide valuable molecular markers and microbial indicators for selective breeding and health monitoring, offering a scientific basis for improving the resilience of P. maxima aquaculture under changing environmental conditions.
Additional Links: PMID-42791706
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@article {pmid42791706,
year = {2026},
author = {Huang, J and Zhang, T and Xie, D and Zheng, Z and Yang, C and Liao, Y and Wang, Q and Deng, Y},
title = {Transcriptomic Landscape of Gut Microbiota-Host Interactions Reveals Domestication-Related Changes in the Pearl Oyster Pinctada maxima.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {18},
pages = {},
doi = {10.3390/ani16182849},
pmid = {42791706},
issn = {2076-2615},
abstract = {The offspring of domesticated Pinctada maxima exhibited various physiological and microbial adjustments to the complex and dynamic conditions of coastal environments. To support the restoration of P. maxima genetic resources and explore the molecular mechanisms underlying these phenotypic responses, we conducted a comparative analysis of the intestinal transcriptome and microbiota of wild parental and domesticated generations. Each sample generated an average of 43,600,525 clean reads, which were mapped to the P. maxima reference genome with mapping rates ranging from 63.91% to 79.48%, and a total of 3007 differentially expressed genes (DEGs) were subsequently identified. Gene Ontology analysis revealed that the DEGs were enriched in organic acid metabolism, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that the DEGs were enriched in glycosphingolipid biosynthesis and xenobiotic metabolism via cytochrome P450. Microbiota profiling revealed significant compositional shifts at phylum and genus levels, with increased alpha diversity in F1; dominant phyla transitioned towards Spirochaetota and Bacteroidota, and functional predictions pointed to enhanced metabolic and immune capacities. Quantitative validated the up-regulation of immune genes (PmHR96h, PmIAP) and down-regulation of calcium-signaling genes (PmCaM, PmHSP90), consistent with RNA-seq data. Collectively, these coordinated transcriptomic and microbial alterations reflect a multifaceted host-microbiome adaptive response to nearshore conditions. Our findings provide valuable molecular markers and microbial indicators for selective breeding and health monitoring, offering a scientific basis for improving the resilience of P. maxima aquaculture under changing environmental conditions.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Characterization of the Healthy Ocular Mycobiome of Purebred Lusitano Horses Using Oxford Nanopore Long-Read Sequencing.
Animals : an open access journal from MDPI, 16(18): pii:ani16182913.
The ocular surface represents a unique microbial ecosystem continuously exposed to environmental microorganisms; however, the fungal component of the healthy equine ocular microbiome remains poorly characterized. This study aimed to characterize the ocular surface mycobiome of 12 clinically healthy Purebred Lusitano horses from three geographical regions in Portugal kept in two housing systems using Oxford Nanopore long-read sequencing and conventional fungal culture. Sequencing revealed a highly diverse fungal community with marked inter-individual variability. The most abundant genera were Wallemia, Podosphaera, Debaromyces, Aspergillus, Filobasidium, Kurtzmaniella, Metschnikowia, Malassezia and Spathaspora. Patterns of fungal community composition suggested that local environmental conditions may contribute to the observed inter-individual variability. Genera commonly associated with equine fungal keratitis, including Aspergillus, Fusarium and Penicillium, were detected in healthy horses irrespective of housing system. Overall, the healthy equine ocular surface was characterized by a diverse mycobiome dominated by environmentally associated fungi. There findings provide a baseline for future studies investigating ocular microbial dysbiosis, environmental determinants of fungal community structure, and equine ocular health.
Additional Links: PMID-42791770
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PubMed:
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@article {pmid42791770,
year = {2026},
author = {Magalhães, MT and Abreu, ME and Nunes, M and Pascoal, P and Pereira, M and Dias, R and Rosa, T and Delgado, E and Oliveira, M and Lamas, LP},
title = {Characterization of the Healthy Ocular Mycobiome of Purebred Lusitano Horses Using Oxford Nanopore Long-Read Sequencing.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {18},
pages = {},
doi = {10.3390/ani16182913},
pmid = {42791770},
issn = {2076-2615},
support = {//Centro de Investigação Interdisciplinar em Sanidade Animal/ ; },
abstract = {The ocular surface represents a unique microbial ecosystem continuously exposed to environmental microorganisms; however, the fungal component of the healthy equine ocular microbiome remains poorly characterized. This study aimed to characterize the ocular surface mycobiome of 12 clinically healthy Purebred Lusitano horses from three geographical regions in Portugal kept in two housing systems using Oxford Nanopore long-read sequencing and conventional fungal culture. Sequencing revealed a highly diverse fungal community with marked inter-individual variability. The most abundant genera were Wallemia, Podosphaera, Debaromyces, Aspergillus, Filobasidium, Kurtzmaniella, Metschnikowia, Malassezia and Spathaspora. Patterns of fungal community composition suggested that local environmental conditions may contribute to the observed inter-individual variability. Genera commonly associated with equine fungal keratitis, including Aspergillus, Fusarium and Penicillium, were detected in healthy horses irrespective of housing system. Overall, the healthy equine ocular surface was characterized by a diverse mycobiome dominated by environmentally associated fungi. There findings provide a baseline for future studies investigating ocular microbial dysbiosis, environmental determinants of fungal community structure, and equine ocular health.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Global Research Trends and the Association Between Feed Efficiency and Enteric Methane Emissions in Ruminants: A Bibliometric and Thematic Review.
Animals : an open access journal from MDPI, 16(18): pii:ani16182957.
Enteric methane emissions and feed efficiency are increasingly being investigated as complementary traits for improving the environmental sustainability and productivity of ruminant systems. This study conducted a bibliometric and thematic review of scientific literature published between 2016 and 2025 to characterize research trends and synthesize evidence on the association between feed efficiency and enteric methane emissions in ruminants. Publications retrieved from Scopus and Web of Science were analyzed using Bibliometrix and VOSviewer, including scientific production, collaboration networks, keyword co-occurrence, thematic evolution, and burst analyses. A total of 659 publications from 158 sources were identified, with an annual growth rate of 13.97% and 40.36% international co-authorship. Scientific production increased from 37 publications in 2016 to 120 in 2025. Thematic analyses revealed a transition from the characterization of feed-efficiency and methane traits toward integrated approaches involving methane mitigation, nutrient utilization, rumen microbiology, genomics, and precision phenotyping. Evidence indicates that improved feed efficiency can contribute to lower absolute methane emissions, particularly through reduced feed intake, but does not consistently imply lower methane production relative to feed intake or productive output. Feed efficiency and methane emissions should therefore be considered complementary rather than interchangeable traits when developing sustainable breeding, nutritional, and management strategies.
Additional Links: PMID-42791812
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PubMed:
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@article {pmid42791812,
year = {2026},
author = {Botelho, ET and Santos, KFD and Barroso, LL and Cordeiro, MJP and Sousa, LT and Guimarães, BAF and Souza, HF and Sousa, AR and Nunes, GB and Gonçalves, LF and Santos, JGA and Ferreira, J},
title = {Global Research Trends and the Association Between Feed Efficiency and Enteric Methane Emissions in Ruminants: A Bibliometric and Thematic Review.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {18},
pages = {},
doi = {10.3390/ani16182957},
pmid = {42791812},
issn = {2076-2615},
abstract = {Enteric methane emissions and feed efficiency are increasingly being investigated as complementary traits for improving the environmental sustainability and productivity of ruminant systems. This study conducted a bibliometric and thematic review of scientific literature published between 2016 and 2025 to characterize research trends and synthesize evidence on the association between feed efficiency and enteric methane emissions in ruminants. Publications retrieved from Scopus and Web of Science were analyzed using Bibliometrix and VOSviewer, including scientific production, collaboration networks, keyword co-occurrence, thematic evolution, and burst analyses. A total of 659 publications from 158 sources were identified, with an annual growth rate of 13.97% and 40.36% international co-authorship. Scientific production increased from 37 publications in 2016 to 120 in 2025. Thematic analyses revealed a transition from the characterization of feed-efficiency and methane traits toward integrated approaches involving methane mitigation, nutrient utilization, rumen microbiology, genomics, and precision phenotyping. Evidence indicates that improved feed efficiency can contribute to lower absolute methane emissions, particularly through reduced feed intake, but does not consistently imply lower methane production relative to feed intake or productive output. Feed efficiency and methane emissions should therefore be considered complementary rather than interchangeable traits when developing sustainable breeding, nutritional, and management strategies.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Optimized Organic Fertilization Mitigates Antibiotic Resistance Gene Dissemination in Manure-Amended Soils: A Field Study on Nutrient-Microbiome-Antibiotic Resistance Gene Nexus During Cabbage Reproductive Cycle.
Antibiotics (Basel, Switzerland), 15(9): pii:antibiotics15090821.
Background: Manure-amended agricultural soil is a critical reservoir of antibiotic resistance genes (ARGs), posing escalating threats to environmental health and food safety. However, the temporal trajectories of ARG prevalence throughout the complete reproductive cycle of cash crops, and their mechanistic linkages with fertilization regimes and microbial community succession, remain inadequately understood. Methods: To bridge this knowledge gap, we conducted an in situ field experiment over the entire growth period of Chinese cabbage at a long-term manure-amended farm in Tianjin, China. Six contrasting fertilization strategies were evaluated: unfertilized control (CK1), unfertilized baseline control (CK2), traditional full-rate combined manure-chemical fertilization (TF), traditional half-rate combined manure-chemical fertilization (T1), half-dose sole manure fertilizer (T2), and half-dose sole chemical fertilizer only (T3). Results: Our results demonstrated that ARG abundance and associated mobile genetic elements (MGEs) exhibited a pronounced transient surge immediately post-fertilization, yet reverted to baseline levels by harvest, revealing a tangible resilience of the soil resistome. Notably, the optimized half-organic fertilization (T2) effectively curtailed the proliferation of manure-derived pathogenic taxa while preserving beneficial keystone phyla (e.g., Acidobacteria and Proteobacteria), indicating a trade-off between nutrient provisioning and ecological filtering. Co-occurrence network analysis further identified MB-A2-108, Saccharimonadales, and Rokubacteriales as pivotal hosts for multidrug-resistant ARGs, underscoring that microbial interspecific interactions-rather than taxonomic richness alone-are the primary drivers of resistome succession. Quantitative risk assessment confirmed that the T2 regimen reduced the composite ARG contamination index (CFzone) by 25% relative to conventional full fertilization (TF), while maintaining comparable cabbage yields. Conclusions: Collectively, our findings advocate for precision organic fertilization as a nature-based solution that synchronizes nutrient supply with crop demand, curtails ARG propagation, and mitigates long-term agroecological risks.
Additional Links: PMID-42791971
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PubMed:
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@article {pmid42791971,
year = {2026},
author = {Wang, H and Zhang, K and Liu, M and Cheng, S and Cordeiro, CM and Sindhøj, E and Liang, J and Zeng, Y and Shen, S and Zhi, S},
title = {Optimized Organic Fertilization Mitigates Antibiotic Resistance Gene Dissemination in Manure-Amended Soils: A Field Study on Nutrient-Microbiome-Antibiotic Resistance Gene Nexus During Cabbage Reproductive Cycle.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {9},
pages = {},
doi = {10.3390/antibiotics15090821},
pmid = {42791971},
issn = {2079-6382},
support = {24YFZCSN00270//Tianjin Key Research and Development Program Project/ ; 2023YFD1702000//National Key Research and Development Plan Project/ ; 202402AE090032//Yunnan Science & Technology Planning Project/ ; //the Science and Technology Innovation Project of Chinese Academy of Agricultural Sciences./ ; 202301AT070245//Basic Research Program of Yunnan Province/ ; },
abstract = {Background: Manure-amended agricultural soil is a critical reservoir of antibiotic resistance genes (ARGs), posing escalating threats to environmental health and food safety. However, the temporal trajectories of ARG prevalence throughout the complete reproductive cycle of cash crops, and their mechanistic linkages with fertilization regimes and microbial community succession, remain inadequately understood. Methods: To bridge this knowledge gap, we conducted an in situ field experiment over the entire growth period of Chinese cabbage at a long-term manure-amended farm in Tianjin, China. Six contrasting fertilization strategies were evaluated: unfertilized control (CK1), unfertilized baseline control (CK2), traditional full-rate combined manure-chemical fertilization (TF), traditional half-rate combined manure-chemical fertilization (T1), half-dose sole manure fertilizer (T2), and half-dose sole chemical fertilizer only (T3). Results: Our results demonstrated that ARG abundance and associated mobile genetic elements (MGEs) exhibited a pronounced transient surge immediately post-fertilization, yet reverted to baseline levels by harvest, revealing a tangible resilience of the soil resistome. Notably, the optimized half-organic fertilization (T2) effectively curtailed the proliferation of manure-derived pathogenic taxa while preserving beneficial keystone phyla (e.g., Acidobacteria and Proteobacteria), indicating a trade-off between nutrient provisioning and ecological filtering. Co-occurrence network analysis further identified MB-A2-108, Saccharimonadales, and Rokubacteriales as pivotal hosts for multidrug-resistant ARGs, underscoring that microbial interspecific interactions-rather than taxonomic richness alone-are the primary drivers of resistome succession. Quantitative risk assessment confirmed that the T2 regimen reduced the composite ARG contamination index (CFzone) by 25% relative to conventional full fertilization (TF), while maintaining comparable cabbage yields. Conclusions: Collectively, our findings advocate for precision organic fertilization as a nature-based solution that synchronizes nutrient supply with crop demand, curtails ARG propagation, and mitigates long-term agroecological risks.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Research Trends in Antimicrobial Oral Hygiene Products, the Oral Microbiome, and Dental Biofilm: A Bibliometric Analysis (2006-2025).
Antibiotics (Basel, Switzerland), 15(9): pii:antibiotics15090839.
Objective: This study aims to provide a global landscape of research into oral hygiene products with antimicrobial or microbiome-modulating activity through a comprehensive bibliometric analysis to identify trends and hotspots that may influence future research frontiers. Methods: A structured bibliographic search was conducted within the Web of Science Core Collection database from 2006 to 2025. Manual screening was performed to exclude duplicate records, studies that did not align with the core topic, and those failing to meet the predefined inclusion criteria. Bibliometric and visual analyses were performed using VOSviewer, CiteSpace, and the R package 'bibliometrix' to evaluate production metrics, citation networks, and multi-level collaboration patterns. Results: The analysis included 1007 publications. Sreenivasan PK was the most productive author, and Lundberg JO was the most cited. The United States, followed by India, Brazil, and China, led global research volume, while the United Kingdom and the Netherlands led in total citations. The International Journal of Dental Hygiene was the most productive journal (n = 48), and the Journal of Dentistry was the most cited (n = 1356). Burgeoning research hotspots include the impact of mouthwashes on the oral microbiome and systemic disorders, the controlled clinical use of chlorhexidine, and alternative formulations incorporating probiotics, herbal extracts, or hyaluronic acid. Conclusions: This study underscores a global shift in dental research priorities from traditional bacterial elimination toward preserving oral microbiota eubiosis. While chlorhexidine remains a subject of research due to its widespread use for therapeutic benefits, bibliometric research highlights its potential systemic consequences as a hotspot. Therefore, future research should focus on innovative antimicrobial formulations for mouthwashes and toothpastes that maintain oral health without causing dysbiosis.
Additional Links: PMID-42791989
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PubMed:
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@article {pmid42791989,
year = {2026},
author = {Baca-García, A and Baca, P and Abellán, A and Arias-Moliz, MT and Valderrama, P},
title = {Research Trends in Antimicrobial Oral Hygiene Products, the Oral Microbiome, and Dental Biofilm: A Bibliometric Analysis (2006-2025).},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {9},
pages = {},
doi = {10.3390/antibiotics15090839},
pmid = {42791989},
issn = {2079-6382},
support = {PID2023-149087NB-I00//Spanish State Research Agency/ ; },
abstract = {Objective: This study aims to provide a global landscape of research into oral hygiene products with antimicrobial or microbiome-modulating activity through a comprehensive bibliometric analysis to identify trends and hotspots that may influence future research frontiers. Methods: A structured bibliographic search was conducted within the Web of Science Core Collection database from 2006 to 2025. Manual screening was performed to exclude duplicate records, studies that did not align with the core topic, and those failing to meet the predefined inclusion criteria. Bibliometric and visual analyses were performed using VOSviewer, CiteSpace, and the R package 'bibliometrix' to evaluate production metrics, citation networks, and multi-level collaboration patterns. Results: The analysis included 1007 publications. Sreenivasan PK was the most productive author, and Lundberg JO was the most cited. The United States, followed by India, Brazil, and China, led global research volume, while the United Kingdom and the Netherlands led in total citations. The International Journal of Dental Hygiene was the most productive journal (n = 48), and the Journal of Dentistry was the most cited (n = 1356). Burgeoning research hotspots include the impact of mouthwashes on the oral microbiome and systemic disorders, the controlled clinical use of chlorhexidine, and alternative formulations incorporating probiotics, herbal extracts, or hyaluronic acid. Conclusions: This study underscores a global shift in dental research priorities from traditional bacterial elimination toward preserving oral microbiota eubiosis. While chlorhexidine remains a subject of research due to its widespread use for therapeutic benefits, bibliometric research highlights its potential systemic consequences as a hotspot. Therefore, future research should focus on innovative antimicrobial formulations for mouthwashes and toothpastes that maintain oral health without causing dysbiosis.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Building-Scale Wastewater Metagenomics Reveals Temporal Patterns in Resistance and Virulence Genes.
Antibiotics (Basel, Switzerland), 15(9): pii:antibiotics15090878.
