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RJR: Recommended Bibliography 16 Aug 2026 at 01:52 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: 2026-08-14
Nanoparticles in climate-resilient agriculture: Biological mechanisms, rhizosphere interactions, and yield enhancement under abiotic stress.
Microbiological research, 313:128683 pii:S0944-5013(26)00247-8 [Epub ahead of print].
Climate change intensifies abiotic stresses that limit crop productivity, requiring innovative strategies to enhance resilience without compromising sustainability. Nanoparticles (NPs) have emerged as potential modulators of plant stress responses by influencing molecular regulation, physiological adaptation, and stress resilience. However, current evidence remains fragmented because studies are dispersed across different NP types, crop species, abiotic stress conditions, and omics platforms, with most investigations conducted under controlled experimental conditions and few integrating molecular responses with agronomic performance. In this study, we synthesize evidence from plant physiology, omics (including transcriptomics, proteomics, metabolomics, and soil microbiome analyses), and agronomic studies to provide an integrated conceptual synthesis linking NPs' physicochemical properties with multi-omics reprogramming and yield-related outcomes under abiotic stress. Collectively, the available evidence indicates that NP size, surface charge, composition, and redox activity strongly influence uptake behavior, intracellular interactions, and signaling intensity, thereby shaping coordinated system-level responses rather than isolated modifications in individual genes, proteins, or metabolites. Across abiotic stresses, NPs modulate stress responses through effects on redox homeostasis, hormonal signaling, ion transport, metabolic flexibility, and rhizosphere interactions. However, their effects vary with NP properties, application conditions, plant species, and stress environments, ranging from stress mitigation to growth inhibition. These responses can improve photosynthetic stability, reproductive performance, and resource allocation, contributing to partial recovery of growth and yield under certain stress conditions. Conversely, excessive or poorly controlled NP exposure disrupts redox balance and growth, underscoring the importance of narrow efficacy windows. We further identify key limitations in the existing literature, including dose and crop specificity, short-term experimental designs, limited field validation, and limited mechanistic linkage between multi-omics responses and agronomic performance, highlighting the need for synchronized multi-omics validation. We contend that future advancements require a transition from proof-of-concept demonstrations to predictive, system-level approaches that integrate multi-omics with developmental stage, environmental context, and yield stability. By reframing NPs as context-dependent modulators of stress resilience rather than universal growth enhancers, this review provides a conceptual foundation for their responsible evaluation and potential application in climate-resilient agriculture.
Additional Links: PMID-42600524
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PubMed:
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@article {pmid42600524,
year = {2026},
author = {Khan, R and Uddin, N and Srivastava, AK and Iqbal, A and Riaz, A and Kamran, A and Xie, X and Yang, S},
title = {Nanoparticles in climate-resilient agriculture: Biological mechanisms, rhizosphere interactions, and yield enhancement under abiotic stress.},
journal = {Microbiological research},
volume = {313},
number = {},
pages = {128683},
doi = {10.1016/j.micres.2026.128683},
pmid = {42600524},
issn = {1618-0623},
abstract = {Climate change intensifies abiotic stresses that limit crop productivity, requiring innovative strategies to enhance resilience without compromising sustainability. Nanoparticles (NPs) have emerged as potential modulators of plant stress responses by influencing molecular regulation, physiological adaptation, and stress resilience. However, current evidence remains fragmented because studies are dispersed across different NP types, crop species, abiotic stress conditions, and omics platforms, with most investigations conducted under controlled experimental conditions and few integrating molecular responses with agronomic performance. In this study, we synthesize evidence from plant physiology, omics (including transcriptomics, proteomics, metabolomics, and soil microbiome analyses), and agronomic studies to provide an integrated conceptual synthesis linking NPs' physicochemical properties with multi-omics reprogramming and yield-related outcomes under abiotic stress. Collectively, the available evidence indicates that NP size, surface charge, composition, and redox activity strongly influence uptake behavior, intracellular interactions, and signaling intensity, thereby shaping coordinated system-level responses rather than isolated modifications in individual genes, proteins, or metabolites. Across abiotic stresses, NPs modulate stress responses through effects on redox homeostasis, hormonal signaling, ion transport, metabolic flexibility, and rhizosphere interactions. However, their effects vary with NP properties, application conditions, plant species, and stress environments, ranging from stress mitigation to growth inhibition. These responses can improve photosynthetic stability, reproductive performance, and resource allocation, contributing to partial recovery of growth and yield under certain stress conditions. Conversely, excessive or poorly controlled NP exposure disrupts redox balance and growth, underscoring the importance of narrow efficacy windows. We further identify key limitations in the existing literature, including dose and crop specificity, short-term experimental designs, limited field validation, and limited mechanistic linkage between multi-omics responses and agronomic performance, highlighting the need for synchronized multi-omics validation. We contend that future advancements require a transition from proof-of-concept demonstrations to predictive, system-level approaches that integrate multi-omics with developmental stage, environmental context, and yield stability. By reframing NPs as context-dependent modulators of stress resilience rather than universal growth enhancers, this review provides a conceptual foundation for their responsible evaluation and potential application in climate-resilient agriculture.},
}
RevDate: 2026-08-14
The Early Post-Transplantation Lung Microbiome and CXCL10 are Associated with Chronic Lung Allograft Dysfunction: A Prospective Study with 5-year Follow-Up.
American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons pii:S1600-6135(26)02730-9 [Epub ahead of print].
Chronic lung allograft dysfunction (CLAD) is the major barrier to long-term lung transplantation success. Microbial factors have been linked to CLAD risk, and sequence-based methods have been applied recently to identify potential microbial drivers, though patient heterogeneity and follow-up time have been limitations. We undertook a longitudinal cohort study of 186 patients transplanted for diseases other than cystic fibrosis. Dense lung sampling was done over the first-year and patients were followed for 6.04 (median) years. Bronchoalveolar lavage (BAL) was analyzed by bacterial 16S rRNA gene sequencing and quantification. Post-implantation BAL was assayed for cytokines and metabolomics. Seventy patients (38%) developed CLAD. CLAD development and shorter time-to-CLAD were associated with higher lung bacterial burden particularly 6-months post-transplant, low Streptococcus/Prevotella ratio in lung six-weeks post-transplant, and elevated lung IP10/CXCL10 immediately post-implantation. Each factor associated with distinct CLAD timing. These factors, together with previously-recognized clinical features, stratify patients into groups differing by >3-fold CLAD risk. Thus, increased lung bacteria and altered composition during the first-year post-transplantation and immediate post-implantation IP10/CXCL10 associate with CLAD after transplantation for non-CF lung disease. Early events in the allograft may establish conditions impacting later graft failure, identify potentially modifiable mechanisms of injury, and provide biomarkers of CLAD risk.
Additional Links: PMID-42600695
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PubMed:
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@article {pmid42600695,
year = {2026},
author = {Merenstein, C and McGinniss, JE and Gallop, R and Whiteside, SA and Pandya, K and Oyster, M and Graham-Wooten, J and Kalman, L and Clausen, E and Cantu, E and Diamond, JM and Bushman, FD and Christie, JD and Collman, RG},
title = {The Early Post-Transplantation Lung Microbiome and CXCL10 are Associated with Chronic Lung Allograft Dysfunction: A Prospective Study with 5-year Follow-Up.},
journal = {American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ajt.2026.08.009},
pmid = {42600695},
issn = {1600-6143},
abstract = {Chronic lung allograft dysfunction (CLAD) is the major barrier to long-term lung transplantation success. Microbial factors have been linked to CLAD risk, and sequence-based methods have been applied recently to identify potential microbial drivers, though patient heterogeneity and follow-up time have been limitations. We undertook a longitudinal cohort study of 186 patients transplanted for diseases other than cystic fibrosis. Dense lung sampling was done over the first-year and patients were followed for 6.04 (median) years. Bronchoalveolar lavage (BAL) was analyzed by bacterial 16S rRNA gene sequencing and quantification. Post-implantation BAL was assayed for cytokines and metabolomics. Seventy patients (38%) developed CLAD. CLAD development and shorter time-to-CLAD were associated with higher lung bacterial burden particularly 6-months post-transplant, low Streptococcus/Prevotella ratio in lung six-weeks post-transplant, and elevated lung IP10/CXCL10 immediately post-implantation. Each factor associated with distinct CLAD timing. These factors, together with previously-recognized clinical features, stratify patients into groups differing by >3-fold CLAD risk. Thus, increased lung bacteria and altered composition during the first-year post-transplantation and immediate post-implantation IP10/CXCL10 associate with CLAD after transplantation for non-CF lung disease. Early events in the allograft may establish conditions impacting later graft failure, identify potentially modifiable mechanisms of injury, and provide biomarkers of CLAD risk.},
}
RevDate: 2026-08-15
Prospective associations of tea consumption with skeletal muscle mass and strength: Insights from the gut microbiome and proteomics.
Pharmacological research, 231:108398 pii:S1043-6618(26)00313-0 [Epub ahead of print].
Tea consumption may be associated with skeletal muscle health, but longitudinal evidence based on repeated assessments remains limited. We examined the associations of tea intake and serum biomarkers with repeated skeletal muscle measures and explored whether these associations might be partly explained by multi-omics features. In this prospective cohort, 3408 adults were followed for approximately 12 years. Skeletal muscle mass was measured by dual-energy X-ray absorptiometry, handgrip strength by digital dynamometry, gut microbial taxonomic and functional profiles by shotgun metagenomic sequencing, serum proteins by data-independent acquisition mass spectrometry, and fecal metabolites by targeted UPLC-MS/MS metabolomics. Linear mixed-effects models examined longitudinal associations, and mediation analyses estimated indirect effects. In longitudinal analyses, higher tea consumption frequency was associated with greater appendicular skeletal muscle mass, appendicular skeletal muscle index, and handgrip strength (β: 0.037-0.140; 95% CI: 0.002-0.205). Higher circulating flavan-3-ols showed similar associations with these muscle-related outcomes (β: 0.085-0.174; 95% CI: 0.007-0.254), whereas no significant associations were observed with walking speed. Exploratory multi-omics analyses identified tea-related differences in gut microbial species and functional pathways, fecal metabolites, and circulating proteins, including Gemmiger formicilis, amino acid biosynthesis pathways, fructose 1,6-bisphosphate, VTN, CFI, CNDP1, and ITIH4. Exploratory mediation analyses identified statistical indirect associations involving multi-omics features, with estimated proportions mediated ranging from 4.5% to 19.0%. Overall, higher tea consumption and circulating biomarkers were associated with greater skeletal muscle mass and strength, accompanied by distinct multi-omics features that may provide potential biological links between tea exposure and muscle-related outcomes.
Additional Links: PMID-42600761
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PubMed:
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@article {pmid42600761,
year = {2026},
author = {Hong, Z and Lu, Z and Shi, R and Zheng, S and Luo, J and Chen, J and Xie, Z and Zheng, JS and Chen, YM and Zhang, Z},
title = {Prospective associations of tea consumption with skeletal muscle mass and strength: Insights from the gut microbiome and proteomics.},
journal = {Pharmacological research},
volume = {231},
number = {},
pages = {108398},
doi = {10.1016/j.phrs.2026.108398},
pmid = {42600761},
issn = {1096-1186},
abstract = {Tea consumption may be associated with skeletal muscle health, but longitudinal evidence based on repeated assessments remains limited. We examined the associations of tea intake and serum biomarkers with repeated skeletal muscle measures and explored whether these associations might be partly explained by multi-omics features. In this prospective cohort, 3408 adults were followed for approximately 12 years. Skeletal muscle mass was measured by dual-energy X-ray absorptiometry, handgrip strength by digital dynamometry, gut microbial taxonomic and functional profiles by shotgun metagenomic sequencing, serum proteins by data-independent acquisition mass spectrometry, and fecal metabolites by targeted UPLC-MS/MS metabolomics. Linear mixed-effects models examined longitudinal associations, and mediation analyses estimated indirect effects. In longitudinal analyses, higher tea consumption frequency was associated with greater appendicular skeletal muscle mass, appendicular skeletal muscle index, and handgrip strength (β: 0.037-0.140; 95% CI: 0.002-0.205). Higher circulating flavan-3-ols showed similar associations with these muscle-related outcomes (β: 0.085-0.174; 95% CI: 0.007-0.254), whereas no significant associations were observed with walking speed. Exploratory multi-omics analyses identified tea-related differences in gut microbial species and functional pathways, fecal metabolites, and circulating proteins, including Gemmiger formicilis, amino acid biosynthesis pathways, fructose 1,6-bisphosphate, VTN, CFI, CNDP1, and ITIH4. Exploratory mediation analyses identified statistical indirect associations involving multi-omics features, with estimated proportions mediated ranging from 4.5% to 19.0%. Overall, higher tea consumption and circulating biomarkers were associated with greater skeletal muscle mass and strength, accompanied by distinct multi-omics features that may provide potential biological links between tea exposure and muscle-related outcomes.},
}
RevDate: 2026-08-14
Forest conversion is more strongly associated with soil microbial functioning than chronic trace element exposure in an industrialized coastal Mediterranean ecosystem.
Environmental pollution (Barking, Essex : 1987) pii:S0269-7491(26)01333-3 [Epub ahead of print].
Forest soils in industrialized coastal zones can experience chronic diffuse trace element (TE) exposure, yet how vegetation replacement influences soil microbial communities under these conditions remains poorly understood. This study compared soils from native sclerophyllous forests and exotic pine plantations in the Hualpén Peninsula Nature Sanctuary (Chile), located near an industrial complex characterized by oil refining, petrochemical, steel, and port activities. Twenty-two soil sites were evaluated for TE concentrations, contamination indices, physicochemical properties, microbial biomass, enzymatic activities, and bacterial community composition using 16S rRNA gene sequencing. Native forest soils contained 89% more organic matter (14.4% vs. 7.6%) and nearly twice the available N (53.6 vs. 26.2 mg kg[-1]) than plantation soils. These soils also exhibited greater respiration and microbial biomass carbon, whereas plantation soils showed higher metabolic quotients (qCO2), indicating lower microbial metabolic efficiency. Soil pH remained acidic in both systems (5.6-5.8). Mn and Zn were the most abundant elements, while contamination factors were highest for Pb, Cr, and Mn, indicating persistent trace element enrichment across the study area. Bacterial communities were dominated by Proteobacteria, Actinobacteriota, and Acidobacteriota, with native forest soils showing significantly higher Faith phylogenetic diversity (p = 0.041). Redundancy analysis revealed that bacterial community structure was more strongly associated with nutrient availability and microbial functional indicators than with trace element enrichment. However, Cr showed a significant secondary association (envfit r[2] = 0.53, p = 0.032). Overall, the results indicate that variation in soil microbial functioning was more closely associated with vegetation type and related soil properties than with chronic trace element enrichment. These findings highlight the importance of considering land-use change, soil quality, and contamination together when evaluating microbial responses in industrially influenced forest ecosystems.