Background/Objectives: Antimicrobial resistance (AMR) and virulence represent co-evolving dimensions of microbial pathogenic potential whose ecological organization in building-scale wastewater systems remains poorly understood. Methods: Using shotgun metagenomic sequencing, we characterized the temporal dynamics and ecological associations of antimicrobial resistance genes (ARGs) and virulence factors (VFs) in 12 wastewater grab samples (2 per semester) collected from a university residence hall designated for COVID-19 quarantine between 2021 and 2023. Results: The wastewater microbiome was anchored by a stable core of gut-associated anaerobic bacteria, with community composition exhibiting significant Spring-versus-Fall structuring and a year × semester interaction that explained 60% of the community variation. A marked shift toward opportunistic taxa, particularly Acinetobacter, during Fall 2023 represented the most pronounced temporal perturbation. Total ARG abundance remained stable across semesters, while resistome composition shifted significantly, indicating that temporal dynamics were driven by compositional turnover rather than changes in overall resistance burden. VF functional categories were broadly conserved across sampling periods, consistent with their structural embedding within the persistent fecal core microbiome. Correlation and network analyses revealed modular ecological coupling between resistance and virulence functional categories, with metal/co-resistance and fosfomycin classes showing the strongest associations with virulence functions. At the community level, a Benjamini-Hochberg-corrected co-occurrence network resolved into taxa-anchored resistance modules and separate virulence-function clusters, with Acinetobacter and fluoroquinolone resistance as the principal connectors. Conclusions: These findings indicate that building-scale wastewater metagenomics can capture ecologically structured functional gene dynamics, highlighting its potential as a surveillance tool for monitoring AMR and virulence in built environments.
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PubMed:
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@article {pmid42792028,
year = {2026},
author = {Morikwe, UC and Kiki, LC and Ezeanowai, FC and Hall, S and Bhatia, S and Maswanganye, TN and Jeje, O and Hill, MS and Graves, JL and Deng, D and Jeffers-Francis, L},
title = {Building-Scale Wastewater Metagenomics Reveals Temporal Patterns in Resistance and Virulence Genes.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {9},
pages = {},
doi = {10.3390/antibiotics15090878},
pmid = {42792028},
issn = {2079-6382},
support = {EEC-2133504//U.S. National Science Foundation/ ; },
abstract = {Background/Objectives: Antimicrobial resistance (AMR) and virulence represent co-evolving dimensions of microbial pathogenic potential whose ecological organization in building-scale wastewater systems remains poorly understood. Methods: Using shotgun metagenomic sequencing, we characterized the temporal dynamics and ecological associations of antimicrobial resistance genes (ARGs) and virulence factors (VFs) in 12 wastewater grab samples (2 per semester) collected from a university residence hall designated for COVID-19 quarantine between 2021 and 2023. Results: The wastewater microbiome was anchored by a stable core of gut-associated anaerobic bacteria, with community composition exhibiting significant Spring-versus-Fall structuring and a year × semester interaction that explained 60% of the community variation. A marked shift toward opportunistic taxa, particularly Acinetobacter, during Fall 2023 represented the most pronounced temporal perturbation. Total ARG abundance remained stable across semesters, while resistome composition shifted significantly, indicating that temporal dynamics were driven by compositional turnover rather than changes in overall resistance burden. VF functional categories were broadly conserved across sampling periods, consistent with their structural embedding within the persistent fecal core microbiome. Correlation and network analyses revealed modular ecological coupling between resistance and virulence functional categories, with metal/co-resistance and fosfomycin classes showing the strongest associations with virulence functions. At the community level, a Benjamini-Hochberg-corrected co-occurrence network resolved into taxa-anchored resistance modules and separate virulence-function clusters, with Acinetobacter and fluoroquinolone resistance as the principal connectors. Conclusions: These findings indicate that building-scale wastewater metagenomics can capture ecologically structured functional gene dynamics, highlighting its potential as a surveillance tool for monitoring AMR and virulence in built environments.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Postbiotics and Paraprobiotics as Next-Generation Gut Microbiome Modulators in Sustainable Aquaculture Health.
Antibiotics (Basel, Switzerland), 15(9): pii:antibiotics15090887.
Widespread antibiotic use in aquaculture has increased selective pressure on resident bacterial communities, accelerating the emergence of resistance in key pathogens and raising concerns for animal health, environmental microbiomes, and food-chain safety. Reducing dependence on therapeutic antimicrobials requires alternative strategies that remain effective under the processing and biosafety constraints of intensive production systems, where recurrent bacterial diseases continue to cause substantial economic losses. Live probiotics, currently the most extensively studied microbiome-based intervention, have practical limitations, including reduced viability during feed pelleting and extrusion, transient gut colonization, strain-specific host responses, biosafety concerns related to horizontal transfer of antimicrobial-resistance genes, and variable regulatory requirements across regions. Postbiotics, defined as preparations of non-viable microbial biomass, with or without metabolites, that confer a demonstrated health benefit in the target host, and paraprobiotics, which emphasize inactivated whole-cell preparations that preserve surface-associated microbial molecular patterns, may help address several of these constraints. These approaches offer improved compositional definition, greater feed-processing stability, and a potentially more favorable biosafety profile. Because they are non-viable, their anti-pathogen effects do not depend on growth or competitive colonization but may instead involve preformed antimicrobial compounds retained in some preparations, interference with pathogen attachment, modulation of the intestinal environment, reinforcement of barrier function, and stimulation of host immune responses. This review synthesizes current evidence on postbiotics and paraprobiotics in aquaculture, with emphasis on structural classification, pattern-recognition receptor signaling, intestinal barrier function, innate immune priming, encapsulation technologies, and translational readiness. Taken together, available evidence supports postbiotics and paraprobiotics as promising, but not yet fully characterized, alternatives to live probiotics within antibiotic-reduction strategies for aquaculture. Progress toward commercial application will depend on resolving key questions related to dose-response relationships, processing stability in formulated feeds, and species-specific efficacy.
Additional Links: PMID-42792037
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PubMed:
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@article {pmid42792037,
year = {2026},
author = {Linh, NV and Khang, LTP and Permpoonpattana, P and Dinh-Hung, N},
title = {Postbiotics and Paraprobiotics as Next-Generation Gut Microbiome Modulators in Sustainable Aquaculture Health.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {9},
pages = {},
doi = {10.3390/antibiotics15090887},
pmid = {42792037},
issn = {2079-6382},
support = {//Prince of Songkla University/ ; },
abstract = {Widespread antibiotic use in aquaculture has increased selective pressure on resident bacterial communities, accelerating the emergence of resistance in key pathogens and raising concerns for animal health, environmental microbiomes, and food-chain safety. Reducing dependence on therapeutic antimicrobials requires alternative strategies that remain effective under the processing and biosafety constraints of intensive production systems, where recurrent bacterial diseases continue to cause substantial economic losses. Live probiotics, currently the most extensively studied microbiome-based intervention, have practical limitations, including reduced viability during feed pelleting and extrusion, transient gut colonization, strain-specific host responses, biosafety concerns related to horizontal transfer of antimicrobial-resistance genes, and variable regulatory requirements across regions. Postbiotics, defined as preparations of non-viable microbial biomass, with or without metabolites, that confer a demonstrated health benefit in the target host, and paraprobiotics, which emphasize inactivated whole-cell preparations that preserve surface-associated microbial molecular patterns, may help address several of these constraints. These approaches offer improved compositional definition, greater feed-processing stability, and a potentially more favorable biosafety profile. Because they are non-viable, their anti-pathogen effects do not depend on growth or competitive colonization but may instead involve preformed antimicrobial compounds retained in some preparations, interference with pathogen attachment, modulation of the intestinal environment, reinforcement of barrier function, and stimulation of host immune responses. This review synthesizes current evidence on postbiotics and paraprobiotics in aquaculture, with emphasis on structural classification, pattern-recognition receptor signaling, intestinal barrier function, innate immune priming, encapsulation technologies, and translational readiness. Taken together, available evidence supports postbiotics and paraprobiotics as promising, but not yet fully characterized, alternatives to live probiotics within antibiotic-reduction strategies for aquaculture. Progress toward commercial application will depend on resolving key questions related to dose-response relationships, processing stability in formulated feeds, and species-specific efficacy.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Antimicrobial Resistance and Associated Genetic Determinants of Aliivibrio Colonizing the Gastrointestinal Tract of Farmed Atlantic Salmon (Salmo salar L.).
Antibiotics (Basel, Switzerland), 15(9): pii:antibiotics15090888.
BACKGROUND/OBJECTIVES: Currently, readily available data on antimicrobial resistance in bacteria colonizing farmed Atlantic salmon (Salmo salar L.) are limited. Recent data indicate that the gastrointestinal tract mucosa of adult Atlantic salmon farmed in Tasmania (Australia) is consistently colonized by Aliivibrio species. Aliivibrio and other Vibrionaceae may contribute to gut dysbiosis through overgrowth. We investigated Aliivibrio isolates and other Aliivibrio species to link antimicrobial resistance (AMR) phenotypes with the presence of antimicrobial resistance genes (ARGs).
METHODS: We performed antimicrobial susceptibility testing on Atlantic salmon bacterial isolates (n = 50). We surveyed ARGs in representative genome-sequenced strains (n = 21) and across the genus Aliivibrio (n = 112 strains) using a range of bioinformatic approaches.
RESULTS: Salmon Aliivibrio isolates had high MIC values for multiple antimicrobial drug classes (penams, tetracyclines, sulfonamides, macrolides, and aminoglycosides), including antimicrobials important for aquaculture prophylaxis. The greatest susceptibility was observed for chloramphenicol, oxolinic acid, ciprofloxacin, rifampicin, meropenem, trimethoprim, and trimethoprim-sulfamethoxazole. Provisional analysis suggests that the resistance profile of Aliivibrio isolates matches a core set of predicted ARGs common to the genus Aliivibrio. Among the isolates, plasmids and integrons did not include genes similar to known ARGs. Based on available genome data, strains of several Aliivibrio species carried predicted ARGs on integrons, including genes providing potential resistance to chloramphenicol (cpt, catB), tetracyclines (tetE), sulfonamides (sul2), and trimethoprim (dfrA1).
CONCLUSIONS: Based on these results, we estimated provisional epidemiological cutoff values for several antimicrobials for Aliivibrio isolates predominant in Atlantic salmon farmed in Tasmania. Furthermore, available data show no evidence that plasmid- or integron-associated ARGs are prevalent and suggest that they are, overall, uncommon in the genus Aliivibrio. The data presented provide a foundation for monitoring AMR in Atlantic salmon gut-associated commensal bacteria.
Additional Links: PMID-42792038
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PubMed:
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@article {pmid42792038,
year = {2026},
author = {Hamlett, JK and Bowman, JP},
title = {Antimicrobial Resistance and Associated Genetic Determinants of Aliivibrio Colonizing the Gastrointestinal Tract of Farmed Atlantic Salmon (Salmo salar L.).},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {9},
pages = {},
doi = {10.3390/antibiotics15090888},
pmid = {42792038},
issn = {2079-6382},
abstract = {BACKGROUND/OBJECTIVES: Currently, readily available data on antimicrobial resistance in bacteria colonizing farmed Atlantic salmon (Salmo salar L.) are limited. Recent data indicate that the gastrointestinal tract mucosa of adult Atlantic salmon farmed in Tasmania (Australia) is consistently colonized by Aliivibrio species. Aliivibrio and other Vibrionaceae may contribute to gut dysbiosis through overgrowth. We investigated Aliivibrio isolates and other Aliivibrio species to link antimicrobial resistance (AMR) phenotypes with the presence of antimicrobial resistance genes (ARGs).
METHODS: We performed antimicrobial susceptibility testing on Atlantic salmon bacterial isolates (n = 50). We surveyed ARGs in representative genome-sequenced strains (n = 21) and across the genus Aliivibrio (n = 112 strains) using a range of bioinformatic approaches.
RESULTS: Salmon Aliivibrio isolates had high MIC values for multiple antimicrobial drug classes (penams, tetracyclines, sulfonamides, macrolides, and aminoglycosides), including antimicrobials important for aquaculture prophylaxis. The greatest susceptibility was observed for chloramphenicol, oxolinic acid, ciprofloxacin, rifampicin, meropenem, trimethoprim, and trimethoprim-sulfamethoxazole. Provisional analysis suggests that the resistance profile of Aliivibrio isolates matches a core set of predicted ARGs common to the genus Aliivibrio. Among the isolates, plasmids and integrons did not include genes similar to known ARGs. Based on available genome data, strains of several Aliivibrio species carried predicted ARGs on integrons, including genes providing potential resistance to chloramphenicol (cpt, catB), tetracyclines (tetE), sulfonamides (sul2), and trimethoprim (dfrA1).
CONCLUSIONS: Based on these results, we estimated provisional epidemiological cutoff values for several antimicrobials for Aliivibrio isolates predominant in Atlantic salmon farmed in Tasmania. Furthermore, available data show no evidence that plasmid- or integron-associated ARGs are prevalent and suggest that they are, overall, uncommon in the genus Aliivibrio. The data presented provide a foundation for monitoring AMR in Atlantic salmon gut-associated commensal bacteria.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Glycerol Monolaurate Supplementation in Extruded Diets Enhances Immune Function and Antioxidant Capacity and Alters the Gut Microbiota and Fecal Metabolome in Cats.
Antioxidants (Basel, Switzerland), 15(9): pii:antiox15091169.
This study evaluated the effects of dietary glycerol monolaurate (GML) supplementation on feline growth performance and intestinal health. Twenty-four adult British Shorthair cats (3.03 ± 0.07 kg) were initially enrolled. Following a 56-day pre-feeding period, 18 eligible cats were allocated to two dietary groups, of which 12 cats were prespecified for final sample collection and statistical analysis (n = 6): a control group (CON, basal diet) and an experimental group (EXP, basal diet + 2000 mg/kg GML product) for a 28-day trial. Dietary GML significantly increased the average daily feed intake. GML supplementation significantly increased the changes in fecal score and fecal pH, and a significant GML × day interaction was observed for the change in fecal pH. GML improved the apparent digestibility of dry matter, gross energy, crude fat, and crude protein. Furthermore, serum albumin increased within the normal range. Cats in the EXP group showed elevated antioxidant enzyme activities, alongside lower malondialdehyde concentrations. GML also elevated serum immunoglobulin A and reduced pro-inflammatory cytokines. Fecal analyses showed reduced acetic acid and total volatile fatty acids, but elevated propionic acid. Microbiome and metabolomic profiling revealed that GML decreased the relative abundance of Streptococcus and metabolites such as Linoleic Acid and 12,13-Epome, while increasing the relative abundances of Collinsella, Peptoclostridium, Clostridium, and (-)-Jasmonic Acid. These findings provide a theoretical foundation for applying GML in pet foods to optimize companion animal extruded diets.
Additional Links: PMID-42792208
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PubMed:
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@article {pmid42792208,
year = {2026},
author = {Jiang, H and Liu, B and Zhang, J and Ge, X and Jin, Z and Han, S and Liu, S},
title = {Glycerol Monolaurate Supplementation in Extruded Diets Enhances Immune Function and Antioxidant Capacity and Alters the Gut Microbiota and Fecal Metabolome in Cats.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {15},
number = {9},
pages = {},
doi = {10.3390/antiox15091169},
pmid = {42792208},
issn = {2076-3921},
abstract = {This study evaluated the effects of dietary glycerol monolaurate (GML) supplementation on feline growth performance and intestinal health. Twenty-four adult British Shorthair cats (3.03 ± 0.07 kg) were initially enrolled. Following a 56-day pre-feeding period, 18 eligible cats were allocated to two dietary groups, of which 12 cats were prespecified for final sample collection and statistical analysis (n = 6): a control group (CON, basal diet) and an experimental group (EXP, basal diet + 2000 mg/kg GML product) for a 28-day trial. Dietary GML significantly increased the average daily feed intake. GML supplementation significantly increased the changes in fecal score and fecal pH, and a significant GML × day interaction was observed for the change in fecal pH. GML improved the apparent digestibility of dry matter, gross energy, crude fat, and crude protein. Furthermore, serum albumin increased within the normal range. Cats in the EXP group showed elevated antioxidant enzyme activities, alongside lower malondialdehyde concentrations. GML also elevated serum immunoglobulin A and reduced pro-inflammatory cytokines. Fecal analyses showed reduced acetic acid and total volatile fatty acids, but elevated propionic acid. Microbiome and metabolomic profiling revealed that GML decreased the relative abundance of Streptococcus and metabolites such as Linoleic Acid and 12,13-Epome, while increasing the relative abundances of Collinsella, Peptoclostridium, Clostridium, and (-)-Jasmonic Acid. These findings provide a theoretical foundation for applying GML in pet foods to optimize companion animal extruded diets.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Probiotics and Extracellular Vesicles as Redox Modulators in Wound Healing: From Microbial Therapeutics to Engineered Nanotherapeutic Strategies.
Antioxidants (Basel, Switzerland), 15(9): pii:antiox15091172.
Chronic wounds are characterized by prolonged inflammation, excess oxidative stress, unregulated angiogenesis, and faulty tissue regeneration that are associated with slow wound healing and poor clinical outcomes. Reactive oxygen species (ROS) signaling deregulation is involved in the pathway of chronic wound pathophysiology, altering redox balance, augmenting the inflammatory response, and inhibiting the cellular response. In this review, a structured literature search and evidence-screening process was used to synthesize evidence on probiotics, EVs, and engineered EVs derived from probiotics in the context of wound healing. Studies suggest that EVs from probiotics may impact redox-sensitive processes of wound healing, including changes associated with Nrf2/HO-1, NF-κB signaling, modulation of mitochondrial ROS, macrophage polarization, and repair of the epithelial barrier. Many of these mechanistic links are derived from pathway-based markers or indirect experiments, however, and will need further mechanistic validation. Probiotic-EVs may offer potential advantages over traditional antioxidant delivery and mammalian-EV systems, including being cell-free, compatible with the microbiome, and easy to engineer. Recent progress in synthetic biology, cargo loading, biomaterial-assisted delivery systems, and ROS-responsive platforms may enable engineered probiotic-EVs to serve as programmable redox nanotherapies. However, major issues regarding EV standardization, biosafety, biodistribution, pharmacokinetics, and clinical validation remain unresolved. Importantly, the evidence for the application of probiotic-derived EVs to wound healing is predominantly preclinical, and there is a lack of direct clinical evidence to date. Collectively, EVs secreted from probiotics might hold potential for chronic wound care and redox-oriented regenerative medicine as a therapeutic platform.
Additional Links: PMID-42792211
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PubMed:
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@article {pmid42792211,
year = {2026},
author = {Wang, AYL and Aviña, AE and Lin, JT and Liu, YY and Lin, MH and Kao, HK},
title = {Probiotics and Extracellular Vesicles as Redox Modulators in Wound Healing: From Microbial Therapeutics to Engineered Nanotherapeutic Strategies.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {15},
number = {9},
pages = {},
doi = {10.3390/antiox15091172},
pmid = {42792211},
issn = {2076-3921},
support = {NSTC 112-2314-B-182A-045-MY3//National Science and Technology Council/ ; },
abstract = {Chronic wounds are characterized by prolonged inflammation, excess oxidative stress, unregulated angiogenesis, and faulty tissue regeneration that are associated with slow wound healing and poor clinical outcomes. Reactive oxygen species (ROS) signaling deregulation is involved in the pathway of chronic wound pathophysiology, altering redox balance, augmenting the inflammatory response, and inhibiting the cellular response. In this review, a structured literature search and evidence-screening process was used to synthesize evidence on probiotics, EVs, and engineered EVs derived from probiotics in the context of wound healing. Studies suggest that EVs from probiotics may impact redox-sensitive processes of wound healing, including changes associated with Nrf2/HO-1, NF-κB signaling, modulation of mitochondrial ROS, macrophage polarization, and repair of the epithelial barrier. Many of these mechanistic links are derived from pathway-based markers or indirect experiments, however, and will need further mechanistic validation. Probiotic-EVs may offer potential advantages over traditional antioxidant delivery and mammalian-EV systems, including being cell-free, compatible with the microbiome, and easy to engineer. Recent progress in synthetic biology, cargo loading, biomaterial-assisted delivery systems, and ROS-responsive platforms may enable engineered probiotic-EVs to serve as programmable redox nanotherapies. However, major issues regarding EV standardization, biosafety, biodistribution, pharmacokinetics, and clinical validation remain unresolved. Importantly, the evidence for the application of probiotic-derived EVs to wound healing is predominantly preclinical, and there is a lack of direct clinical evidence to date. Collectively, EVs secreted from probiotics might hold potential for chronic wound care and redox-oriented regenerative medicine as a therapeutic platform.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Guanidinoacetic Acid and Cysteamine Hydrochloride Improve Beef Cattle Growth and Antioxidant Capacity via Fecal Microbiome and Serum Metabolome.
Antioxidants (Basel, Switzerland), 15(9): pii:antiox15091178.
Balancing muscle growth and antioxidant/anti-inflammatory homeostasis is a core requirement for modern beef production. This study investigated whether cysteamine hydrochloride (CSH) co-supplementation with guanidinoacetic acid (GAA) enhances growth and antioxidant status through fecal microbiome and serum metabolome modulation in Simmental beef cattle. A 60-day trial randomly assigned 45 10-month-old cattle to control (CON), GAA-supplemented, and GAA + CSH-supplemented groups (n = 15 per group). Growth performance was recorded throughout the trial. Fecal samples were collected for 16S rRNA sequencing, and serum samples for non-targeted metabolomics. Both GAA and GAA + CSH (GCSH) improved growth performance versus CON (p < 0.05), with no differences between supplemented groups. However, GCSH uniquely elevated antioxidant enzymes and reduced malondialdehyde (p < 0.05). GCSH treatment was associated with higher abundance of Adlercreutzia, Anaerofustis, and Monoglobus, alongside elevated indole-3-propionic acid and salicylsulfuric acid. In contrast, GAA reduced phenylacetyl-L-glutamine and indole-3-acetic acid. iCAMP analysis revealed that GCSH relieved homogenizing selection while enhancing heterogeneous selection, promoting beneficial taxa colonization. GAA primarily enhances nitrogen utilization, while CSH enriches beneficial microbiota and antioxidant metabolites. These findings suggest that GAA and CSH co-supplementation improves growth and antioxidant homeostasis through complementary mechanisms.
Additional Links: PMID-42792217
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PubMed:
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@article {pmid42792217,
year = {2026},
author = {Feng, B and Zhang, H and Guo, J and Tan, M and Mao, S and Yu, B and Xu, Y and Wang, Y and Feng, M and Song, L and Zhou, Y and Xu, H},
title = {Guanidinoacetic Acid and Cysteamine Hydrochloride Improve Beef Cattle Growth and Antioxidant Capacity via Fecal Microbiome and Serum Metabolome.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {15},
number = {9},
pages = {},
doi = {10.3390/antiox15091178},
pmid = {42792217},
issn = {2076-3921},
support = {264Z6601G//the Central Government Guides Local Science and Technology Development Fund Project-Key Technology Integration, Innovation, and Demonstration for Efficient Ecological Beef Cattle Farm-ing/ ; },
abstract = {Balancing muscle growth and antioxidant/anti-inflammatory homeostasis is a core requirement for modern beef production. This study investigated whether cysteamine hydrochloride (CSH) co-supplementation with guanidinoacetic acid (GAA) enhances growth and antioxidant status through fecal microbiome and serum metabolome modulation in Simmental beef cattle. A 60-day trial randomly assigned 45 10-month-old cattle to control (CON), GAA-supplemented, and GAA + CSH-supplemented groups (n = 15 per group). Growth performance was recorded throughout the trial. Fecal samples were collected for 16S rRNA sequencing, and serum samples for non-targeted metabolomics. Both GAA and GAA + CSH (GCSH) improved growth performance versus CON (p < 0.05), with no differences between supplemented groups. However, GCSH uniquely elevated antioxidant enzymes and reduced malondialdehyde (p < 0.05). GCSH treatment was associated with higher abundance of Adlercreutzia, Anaerofustis, and Monoglobus, alongside elevated indole-3-propionic acid and salicylsulfuric acid. In contrast, GAA reduced phenylacetyl-L-glutamine and indole-3-acetic acid. iCAMP analysis revealed that GCSH relieved homogenizing selection while enhancing heterogeneous selection, promoting beneficial taxa colonization. GAA primarily enhances nitrogen utilization, while CSH enriches beneficial microbiota and antioxidant metabolites. These findings suggest that GAA and CSH co-supplementation improves growth and antioxidant homeostasis through complementary mechanisms.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Combined Probiotics and Antioxidants Attenuate LPS-Induced Acute Intestinal Inflammation via Multi-Pathway Regulation in a Preventive Mouse Model.
Antioxidants (Basel, Switzerland), 15(9): pii:antiox15091201.
Objectives: This study aimed to explore the combined regulatory effects of probiotics combined with bioactive compounds on intestinal immunity and mucosal barrier function. Methods: Fifty specific-pathogen-free (SPF) male Kunming mice (5-6 weeks old, weighing 20 ± 2 g) were randomly assigned to five groups (n = 10 per group): blank control (C), lipopolysaccharide-induced model (LPS), probiotic (PB), antioxidant (AO), and combined treatment (PB/AO). The C and LPS groups received daily oral gavage of 0.5 mL sterile 0.9% saline. The PB group received a daily gavage of 1 × 10[8] CFU/mL Pediococcus acidilactici lindner and Lactobacillus plantarum. The AO group was administered a daily gavage of berberine (30 mg/kg BW), wogonin (30 mg/kg BW), and sodium butyrate (200 mg/kg BW). The PB/AO group received a daily gavage combining the probiotic mixture (1 × 10[8] CFU/mL) with the plant extracts (30 mg/kg BW berberine, 30 mg/kg BW wogonin, and 200 mg/kg BW sodium butyrate). Following a 14-day preventive intervention, all groups except C were intraperitoneally injected with LPS to induce inflammation. Indices of visceral organs, serum antioxidant and immune parameters, ileal histomorphology, gut microbiota composition, and the expression of key barrier- and inflammation-related genes were comprehensively evaluated. Results: LPS exposure increased liver and spleen coefficients. PB/AO treatment significantly reduced the LPS-induced elevation of liver coefficient to a level comparable to that of the C group; however, no significant improvement in spleen coefficient was observed. In terms of antioxidant and immune indices, all intervention groups increased the levels of SOD, GSH-Px, and T-AOC to varying degrees, and decreased the levels of MDA and inflammatory factors (TNF-α, IL-1β, IL-6, and DAO), with the PB/AO group showing the most significant improvement (p < 0.01). Ileal microbiome analysis showed that PB/AO treatment enriched Firmicutes, Lactococcus and Lactobacillus but decreased Proteobacteria, with Clostridia as signature taxa. Mechanistically, PB/AO suppressed the transcription of NF-κB pathway-related genes (TLR4, MyD88 and NF-κB) and upregulated the expression of tight junction proteins (ZO-1, Claudin-1 and Occludin), thereby strengthening the intestinal barrier. Conclusions: In conclusion, co-administration of microbial probiotics and antioxidants achieves optimal protection against LPS-induced intestinal inflammation by jointly driving anti-inflammatory and antioxidative responses, modulating gut microbiota, and reinforcing barrier integrity.
Additional Links: PMID-42792239
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PubMed:
Citation:
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@article {pmid42792239,
year = {2026},
author = {Gao, J and Tuo, Y and An, J and Abudukaiyoumu, K and Yi, Y and Yang, Y and Guo, T},
title = {Combined Probiotics and Antioxidants Attenuate LPS-Induced Acute Intestinal Inflammation via Multi-Pathway Regulation in a Preventive Mouse Model.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {15},
number = {9},
pages = {},
doi = {10.3390/antiox15091201},
pmid = {42792239},
issn = {2076-3921},
support = {2022B02042-4//Key Research and Development Program Project of the Xinjiang Uygur Autonomous Region/ ; XJARS-11-01//Modern Agricultural Industry Technology System of Xinjiang Uygur Autonomous Region/ ; },
abstract = {Objectives: This study aimed to explore the combined regulatory effects of probiotics combined with bioactive compounds on intestinal immunity and mucosal barrier function. Methods: Fifty specific-pathogen-free (SPF) male Kunming mice (5-6 weeks old, weighing 20 ± 2 g) were randomly assigned to five groups (n = 10 per group): blank control (C), lipopolysaccharide-induced model (LPS), probiotic (PB), antioxidant (AO), and combined treatment (PB/AO). The C and LPS groups received daily oral gavage of 0.5 mL sterile 0.9% saline. The PB group received a daily gavage of 1 × 10[8] CFU/mL Pediococcus acidilactici lindner and Lactobacillus plantarum. The AO group was administered a daily gavage of berberine (30 mg/kg BW), wogonin (30 mg/kg BW), and sodium butyrate (200 mg/kg BW). The PB/AO group received a daily gavage combining the probiotic mixture (1 × 10[8] CFU/mL) with the plant extracts (30 mg/kg BW berberine, 30 mg/kg BW wogonin, and 200 mg/kg BW sodium butyrate). Following a 14-day preventive intervention, all groups except C were intraperitoneally injected with LPS to induce inflammation. Indices of visceral organs, serum antioxidant and immune parameters, ileal histomorphology, gut microbiota composition, and the expression of key barrier- and inflammation-related genes were comprehensively evaluated. Results: LPS exposure increased liver and spleen coefficients. PB/AO treatment significantly reduced the LPS-induced elevation of liver coefficient to a level comparable to that of the C group; however, no significant improvement in spleen coefficient was observed. In terms of antioxidant and immune indices, all intervention groups increased the levels of SOD, GSH-Px, and T-AOC to varying degrees, and decreased the levels of MDA and inflammatory factors (TNF-α, IL-1β, IL-6, and DAO), with the PB/AO group showing the most significant improvement (p < 0.01). Ileal microbiome analysis showed that PB/AO treatment enriched Firmicutes, Lactococcus and Lactobacillus but decreased Proteobacteria, with Clostridia as signature taxa. Mechanistically, PB/AO suppressed the transcription of NF-κB pathway-related genes (TLR4, MyD88 and NF-κB) and upregulated the expression of tight junction proteins (ZO-1, Claudin-1 and Occludin), thereby strengthening the intestinal barrier. Conclusions: In conclusion, co-administration of microbial probiotics and antioxidants achieves optimal protection against LPS-induced intestinal inflammation by jointly driving anti-inflammatory and antioxidative responses, modulating gut microbiota, and reinforcing barrier integrity.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Monochromatic Blue Light Enhances Antioxidant Status and Remodels the Gut Microbiome in Association with Increased Plasma Melatonin in Broiler Chickens.
Antioxidants (Basel, Switzerland), 15(9): pii:antiox15091204.
The intestinal microbiome of broiler chickens has potential to regulate host health and growth performance. Although previous studies have revealed that the intestinal microbiota composition is affected by different factors including monochromatic light, the underlying mechanisms remain poorly understood, particularly regarding the causal role of light-sensitive hormones such as melatonin. To address this gap, a 2 × 4 factorial design was adopted in the present study, with two surgical treatments (sham-operation or pinealectomy) and four light conditions (white, blue, green, and red light), to investigate whether blue light modulates gut microbiota and antioxidant status through melatonin-dependent pathways. Broilers were reared under different monochromatic light conditions. On day 3 post-hatching, we ablated circulating melatonin production by conducting a pinealectomy or control sham-operation model. Accordingly, the broilers were assigned to eight groups: white light + sham-operation (WL), white light + pinealectomy (WP), blue light + sham-operation (BL), blue light + pinealectomy (BP), green light + sham-operation (GL), green light + pinealectomy (GP), red light + sham-operation (RL), and red light + pinealectomy (RP). On day 35, blue light was found to most effectively elevate plasma melatonin, which activated the Mel 1a/Nrf2/NQO1 pathway to reduce oxidative stress and remodel the jejunal microbiota. Metagenomic analysis identified Akkermansia muciniphila, Bifidobacterium longum and Ligilactobacillus aviarius as key bacteria enriched in blue light. Consequently, classes of microbiota-derived metabolites like stearidonic acid and indole propionic acid triggered the variation of tryptophan, bile acid and lipid metabolism, which contributed to broiler growth promotion. Moreover, pinealectomy accompanied by plasma melatonin deprivation significantly nullified the blue-light-induced effects. These insights confirm blue light is more effective in microbiota modulation by inducing melatonin secretion and providing a new strategy for light management in the broiler industry.
Additional Links: PMID-42792243
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PubMed:
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@article {pmid42792243,
year = {2026},
author = {Tang, W and Wang, Z and Dong, Y and Cao, J and Chen, Y},
title = {Monochromatic Blue Light Enhances Antioxidant Status and Remodels the Gut Microbiome in Association with Increased Plasma Melatonin in Broiler Chickens.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {15},
number = {9},
pages = {},
doi = {10.3390/antiox15091204},
pmid = {42792243},
issn = {2076-3921},
support = {32172801//National Natural Science Foundation of China/ ; 32372954//National Natural Science Foundation of China/ ; 32573308//National Natural Science Foundation of China/ ; },
abstract = {The intestinal microbiome of broiler chickens has potential to regulate host health and growth performance. Although previous studies have revealed that the intestinal microbiota composition is affected by different factors including monochromatic light, the underlying mechanisms remain poorly understood, particularly regarding the causal role of light-sensitive hormones such as melatonin. To address this gap, a 2 × 4 factorial design was adopted in the present study, with two surgical treatments (sham-operation or pinealectomy) and four light conditions (white, blue, green, and red light), to investigate whether blue light modulates gut microbiota and antioxidant status through melatonin-dependent pathways. Broilers were reared under different monochromatic light conditions. On day 3 post-hatching, we ablated circulating melatonin production by conducting a pinealectomy or control sham-operation model. Accordingly, the broilers were assigned to eight groups: white light + sham-operation (WL), white light + pinealectomy (WP), blue light + sham-operation (BL), blue light + pinealectomy (BP), green light + sham-operation (GL), green light + pinealectomy (GP), red light + sham-operation (RL), and red light + pinealectomy (RP). On day 35, blue light was found to most effectively elevate plasma melatonin, which activated the Mel 1a/Nrf2/NQO1 pathway to reduce oxidative stress and remodel the jejunal microbiota. Metagenomic analysis identified Akkermansia muciniphila, Bifidobacterium longum and Ligilactobacillus aviarius as key bacteria enriched in blue light. Consequently, classes of microbiota-derived metabolites like stearidonic acid and indole propionic acid triggered the variation of tryptophan, bile acid and lipid metabolism, which contributed to broiler growth promotion. Moreover, pinealectomy accompanied by plasma melatonin deprivation significantly nullified the blue-light-induced effects. These insights confirm blue light is more effective in microbiota modulation by inducing melatonin secretion and providing a new strategy for light management in the broiler industry.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Scoping Review on Traditional Fermented Cereals as Catalysts of Precision Nutrition: Mapping Evidence on Probiotic Activity, Gut Microbiota Modulation, and Human Health in Sub-Saharan Africa.
Biology, 15(18): pii:biology15181582.
Traditional fermented cereals are affordable, embedded foods that may provide viable microorganisms, fermentable substrates, and bioactive metabolites that can influence the gut microbiota and human physiology. However, evidence linking indigenous cereal fermentations in Sub-Saharan Africa (SSA) to microbiome-mediated health outcomes and precision nutrition applications remains limited. This scoping review mapped the types of traditional fermented cereal foods studied in SSA; their microbial communities and probiotic attributes; the reported effects on gut microbiota composition and function; the documented health outcomes; and the geographic gaps. The review followed the Arksey and O'Malley framework, subsequent methodological refinements, and the PRISMA-ScR reporting guideline. Searches were conducted in Scopus, PubMed, Web of Science, ScienceDirect, and Google Scholar from 2000 to mid-2026, complemented by citation searching. Eligible human, animals, and in vitro studies examined SSA-fermented cereal products and reported microbial, probiotic, gut microbiota, metabolite, or health-related outcomes. After deduplication and screening, 53 studies were included. The evidence was concentrated in SSA, particularly in cereal-based foods. Lactic acid bacteria and yeasts dominated reported fermentation communities, but strain-level validation, dose definition, and controlled human studies were uncommon. Evidence for direct gut-microbiota modulation and clinically important health effects was substantially weaker than evidence for food-level microbial diversity, in vitro probiotic properties, and improved nutrient bioaccessibility. Overall, traditional fermented cereals in sub-Saharan Africa demonstrate promising microbial, nutritional, and functional properties, but current evidence remains heterogeneous and insufficient to establish consistent effects on gut microbiota and human health. Further well-designed human studies integrating dietary, microbiome, and metabolic outcomes are needed to clarify their potential role in precision nutrition.