Additional Links: PMID-42600831
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PubMed:
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@article {pmid42600831,
year = {2026},
author = {Fabian Plaza, S and Gonzalo Tortella, F and Larama, G and Rodriguez, R and Lebeau, T and Lapie, C and Valdivia, W and Fajardo, E and Fernández-Baldo, M and Hirzel, J and Santoyo, G and Schoebitz, M},
title = {Forest conversion is more strongly associated with soil microbial functioning than chronic trace element exposure in an industrialized coastal Mediterranean ecosystem.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {128963},
doi = {10.1016/j.envpol.2026.128963},
pmid = {42600831},
issn = {1873-6424},
abstract = {Forest soils in industrialized coastal zones can experience chronic diffuse trace element (TE) exposure, yet how vegetation replacement influences soil microbial communities under these conditions remains poorly understood. This study compared soils from native sclerophyllous forests and exotic pine plantations in the Hualpén Peninsula Nature Sanctuary (Chile), located near an industrial complex characterized by oil refining, petrochemical, steel, and port activities. Twenty-two soil sites were evaluated for TE concentrations, contamination indices, physicochemical properties, microbial biomass, enzymatic activities, and bacterial community composition using 16S rRNA gene sequencing. Native forest soils contained 89% more organic matter (14.4% vs. 7.6%) and nearly twice the available N (53.6 vs. 26.2 mg kg[-1]) than plantation soils. These soils also exhibited greater respiration and microbial biomass carbon, whereas plantation soils showed higher metabolic quotients (qCO2), indicating lower microbial metabolic efficiency. Soil pH remained acidic in both systems (5.6-5.8). Mn and Zn were the most abundant elements, while contamination factors were highest for Pb, Cr, and Mn, indicating persistent trace element enrichment across the study area. Bacterial communities were dominated by Proteobacteria, Actinobacteriota, and Acidobacteriota, with native forest soils showing significantly higher Faith phylogenetic diversity (p = 0.041). Redundancy analysis revealed that bacterial community structure was more strongly associated with nutrient availability and microbial functional indicators than with trace element enrichment. However, Cr showed a significant secondary association (envfit r[2] = 0.53, p = 0.032). Overall, the results indicate that variation in soil microbial functioning was more closely associated with vegetation type and related soil properties than with chronic trace element enrichment. These findings highlight the importance of considering land-use change, soil quality, and contamination together when evaluating microbial responses in industrially influenced forest ecosystems.},
}
RevDate: 2026-08-14
Metagenomics reveals rumen residues as a superior inoculum for volatile fatty acid production in vitro.
Bioresource technology pii:S0960-8524(26)01709-8 [Epub ahead of print].
Rumen microbiome is widely recognized as an efficient system for lignocellulose degradation. Rumen fluid (RF) has been often used as the inoculum in previous study of bioprocesses, however, the potential of rumen solids (RS) to enhance volatile fatty acid (VFA) production remains underexplored. The anaerobic fermentation performance of RS, RF, and RF + RS mixture as inocula was compared using corn stover as substrate, with RS addition at 5%, 10%, or 20% (w/w) to corn stover and RF addition at 1:2 (v/v) to buffer solution. At a corn stover content of 2.5% (w/v, based on final working volume), the highest VFA concentration of 10.05 g/L was achieved with 20% RS as inoculum, outperforming those with both RF and RF + RS. Metagenomic analysis revealed significant differences in bacterial, fungal, and archaeal community structures with 20% RS and RF. With 20% RS, hydrolytic bacteria (e.g., Enterobacter) dominated the ecological niche, microbial co-occurrence network analysis of the 2,000 most abundant genera revealed a simpler network with fewer negative associations, and functional analysis demonstrated a notable increase in relative abundance of glycosyltransferase (GT) families within carbohydrate-active enzymes (CAZymes). With 20% RS, enrichment in glycolysis-related genes was observed, indicating a preference for carbohydrate degradation, while acid-producing pathways were enriched such as pyruvate metabolism with RF. Rumen solids, as a superior inoculum for VFA production, effectively enhanced lignocellulose bioconversion by enriching specific low-abundance microbial taxa, forming a microbial network with fewer negative associations, increasing the relative abundance of GT families, and strengthening the systemic hydrolysis capacity.
Additional Links: PMID-42600856
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PubMed:
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@article {pmid42600856,
year = {2026},
author = {Li, Y and Chen, L and Zhang, J and Zhang, Y and Wang, M and Zhang, R and Fang, W and Zhang, P and Zhang, G},
title = {Metagenomics reveals rumen residues as a superior inoculum for volatile fatty acid production in vitro.},
journal = {Bioresource technology},
volume = {},
number = {},
pages = {135627},
doi = {10.1016/j.biortech.2026.135627},
pmid = {42600856},
issn = {1873-2976},
abstract = {Rumen microbiome is widely recognized as an efficient system for lignocellulose degradation. Rumen fluid (RF) has been often used as the inoculum in previous study of bioprocesses, however, the potential of rumen solids (RS) to enhance volatile fatty acid (VFA) production remains underexplored. The anaerobic fermentation performance of RS, RF, and RF + RS mixture as inocula was compared using corn stover as substrate, with RS addition at 5%, 10%, or 20% (w/w) to corn stover and RF addition at 1:2 (v/v) to buffer solution. At a corn stover content of 2.5% (w/v, based on final working volume), the highest VFA concentration of 10.05 g/L was achieved with 20% RS as inoculum, outperforming those with both RF and RF + RS. Metagenomic analysis revealed significant differences in bacterial, fungal, and archaeal community structures with 20% RS and RF. With 20% RS, hydrolytic bacteria (e.g., Enterobacter) dominated the ecological niche, microbial co-occurrence network analysis of the 2,000 most abundant genera revealed a simpler network with fewer negative associations, and functional analysis demonstrated a notable increase in relative abundance of glycosyltransferase (GT) families within carbohydrate-active enzymes (CAZymes). With 20% RS, enrichment in glycolysis-related genes was observed, indicating a preference for carbohydrate degradation, while acid-producing pathways were enriched such as pyruvate metabolism with RF. Rumen solids, as a superior inoculum for VFA production, effectively enhanced lignocellulose bioconversion by enriching specific low-abundance microbial taxa, forming a microbial network with fewer negative associations, increasing the relative abundance of GT families, and strengthening the systemic hydrolysis capacity.},
}
RevDate: 2026-08-14
Snail immunity to schistosomes: insights from omics studies.
Developmental and comparative immunology pii:S0145-305X(26)00167-9 [Epub ahead of print].
Schistosomiasis is a serious public health concern, with transmission facilitated by a small number of freshwater snail intermediate host species. Infection outcomes vary greatly across the primary vector genera, Biomphalaria (for Schistosoma mansoni), Bulinus (for S. haematobium), and Oncomelania (for S. japonicum), even within species, ranging from full resistance to high compatibility. Omics methods have altered this field by correlating host genotype, baseline immunological status, and time-resolved responses to whether invading miracidia are eliminated or develop sporocysts. Evidence from genomes, transcriptomics, proteomics, and epigenomics suggests that resistance is frequently primed prior to exposure. However, the clearest divergence between resistant and susceptible trajectories occurs during a small early window (<12-48 h) after penetration. During this time, recognition, hemocyte recruitment, and soluble effector deployment either come together quickly or are delayed and guided by parasite-derived modulators. Established infections cause the host to adapt to chronic conditions through immune regulation, metabolic reprogramming, tissue and neuroendocrine remodeling, microbiome modification, and parasite castration. Comparative genomics reveals that each vector genus has evolved its own immunogenomic profile, which includes lineage-specific expansions of recognition and effector gene families. Together, these findings can help with field surveillance and intervention by providing molecular compatibility markers, functional tools for testing candidate genes, and tactics that target parasite-derived immune modulators. Integrated multi-omics approaches are a top priority, yet they are still limited in snail vectors compared to other disease vector systems.
Additional Links: PMID-42600959
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PubMed:
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@article {pmid42600959,
year = {2026},
author = {Habib, MR},
title = {Snail immunity to schistosomes: insights from omics studies.},
journal = {Developmental and comparative immunology},
volume = {},
number = {},
pages = {105711},
doi = {10.1016/j.dci.2026.105711},
pmid = {42600959},
issn = {1879-0089},
abstract = {Schistosomiasis is a serious public health concern, with transmission facilitated by a small number of freshwater snail intermediate host species. Infection outcomes vary greatly across the primary vector genera, Biomphalaria (for Schistosoma mansoni), Bulinus (for S. haematobium), and Oncomelania (for S. japonicum), even within species, ranging from full resistance to high compatibility. Omics methods have altered this field by correlating host genotype, baseline immunological status, and time-resolved responses to whether invading miracidia are eliminated or develop sporocysts. Evidence from genomes, transcriptomics, proteomics, and epigenomics suggests that resistance is frequently primed prior to exposure. However, the clearest divergence between resistant and susceptible trajectories occurs during a small early window (<12-48 h) after penetration. During this time, recognition, hemocyte recruitment, and soluble effector deployment either come together quickly or are delayed and guided by parasite-derived modulators. Established infections cause the host to adapt to chronic conditions through immune regulation, metabolic reprogramming, tissue and neuroendocrine remodeling, microbiome modification, and parasite castration. Comparative genomics reveals that each vector genus has evolved its own immunogenomic profile, which includes lineage-specific expansions of recognition and effector gene families. Together, these findings can help with field surveillance and intervention by providing molecular compatibility markers, functional tools for testing candidate genes, and tactics that target parasite-derived immune modulators. Integrated multi-omics approaches are a top priority, yet they are still limited in snail vectors compared to other disease vector systems.},
}
RevDate: 2026-08-14
Enhancing Anthocyanin Bioavailability Unlocks the Cardiovascular Potential of Grape Pomace: A Review.
The Journal of nutrition pii:S0022-3166(26)00433-5 [Epub ahead of print].
Grape pomace (GP) is a major byproduct of the wine industry, rich in bioactive compounds such as polyphenols, anthocyanins (ACYs), and fiber, all of which have important functional properties. GP is composed of stalks, seeds, and skins. ACYs, a major component of GP, are key contributors to its functional properties, particularly in supporting cardiovascular health. However, a significant challenge with ACYs is their limited stability and bioavailability. This review explores the chemistry, extraction, and purification of ACYs, primarily from GP, where they are often bound within the plant cell wall. The cell wall matrix hinders the release and absorption of ACYs in the gastrointestinal tract, resulting in low natural bioavailability. Non-thermal extraction techniques designed to liberate ACYs from this matrix are highlighted for their potential to enhance bioavailability. The review also discusses encapsulation methods and novel approaches such as electrospinning, which may further improve ACY stability and controlled release. Additionally, the antioxidant and anti-inflammatory effects of GP, its influence on short-chain fatty acid production, and findings from recent in vitro, in vivo, and human studies are summarized. Finally, the potential mechanisms by which ACYs in GP may benefit cardiovascular health are explored. Nonetheless, further research is needed to clarify the specific metabolites, underlying mechanisms, and unique properties of ACYs found in GP.
Additional Links: PMID-42600988
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PubMed:
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@article {pmid42600988,
year = {2026},
author = {Ghanta, CC and Thapa, A and Tao, Z and Rohatgi, A and Mineo, C and Kalbasi-Ashtari, A and Pahlavani, M},
title = {Enhancing Anthocyanin Bioavailability Unlocks the Cardiovascular Potential of Grape Pomace: A Review.},
journal = {The Journal of nutrition},
volume = {},
number = {},
pages = {101784},
doi = {10.1016/j.tjnut.2026.101784},
pmid = {42600988},
issn = {1541-6100},
abstract = {Grape pomace (GP) is a major byproduct of the wine industry, rich in bioactive compounds such as polyphenols, anthocyanins (ACYs), and fiber, all of which have important functional properties. GP is composed of stalks, seeds, and skins. ACYs, a major component of GP, are key contributors to its functional properties, particularly in supporting cardiovascular health. However, a significant challenge with ACYs is their limited stability and bioavailability. This review explores the chemistry, extraction, and purification of ACYs, primarily from GP, where they are often bound within the plant cell wall. The cell wall matrix hinders the release and absorption of ACYs in the gastrointestinal tract, resulting in low natural bioavailability. Non-thermal extraction techniques designed to liberate ACYs from this matrix are highlighted for their potential to enhance bioavailability. The review also discusses encapsulation methods and novel approaches such as electrospinning, which may further improve ACY stability and controlled release. Additionally, the antioxidant and anti-inflammatory effects of GP, its influence on short-chain fatty acid production, and findings from recent in vitro, in vivo, and human studies are summarized. Finally, the potential mechanisms by which ACYs in GP may benefit cardiovascular health are explored. Nonetheless, further research is needed to clarify the specific metabolites, underlying mechanisms, and unique properties of ACYs found in GP.},
}
RevDate: 2026-08-14
Late-Onset Neonatal Sepsis: Contemporary Epidemiology, Diagnosis, Prevention, and Precision Therapeutics.
American journal of perinatology [Epub ahead of print].
OBJECTIVES: Late-onset neonatal sepsis (LOS) remains a major challenge in modern neonatal intensive care units (NICUs), disproportionately affecting very low birth weight (VLBW) and extremely preterm infants. Despite advances in perinatal care, LOS continues to contribute to high mortality, prolonged hospitalization, and long-term neurodevelopmental impairment. Emerging trends-including evolving pathogen profiles, increased antimicrobial resistance (AMR), and widespread microbiome disruption-highlight persistent clinical and public health concerns. This review synthesizes current evidence on the epidemiology, pathophysiology, diagnosis, and management of LOS, with emphasis on evolving diagnostics, antimicrobial stewardship, prevention strategies, and emerging precision approaches. Key gaps and research priorities are highlighted to inform future clinical practice and neonatal health policy.
STUDY DESIGN: This narrative review synthesizes contemporary literature, including multicenter cohort studies, national registries, and emerging diagnostic and predictive technologies.
RESULTS: LOS arises from the complex interplay between neonatal immune immaturity, invasive NICU interventions, and microbial exposure. Gram-positive organisms predominate in high-income settings, while multidrug-resistant Gram-negative pathogens are increasingly reported in low- and middle-income countries, contributing to higher morbidity and mortality. Early-life antibiotic exposure and dysbiosis compromise the gut microbiome, further increasing susceptibility. Clinical recognition remains challenging due to nonspecific signs, often leading to delayed or excessive empiric antibiotic therapy. Rapid molecular diagnostics, emerging predictive tools, including early-warning models, and serial biomarker monitoring offer opportunities for pathogen-directed therapy, individualized pharmacokinetic optimization, and safe antimicrobial stewardship. Prevention through central-line bundles, human milk feeding, probiotics, strict hand hygiene, and context-specific infection-control strategies remains central to reducing LOS incidence.
CONCLUSIONS: LOS represents a multifactorial syndrome with profound implications for survival and neurodevelopment in preterm and VLBW infants. Effective management requires integration of precision diagnostics, individualized therapy, microbiome-preserving strategies, neuroprotective interventions, and equitable implementation of prevention and stewardship programs. Bridging mechanistic understanding with scalable, context-sensitive approaches is critical to improving survival, reducing morbidity, and optimizing long-term outcomes.