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@article {pmid42792528,
year = {2026},
author = {Olamiti, G},
title = {Scoping Review on Traditional Fermented Cereals as Catalysts of Precision Nutrition: Mapping Evidence on Probiotic Activity, Gut Microbiota Modulation, and Human Health in Sub-Saharan Africa.},
journal = {Biology},
volume = {15},
number = {18},
pages = {},
doi = {10.3390/biology15181582},
pmid = {42792528},
issn = {2079-7737},
support = {PDRF Programme (PR 48)//University of Venda/ ; },
abstract = {Traditional fermented cereals are affordable, embedded foods that may provide viable microorganisms, fermentable substrates, and bioactive metabolites that can influence the gut microbiota and human physiology. However, evidence linking indigenous cereal fermentations in Sub-Saharan Africa (SSA) to microbiome-mediated health outcomes and precision nutrition applications remains limited. This scoping review mapped the types of traditional fermented cereal foods studied in SSA; their microbial communities and probiotic attributes; the reported effects on gut microbiota composition and function; the documented health outcomes; and the geographic gaps. The review followed the Arksey and O'Malley framework, subsequent methodological refinements, and the PRISMA-ScR reporting guideline. Searches were conducted in Scopus, PubMed, Web of Science, ScienceDirect, and Google Scholar from 2000 to mid-2026, complemented by citation searching. Eligible human, animals, and in vitro studies examined SSA-fermented cereal products and reported microbial, probiotic, gut microbiota, metabolite, or health-related outcomes. After deduplication and screening, 53 studies were included. The evidence was concentrated in SSA, particularly in cereal-based foods. Lactic acid bacteria and yeasts dominated reported fermentation communities, but strain-level validation, dose definition, and controlled human studies were uncommon. Evidence for direct gut-microbiota modulation and clinically important health effects was substantially weaker than evidence for food-level microbial diversity, in vitro probiotic properties, and improved nutrient bioaccessibility. Overall, traditional fermented cereals in sub-Saharan Africa demonstrate promising microbial, nutritional, and functional properties, but current evidence remains heterogeneous and insufficient to establish consistent effects on gut microbiota and human health. Further well-designed human studies integrating dietary, microbiome, and metabolic outcomes are needed to clarify their potential role in precision nutrition.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Integrative Analysis of Gut Microbiota and Metabolome Reveals Health Benefits of Postbiotic Supplementation in Asian Seabass (Lates calcarifer).
Biology, 15(18): pii:biology15181605.
This study evaluated the effects of dietary SYNSEA Premium postbiotics on growth, immunity, disease resistance, intestinal microbiota, and host metabolism in Asian seabass (Lates calcarifer). Fish were fed a control diet or diets supplemented with heat-killed Lactiplantibacillus plantarum LP28, L. plantarum LP1008, and Bacillus subtilis at 10[8] (LSP) or 10[9] (HSP) cells kg[-1] diet for 56 days. Postbiotic supplementation did not significantly affect growth performance, feed efficiency, production, condition factor, or dorsal muscle composition, but significantly improved survival. Fish receiving postbiotics also exhibited higher survival following Vibrio alginolyticus and iridovirus challenges. These protective effects were accompanied by enhanced superoxide dismutase, phagocytic, and lysozyme activities and modulation of immune-related genes, including tgf-β1, tnf, ifn-γ1, c3, and mx. Exploratory microbiome and metabolome analyses, which were restricted to the control and LSP groups, identified differences in the relative abundance of specific intestinal microbial taxa and associations between microbial composition and host metabolic profiles. The LSP group showed lower relative abundances of potential pathogens such as Salmonella enterica, Lactococcus garvieae, and Staphylococcus warneri, although the overall microbial community structure did not differ significantly between groups. Metabolomic analysis of the LSP group further showed changes in D-glucose, pentose phosphate pathway intermediates, reduced glutathione, CoA, and 2-methylacetoacetyl-CoA relative to the control. Collectively, SYNSEA Premium improved survival, immune responses, and resistance to bacterial and viral infections without significantly affecting growth performance, while exploratory omics analysis of the LSP treatment identified associated microbial and metabolic changes.
Additional Links: PMID-42792551
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PubMed:
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@article {pmid42792551,
year = {2026},
author = {Huang, KC and Ballantyne, R and Chumpati, N and Punchanokkul, J and Tu, YL and Chang, HT and Lin, JS and Lee, JW and Kantha, P and Liu, CH},
title = {Integrative Analysis of Gut Microbiota and Metabolome Reveals Health Benefits of Postbiotic Supplementation in Asian Seabass (Lates calcarifer).},
journal = {Biology},
volume = {15},
number = {18},
pages = {},
doi = {10.3390/biology15181605},
pmid = {42792551},
issn = {2079-7737},
support = {NO NUMBER//SYNBIOTEC INC./ ; 113-2313-B-020 -007 -MY3//National Science and Technology Council/ ; },
abstract = {This study evaluated the effects of dietary SYNSEA Premium postbiotics on growth, immunity, disease resistance, intestinal microbiota, and host metabolism in Asian seabass (Lates calcarifer). Fish were fed a control diet or diets supplemented with heat-killed Lactiplantibacillus plantarum LP28, L. plantarum LP1008, and Bacillus subtilis at 10[8] (LSP) or 10[9] (HSP) cells kg[-1] diet for 56 days. Postbiotic supplementation did not significantly affect growth performance, feed efficiency, production, condition factor, or dorsal muscle composition, but significantly improved survival. Fish receiving postbiotics also exhibited higher survival following Vibrio alginolyticus and iridovirus challenges. These protective effects were accompanied by enhanced superoxide dismutase, phagocytic, and lysozyme activities and modulation of immune-related genes, including tgf-β1, tnf, ifn-γ1, c3, and mx. Exploratory microbiome and metabolome analyses, which were restricted to the control and LSP groups, identified differences in the relative abundance of specific intestinal microbial taxa and associations between microbial composition and host metabolic profiles. The LSP group showed lower relative abundances of potential pathogens such as Salmonella enterica, Lactococcus garvieae, and Staphylococcus warneri, although the overall microbial community structure did not differ significantly between groups. Metabolomic analysis of the LSP group further showed changes in D-glucose, pentose phosphate pathway intermediates, reduced glutathione, CoA, and 2-methylacetoacetyl-CoA relative to the control. Collectively, SYNSEA Premium improved survival, immune responses, and resistance to bacterial and viral infections without significantly affecting growth performance, while exploratory omics analysis of the LSP treatment identified associated microbial and metabolic changes.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Spatial Variation in Stream-Water Bacterial Communities Across Sites Differing in Wild Chinese Giant Salamander Detection Frequency.
Biology, 15(18): pii:biology15181647.
Wildlife monitoring and environmental microbiome profiling provide complementary perspectives for assessing habitats of protected aquatic species. This study integrated long-term computer vision monitoring, 16S rRNA amplicon sequencing, and water-quality measurements to examine stream sites differing in the camera-confirmed detection frequency of wild Chinese giant salamanders (Andrias davidianus). Monitoring from July 2024 to January 2026 recorded 47 independent detection events, of which 35 occurred at S1. S1 was therefore designated as the high-frequency detection site, while S2-S6 served as comparison sites. Stream-water bacterial communities were characterized from one composite sample per site, together with measurements of water temperature, pH, dissolved oxygen, conductivity, ammonia nitrogen, and nitrate nitrogen. S1 differed from several comparison sites in bacterial taxonomic composition, alpha-diversity estimates, and site-specific ASVs. Comamonadaceae, Rhodoferax, and Flavobacterium showed relatively high abundances at S1. However, RDA, envfit, Mantel, partial RDA, and variation-partitioning analyses found no significant independent relationship between the measured water-quality variables and bacterial-community variation. The observed spatial patterns likely reflect interactions among water quality, hydrology, substrate, riparian shading, refuge availability, organic-matter inputs, and anthropogenic disturbance. These results establish an exploratory spatial baseline and support the use of stream-water bacterial communities as a complementary component of Chinese giant salamander habitat monitoring.
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@article {pmid42792592,
year = {2026},
author = {Yang, X and Chen, J and Chen, S and Liu, S and Qiu, D and Qin, Z and Tuo, X and Chen, L and He, L},
title = {Spatial Variation in Stream-Water Bacterial Communities Across Sites Differing in Wild Chinese Giant Salamander Detection Frequency.},
journal = {Biology},
volume = {15},
number = {18},
pages = {},
doi = {10.3390/biology15181647},
pmid = {42792592},
issn = {2079-7737},
support = {MYK2025023//the Graduate Research and Innovation Project of Hubei University for Nationalities/ ; 2024WA064//the China University Industry-University-Research Innovation Fund-Intelligent Internet of Things Innovation Education Project/ ; },
abstract = {Wildlife monitoring and environmental microbiome profiling provide complementary perspectives for assessing habitats of protected aquatic species. This study integrated long-term computer vision monitoring, 16S rRNA amplicon sequencing, and water-quality measurements to examine stream sites differing in the camera-confirmed detection frequency of wild Chinese giant salamanders (Andrias davidianus). Monitoring from July 2024 to January 2026 recorded 47 independent detection events, of which 35 occurred at S1. S1 was therefore designated as the high-frequency detection site, while S2-S6 served as comparison sites. Stream-water bacterial communities were characterized from one composite sample per site, together with measurements of water temperature, pH, dissolved oxygen, conductivity, ammonia nitrogen, and nitrate nitrogen. S1 differed from several comparison sites in bacterial taxonomic composition, alpha-diversity estimates, and site-specific ASVs. Comamonadaceae, Rhodoferax, and Flavobacterium showed relatively high abundances at S1. However, RDA, envfit, Mantel, partial RDA, and variation-partitioning analyses found no significant independent relationship between the measured water-quality variables and bacterial-community variation. The observed spatial patterns likely reflect interactions among water quality, hydrology, substrate, riparian shading, refuge availability, organic-matter inputs, and anthropogenic disturbance. These results establish an exploratory spatial baseline and support the use of stream-water bacterial communities as a complementary component of Chinese giant salamander habitat monitoring.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Maternal Lactobacillus johnsonii Supplementation Is Associated with Altered Offspring Cecal Microbiome and Reduced Cockroach Allergen-Induced Airway Responses in Mice.
Biomedicines, 14(9): pii:biomedicines14091892.
Background: Early-life microbial exposures shape immune maturation and can influence later susceptibility to allergic airway disease. While probiotics can modulate host immunity, determining whether maternal probiotic supplementation alone promotes changes in offspring microbiomes and the immune functions that reduce allergic disease remains incompletely defined. Methods: Female mice were gavaged with Lactobacillus johnsonii (Lj) daily for 7 days prior to mating, and then twice weekly until delivery. Offspring were sensitized and challenged with cockroach allergen (CRA), beginning at 5 weeks of age, for 3 weeks to initiate asthmatic-type responses. Airway physiology (methacholine-induced airway hyperreactivity; AHR), lung-mucus-related gene expression (Muc5ac, Gob5), and lymph node restimulation responses were assessed. Results: Offspring from Lj-supplemented dams exhibited reduced AHR and decreased induction of Muc5ac and Gob5 following the final CRA challenge, accompanied by diminished Th cell cytokine production upon lymph node restimulation. Maternal Lj supplementation produced a significant shift in offspring cecal microbiome structure at 5 weeks, including altered phylum-level composition and a discrete set of significantly changed OTUs, including Akkermansia. PICRUSt2 analyses predicted coordinated differences in microbial metabolic potential across multiple pathways, consistent with functional reprogramming of the gut microbiome. Bone marrow dendritic cells (BMDC) derived from adult offspring of Lj-supplemented dams showed attenuated inflammatory programming after RSV or TLR7 stimulation, with reduced expression of innate immune cytokines compared to PBS-supplemented dams. Conclusions: The relatively long-term effects were associated with reduced allergic airway disease severity, supporting maternal probiotic supplementation as a potential strategy to lower offsprings' risk of allergic airway pathology.
Additional Links: PMID-42792635
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@article {pmid42792635,
year = {2026},
author = {Arzola Martínez, L and Ethridge, AD and Rasky, AJ and Morris, S and Yagi, K and Ptaschinski, C and Fonseca, W and Lukacs, NW},
title = {Maternal Lactobacillus johnsonii Supplementation Is Associated with Altered Offspring Cecal Microbiome and Reduced Cockroach Allergen-Induced Airway Responses in Mice.},
journal = {Biomedicines},
volume = {14},
number = {9},
pages = {},
doi = {10.3390/biomedicines14091892},
pmid = {42792635},
issn = {2227-9059},
support = {5P01AI089473-10/NH/NIH HHS/United States ; 5R01AI138348-05/NH/NIH HHS/United States ; },
abstract = {Background: Early-life microbial exposures shape immune maturation and can influence later susceptibility to allergic airway disease. While probiotics can modulate host immunity, determining whether maternal probiotic supplementation alone promotes changes in offspring microbiomes and the immune functions that reduce allergic disease remains incompletely defined. Methods: Female mice were gavaged with Lactobacillus johnsonii (Lj) daily for 7 days prior to mating, and then twice weekly until delivery. Offspring were sensitized and challenged with cockroach allergen (CRA), beginning at 5 weeks of age, for 3 weeks to initiate asthmatic-type responses. Airway physiology (methacholine-induced airway hyperreactivity; AHR), lung-mucus-related gene expression (Muc5ac, Gob5), and lymph node restimulation responses were assessed. Results: Offspring from Lj-supplemented dams exhibited reduced AHR and decreased induction of Muc5ac and Gob5 following the final CRA challenge, accompanied by diminished Th cell cytokine production upon lymph node restimulation. Maternal Lj supplementation produced a significant shift in offspring cecal microbiome structure at 5 weeks, including altered phylum-level composition and a discrete set of significantly changed OTUs, including Akkermansia. PICRUSt2 analyses predicted coordinated differences in microbial metabolic potential across multiple pathways, consistent with functional reprogramming of the gut microbiome. Bone marrow dendritic cells (BMDC) derived from adult offspring of Lj-supplemented dams showed attenuated inflammatory programming after RSV or TLR7 stimulation, with reduced expression of innate immune cytokines compared to PBS-supplemented dams. Conclusions: The relatively long-term effects were associated with reduced allergic airway disease severity, supporting maternal probiotic supplementation as a potential strategy to lower offsprings' risk of allergic airway pathology.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Diagnostic and Therapeutic Approaches in Periodontology: From Traditional Concepts to Modern Innovations.
Biomedicines, 14(9): pii:biomedicines14091916.
Objectives: To synthesize current evidence regarding advances in periodontal diagnosis and therapy, with emphasis on molecular biomarkers, omics technologies, microbiome profiling, digital imaging, and artificial intelligence-based analytical models that support the transition toward precision periodontology. Methods: This narrative review examines contemporary evidence on emerging molecular, microbiological, and digital technologies applied to periodontal diagnosis, prognostic assessment, and therapeutic planning. The review includes studies addressing salivary and gingival crevicular fluid biomarkers, microbiome characterization, omics approaches, cone-beam computed tomography, three-dimensional imaging, machine-learning algorithms, and personalized periodontal therapies. Relevant literature was identified through searches in major biomedical databases, including PubMed/MEDLINE, Scopus, and Web of Science, focusing on studies published on periodontal diagnostics, biomarkers, digital technologies, artificial intelligence, and precision medicine approaches in periodontology. Results: Peer-reviewed articles addressing innovative diagnostic and therapeutic approaches in periodontology were considered. Priority was given to studies evaluating clinical applicability, diagnostic performance, prognostic utility, and personalized treatment strategies integrating molecular and digital technologies. Conclusions: Emerging molecular and digital technologies are reshaping periodontal diagnosis and therapy by improving disease detection, risk prediction, and individualized treatment planning. Biomarkers, omics technologies, microbiome profiling, and artificial intelligence-assisted imaging may enhance diagnostic precision and clinical decision-making. These developments support the implementation of precision periodontology; however, challenges related to biomarker validation, algorithm standardization, cost, and accessibility remain barriers to routine clinical adoption. Further research is necessary to validate these approaches and facilitate their integration into periodontal practice. The integration of biomarkers, omics technologies, advanced imaging, and artificial intelligence may improve early periodontal diagnosis, prognostic assessment, and personalized treatment planning. These innovations support the transition toward precision periodontology and have the potential to enhance clinical decision-making, treatment outcomes, and long-term periodontal health in routine dental practice.