Additional Links: PMID-42601049
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PubMed:
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@article {pmid42601049,
year = {2026},
author = {Dixit, S and Dixit, S and Rao, YK and Das, A},
title = {Late-Onset Neonatal Sepsis: Contemporary Epidemiology, Diagnosis, Prevention, and Precision Therapeutics.},
journal = {American journal of perinatology},
volume = {},
number = {},
pages = {},
doi = {10.1055/a-2938-3600},
pmid = {42601049},
issn = {1098-8785},
abstract = {OBJECTIVES: Late-onset neonatal sepsis (LOS) remains a major challenge in modern neonatal intensive care units (NICUs), disproportionately affecting very low birth weight (VLBW) and extremely preterm infants. Despite advances in perinatal care, LOS continues to contribute to high mortality, prolonged hospitalization, and long-term neurodevelopmental impairment. Emerging trends-including evolving pathogen profiles, increased antimicrobial resistance (AMR), and widespread microbiome disruption-highlight persistent clinical and public health concerns. This review synthesizes current evidence on the epidemiology, pathophysiology, diagnosis, and management of LOS, with emphasis on evolving diagnostics, antimicrobial stewardship, prevention strategies, and emerging precision approaches. Key gaps and research priorities are highlighted to inform future clinical practice and neonatal health policy.
STUDY DESIGN: This narrative review synthesizes contemporary literature, including multicenter cohort studies, national registries, and emerging diagnostic and predictive technologies.
RESULTS: LOS arises from the complex interplay between neonatal immune immaturity, invasive NICU interventions, and microbial exposure. Gram-positive organisms predominate in high-income settings, while multidrug-resistant Gram-negative pathogens are increasingly reported in low- and middle-income countries, contributing to higher morbidity and mortality. Early-life antibiotic exposure and dysbiosis compromise the gut microbiome, further increasing susceptibility. Clinical recognition remains challenging due to nonspecific signs, often leading to delayed or excessive empiric antibiotic therapy. Rapid molecular diagnostics, emerging predictive tools, including early-warning models, and serial biomarker monitoring offer opportunities for pathogen-directed therapy, individualized pharmacokinetic optimization, and safe antimicrobial stewardship. Prevention through central-line bundles, human milk feeding, probiotics, strict hand hygiene, and context-specific infection-control strategies remains central to reducing LOS incidence.
CONCLUSIONS: LOS represents a multifactorial syndrome with profound implications for survival and neurodevelopment in preterm and VLBW infants. Effective management requires integration of precision diagnostics, individualized therapy, microbiome-preserving strategies, neuroprotective interventions, and equitable implementation of prevention and stewardship programs. Bridging mechanistic understanding with scalable, context-sensitive approaches is critical to improving survival, reducing morbidity, and optimizing long-term outcomes.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
The microbial communities of a tomato crop grown in Veggie under different lighting regimes on the International Space Station.
Life sciences in space research, 52:84-97.
Customized lighting treatments are being investigated to help optimize space crop production. The VEG-05 experiment on the International Space Station (ISS) investigated the effect of red-rich and blue-rich lighting in the Veggie plant-growth chamber on the microbial communities of a dwarf tomato variety Solanum lycopersicum cv. Red Robin. The microbial communities were investigated using bacterial 16S rRNA and fungal internal transcribed spacer (ITS) sequencing methods to identify bacterial and fungal communities from tomato fruit, leaves, roots, rooting substrate, and Veggie chamber surfaces grown under red-rich or blue-rich lighting. The plants were also screened using culture-based methods for potential food-borne pathogens and plate counts for bacteria and fungi. Differences in microbial load were compared between lighting conditions, as well as between ISS and ground-control treatments. Fruit production was lower on ISS-grown plants, thus limiting the number of samples available for analyses from flight plants. These analyses determined the microbiological food safety for tomato plants grown under a red-rich or a blue-rich lighting treatment and microgravity conditions. The potential core microbiome for flight tomato plants included the genera Rhizobium, Azospirillum, Burkholderia, Dyadobacter, Methylobacterium/Methylorubrum, Sphingomonas, and the family Erwiniacea. Pseudomonas was the only genus common to all ground-control plants, due to low microbial diversity on leaf samples. Culture-based pathogen screening, corroborated by 16S rRNA and ITS sequencing, yielded negative results. Our results indicate flight microbial communities show increased colonization compared to ground controls, and this increase was associated with red-rich light treatment more so than blue-rich light treatment. This experiment provides valuable data for a fruiting crop grown on the ISS and how the plant microbial community may change due to different lighting conditions.
Additional Links: PMID-42601164
Publisher:
PubMed:
Citation:
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@article {pmid42601164,
year = {2026},
author = {Spern, CJ and Hummerick, ME and Khodadad, CL and Morales, CJ and Dixit, AR and Spencer, LE and Mitchell, CA and Morrow, RC and Wheeler, RM and Massa, GD},
title = {The microbial communities of a tomato crop grown in Veggie under different lighting regimes on the International Space Station.},
journal = {Life sciences in space research},
volume = {52},
number = {},
pages = {84-97},
doi = {10.1016/j.lssr.2026.01.010},
pmid = {42601164},
issn = {2214-5532},
mesh = {*Solanum lycopersicum/microbiology/growth & development/radiation effects ; RNA, Ribosomal, 16S/genetics ; *Lighting ; Space Flight ; Red Light ; Bacteria/genetics/isolation & purification ; Spacecraft ; *Microbiota ; Blue Light ; Fungi/genetics/isolation & purification ; Light ; },
abstract = {Customized lighting treatments are being investigated to help optimize space crop production. The VEG-05 experiment on the International Space Station (ISS) investigated the effect of red-rich and blue-rich lighting in the Veggie plant-growth chamber on the microbial communities of a dwarf tomato variety Solanum lycopersicum cv. Red Robin. The microbial communities were investigated using bacterial 16S rRNA and fungal internal transcribed spacer (ITS) sequencing methods to identify bacterial and fungal communities from tomato fruit, leaves, roots, rooting substrate, and Veggie chamber surfaces grown under red-rich or blue-rich lighting. The plants were also screened using culture-based methods for potential food-borne pathogens and plate counts for bacteria and fungi. Differences in microbial load were compared between lighting conditions, as well as between ISS and ground-control treatments. Fruit production was lower on ISS-grown plants, thus limiting the number of samples available for analyses from flight plants. These analyses determined the microbiological food safety for tomato plants grown under a red-rich or a blue-rich lighting treatment and microgravity conditions. The potential core microbiome for flight tomato plants included the genera Rhizobium, Azospirillum, Burkholderia, Dyadobacter, Methylobacterium/Methylorubrum, Sphingomonas, and the family Erwiniacea. Pseudomonas was the only genus common to all ground-control plants, due to low microbial diversity on leaf samples. Culture-based pathogen screening, corroborated by 16S rRNA and ITS sequencing, yielded negative results. Our results indicate flight microbial communities show increased colonization compared to ground controls, and this increase was associated with red-rich light treatment more so than blue-rich light treatment. This experiment provides valuable data for a fruiting crop grown on the ISS and how the plant microbial community may change due to different lighting conditions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Solanum lycopersicum/microbiology/growth & development/radiation effects
RNA, Ribosomal, 16S/genetics
*Lighting
Space Flight
Red Light
Bacteria/genetics/isolation & purification
Spacecraft
*Microbiota
Blue Light
Fungi/genetics/isolation & purification
Light
RevDate: 2026-08-14
CmpDate: 2026-08-15
Enhanced salivary correlation between Streptococcus mutans and herpes simplex virus-1 in oral squamous cell carcinoma: a case-control study.
BMC oral health, 26(1):.
BACKGROUND: Streptococcus mutans modulates local immune responses in the oral mucosa and has been implicated in oral squamous cell carcinoma (OSCC) pathogenesis. Emerging evidence suggests that certain oral bacteria can influence viral infections through immune modulation. This case-control study aimed to determine whether the correlation between S. mutans and herpes simplex virus type 1 (HSV-1) differs between OSCC patients and non-tumor controls, thereby elucidating potential bacterial-viral association in the tumor microenvironment.
METHODS: Unstimulated whole saliva samples were collected from 121 individuals, including 60 non-tumor controls and 61 OSCC patients. Real-time qPCR was used to quantify S. mutans 16S rRNA abundance and HSV-1 glycoprotein D (gD) mRNA levels. Mann-Whitney U tests assessed differences between groups, and Pearson's correlation analyses evaluated bacterial-viral associations. Analysis of covariance (ANCOVA) adjusted for age and sex. Subgroup analyses examined correlations across clinical and demographic factors.
RESULTS: Salivary S. mutans 16S rRNA abundance and HSV-1 gD mRNA levels were significantly higher in OSCC patients than in controls (P = 0.0145 and P = 0.0257, respectively). A moderate correlation was observed between S. mutans and HSV-1 in non-tumor controls (r = 0.3806, P = 0.0027), whereas a substantially stronger correlation was evident in OSCC patients (r = 0.7878, P < 0.0001). Subgroup analyses revealed particularly strong correlations in individuals with alcohol consumption (r = 0.9109, P < 0.0001) and smoking history (r = 0.9062, P < 0.0001).
CONCLUSIONS: This study demonstrates a significantly stronger association between S. mutans and HSV-1 in OSCC than in non-tumor controls. These findings suggest that salivary bacterial-viral co-enrichment warrants further evaluation as a potential biomarker pair and may inform future microbiome-based strategies for OSCC risk assessment and prevention.
Additional Links: PMID-42601617
PubMed:
Citation:
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@article {pmid42601617,
year = {2026},
author = {Kim, TL and Shin, CG and Oh, SY and Lee, HJ and Kwak, S and Kwon, TG and Kim, JW and Choi, SY and Hong, SH},
title = {Enhanced salivary correlation between Streptococcus mutans and herpes simplex virus-1 in oral squamous cell carcinoma: a case-control study.},
journal = {BMC oral health},
volume = {26},
number = {1},
pages = {},
pmid = {42601617},
issn = {1472-6831},
support = {2022R1A2C2006728//National Research Foundation of Korea/ ; },
mesh = {Humans ; *Herpesvirus 1, Human/isolation & purification ; *Saliva/microbiology/virology ; Case-Control Studies ; Male ; Female ; *Carcinoma, Squamous Cell/microbiology/virology ; *Streptococcus mutans/isolation & purification ; *Mouth Neoplasms/microbiology/virology ; Middle Aged ; Aged ; Adult ; Viral Envelope Proteins ; },
abstract = {BACKGROUND: Streptococcus mutans modulates local immune responses in the oral mucosa and has been implicated in oral squamous cell carcinoma (OSCC) pathogenesis. Emerging evidence suggests that certain oral bacteria can influence viral infections through immune modulation. This case-control study aimed to determine whether the correlation between S. mutans and herpes simplex virus type 1 (HSV-1) differs between OSCC patients and non-tumor controls, thereby elucidating potential bacterial-viral association in the tumor microenvironment.
METHODS: Unstimulated whole saliva samples were collected from 121 individuals, including 60 non-tumor controls and 61 OSCC patients. Real-time qPCR was used to quantify S. mutans 16S rRNA abundance and HSV-1 glycoprotein D (gD) mRNA levels. Mann-Whitney U tests assessed differences between groups, and Pearson's correlation analyses evaluated bacterial-viral associations. Analysis of covariance (ANCOVA) adjusted for age and sex. Subgroup analyses examined correlations across clinical and demographic factors.
RESULTS: Salivary S. mutans 16S rRNA abundance and HSV-1 gD mRNA levels were significantly higher in OSCC patients than in controls (P = 0.0145 and P = 0.0257, respectively). A moderate correlation was observed between S. mutans and HSV-1 in non-tumor controls (r = 0.3806, P = 0.0027), whereas a substantially stronger correlation was evident in OSCC patients (r = 0.7878, P < 0.0001). Subgroup analyses revealed particularly strong correlations in individuals with alcohol consumption (r = 0.9109, P < 0.0001) and smoking history (r = 0.9062, P < 0.0001).
CONCLUSIONS: This study demonstrates a significantly stronger association between S. mutans and HSV-1 in OSCC than in non-tumor controls. These findings suggest that salivary bacterial-viral co-enrichment warrants further evaluation as a potential biomarker pair and may inform future microbiome-based strategies for OSCC risk assessment and prevention.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Herpesvirus 1, Human/isolation & purification
*Saliva/microbiology/virology
Case-Control Studies
Male
Female
*Carcinoma, Squamous Cell/microbiology/virology
*Streptococcus mutans/isolation & purification
*Mouth Neoplasms/microbiology/virology
Middle Aged
Aged
Adult
Viral Envelope Proteins
RevDate: 2026-08-15
Optimizing delivery to the gastrointestinal tract: a mechanistic approach to nutraceutical design and development.
Expert opinion on drug delivery [Epub ahead of print].
INTRODUCTION: Nutraceuticals have garnered increasing scientific and commercial interest for their potential roles in health promotion, disease prevention and adjunctive disease management. However, the complex physicochemical and biological environment of the gastrointestinal (GI) tract presents formidable barriers to their effective oral delivery, contributing to a persistent gap between preclinical promise and clinical efficacy. A mechanistic understanding of GI physiology, nutraceutical-specific delivery challenges and available formulation strategies is therefore essential to advance the field.
AREAS COVERED: Preclinical and clinical studies exploring the oral delivery of nutraceuticals were identified through targeted PubMed, Scopus and Web of Science searches to examine the GI tract as a dynamic delivery environment. Nutraceuticals are classified according to their primary delivery challenges, including lipophilicity, chemical and enzymatic lability and requirements for colon-targeted or microbiome-directed delivery. Formulation strategies are reviewed mechanistically, with particular attention to lipid-based systems, polymeric nanoparticles, hydrogel and hybrid biomaterials and colon-targeted delivery platforms.
EXPERT OPINION: Advancing nutraceutical science requires moving toward a formulation-driven approach to overcome the biological barriers faced by oral delivery. There is a critical need for regulatory oversight to ensure that marketed claims are backed by scientific evidence relating to nutraceutical pharmacokinetics, pharmacodynamics and safety evaluations.
Additional Links: PMID-42601804
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PubMed:
Citation:
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@article {pmid42601804,
year = {2026},
author = {Hunter, A and Ariaee, A and Wignall, A and Paxton, K and Bremmell, K and Prestidge, C and Joyce, P},
title = {Optimizing delivery to the gastrointestinal tract: a mechanistic approach to nutraceutical design and development.},
journal = {Expert opinion on drug delivery},
volume = {},
number = {},
pages = {},
doi = {10.1080/17425247.2026.2719683},
pmid = {42601804},
issn = {1744-7593},
abstract = {INTRODUCTION: Nutraceuticals have garnered increasing scientific and commercial interest for their potential roles in health promotion, disease prevention and adjunctive disease management. However, the complex physicochemical and biological environment of the gastrointestinal (GI) tract presents formidable barriers to their effective oral delivery, contributing to a persistent gap between preclinical promise and clinical efficacy. A mechanistic understanding of GI physiology, nutraceutical-specific delivery challenges and available formulation strategies is therefore essential to advance the field.
AREAS COVERED: Preclinical and clinical studies exploring the oral delivery of nutraceuticals were identified through targeted PubMed, Scopus and Web of Science searches to examine the GI tract as a dynamic delivery environment. Nutraceuticals are classified according to their primary delivery challenges, including lipophilicity, chemical and enzymatic lability and requirements for colon-targeted or microbiome-directed delivery. Formulation strategies are reviewed mechanistically, with particular attention to lipid-based systems, polymeric nanoparticles, hydrogel and hybrid biomaterials and colon-targeted delivery platforms.