Additional Links: PMID-42792659
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@article {pmid42792659,
year = {2026},
author = {Chacón, T and Zuluaga-López, Ó and Sandoval-Llanos, GM and Piedrahita Posada, MC and Herrera-Serna, BY},
title = {Diagnostic and Therapeutic Approaches in Periodontology: From Traditional Concepts to Modern Innovations.},
journal = {Biomedicines},
volume = {14},
number = {9},
pages = {},
doi = {10.3390/biomedicines14091916},
pmid = {42792659},
issn = {2227-9059},
abstract = {Objectives: To synthesize current evidence regarding advances in periodontal diagnosis and therapy, with emphasis on molecular biomarkers, omics technologies, microbiome profiling, digital imaging, and artificial intelligence-based analytical models that support the transition toward precision periodontology. Methods: This narrative review examines contemporary evidence on emerging molecular, microbiological, and digital technologies applied to periodontal diagnosis, prognostic assessment, and therapeutic planning. The review includes studies addressing salivary and gingival crevicular fluid biomarkers, microbiome characterization, omics approaches, cone-beam computed tomography, three-dimensional imaging, machine-learning algorithms, and personalized periodontal therapies. Relevant literature was identified through searches in major biomedical databases, including PubMed/MEDLINE, Scopus, and Web of Science, focusing on studies published on periodontal diagnostics, biomarkers, digital technologies, artificial intelligence, and precision medicine approaches in periodontology. Results: Peer-reviewed articles addressing innovative diagnostic and therapeutic approaches in periodontology were considered. Priority was given to studies evaluating clinical applicability, diagnostic performance, prognostic utility, and personalized treatment strategies integrating molecular and digital technologies. Conclusions: Emerging molecular and digital technologies are reshaping periodontal diagnosis and therapy by improving disease detection, risk prediction, and individualized treatment planning. Biomarkers, omics technologies, microbiome profiling, and artificial intelligence-assisted imaging may enhance diagnostic precision and clinical decision-making. These developments support the implementation of precision periodontology; however, challenges related to biomarker validation, algorithm standardization, cost, and accessibility remain barriers to routine clinical adoption. Further research is necessary to validate these approaches and facilitate their integration into periodontal practice. The integration of biomarkers, omics technologies, advanced imaging, and artificial intelligence may improve early periodontal diagnosis, prognostic assessment, and personalized treatment planning. These innovations support the transition toward precision periodontology and have the potential to enhance clinical decision-making, treatment outcomes, and long-term periodontal health in routine dental practice.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Interorgan Crosstalk in MASLD: A Narrative Review.
Biomedicines, 14(9): pii:biomedicines14091949.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a systemic disorder shaped by interorgan crosstalk: dynamic, bidirectional communication through which the liver and endocrine organs, gut, adipose tissue, brain, kidney, skeletal muscle, bone, and heart exchange signals to coordinate metabolism, immunity, and tissue homeostasis. Across these axes, neural circuits, hormones, cytokines, adipokines, hepatokines, myokines, osteokines, bile acids, microbial metabolites, lipids, extracellular vesicles, and microRNAs integrate nutrient handling, insulin action, immunity, mitochondrial function, and tissue remodeling. Perturbation of these networks converts physiological homeostasis into self-reinforcing loops of substrate overflow, endocrine dysregulation, dysbiosis, inflammation, and fibrogenesis, while hepatic dysfunction propagates renal, neurocognitive, cardiometabolic, and musculoskeletal complications. This framework helps explain why individuals with comparable steatosis show divergent trajectories of metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, extrahepatic disease, and treatment response. It also highlights tractable points of intervention, including restoration of adipose buffering, modulation of gut microbial and bile-acid signaling, correction of endocrine drivers, preservation of muscle and bone, and integrated cardio-kidney-liver risk reduction across different disease stages and clinical phenotypes. We argue that precision hepatology should move beyond isolated assessment of liver fat and fibrosis towards multidimensional phenotyping of dominant crosstalk mechanisms. Longitudinal multi-omic studies and trials incorporating outcomes across organs are now required to distinguish causal signals from disease correlates, define clinically actionable endotypes, and test whether targeting one node can restore durable metabolic and functional resilience throughout the interconnected MASLD network, while improving patient-centered outcomes across the disease course.
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@article {pmid42792691,
year = {2026},
author = {Lonardo, A and Weiskirchen, R},
title = {Interorgan Crosstalk in MASLD: A Narrative Review.},
journal = {Biomedicines},
volume = {14},
number = {9},
pages = {},
doi = {10.3390/biomedicines14091949},
pmid = {42792691},
issn = {2227-9059},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) is a systemic disorder shaped by interorgan crosstalk: dynamic, bidirectional communication through which the liver and endocrine organs, gut, adipose tissue, brain, kidney, skeletal muscle, bone, and heart exchange signals to coordinate metabolism, immunity, and tissue homeostasis. Across these axes, neural circuits, hormones, cytokines, adipokines, hepatokines, myokines, osteokines, bile acids, microbial metabolites, lipids, extracellular vesicles, and microRNAs integrate nutrient handling, insulin action, immunity, mitochondrial function, and tissue remodeling. Perturbation of these networks converts physiological homeostasis into self-reinforcing loops of substrate overflow, endocrine dysregulation, dysbiosis, inflammation, and fibrogenesis, while hepatic dysfunction propagates renal, neurocognitive, cardiometabolic, and musculoskeletal complications. This framework helps explain why individuals with comparable steatosis show divergent trajectories of metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, extrahepatic disease, and treatment response. It also highlights tractable points of intervention, including restoration of adipose buffering, modulation of gut microbial and bile-acid signaling, correction of endocrine drivers, preservation of muscle and bone, and integrated cardio-kidney-liver risk reduction across different disease stages and clinical phenotypes. We argue that precision hepatology should move beyond isolated assessment of liver fat and fibrosis towards multidimensional phenotyping of dominant crosstalk mechanisms. Longitudinal multi-omic studies and trials incorporating outcomes across organs are now required to distinguish causal signals from disease correlates, define clinically actionable endotypes, and test whether targeting one node can restore durable metabolic and functional resilience throughout the interconnected MASLD network, while improving patient-centered outcomes across the disease course.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Mechanistic Links Between Natural Bioactive Molecules and Tumor Immune Microenvironment States in PD-1/PD-L1 Resistance.
Biomedicines, 14(9): pii:biomedicines14091955.
Programmed cell death protein 1/programmed death ligand 1 (PD-1/PD-L1) blockade can produce durable responses, but primary and acquired resistance are common. Treatment outcome is influenced by antigen presentation, T-cell localization, suppressive myeloid populations, metabolic stress, and the gut microbiome, all of which shape the tumor immune microenvironment (TIME). This review examines natural bioactive molecules in relation to these resistance features rather than grouping them by chemical class. Castalagin/camu-camu, ginseng polysaccharides, and ginsenoside Rh2 have the clearest preclinical evidence from direct PD-1/PD-L1-combination studies; evidence for the curcumin-gasdermin E (GSDME) axis comes from one recent study. Demethylzeylasteral has a well-supported ubiquitin-specific peptidase 22 (USP22)-PD-L1 degradation mechanism, but the reported antibody combination used cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) rather than PD-1/PD-L1. ACT001, berberine, baicalein, and several other candidates are supported mainly by indirect evidence of PD-L1 regulation or TIME remodeling. The translational value of these findings depends on exposure, target engagement, model selection, biomarker design, and material quality. Relating each candidate to a defined resistance setting helps distinguish promising combinations from mechanistic leads that still require direct testing.
Additional Links: PMID-42792697
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@article {pmid42792697,
year = {2026},
author = {Cheng, H and Chen, M and Xiao, M and Zhang, H and Zhang, Z and Jiang, D and Wan, AH and Wang, Q and Wan, G},
title = {Mechanistic Links Between Natural Bioactive Molecules and Tumor Immune Microenvironment States in PD-1/PD-L1 Resistance.},
journal = {Biomedicines},
volume = {14},
number = {9},
pages = {},
doi = {10.3390/biomedicines14091955},
pmid = {42792697},
issn = {2227-9059},
support = {82473938//National Natural Science Foundation of China/ ; },
abstract = {Programmed cell death protein 1/programmed death ligand 1 (PD-1/PD-L1) blockade can produce durable responses, but primary and acquired resistance are common. Treatment outcome is influenced by antigen presentation, T-cell localization, suppressive myeloid populations, metabolic stress, and the gut microbiome, all of which shape the tumor immune microenvironment (TIME). This review examines natural bioactive molecules in relation to these resistance features rather than grouping them by chemical class. Castalagin/camu-camu, ginseng polysaccharides, and ginsenoside Rh2 have the clearest preclinical evidence from direct PD-1/PD-L1-combination studies; evidence for the curcumin-gasdermin E (GSDME) axis comes from one recent study. Demethylzeylasteral has a well-supported ubiquitin-specific peptidase 22 (USP22)-PD-L1 degradation mechanism, but the reported antibody combination used cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) rather than PD-1/PD-L1. ACT001, berberine, baicalein, and several other candidates are supported mainly by indirect evidence of PD-L1 regulation or TIME remodeling. The translational value of these findings depends on exposure, target engagement, model selection, biomarker design, and material quality. Relating each candidate to a defined resistance setting helps distinguish promising combinations from mechanistic leads that still require direct testing.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Mitochondria Meet the Lung Microbiome: A Bidirectional Dialogue in Inflammation and Respiratory Diseases.
Biomedicines, 14(9): pii:biomedicines14091965.
The respiratory tract is a dynamic biological interface where microbiome, environmental exposure, epithelial integrity, and host metabolic regulation converge to maintain pulmonary homeostasis. Once considered sterile, the lung is now recognized as a low-biomass yet structured microbial ecosystem that contributes to immune calibration, colonization resistance, epithelial barrier function, and tissue resilience. Disruption of this equilibrium, known as pulmonary dysbiosis, has been increasingly associated with acute and chronic lung diseases, including cystic fibrosis, chronic obstructive pulmonary disease, acute respiratory distress syndrome, idiopathic pulmonary fibrosis, asthma, bronchiectasis, and lung cancer. In parallel, mitochondria have emerged as central regulators of pulmonary cell function, extending beyond ATP production to control redox signaling, apoptosis, innate immunity, epithelial repair, and inflammatory responses. This review examines the bidirectional crosstalk between the respiratory microbiome and mitochondria as an integrated pathogenic axis in lung disease. Dysbiotic microbial communities and respiratory pathogens can induce mitochondrial stress through toxins, virulence factors, microbial metabolites, and pattern-recognition receptor activation, leading to mitochondrial alteration and the release of mitochondrial damage-associated molecular patterns. Conversely, dysfunctional mitochondria reshape the pulmonary microenvironment by altering oxygen consumption, nutrient availability, cytokine production, redox balance, and barrier repair, thereby favoring pathogen persistence and chronic inflammation. Understanding mitochondria-microbiome interactions may support precision medicine strategies that integrate microbial, metabolic, inflammatory, and bioenergetic biomarkers to improve the diagnosis, prognosis, and treatment of inflammatory-related lung diseases.
Additional Links: PMID-42792707
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@article {pmid42792707,
year = {2026},
author = {Parolin, C and Gentile, E and Pellegrino, C and Spada, V and Bassi, C and Sabbioni, S and Vitali, B and Pinton, P and Rimessi, A},
title = {Mitochondria Meet the Lung Microbiome: A Bidirectional Dialogue in Inflammation and Respiratory Diseases.},
journal = {Biomedicines},
volume = {14},
number = {9},
pages = {},
doi = {10.3390/biomedicines14091965},
pmid = {42792707},
issn = {2227-9059},
support = {PRIN2017E5L5P3//Ministry of Universities and Research/ ; PRIN2020RRJP5L003//Ministry of Universities and Research/ ; CUP E83C22004670001//Ministry of Universities and Research/ ; CUP C93C22002780006//Ministry of Universities and Research/ ; IG-23670//Italian Association for Cancer Research/ ; CUP F53D23008660001-PRIN 2022 PNRR//Ministry of Universities and Research/ ; CUP F53D23003780006-PRIN 2022//Ministry of Universities and Research/ ; FIRD-2026//University of Ferrara/ ; },
abstract = {The respiratory tract is a dynamic biological interface where microbiome, environmental exposure, epithelial integrity, and host metabolic regulation converge to maintain pulmonary homeostasis. Once considered sterile, the lung is now recognized as a low-biomass yet structured microbial ecosystem that contributes to immune calibration, colonization resistance, epithelial barrier function, and tissue resilience. Disruption of this equilibrium, known as pulmonary dysbiosis, has been increasingly associated with acute and chronic lung diseases, including cystic fibrosis, chronic obstructive pulmonary disease, acute respiratory distress syndrome, idiopathic pulmonary fibrosis, asthma, bronchiectasis, and lung cancer. In parallel, mitochondria have emerged as central regulators of pulmonary cell function, extending beyond ATP production to control redox signaling, apoptosis, innate immunity, epithelial repair, and inflammatory responses. This review examines the bidirectional crosstalk between the respiratory microbiome and mitochondria as an integrated pathogenic axis in lung disease. Dysbiotic microbial communities and respiratory pathogens can induce mitochondrial stress through toxins, virulence factors, microbial metabolites, and pattern-recognition receptor activation, leading to mitochondrial alteration and the release of mitochondrial damage-associated molecular patterns. Conversely, dysfunctional mitochondria reshape the pulmonary microenvironment by altering oxygen consumption, nutrient availability, cytokine production, redox balance, and barrier repair, thereby favoring pathogen persistence and chronic inflammation. Understanding mitochondria-microbiome interactions may support precision medicine strategies that integrate microbial, metabolic, inflammatory, and bioenergetic biomarkers to improve the diagnosis, prognosis, and treatment of inflammatory-related lung diseases.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Gut Microbiota and Brain Aging: Identifying Keystone Biomarkers for Cognitive Health.
Biomedicines, 14(9): pii:biomedicines14091975.
The fact that the population is getting older has greatly increased the occurrence of cognitive decline and neurodegenerative diseases, underlining the importance of having reliable biomarkers that can measure biological aging before irreversible neurological damage takes place. New evidence shows that brain aging is not just the result of changes within neurons themselves but is also greatly affected by the gut microbiota via immune, metabolic, endocrine, and neurovascular signaling. This review brings together the existing knowledge about biomarkers of biological aging-such as telomere shortening, epigenetic clocks, oxidative stress, inflammation, cellular senescence, and metabolic dysfunction-as well as established cognitive biomarkers obtained from neuroimaging, cerebrospinal fluid, blood, genetic evaluations, and neuropsychological tests. We also point out that changes associated with age in the composition of the gut microbiota and the metabolites it produces are becoming more and more involved in the mechanisms connecting intestinal dysbiosis, dysfunction of the blood-brain barrier (BBB), neuroinflammation, and age-related cognitive decline. Through this approach of combined and complementary biomarker systems, we hypothesize that the gut microbiota has emerged as a central regulator of biological and cognitive aging and may provide a useful source for development of biomarkers of cognitive resilience and risk of neurodegenerative diseases. Lastly, we consider microbiome-based interventions, including probiotics, prebiotics, dietary changes, fecal microbial transplant, and new treatment modalities derived from molecular studies, as possible approaches to the prevention and management of age-related cognitive decline. Collectively, this review provides a comprehensive framework linking aging biology, microbiome science, and cognitive biomarkers to advance biomarker-driven precision medicine for healthy brain aging.
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@article {pmid42792717,
year = {2026},
author = {Bhatia, M and Mishra, SP and Mishra, RK and Jain, S and Yadav, H and Tomar, RS},
title = {Gut Microbiota and Brain Aging: Identifying Keystone Biomarkers for Cognitive Health.},
journal = {Biomedicines},
volume = {14},
number = {9},
pages = {},
doi = {10.3390/biomedicines14091975},
pmid = {42792717},
issn = {2227-9059},
abstract = {The fact that the population is getting older has greatly increased the occurrence of cognitive decline and neurodegenerative diseases, underlining the importance of having reliable biomarkers that can measure biological aging before irreversible neurological damage takes place. New evidence shows that brain aging is not just the result of changes within neurons themselves but is also greatly affected by the gut microbiota via immune, metabolic, endocrine, and neurovascular signaling. This review brings together the existing knowledge about biomarkers of biological aging-such as telomere shortening, epigenetic clocks, oxidative stress, inflammation, cellular senescence, and metabolic dysfunction-as well as established cognitive biomarkers obtained from neuroimaging, cerebrospinal fluid, blood, genetic evaluations, and neuropsychological tests. We also point out that changes associated with age in the composition of the gut microbiota and the metabolites it produces are becoming more and more involved in the mechanisms connecting intestinal dysbiosis, dysfunction of the blood-brain barrier (BBB), neuroinflammation, and age-related cognitive decline. Through this approach of combined and complementary biomarker systems, we hypothesize that the gut microbiota has emerged as a central regulator of biological and cognitive aging and may provide a useful source for development of biomarkers of cognitive resilience and risk of neurodegenerative diseases. Lastly, we consider microbiome-based interventions, including probiotics, prebiotics, dietary changes, fecal microbial transplant, and new treatment modalities derived from molecular studies, as possible approaches to the prevention and management of age-related cognitive decline. Collectively, this review provides a comprehensive framework linking aging biology, microbiome science, and cognitive biomarkers to advance biomarker-driven precision medicine for healthy brain aging.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Short-Chain Fatty Acids in Sepsis: Mechanisms of Action and Therapeutic Advances.
Biomedicines, 14(9): pii:biomedicines14091992.
Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Its development and progression involve multiple interconnected mechanisms, including uncontrolled inflammation, immunosuppression, metabolic reprogramming, intestinal barrier disruption, and multi-organ injury. Short-chain fatty acids (SCFAs), primarily acetate, propionate, and butyrate, are important metabolites produced by the anaerobic fermentation of dietary fiber and indigestible carbohydrates by gut microbiota. During sepsis, antibiotic exposure, intestinal hypoperfusion, insufficient nutritional substrates, and microbial dysbiosis may deplete SCFA-producing bacteria and lower SCFA levels, thereby aggravating intestinal barrier dysfunction, endotoxin translocation, and systemic inflammatory responses. SCFAs can influence sepsis-associated intestinal, pulmonary, cardiac, hepatic, renal, and cerebral injury by activating receptors such as free fatty acid receptor 2 (FFAR2)/G protein-coupled receptor 43 (GPR43), free fatty acid receptor 3 (FFAR3)/G protein-coupled receptor 41 (GPR41), and G protein-coupled receptor 109A (GPR109A); inhibiting histone deacetylases; and regulating immune-cell metabolism, inflammasome activation, oxidative stress, mitochondrial function, and modes of cell death. In recent years, strategies such as direct SCFA supplementation, promotion of endogenous SCFA production, restoration of SCFA-producing microbial communities, and targeting of SCFA receptors and downstream signaling pathways have shown therapeutic potential. However, their clinical translation remains limited by uncertainties regarding dose, timing, route of administration, patient stratification, and safety. This review systematically summarizes the mechanisms of action and therapeutic advances of SCFAs in sepsis, aiming to provide a reference for microbiome-based interventions and metabolism-targeted therapies in sepsis.