EXPERT OPINION: Advancing nutraceutical science requires moving toward a formulation-driven approach to overcome the biological barriers faced by oral delivery. There is a critical need for regulatory oversight to ensure that marketed claims are backed by scientific evidence relating to nutraceutical pharmacokinetics, pharmacodynamics and safety evaluations.},
}
RevDate: 2026-08-15
CmpDate: 2026-08-15
Commentary: Correlation between the gut microbiota composition and cognitive frailty: a case-control study in community-dwelling older adults.
Frontiers in nutrition, 13:1929141.
Additional Links: PMID-42601860
PubMed:
Citation:
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@article {pmid42601860,
year = {2026},
author = {Georgiadou, N and Sultan, O and Harris, BHL and Koizia, LJ},
title = {Commentary: Correlation between the gut microbiota composition and cognitive frailty: a case-control study in community-dwelling older adults.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1929141},
pmid = {42601860},
issn = {2296-861X},
}
RevDate: 2026-08-15
CmpDate: 2026-08-15
Seasonal dynamics of the gut microbiota in Apis mellifera ligustica: a two-year longitudinal study.
Frontiers in insect science, 6:1920906.
The honey bee gut microbiota plays a crucial role in host nutrition, immunity, and colony health, yet the relative influence of seasonal and colony-specific factors on its long-term dynamics remains incompletely understood. This study investigated temporal variation in the gut bacterial community of three Apis mellifera ligustica colonies maintained in the same apiary and monitored over two consecutive years (2022-2023). Worker bees were sampled during eight seasonal periods, and gut microbiota composition was characterized using 16S rRNA gene amplicon sequencing. Across all sampling periods, the microbiome was consistently dominated by the characteristic honey bee-associated genera Gilliamella, Snodgrassella, Bartonella, Frischella, Commensalibacter, and Lactobacillus, indicating the persistence of a conserved core bacterial community. Seasonal variation was primarily associated with changes in the relative abundance of dominant taxa rather than with major changes in community composition. In particular, Gilliamella apicola and Snodgrassella alvi exhibited complementary seasonal patterns, with Gilliamella reaching its highest abundance during autumn, particularly in autumn 2023, whereas Snodgrassella predominated during spring and winter. Alpha-diversity metrics (Observed OTUs, Chao1, Shannon, and Simpson indices) showed limited seasonal variation, whereas beta-diversity analyses detected significant differences in community composition among seasons. Principal Coordinates Analysis and PERMANOVA identified season as the factor most strongly associated with microbiome variation, while colony identity did not significantly influence bacterial community composition under the standardized experimental conditions adopted in this study. Overall, these findings show that the gut microbiome of A. mellifera ligustica maintains a conserved core bacterial community while exhibiting reproducible seasonal variation in the relative abundance of its dominant members. This study provides a longitudinal baseline for future investigations aimed at understanding the ecological mechanisms underlying seasonal microbiome dynamics and their relationship with honey bee biology and environmental change.
Additional Links: PMID-42601898
PubMed:
Citation:
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@article {pmid42601898,
year = {2026},
author = {Iorizzo, M and Pannella, G and Succi, M and Ganassi, S and Di Criscio, D and Tedino, C and Albanese, G and De Cristofaro, A},
title = {Seasonal dynamics of the gut microbiota in Apis mellifera ligustica: a two-year longitudinal study.},
journal = {Frontiers in insect science},
volume = {6},
number = {},
pages = {1920906},
pmid = {42601898},
issn = {2673-8600},
abstract = {The honey bee gut microbiota plays a crucial role in host nutrition, immunity, and colony health, yet the relative influence of seasonal and colony-specific factors on its long-term dynamics remains incompletely understood. This study investigated temporal variation in the gut bacterial community of three Apis mellifera ligustica colonies maintained in the same apiary and monitored over two consecutive years (2022-2023). Worker bees were sampled during eight seasonal periods, and gut microbiota composition was characterized using 16S rRNA gene amplicon sequencing. Across all sampling periods, the microbiome was consistently dominated by the characteristic honey bee-associated genera Gilliamella, Snodgrassella, Bartonella, Frischella, Commensalibacter, and Lactobacillus, indicating the persistence of a conserved core bacterial community. Seasonal variation was primarily associated with changes in the relative abundance of dominant taxa rather than with major changes in community composition. In particular, Gilliamella apicola and Snodgrassella alvi exhibited complementary seasonal patterns, with Gilliamella reaching its highest abundance during autumn, particularly in autumn 2023, whereas Snodgrassella predominated during spring and winter. Alpha-diversity metrics (Observed OTUs, Chao1, Shannon, and Simpson indices) showed limited seasonal variation, whereas beta-diversity analyses detected significant differences in community composition among seasons. Principal Coordinates Analysis and PERMANOVA identified season as the factor most strongly associated with microbiome variation, while colony identity did not significantly influence bacterial community composition under the standardized experimental conditions adopted in this study. Overall, these findings show that the gut microbiome of A. mellifera ligustica maintains a conserved core bacterial community while exhibiting reproducible seasonal variation in the relative abundance of its dominant members. This study provides a longitudinal baseline for future investigations aimed at understanding the ecological mechanisms underlying seasonal microbiome dynamics and their relationship with honey bee biology and environmental change.},
}
RevDate: 2026-08-15
CmpDate: 2026-08-15
L-carvone supplementation reduces methane production and modulates rumen fermentation, digestibility and microbial communities in vitro.
Frontiers in veterinary science, 13:1900394.
INTRODUCTION: Natural feed additives are increasingly explored to reduce ruminal methane emissions. This study evaluated L-carvone (LC), a monoterpene compound present in essential oils, for its effects at different inclusion levels on rumen fermentation, in vitro dry matter digestibility (IVDMD), methane production, and microbiota composition.
METHODS: Three treatments were tested: a basal diet (total mixed ration; TMR + 0 μL/L LC), LC250 (TMR + 250 μL/L LC), and LC500 (TMR + 500 μL/L LC), using a 59:41 concentrate-to-forage substrate. Fermentation parameters were analysed using the Gas Endeavour system and 16 S rRNA gene sequencing was applied to investigate the ruminal microbiota profile. Data were analysed using linear mixed models, with treatment included as a fixed effect and experimental runs as a random effect. Pairwise comparisons were conducted using Bonferroni correction, with p value below 0.05 considered significant.
RESULTS: Total gas production decreased progressively with increasing LC inclusion (p < 0.001), whereas methane production was significantly reduced only in LC500 (p < 0.001). LC500 reduced methane production by 28% compared with TMR (p < 0.001) and decreased IVDMD by approximately 15%, while LC250 showed a numerical but non-significant reduction in methane production without affecting IVDMD. Total volatile fatty acid (TVFA) concentration was lower in LC500compared with TMR (p < 0.01), whereas LC250 showed intermediate values. This reduction was mainly due to lower propionate, iso-butyrate, and iso-valerate concentrations. The proportion of butyrate increased in LC500 (p < 0.01). In addition, ammonia nitrogen concentration was lower in LC500 than in LC250 (p = 0.040), while TMR remained intermediate. At the phylum level, increasing LC supplementation reduced the abundance of Bacteroidota and increased Firmicutes. At the genus level, Prevotella abundance decreased with LC inclusion, whereas butyrate-producing genera including Butyrivibrio, Pseudobutyrivibrio, and Ruminococcus increased. Alpha diversity analysis showed that richness indices (observed OTUs and Faith's phylogenetic diversity) were highest in LC250, whereas Shannon diversity and Pielou's evenness were similarly higher in LC250 and LC500 compared with TMR.