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PubMed:
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@article {pmid42792734,
year = {2026},
author = {Wang, Z and Wen, X and Yuan, S and Zhang, J and Xu, D},
title = {Short-Chain Fatty Acids in Sepsis: Mechanisms of Action and Therapeutic Advances.},
journal = {Biomedicines},
volume = {14},
number = {9},
pages = {},
doi = {10.3390/biomedicines14091992},
pmid = {42792734},
issn = {2227-9059},
abstract = {Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Its development and progression involve multiple interconnected mechanisms, including uncontrolled inflammation, immunosuppression, metabolic reprogramming, intestinal barrier disruption, and multi-organ injury. Short-chain fatty acids (SCFAs), primarily acetate, propionate, and butyrate, are important metabolites produced by the anaerobic fermentation of dietary fiber and indigestible carbohydrates by gut microbiota. During sepsis, antibiotic exposure, intestinal hypoperfusion, insufficient nutritional substrates, and microbial dysbiosis may deplete SCFA-producing bacteria and lower SCFA levels, thereby aggravating intestinal barrier dysfunction, endotoxin translocation, and systemic inflammatory responses. SCFAs can influence sepsis-associated intestinal, pulmonary, cardiac, hepatic, renal, and cerebral injury by activating receptors such as free fatty acid receptor 2 (FFAR2)/G protein-coupled receptor 43 (GPR43), free fatty acid receptor 3 (FFAR3)/G protein-coupled receptor 41 (GPR41), and G protein-coupled receptor 109A (GPR109A); inhibiting histone deacetylases; and regulating immune-cell metabolism, inflammasome activation, oxidative stress, mitochondrial function, and modes of cell death. In recent years, strategies such as direct SCFA supplementation, promotion of endogenous SCFA production, restoration of SCFA-producing microbial communities, and targeting of SCFA receptors and downstream signaling pathways have shown therapeutic potential. However, their clinical translation remains limited by uncertainties regarding dose, timing, route of administration, patient stratification, and safety. This review systematically summarizes the mechanisms of action and therapeutic advances of SCFAs in sepsis, aiming to provide a reference for microbiome-based interventions and metabolism-targeted therapies in sepsis.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Mesenteric Panniculitis and the Gut-Mesentery-Metabolic Axis: A Hypothesis-Generating Narrative Review.
Biomedicines, 14(9): pii:biomedicines14092017.
Mesenteric panniculitis (MP) is an uncommon inflammatory disorder of mesenteric adipose tissue. Its pathophysiology remains unclear. Gut dysbiosis, intestinal barrier dysfunction, metabolic endotoxemia, glycemic variability (GV), and vascular dysfunction have been implicated in inflammatory and metabolic disorders, but their specific involvement in MP has not been established. This narrative review integrates MP-specific clinical evidence with indirect mechanistic evidence from related metabolic, inflammatory, and experimental settings to examine the possible relationships between these mechanisms and MP and their integration within a proposed gut-mesentery-metabolic axis. The literature was reviewed through structured searches of PubMed, Scopus, and Web of Science for relevant publications from 2018 to 2026, supplemented by earlier foundational studies identified through reference-list screening and targeted searches. Current data suggest that dysbiosis and impaired intestinal barrier function may facilitate microbial-product translocation and lipopolysaccharide-mediated inflammatory signaling, while GV may contribute to oxidative stress, endothelial dysfunction, and pro-inflammatory responses. Mesenteric vascular anatomy and impaired regional perfusion may represent additional factors influencing local tissue susceptibility. Recent randomized controlled trials of microbiome-targeted interventions in metabolic disorders have shown heterogeneous effects on glycemic, inflammatory, and microbiota-related outcomes, indicating a need for further investigation of individualized microbiome-directed strategies. Direct evidence that microbial, metabolic, or vascular mechanisms initiate or sustain MP is currently limited. Accordingly, the proposed gut-mesentery-metabolic axis should be interpreted as a hypothesis-generating framework rather than an established causal model. Prospective MP-specific studies integrating microbiome profiling, validated measures of intestinal barrier function, metabolic phenotyping, GV, vascular assessment, and imaging are required to test the proposed relationships.
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@article {pmid42792759,
year = {2026},
author = {Ispas, S and Maggio, V and Rabbani, SA and Wali, AF and Bhongade, BA and Talath, S and Rangraze, IR and Satyam, SM and Avagimyan, A and Hoffmann, K and Ilias, I and Paczkowska, A and El-Tanani, M and Rizzo, M},
title = {Mesenteric Panniculitis and the Gut-Mesentery-Metabolic Axis: A Hypothesis-Generating Narrative Review.},
journal = {Biomedicines},
volume = {14},
number = {9},
pages = {},
doi = {10.3390/biomedicines14092017},
pmid = {42792759},
issn = {2227-9059},
abstract = {Mesenteric panniculitis (MP) is an uncommon inflammatory disorder of mesenteric adipose tissue. Its pathophysiology remains unclear. Gut dysbiosis, intestinal barrier dysfunction, metabolic endotoxemia, glycemic variability (GV), and vascular dysfunction have been implicated in inflammatory and metabolic disorders, but their specific involvement in MP has not been established. This narrative review integrates MP-specific clinical evidence with indirect mechanistic evidence from related metabolic, inflammatory, and experimental settings to examine the possible relationships between these mechanisms and MP and their integration within a proposed gut-mesentery-metabolic axis. The literature was reviewed through structured searches of PubMed, Scopus, and Web of Science for relevant publications from 2018 to 2026, supplemented by earlier foundational studies identified through reference-list screening and targeted searches. Current data suggest that dysbiosis and impaired intestinal barrier function may facilitate microbial-product translocation and lipopolysaccharide-mediated inflammatory signaling, while GV may contribute to oxidative stress, endothelial dysfunction, and pro-inflammatory responses. Mesenteric vascular anatomy and impaired regional perfusion may represent additional factors influencing local tissue susceptibility. Recent randomized controlled trials of microbiome-targeted interventions in metabolic disorders have shown heterogeneous effects on glycemic, inflammatory, and microbiota-related outcomes, indicating a need for further investigation of individualized microbiome-directed strategies. Direct evidence that microbial, metabolic, or vascular mechanisms initiate or sustain MP is currently limited. Accordingly, the proposed gut-mesentery-metabolic axis should be interpreted as a hypothesis-generating framework rather than an established causal model. Prospective MP-specific studies integrating microbiome profiling, validated measures of intestinal barrier function, metabolic phenotyping, GV, vascular assessment, and imaging are required to test the proposed relationships.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Periodontal Dysbiosis and Premature Atherosclerosis: A Critical Appraisal of the Oral-Gut-Vascular Axis.
Biomedicines, 14(9): pii:biomedicines14092051.
Background/Objectives: Premature coronary artery disease (PCAD) is not fully explained by conventional risk factors, particularly in younger adults with residual inflammatory risk. This review evaluates the oral-gut-vascular axis as a mechanistic framework linking periodontal dysbiosis to premature atherosclerosis. Methods: A structured narrative search of PubMed/MEDLINE, Scopus, Embase, and Web of Science was conducted for English-language publications issued between January 2015 and June 2026. Human observational and interventional studies, mechanistic studies, systematic reviews, meta-analyses, and major scientific statements addressing periodontal disease, gut dysbiosis, barrier dysfunction, microbial metabolites, and vascular outcomes were considered. Results: Current evidence supports the biological plausibility of interconnected pathways involving periodontal pathobionts, microbial translocation, intestinal dysbiosis, increased epithelial permeability, endotoxemia, TLR2/TLR4 signaling, TMAO metabolism, oxidative stress, immune dysregulation, endothelial dysfunction, and plaque development. Candidate translational markers include hsCRP, IL-6, LPS, LBP, TMAO, oxidized LDL, adhesion molecules, salivary microbial signatures, and vascular imaging indices. Periodontal treatment and microbiome-directed strategies may reduce inflammatory burden, although effects on major cardiovascular outcomes remain unproven. Conclusions: The oral-gut-vascular axis is biologically plausible but not yet causally established in humans, and its specific relevance to PCAD remains largely inferential. Prospective PCAD-specific cohorts, standardized multi-omics, validated biomarkers, vascular imaging, and externally validated artificial-intelligence models are required to establish clinical utility and inform integrated cardio-dental prevention in younger populations.
Additional Links: PMID-42792792
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@article {pmid42792792,
year = {2026},
author = {Anghel, L and Bele, DN and Sascău, RA and Benchea, LC and Scutariu, MM and Prisacariu, C and Radu, R and Balasanian, MO and Stătescu, C},
title = {Periodontal Dysbiosis and Premature Atherosclerosis: A Critical Appraisal of the Oral-Gut-Vascular Axis.},
journal = {Biomedicines},
volume = {14},
number = {9},
pages = {},
doi = {10.3390/biomedicines14092051},
pmid = {42792792},
issn = {2227-9059},
abstract = {Background/Objectives: Premature coronary artery disease (PCAD) is not fully explained by conventional risk factors, particularly in younger adults with residual inflammatory risk. This review evaluates the oral-gut-vascular axis as a mechanistic framework linking periodontal dysbiosis to premature atherosclerosis. Methods: A structured narrative search of PubMed/MEDLINE, Scopus, Embase, and Web of Science was conducted for English-language publications issued between January 2015 and June 2026. Human observational and interventional studies, mechanistic studies, systematic reviews, meta-analyses, and major scientific statements addressing periodontal disease, gut dysbiosis, barrier dysfunction, microbial metabolites, and vascular outcomes were considered. Results: Current evidence supports the biological plausibility of interconnected pathways involving periodontal pathobionts, microbial translocation, intestinal dysbiosis, increased epithelial permeability, endotoxemia, TLR2/TLR4 signaling, TMAO metabolism, oxidative stress, immune dysregulation, endothelial dysfunction, and plaque development. Candidate translational markers include hsCRP, IL-6, LPS, LBP, TMAO, oxidized LDL, adhesion molecules, salivary microbial signatures, and vascular imaging indices. Periodontal treatment and microbiome-directed strategies may reduce inflammatory burden, although effects on major cardiovascular outcomes remain unproven. Conclusions: The oral-gut-vascular axis is biologically plausible but not yet causally established in humans, and its specific relevance to PCAD remains largely inferential. Prospective PCAD-specific cohorts, standardized multi-omics, validated biomarkers, vascular imaging, and externally validated artificial-intelligence models are required to establish clinical utility and inform integrated cardio-dental prevention in younger populations.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Microbiota-Inflammation Crosstalk in Myeloproliferative Neoplasms: MPN-Specific Human Data, Mechanistic Plausibility and Translational Priorities.
Biomedicines, 14(9): pii:biomedicines14092074.
Myeloproliferative neoplasms (MPNs) are clonal hematopoietic stem cell disorders driven mainly by somatic mutations in JAK2, CALR or MPL, but their clinical phenotype is also shaped by chronic inflammation, immune dysregulation, vascular complications and microenvironmental remodeling. Emerging evidence suggests that the gut microbiota may contribute to this inflammatory and immunometabolic landscape; however, the current literature remains heterogeneous and its translational relevance is still insufficiently defined. This critical narrative review maps the available evidence linking the gut microbiota, microbial metabolites and systemic microbial signatures to MPN biology. We distinguish direct human MPN data from indirect mechanistic evidence derived from studies of intestinal barrier dysfunction, thrombo-inflammation, hematopoietic regulation, allogeneic hematopoietic cell transplantation and infection risk. Across human MPN cohorts, the most consistent findings are not uniform changes in global microbial diversity, but rather alterations in specific immunoregulatory taxa, particularly reduced Firmicutes/Faecalibacterium-related communities and dysbiotic signatures associated with JAK2V617F status. Mechanistically, dysbiosis and impaired intestinal barrier integrity may facilitate low-grade endotoxemia, TLR4/NF-κB activation, cytokine amplification, endothelial activation and platelet priming. In parallel, microbial metabolites may influence hematopoietic stem cell programs, the bone marrow niche, megakaryopoiesis and thrombopoiesis. Treatment exposure and diet are relevant modifiers of the microbiota-inflammation axis, although available interventional data remain preliminary. Mendelian randomization and multi-omics studies provide hypothesis-generating evidence for microbiota-metabolome-MPN interactions, but require longitudinal validation, functional studies and contamination-aware analytical pipelines, especially for low-biomass blood and bone marrow samples. Microbiota-targeted strategies, including nutritional interventions and fecal or washed microbiota transplantation, represent promising but still investigational approaches, particularly in immunocompromised or post-transplant settings. Future studies should integrate microbiome, metabolome, genome, proteome, inflammatory biomarkers and clinical outcomes while controlling for diet, antibiotics, treatment exposure and driver mutation status. Such an approach may clarify whether the microbiota is a biomarker, mediator or therapeutic target in MPNs.
Additional Links: PMID-42792816
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@article {pmid42792816,
year = {2026},
author = {Țîrlea, LG and Lipan, L and Tănase, AD},
title = {Microbiota-Inflammation Crosstalk in Myeloproliferative Neoplasms: MPN-Specific Human Data, Mechanistic Plausibility and Translational Priorities.},
journal = {Biomedicines},
volume = {14},
number = {9},
pages = {},
doi = {10.3390/biomedicines14092074},
pmid = {42792816},
issn = {2227-9059},
abstract = {Myeloproliferative neoplasms (MPNs) are clonal hematopoietic stem cell disorders driven mainly by somatic mutations in JAK2, CALR or MPL, but their clinical phenotype is also shaped by chronic inflammation, immune dysregulation, vascular complications and microenvironmental remodeling. Emerging evidence suggests that the gut microbiota may contribute to this inflammatory and immunometabolic landscape; however, the current literature remains heterogeneous and its translational relevance is still insufficiently defined. This critical narrative review maps the available evidence linking the gut microbiota, microbial metabolites and systemic microbial signatures to MPN biology. We distinguish direct human MPN data from indirect mechanistic evidence derived from studies of intestinal barrier dysfunction, thrombo-inflammation, hematopoietic regulation, allogeneic hematopoietic cell transplantation and infection risk. Across human MPN cohorts, the most consistent findings are not uniform changes in global microbial diversity, but rather alterations in specific immunoregulatory taxa, particularly reduced Firmicutes/Faecalibacterium-related communities and dysbiotic signatures associated with JAK2V617F status. Mechanistically, dysbiosis and impaired intestinal barrier integrity may facilitate low-grade endotoxemia, TLR4/NF-κB activation, cytokine amplification, endothelial activation and platelet priming. In parallel, microbial metabolites may influence hematopoietic stem cell programs, the bone marrow niche, megakaryopoiesis and thrombopoiesis. Treatment exposure and diet are relevant modifiers of the microbiota-inflammation axis, although available interventional data remain preliminary. Mendelian randomization and multi-omics studies provide hypothesis-generating evidence for microbiota-metabolome-MPN interactions, but require longitudinal validation, functional studies and contamination-aware analytical pipelines, especially for low-biomass blood and bone marrow samples. Microbiota-targeted strategies, including nutritional interventions and fecal or washed microbiota transplantation, represent promising but still investigational approaches, particularly in immunocompromised or post-transplant settings. Future studies should integrate microbiome, metabolome, genome, proteome, inflammatory biomarkers and clinical outcomes while controlling for diet, antibiotics, treatment exposure and driver mutation status. Such an approach may clarify whether the microbiota is a biomarker, mediator or therapeutic target in MPNs.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Inhaler Devices as Potential Bacterial Reservoirs: A 30-Day Microbiota Analysis in Non-Cystic Fibrosis Bronchiectasis.
Biomedicines, 14(9): pii:biomedicines14092132.
Background/Objectives: Handheld inhalers are essential for the management of bronchiectasis, yet their role as potential microbial reservoirs remains poorly understood. We aimed to characterize and compare the bacterial communities in pressurized metered-dose inhalers (pMDIs) and Respimat[®] devices after 30 days of clinical use. Methods: In this 30-day prospective study of eight adults with non-cystic fibrosis bronchiectasis, inhaler devices (six pMDIs and four Respimat[®] devices) were analyzed using 16S rRNA gene sequencing of the V4 region. Total bacterial loads (quantitative PCR), α- and β-diversity, differential taxon abundance (ANCOM-BC), and microbial source tracking (SourceTracker2) were compared between device types. Results: After 30 days, pMDIs showed significantly higher bacterial loads than negative controls (adjusted p < 0.05), whereas Respimat[®] loads were indistinguishable from those of controls. Compared to Respimat[®] devices, pMDIs showed a trend toward microbial simplification (α-diversity: Shannon index, p = 0.08). However, overall community structures did not differ significantly (β-diversity: PERMANOVA, adjusted p = 0.18). ANCOM-BC identified 12 amplicon sequence variants (ASVs) significantly enriched in pMDIs, including one belonging to the genus Pseudomonas, compared to only one ASV in Respimat[®] devices. Paired device analyses between two participants who used both devices also revealed differences in the relative abundance of specific potentially pathogenic genera. For instance, in one participant, the pMDI was dominated by Staphylococcus (70.9% vs. 2.5% in the paired Respimat[®]). Conclusions: After 30 days of use by patients with bronchiectasis, bacterial DNA was detected in the liquid contents of both inhaler types. Only pMDIs showed a significant increase in total bacterial load relative to negative controls, and pMDIs harboured more differentially abundant ASVs than Respimat[®] devices, suggesting that pMDIs may be more susceptible to microbial contamination in patients with non-cystic fibrosis bronchiectasis.
Additional Links: PMID-42792872
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@article {pmid42792872,
year = {2026},
author = {Baek, J and Sul, OJ and Choi, HW and Jung, C and Lee, S and Park, J and Koo, H and Kwon, B and Filho, FSL and Ra, SW},
title = {Inhaler Devices as Potential Bacterial Reservoirs: A 30-Day Microbiota Analysis in Non-Cystic Fibrosis Bronchiectasis.},
journal = {Biomedicines},
volume = {14},
number = {9},
pages = {},
doi = {10.3390/biomedicines14092132},
pmid = {42792872},
issn = {2227-9059},
support = {2026-UUHBRI-01//Ulsan University Hospital/ ; 2021R1I1A1A0104430413//National Research Foundation of Korea/ ; 2022R1F1A106275312//National Research Foundation of Korea/ ; },
abstract = {Background/Objectives: Handheld inhalers are essential for the management of bronchiectasis, yet their role as potential microbial reservoirs remains poorly understood. We aimed to characterize and compare the bacterial communities in pressurized metered-dose inhalers (pMDIs) and Respimat[®] devices after 30 days of clinical use. Methods: In this 30-day prospective study of eight adults with non-cystic fibrosis bronchiectasis, inhaler devices (six pMDIs and four Respimat[®] devices) were analyzed using 16S rRNA gene sequencing of the V4 region. Total bacterial loads (quantitative PCR), α- and β-diversity, differential taxon abundance (ANCOM-BC), and microbial source tracking (SourceTracker2) were compared between device types. Results: After 30 days, pMDIs showed significantly higher bacterial loads than negative controls (adjusted p < 0.05), whereas Respimat[®] loads were indistinguishable from those of controls. Compared to Respimat[®] devices, pMDIs showed a trend toward microbial simplification (α-diversity: Shannon index, p = 0.08). However, overall community structures did not differ significantly (β-diversity: PERMANOVA, adjusted p = 0.18). ANCOM-BC identified 12 amplicon sequence variants (ASVs) significantly enriched in pMDIs, including one belonging to the genus Pseudomonas, compared to only one ASV in Respimat[®] devices. Paired device analyses between two participants who used both devices also revealed differences in the relative abundance of specific potentially pathogenic genera. For instance, in one participant, the pMDI was dominated by Staphylococcus (70.9% vs. 2.5% in the paired Respimat[®]). Conclusions: After 30 days of use by patients with bronchiectasis, bacterial DNA was detected in the liquid contents of both inhaler types. Only pMDIs showed a significant increase in total bacterial load relative to negative controls, and pMDIs harboured more differentially abundant ASVs than Respimat[®] devices, suggesting that pMDIs may be more susceptible to microbial contamination in patients with non-cystic fibrosis bronchiectasis.},
}
RevDate: 2026-09-26
CmpDate: 2026-09-26
Gut Microbiota and Metabolic Pathway Signatures for Inflammatory Bowel Disease Identified via Subject-Stratified Random Forest Based on the Longitudinal HMP2 Cohort.
Genes, 17(9): pii:genes17091053.
Background: Inflammatory bowel disease (IBD) is characterised by severe intestinal microbial dysbiosis. Most machine learning diagnostic models built on the longitudinal HMP2 cohort suffer serious data leakage from random sample-level cross-validation splitting, which leads to artificially inflated AUC values. Additionally, incomplete reporting of microbial preprocessing, random forest hyperparameters and multi-dimensional evaluation metrics reduces the reproducibility of existing research. Methods: We re-analysed the public HMP2 (IBDMDB) longitudinal metagenomic dataset containing 130 unique subjects (103 IBD/27 healthy controls) and 1627 longitudinal faecal samples. Raw 585 species were filtered by a minimum relative abundance of 1 × 10[-5] and sample prevalence ≥20%, retaining 89 taxa; all 1135 metabolic pathways were retained. CLR transformation was applied to compositional abundance data. We performed Wilcoxon differential testing with Benjamini-Hochberg FDR correction, alpha/beta diversity analysis, and three random forest models (filtered species, all FDR-significant pathways, strictly filtered pathways). Critical improvements included subject-ID-stratified 5-fold cross-validation repeated 5 times, within-fold training-set-only feature importance calculation, and class weighting to balance unbalanced IBD/control samples. PERMANOVA with subject stratification and PERMDISP dispersion test were implemented with 999 fixed-seed permutations. Results: All four alpha diversity indices were significantly lower in IBD patients (all p < 0.0001). Subject-stratified PERMANOVA showed disease status only explained 1.18% of total Bray-Curtis community variance (R[2] = 0.0118, p = 1); PERMDISP detected significant group dispersion heterogeneity (p = 0.027). We identified 63 differentially abundant species and 695 perturbed pathways at FDR < 0.05. Canonical butyrate producers Faecalibacterium prausnitzii and Roseburia hominis showed no significant inter-group differences. Bootstrap 1000-resampling AUC 95% CIs indicated moderate classification performance: species model (0.626-0.705, mean AUC = 0.665), all-significant-pathway model (0.645-0.712, mean AUC = 0.679), strict-pathway model (0.620-0.685, mean AUC = 0.654). Alistipes putredinis and peptidoglycan biosynthesis I were the top taxonomic and pathway biomarkers, respectively. Conclusions: This study established a leakage-free machine learning pipeline for longitudinal microbiome cohorts via subject-level cross-validation splitting. The moderate AUC values eliminate false high performance caused by sample leakage, and we provide reliable candidate microbial and metabolic biomarkers for IBD. Restricted by single-cohort internal validation and unadjusted medication confounders, these markers still require independent multi-centre external verification before clinical translation.
Additional Links: PMID-42792947
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@article {pmid42792947,
year = {2026},
author = {Du, Q and Xing, L and Zhu, C and Li, P},
title = {Gut Microbiota and Metabolic Pathway Signatures for Inflammatory Bowel Disease Identified via Subject-Stratified Random Forest Based on the Longitudinal HMP2 Cohort.},
journal = {Genes},
volume = {17},
number = {9},
pages = {},
doi = {10.3390/genes17091053},
pmid = {42792947},
issn = {2073-4425},
mesh = {Humans ; *Inflammatory Bowel Diseases/microbiology/metabolism/genetics ; Random Forest ; *Metabolic Networks and Pathways/genetics ; *Gastrointestinal Microbiome/genetics ; Longitudinal Studies ; Feces/microbiology ; Female ; Machine Learning ; },
abstract = {Background: Inflammatory bowel disease (IBD) is characterised by severe intestinal microbial dysbiosis. Most machine learning diagnostic models built on the longitudinal HMP2 cohort suffer serious data leakage from random sample-level cross-validation splitting, which leads to artificially inflated AUC values. Additionally, incomplete reporting of microbial preprocessing, random forest hyperparameters and multi-dimensional evaluation metrics reduces the reproducibility of existing research. Methods: We re-analysed the public HMP2 (IBDMDB) longitudinal metagenomic dataset containing 130 unique subjects (103 IBD/27 healthy controls) and 1627 longitudinal faecal samples. Raw 585 species were filtered by a minimum relative abundance of 1 × 10[-5] and sample prevalence ≥20%, retaining 89 taxa; all 1135 metabolic pathways were retained. CLR transformation was applied to compositional abundance data. We performed Wilcoxon differential testing with Benjamini-Hochberg FDR correction, alpha/beta diversity analysis, and three random forest models (filtered species, all FDR-significant pathways, strictly filtered pathways). Critical improvements included subject-ID-stratified 5-fold cross-validation repeated 5 times, within-fold training-set-only feature importance calculation, and class weighting to balance unbalanced IBD/control samples. PERMANOVA with subject stratification and PERMDISP dispersion test were implemented with 999 fixed-seed permutations. Results: All four alpha diversity indices were significantly lower in IBD patients (all p < 0.0001). Subject-stratified PERMANOVA showed disease status only explained 1.18% of total Bray-Curtis community variance (R[2] = 0.0118, p = 1); PERMDISP detected significant group dispersion heterogeneity (p = 0.027). We identified 63 differentially abundant species and 695 perturbed pathways at FDR < 0.05. Canonical butyrate producers Faecalibacterium prausnitzii and Roseburia hominis showed no significant inter-group differences. Bootstrap 1000-resampling AUC 95% CIs indicated moderate classification performance: species model (0.626-0.705, mean AUC = 0.665), all-significant-pathway model (0.645-0.712, mean AUC = 0.679), strict-pathway model (0.620-0.685, mean AUC = 0.654). Alistipes putredinis and peptidoglycan biosynthesis I were the top taxonomic and pathway biomarkers, respectively. Conclusions: This study established a leakage-free machine learning pipeline for longitudinal microbiome cohorts via subject-level cross-validation splitting. The moderate AUC values eliminate false high performance caused by sample leakage, and we provide reliable candidate microbial and metabolic biomarkers for IBD. Restricted by single-cohort internal validation and unadjusted medication confounders, these markers still require independent multi-centre external verification before clinical translation.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Inflammatory Bowel Diseases/microbiology/metabolism/genetics
Random Forest
*Metabolic Networks and Pathways/genetics
*Gastrointestinal Microbiome/genetics
Longitudinal Studies
Feces/microbiology
Female
Machine Learning
RevDate: 2026-09-26
CmpDate: 2026-09-26
Omics-Based Sperm-Retrieval Prediction in Non-Obstructive Azoospermia: A Critical Narrative Review and Validation Framework.
Genes, 17(9): pii:genes17091088.
In non-obstructive azoospermia (NOA), microdissection testicular sperm extraction can provide sperm for intracytoplasmic sperm injection, but retrieval fails in approximately half of procedures. Genomic, transcriptomic, noncoding RNA, proteomic, metabolomic, and microbiome studies have reported molecular associations and prediction estimates. This critical narrative review examines the requirements for an assay-model system to support preoperative retrieval counseling. A focused PubMed/MEDLINE search updated on 31 August 2026 and targeted reference checking identified representative human reports and methodological guidance. Selected reports mainly illustrate discovery, development, and same-source evaluation. Common limitations include small cohorts, local assay optimization, heterogeneous outcomes, incomplete calibration, and uncertain transportability. Established karyotyping and Y-chromosome testing must be distinguished from discovery-scale genomics, which currently supports etiologic and qualified genotype-specific counseling rather than a universal calibrated retrieval model. A routine-variable multicenter model reported an external-cohort area under the receiver-operating-characteristic curve (AUC) of 0.8301, although cohort provenance, calibration, and clinical utility require independent confirmation. An author-developed seven-gate framework integrates clinical-question definition, assay specification, model development, internal validation, external evaluation, incremental value, and prospective impact. Future omics studies should test incremental value beyond a prespecified routine-variable model in the same patients and assess calibration, threshold consequences, net benefit, assay failure, cost, and patient outcomes.
Additional Links: PMID-42792982
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@article {pmid42792982,
year = {2026},
author = {Kaltsas, A and Kyrgiafini, MA and Markou, E and Chrisofos, M},
title = {Omics-Based Sperm-Retrieval Prediction in Non-Obstructive Azoospermia: A Critical Narrative Review and Validation Framework.},
journal = {Genes},
volume = {17},
number = {9},
pages = {},
doi = {10.3390/genes17091088},
pmid = {42792982},
issn = {2073-4425},
mesh = {Humans ; *Azoospermia/genetics/therapy/metabolism ; Male ; *Sperm Retrieval ; Genomics/methods ; Proteomics/methods ; Sperm Injections, Intracytoplasmic/methods ; Multiomics ; },
abstract = {In non-obstructive azoospermia (NOA), microdissection testicular sperm extraction can provide sperm for intracytoplasmic sperm injection, but retrieval fails in approximately half of procedures. Genomic, transcriptomic, noncoding RNA, proteomic, metabolomic, and microbiome studies have reported molecular associations and prediction estimates. This critical narrative review examines the requirements for an assay-model system to support preoperative retrieval counseling. A focused PubMed/MEDLINE search updated on 31 August 2026 and targeted reference checking identified representative human reports and methodological guidance. Selected reports mainly illustrate discovery, development, and same-source evaluation. Common limitations include small cohorts, local assay optimization, heterogeneous outcomes, incomplete calibration, and uncertain transportability. Established karyotyping and Y-chromosome testing must be distinguished from discovery-scale genomics, which currently supports etiologic and qualified genotype-specific counseling rather than a universal calibrated retrieval model. A routine-variable multicenter model reported an external-cohort area under the receiver-operating-characteristic curve (AUC) of 0.8301, although cohort provenance, calibration, and clinical utility require independent confirmation. An author-developed seven-gate framework integrates clinical-question definition, assay specification, model development, internal validation, external evaluation, incremental value, and prospective impact. Future omics studies should test incremental value beyond a prespecified routine-variable model in the same patients and assess calibration, threshold consequences, net benefit, assay failure, cost, and patient outcomes.},
}
MeSH Terms:
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Humans
*Azoospermia/genetics/therapy/metabolism
Male
*Sperm Retrieval
Genomics/methods
Proteomics/methods
Sperm Injections, Intracytoplasmic/methods
Multiomics
RevDate: 2026-09-26
CmpDate: 2026-09-26
The Epigenetic Aging-Cancer Continuum: Biomarkers, Metabolism, and Therapy.
Genes, 17(9): pii:genes17091130.
Aging and cancer form a biological continuum influenced by epigenomic changes, metabolic dysfunction, inflammation, cellular senescence, and loss of tissue homeostasis. Age-related epigenetic alterations can promote cancer, which exploits plasticity for evolution, immune evasion, metastasis, and resistance. Nutrition and metabolism affect this process through one-carbon metabolism, methyl-donor availability, acetyl-CoA and NAD[+] balance, redox status, microbiome metabolites, and chromatin enzyme activity. Circulating biomarkers such as cell-free DNA methylation, mutation-based ctDNA, fragmentomic features, and non-coding RNAs can detect tumor and host changes linked to aging, inflammation, nutrition, and treatment with minimal invasiveness. This review explores the epigenetic aging-cancer link, how nutrition and metabolism modify pathways, and the potential of circulating biomarkers for diagnosis, prognosis, prediction, and monitoring. The focus is on epigenetic plasticity, drug-tolerant states, resistance, epigenetic drugs, metabolic targeting, and nutritional interventions. New technologies, including single-cell and spatial epigenomics, long-read sequencing, and multimodal computational approaches, aid biomarker discovery and clinical use. Challenges include variability, misclassification, heterogeneity, confounding, reverse causality, overfitting, and limited validation. Clinical applications need standard workflows, representative cohorts, transparent models, and proof that biomarker-guided strategies improve outcomes.
Additional Links: PMID-42793024
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@article {pmid42793024,
year = {2026},
author = {Papaneophytou, C and Pieri, M and Makreli, ME and Charidemou, E and Andreou, EP},
title = {The Epigenetic Aging-Cancer Continuum: Biomarkers, Metabolism, and Therapy.},
journal = {Genes},
volume = {17},
number = {9},
pages = {},
doi = {10.3390/genes17091130},
pmid = {42793024},
issn = {2073-4425},
mesh = {Humans ; *Epigenesis, Genetic ; *Aging/genetics/metabolism ; *Neoplasms/genetics/metabolism/therapy/pathology ; *Biomarkers, Tumor/genetics ; DNA Methylation/genetics ; Epigenomics/methods ; },
abstract = {Aging and cancer form a biological continuum influenced by epigenomic changes, metabolic dysfunction, inflammation, cellular senescence, and loss of tissue homeostasis. Age-related epigenetic alterations can promote cancer, which exploits plasticity for evolution, immune evasion, metastasis, and resistance. Nutrition and metabolism affect this process through one-carbon metabolism, methyl-donor availability, acetyl-CoA and NAD[+] balance, redox status, microbiome metabolites, and chromatin enzyme activity. Circulating biomarkers such as cell-free DNA methylation, mutation-based ctDNA, fragmentomic features, and non-coding RNAs can detect tumor and host changes linked to aging, inflammation, nutrition, and treatment with minimal invasiveness. This review explores the epigenetic aging-cancer link, how nutrition and metabolism modify pathways, and the potential of circulating biomarkers for diagnosis, prognosis, prediction, and monitoring. The focus is on epigenetic plasticity, drug-tolerant states, resistance, epigenetic drugs, metabolic targeting, and nutritional interventions. New technologies, including single-cell and spatial epigenomics, long-read sequencing, and multimodal computational approaches, aid biomarker discovery and clinical use. Challenges include variability, misclassification, heterogeneity, confounding, reverse causality, overfitting, and limited validation. Clinical applications need standard workflows, representative cohorts, transparent models, and proof that biomarker-guided strategies improve outcomes.},
}
MeSH Terms:
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Humans
*Epigenesis, Genetic
*Aging/genetics/metabolism
*Neoplasms/genetics/metabolism/therapy/pathology
*Biomarkers, Tumor/genetics
DNA Methylation/genetics
Epigenomics/methods
RevDate: 2026-09-26
CmpDate: 2026-09-26
Advancing Epidermal Barrier Resilience in Atopic Dermatitis with Isosorbide Di-Fatty Acid Esters: From Disruption to Restoration.
Biomolecules, 16(9): pii:biom16091246.
Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease characterized by epidermal barrier dysfunction, immune dysregulation, microbial imbalance, and severe pruritus. Emerging evidence establishes that barrier disruption is a central pathogenic driver capable of initiating inflammatory signaling, neuroimmune activation, and chronic disease instability. This understanding has shifted therapeutic paradigms toward barrier-directed strategies aimed at restoring epidermal resilience. This narrative review evaluates the mechanistic and clinical evidence surrounding isosorbide fatty acid diester molecules-specifically isosorbide dicaprylate (IDC) and isosorbide di-(linoleate/oleate) (IDL)-as a barrier-first approach for AD management. Early in vitro and ex vivo investigations demonstrated that IDC significantly improves epidermal hydration, transepidermal water loss, and the expression of barrier-associated genes linked to epidermal integrity. Subsequent studies showed that IDL expands these effects through coordinated regulation of keratinocyte differentiation, lipid homeostasis, and inflammatory stress pathways. Furthermore, recent mechanistic data highlight synergistic anti-inflammatory and pruritus-modulating effects involving TRPA1-, TRPV3-, and TSLP-associated pathways, while preserving tissue integrity under cytokine-induced stress. Clinically, these findings are supported by randomized studies in pediatric and adult cohorts demonstrating significant reductions in pruritus, favorable Eczema Area and Severity Index (EASI) responses, decreased topical corticosteroid dependence, and a reduction in the relative abundance of Staphylococcus aureus. Collectively, these findings support a barrier-first therapeutic framework in which restoration of epidermal resilience may beneficially influence multiple interconnected pathways involved in atopic dermatitis.
Additional Links: PMID-42793078
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PubMed:
Citation:
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@article {pmid42793078,
year = {2026},
author = {Chaudhuri, RK and Sivamani, RK},
title = {Advancing Epidermal Barrier Resilience in Atopic Dermatitis with Isosorbide Di-Fatty Acid Esters: From Disruption to Restoration.},
journal = {Biomolecules},
volume = {16},
number = {9},
pages = {},
doi = {10.3390/biom16091246},
pmid = {42793078},
issn = {2218-273X},
mesh = {*Dermatitis, Atopic/drug therapy/metabolism/pathology ; Humans ; *Epidermis/drug effects/metabolism/pathology ; *Isosorbide/pharmacology/therapeutic use/chemistry ; Animals ; *Esters/chemistry ; Pruritus/drug therapy ; },
abstract = {Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease characterized by epidermal barrier dysfunction, immune dysregulation, microbial imbalance, and severe pruritus. Emerging evidence establishes that barrier disruption is a central pathogenic driver capable of initiating inflammatory signaling, neuroimmune activation, and chronic disease instability. This understanding has shifted therapeutic paradigms toward barrier-directed strategies aimed at restoring epidermal resilience. This narrative review evaluates the mechanistic and clinical evidence surrounding isosorbide fatty acid diester molecules-specifically isosorbide dicaprylate (IDC) and isosorbide di-(linoleate/oleate) (IDL)-as a barrier-first approach for AD management. Early in vitro and ex vivo investigations demonstrated that IDC significantly improves epidermal hydration, transepidermal water loss, and the expression of barrier-associated genes linked to epidermal integrity. Subsequent studies showed that IDL expands these effects through coordinated regulation of keratinocyte differentiation, lipid homeostasis, and inflammatory stress pathways. Furthermore, recent mechanistic data highlight synergistic anti-inflammatory and pruritus-modulating effects involving TRPA1-, TRPV3-, and TSLP-associated pathways, while preserving tissue integrity under cytokine-induced stress. Clinically, these findings are supported by randomized studies in pediatric and adult cohorts demonstrating significant reductions in pruritus, favorable Eczema Area and Severity Index (EASI) responses, decreased topical corticosteroid dependence, and a reduction in the relative abundance of Staphylococcus aureus. Collectively, these findings support a barrier-first therapeutic framework in which restoration of epidermal resilience may beneficially influence multiple interconnected pathways involved in atopic dermatitis.},
}
MeSH Terms:
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hide MeSH Terms
*Dermatitis, Atopic/drug therapy/metabolism/pathology
Humans
*Epidermis/drug effects/metabolism/pathology
*Isosorbide/pharmacology/therapeutic use/chemistry
Animals
*Esters/chemistry
Pruritus/drug therapy
RevDate: 2026-09-26
CmpDate: 2026-09-26
β3-Adrenergic Signaling Preserves Postnatal Maturation of the Enteric Nervous System and Gut Microbiome During Neonatal Hyperoxia.
Biomolecules, 16(9): pii:biom16091284.
Oxygen availability is a key regulator of organ maturation during the perinatal period. Disruption of physiological oxygen homeostasis contributes to prematurity-associated disorders, yet its effects on the coordinated maturation of the enteric nervous system (ENS) and gut microbiome remain poorly understood. Because β3-adrenergic receptor (β3-AR) signaling has emerged as a mediator of tissue adaptation to oxygen, we investigated whether activation of this pathway modulates hyperoxia-induced alterations in the developing colon. Newborn rats were exposed to normoxia or hyperoxia (85% O2) from birth to postnatal day 14 and treated with the β3-AR agonist BRL37344 (1 or 3 mg/kg). Enteric neuronal and glial populations were evaluated by quantitative immunofluorescence, whereas the colonic microbiome (CM) was characterized by 16S rRNA gene sequencing. Hyperoxia reduced neuronal density and altered neurochemical coding within the submucosal plexus, disrupted enteric glial organization in both the colonic submucosal plexus and mucosa, and remodeled the intestinal microbiome without affecting overall community diversity. BRL37344 treatment partially preserved submucosal neurochemical coding, modulated neuron-glia organization within the submucosal plexus, prevented the loss of mucosal enteric glial cells, and reshaped microbial composition. Collectively, these findings demonstrate that neonatal hyperoxia disrupts coordinated postnatal maturation of the ENS and CM and indicate that β3-AR signaling may contribute to postnatal intestinal adaptation to neonatal oxygen imbalance.
Additional Links: PMID-42793116
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PubMed:
Citation:
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@article {pmid42793116,
year = {2026},
author = {Nardini, P and Bertorello, S and Filippi, L and Zizi, V and Cioffi, I and Cei, F and Baldi, S and Bani, D and Calvani, M and Fazi, C and Amedei, A and Pini, A},
title = {β3-Adrenergic Signaling Preserves Postnatal Maturation of the Enteric Nervous System and Gut Microbiome During Neonatal Hyperoxia.},
journal = {Biomolecules},
volume = {16},
number = {9},
pages = {},
doi = {10.3390/biom16091284},
pmid = {42793116},
issn = {2218-273X},
support = {OBERON, 2022FYBMEX//Ministry of Universities and Research/ ; 0106182//Meyer Foundation Italy/ ; B/2022/0198).//Intesa Sanpaolo Charity/ ; },
mesh = {Animals ; *Enteric Nervous System/metabolism/growth & development/drug effects ; Animals, Newborn ; Signal Transduction ; *Hyperoxia/metabolism/microbiology ; Rats ; *Gastrointestinal Microbiome/drug effects ; *Receptors, Adrenergic, beta-3/metabolism ; Colon/microbiology/metabolism ; Neurons/metabolism ; Female ; Male ; Neuroglia/metabolism ; Rats, Sprague-Dawley ; },
abstract = {Oxygen availability is a key regulator of organ maturation during the perinatal period. Disruption of physiological oxygen homeostasis contributes to prematurity-associated disorders, yet its effects on the coordinated maturation of the enteric nervous system (ENS) and gut microbiome remain poorly understood. Because β3-adrenergic receptor (β3-AR) signaling has emerged as a mediator of tissue adaptation to oxygen, we investigated whether activation of this pathway modulates hyperoxia-induced alterations in the developing colon. Newborn rats were exposed to normoxia or hyperoxia (85% O2) from birth to postnatal day 14 and treated with the β3-AR agonist BRL37344 (1 or 3 mg/kg). Enteric neuronal and glial populations were evaluated by quantitative immunofluorescence, whereas the colonic microbiome (CM) was characterized by 16S rRNA gene sequencing. Hyperoxia reduced neuronal density and altered neurochemical coding within the submucosal plexus, disrupted enteric glial organization in both the colonic submucosal plexus and mucosa, and remodeled the intestinal microbiome without affecting overall community diversity. BRL37344 treatment partially preserved submucosal neurochemical coding, modulated neuron-glia organization within the submucosal plexus, prevented the loss of mucosal enteric glial cells, and reshaped microbial composition. Collectively, these findings demonstrate that neonatal hyperoxia disrupts coordinated postnatal maturation of the ENS and CM and indicate that β3-AR signaling may contribute to postnatal intestinal adaptation to neonatal oxygen imbalance.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Enteric Nervous System/metabolism/growth & development/drug effects
Animals, Newborn
Signal Transduction
*Hyperoxia/metabolism/microbiology
Rats
*Gastrointestinal Microbiome/drug effects
*Receptors, Adrenergic, beta-3/metabolism
Colon/microbiology/metabolism
Neurons/metabolism
Female
Male
Neuroglia/metabolism
Rats, Sprague-Dawley
RevDate: 2026-09-26
CmpDate: 2026-09-26
The Nexus of Gut Microbiome, Microbial Metabolites, and Colonization Resistance Against Enteric Pathogens.
Biomolecules, 16(9): pii:biom16091291.
The gut microbiome is a complex ecological system crucial to human physiology. Commensal microbes in the gut provide resistance against pathogenic colonization, mainly due to their metabolites. Though studies have revealed a few mechanisms of microbial metabolite-mediated colonization resistance, various commensal microbes in the gut produce versatile metabolites and confront different pathogens. To pave the way for microbial metabolite-based treatment, clarification of what microbes and derived metabolites contribute to colonization resistance is a central topic. This focused review addressed the nexus of the gut microbiome, microbial metabolites, and colonization resistance against three representative pathogens, namely Clostridioides difficile, Salmonella enterica subspecies enterica serovar Typhimurium, and vancomycin-resistant Enterococcus. Different microbes and microbial metabolites involved in colonization resistance against these pathogens are discussed. Microbial metabolites, mainly short-chain fatty acids, secondary bile acids, and bacteriocins, were included. The emerging role of signal molecules in combating pathogenic infections is also addressed. In contrast to others, we further discussed different strategies that can enhance microbial metabolite-mediated colonization resistance, such as precise microbial preparation, targeted proliferation of a protective metabolite-producing microbiome, regulation of dietary patterns to optimize metabolic homeostasis, enhancing the local concentration of metabolites in the gut, and host-matched intervention.
Additional Links: PMID-42793123
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PubMed:
Citation:
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@article {pmid42793123,
year = {2026},
author = {Jiang, M and Yang, M and Du, P and Sun, Z},
title = {The Nexus of Gut Microbiome, Microbial Metabolites, and Colonization Resistance Against Enteric Pathogens.},
journal = {Biomolecules},
volume = {16},
number = {9},
pages = {},
doi = {10.3390/biom16091291},
pmid = {42793123},
issn = {2218-273X},
support = {252301420120//the Science and Technology Research and Development Program Joint Fund/ ; HN2022105//the Henan Province Postdoctoral Research Project Initiation Fund/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; Bacteriocins/metabolism ; Bile Acids and Salts/metabolism ; Animals ; Clostridioides difficile/pathogenicity ; Fatty Acids, Volatile/metabolism ; Salmonella typhimurium/pathogenicity ; Vancomycin-Resistant Enterococci/metabolism ; },
abstract = {The gut microbiome is a complex ecological system crucial to human physiology. Commensal microbes in the gut provide resistance against pathogenic colonization, mainly due to their metabolites. Though studies have revealed a few mechanisms of microbial metabolite-mediated colonization resistance, various commensal microbes in the gut produce versatile metabolites and confront different pathogens. To pave the way for microbial metabolite-based treatment, clarification of what microbes and derived metabolites contribute to colonization resistance is a central topic. This focused review addressed the nexus of the gut microbiome, microbial metabolites, and colonization resistance against three representative pathogens, namely Clostridioides difficile, Salmonella enterica subspecies enterica serovar Typhimurium, and vancomycin-resistant Enterococcus. Different microbes and microbial metabolites involved in colonization resistance against these pathogens are discussed. Microbial metabolites, mainly short-chain fatty acids, secondary bile acids, and bacteriocins, were included. The emerging role of signal molecules in combating pathogenic infections is also addressed. In contrast to others, we further discussed different strategies that can enhance microbial metabolite-mediated colonization resistance, such as precise microbial preparation, targeted proliferation of a protective metabolite-producing microbiome, regulation of dietary patterns to optimize metabolic homeostasis, enhancing the local concentration of metabolites in the gut, and host-matched intervention.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome
Bacteriocins/metabolism
Bile Acids and Salts/metabolism
Animals
Clostridioides difficile/pathogenicity
Fatty Acids, Volatile/metabolism
Salmonella typhimurium/pathogenicity
Vancomycin-Resistant Enterococci/metabolism
RevDate: 2026-09-26
CmpDate: 2026-09-26
Pollutant Burden in Autism Spectrum Disorder: Mechanistic Convergence, Genetic Susceptibility, and Clinical Translation.
Current issues in molecular biology, 48(9): pii:cimb48090878.
Autism spectrum disorder (ASD) risk reflects genetic susceptibility and modifiable environmental exposures acting during fetal and early postnatal critical periods. Building on our prior two-path model, in which folate receptor autoantibody-driven cerebral folate deficiency and oxidative stress/neuroinflammation converge on disrupted neurodevelopment, this review provides the first full mechanistic treatment of environmental pollutants within that framework. We synthesize evidence across seven exposure categories: micro/nanoplastics, plastic-associated endocrine-disrupting chemicals, ambient/indoor air pollution, tire wear particles and 6PPD-quinone, heavy metals and pesticides, industrial chemicals and persistent organic pollutants, and ultra-processed food intake as a parallel, non-pollutant contributor to the same inflammatory pathway. Human biomonitoring of micro/nanoplastics has progressed beyond detection in the placenta, brain and breast milk to direct evidence of placental genotoxicity and fetal endocrine disruption, complementing rodent data linking early-life exposure to impaired corticogenesis, disrupted microglial synaptic pruning, and ASD-relevant behavioral deficits. Across categories, oxidative stress, barrier disruption, neuroinflammation, endocrine disruption, and epigenetic modification recur as convergent mechanisms acting on trimester- and age-specific windows of vulnerability. Genetic variation in folate pathway and mitochondrial genes, as well as folate/vitamin B sufficiency, are proposed as candidate effect modifiers rather than established protective factors to modify susceptibility to this pollutant burden. Most evidence is associational or mechanistic rather than trial-based; we grade evidence strength and translate findings into biomarker-guided clinical and population-level policy guidance.
Additional Links: PMID-42793234
Publisher:
PubMed:
Citation:
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@article {pmid42793234,
year = {2026},
author = {Ayoub, G},
title = {Pollutant Burden in Autism Spectrum Disorder: Mechanistic Convergence, Genetic Susceptibility, and Clinical Translation.},
journal = {Current issues in molecular biology},
volume = {48},
number = {9},
pages = {},
doi = {10.3390/cimb48090878},
pmid = {42793234},
issn = {1467-3045},
abstract = {Autism spectrum disorder (ASD) risk reflects genetic susceptibility and modifiable environmental exposures acting during fetal and early postnatal critical periods. Building on our prior two-path model, in which folate receptor autoantibody-driven cerebral folate deficiency and oxidative stress/neuroinflammation converge on disrupted neurodevelopment, this review provides the first full mechanistic treatment of environmental pollutants within that framework. We synthesize evidence across seven exposure categories: micro/nanoplastics, plastic-associated endocrine-disrupting chemicals, ambient/indoor air pollution, tire wear particles and 6PPD-quinone, heavy metals and pesticides, industrial chemicals and persistent organic pollutants, and ultra-processed food intake as a parallel, non-pollutant contributor to the same inflammatory pathway. Human biomonitoring of micro/nanoplastics has progressed beyond detection in the placenta, brain and breast milk to direct evidence of placental genotoxicity and fetal endocrine disruption, complementing rodent data linking early-life exposure to impaired corticogenesis, disrupted microglial synaptic pruning, and ASD-relevant behavioral deficits. Across categories, oxidative stress, barrier disruption, neuroinflammation, endocrine disruption, and epigenetic modification recur as convergent mechanisms acting on trimester- and age-specific windows of vulnerability. Genetic variation in folate pathway and mitochondrial genes, as well as folate/vitamin B sufficiency, are proposed as candidate effect modifiers rather than established protective factors to modify susceptibility to this pollutant burden. Most evidence is associational or mechanistic rather than trial-based; we grade evidence strength and translate findings into biomarker-guided clinical and population-level policy guidance.},
}
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RJR Experience and Expertise
Researcher
Robbins holds BS, MS, and PhD degrees in the life sciences. He served as a tenured faculty member in the Zoology and Biological Science departments at Michigan State University. He is currently exploring the intersection between genomics, microbial ecology, and biodiversity — an area that promises to transform our understanding of the biosphere.
Educator
Robbins has extensive experience in college-level education: At MSU he taught introductory biology, genetics, and population genetics. At JHU, he was an instructor for a special course on biological database design. At FHCRC, he team-taught a graduate-level course on the history of genetics. At Bellevue College he taught medical informatics.
Administrator
Robbins has been involved in science administration at both the federal and the institutional levels. At NSF he was a program officer for database activities in the life sciences, at DOE he was a program officer for information infrastructure in the human genome project. At the Fred Hutchinson Cancer Research Center, he served as a vice president for fifteen years.
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Robbins has been involved with information technology since writing his first Fortran program as a college student. At NSF he was the first program officer for database activities in the life sciences. At JHU he held an appointment in the CS department and served as director of the informatics core for the Genome Data Base. At the FHCRC he was VP for Information Technology.
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While still at Michigan State, Robbins started his first publishing venture, founding a small company that addressed the short-run publishing needs of instructors in very large undergraduate classes. For more than 20 years, Robbins has been operating The Electronic Scholarly Publishing Project, a web site dedicated to the digital publishing of critical works in science, especially classical genetics.
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Robbins is well-known for his speaking abilities and is often called upon to provide keynote or plenary addresses at international meetings. For example, in July, 2012, he gave a well-received keynote address at the Global Biodiversity Informatics Congress, sponsored by GBIF and held in Copenhagen. The slides from that talk can be seen HERE.
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Robbins is a skilled meeting facilitator. He prefers a participatory approach, with part of the meeting involving dynamic breakout groups, created by the participants in real time: (1) individuals propose breakout groups; (2) everyone signs up for one (or more) groups; (3) the groups with the most interested parties then meet, with reports from each group presented and discussed in a subsequent plenary session.
Designer
Robbins has been engaged with photography and design since the 1960s, when he worked for a professional photography laboratory. He now prefers digital photography and tools for their precision and reproducibility. He designed his first web site more than 20 years ago and he personally designed and implemented this web site. He engages in graphic design as a hobby.
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