CONCLUSION: The LC reduced methane production during a 24-h in vitro rumen fermentation while altering rumen fermentation characteristics, as evidenced by lower total gas production, IVDMD, and VFA concentrations at the highest inclusion level. These changes were accompanied by shifts in the rumen microbiota, including a reduced abundance of Euryarchaeota, a phylum associated with methanogenic archaea. Therefore, optimizing the inclusion level of LC is essential to achieve methane mitigation while minimizing adverse effects on feed digestion.
Additional Links: PMID-42601899
PubMed:
Citation:
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@article {pmid42601899,
year = {2026},
author = {Jalal, H and Pompei, L and Giammarco, M and Malik, MI and Akram, S and Akram, MZ and Di Domenico, M and Ghiaccio, F and Colleluori, R and Pezzi, P and Fusaro, I},
title = {L-carvone supplementation reduces methane production and modulates rumen fermentation, digestibility and microbial communities in vitro.},
journal = {Frontiers in veterinary science},
volume = {13},
number = {},
pages = {1900394},
pmid = {42601899},
issn = {2297-1769},
abstract = {INTRODUCTION: Natural feed additives are increasingly explored to reduce ruminal methane emissions. This study evaluated L-carvone (LC), a monoterpene compound present in essential oils, for its effects at different inclusion levels on rumen fermentation, in vitro dry matter digestibility (IVDMD), methane production, and microbiota composition.
METHODS: Three treatments were tested: a basal diet (total mixed ration; TMR + 0 μL/L LC), LC250 (TMR + 250 μL/L LC), and LC500 (TMR + 500 μL/L LC), using a 59:41 concentrate-to-forage substrate. Fermentation parameters were analysed using the Gas Endeavour system and 16 S rRNA gene sequencing was applied to investigate the ruminal microbiota profile. Data were analysed using linear mixed models, with treatment included as a fixed effect and experimental runs as a random effect. Pairwise comparisons were conducted using Bonferroni correction, with p value below 0.05 considered significant.
RESULTS: Total gas production decreased progressively with increasing LC inclusion (p < 0.001), whereas methane production was significantly reduced only in LC500 (p < 0.001). LC500 reduced methane production by 28% compared with TMR (p < 0.001) and decreased IVDMD by approximately 15%, while LC250 showed a numerical but non-significant reduction in methane production without affecting IVDMD. Total volatile fatty acid (TVFA) concentration was lower in LC500compared with TMR (p < 0.01), whereas LC250 showed intermediate values. This reduction was mainly due to lower propionate, iso-butyrate, and iso-valerate concentrations. The proportion of butyrate increased in LC500 (p < 0.01). In addition, ammonia nitrogen concentration was lower in LC500 than in LC250 (p = 0.040), while TMR remained intermediate. At the phylum level, increasing LC supplementation reduced the abundance of Bacteroidota and increased Firmicutes. At the genus level, Prevotella abundance decreased with LC inclusion, whereas butyrate-producing genera including Butyrivibrio, Pseudobutyrivibrio, and Ruminococcus increased. Alpha diversity analysis showed that richness indices (observed OTUs and Faith's phylogenetic diversity) were highest in LC250, whereas Shannon diversity and Pielou's evenness were similarly higher in LC250 and LC500 compared with TMR.
CONCLUSION: The LC reduced methane production during a 24-h in vitro rumen fermentation while altering rumen fermentation characteristics, as evidenced by lower total gas production, IVDMD, and VFA concentrations at the highest inclusion level. These changes were accompanied by shifts in the rumen microbiota, including a reduced abundance of Euryarchaeota, a phylum associated with methanogenic archaea. Therefore, optimizing the inclusion level of LC is essential to achieve methane mitigation while minimizing adverse effects on feed digestion.},
}
RevDate: 2026-08-15
CmpDate: 2026-08-15
Human relevant platforms for cutaneous wound healing research: current landscape, translational gaps, and emerging frontiers.
Frontiers in bioengineering and biotechnology, 14:1917429.
Cutaneous wound healing is a dynamic, multicellular process that unfolds across four interrelated phases - haemostasis, inflammation, proliferation, and remodellingeach governed by precise intercellular signalling that remains incompletely understood in its human context. Animal models and two-dimensional cell cultures have shaped much of what we know about wound biology, yet both consistently fall short when the question moves from mechanism to translation. They fail to capture the structural organisation of human skin, the particular rhythms of human immune activation and resolution, and above all the multifactorial pathology that makes chronic wounds-diabetic foot ulcers especially, so resistant to treatment. This review traces the development of human-relevant alternative models as a coherent scientific response to those failures: from scratch assays and monocultures through to three-dimensional reconstructed equivalents, organoid platforms, ex vivo tissue preparations, and skin-on-a-chip systems capable of dynamic perfusion and real-time wound monitoring. We assess each class of model not simply on its merits but on what specific biological gap it was designed to close and what gaps remain. Emerging analytical frameworks-multi-omics integration, spatial transcriptomics, microbiome and biofilm modelling, multi-organ-on-a-chip architectures, artificial intelligence, and neuro-immune crosstalk -are examined as the next Frontier. These findings show that no single platform will resolve the translational deficit; what is required is a deliberately combinatorial paradigm in which complementary systems are deployed in tiered sequence, each contributing the biological information it is best positioned to generate.
Additional Links: PMID-42601972
PubMed:
Citation:
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@article {pmid42601972,
year = {2026},
author = {Latheef, F and Suthindhiran, K},
title = {Human relevant platforms for cutaneous wound healing research: current landscape, translational gaps, and emerging frontiers.},
journal = {Frontiers in bioengineering and biotechnology},
volume = {14},
number = {},
pages = {1917429},
pmid = {42601972},
issn = {2296-4185},
abstract = {Cutaneous wound healing is a dynamic, multicellular process that unfolds across four interrelated phases - haemostasis, inflammation, proliferation, and remodellingeach governed by precise intercellular signalling that remains incompletely understood in its human context. Animal models and two-dimensional cell cultures have shaped much of what we know about wound biology, yet both consistently fall short when the question moves from mechanism to translation. They fail to capture the structural organisation of human skin, the particular rhythms of human immune activation and resolution, and above all the multifactorial pathology that makes chronic wounds-diabetic foot ulcers especially, so resistant to treatment. This review traces the development of human-relevant alternative models as a coherent scientific response to those failures: from scratch assays and monocultures through to three-dimensional reconstructed equivalents, organoid platforms, ex vivo tissue preparations, and skin-on-a-chip systems capable of dynamic perfusion and real-time wound monitoring. We assess each class of model not simply on its merits but on what specific biological gap it was designed to close and what gaps remain. Emerging analytical frameworks-multi-omics integration, spatial transcriptomics, microbiome and biofilm modelling, multi-organ-on-a-chip architectures, artificial intelligence, and neuro-immune crosstalk -are examined as the next Frontier. These findings show that no single platform will resolve the translational deficit; what is required is a deliberately combinatorial paradigm in which complementary systems are deployed in tiered sequence, each contributing the biological information it is best positioned to generate.},
}
RevDate: 2026-08-15
CmpDate: 2026-08-15
Persistent gut microbiota dysbiosis and metabolic remodeling after ceftriaxone exposure in mice: a cross-study re-analysis.
Frontiers in cellular and infection microbiology, 16:1822390.
INTRODUCTION: Broad-spectrum antibiotics are known to disrupt the gut microbial environment, which can lead to sustained physiological consequences. Ceftriaxone (CTX) is a β-lactam antibiotic widely used in neuroscience research to enhance expression of the glutamate transporter GLT-1, a key regulator of excitatory neurotransmission in the brain. However, CTX also induces marked alterations in gut microbial composition, yet the consistency and functional consequences of these changes across studies remain poorly defined.
METHODS: Here, we conducted a cross-study re-analysis of four independent, publicly available murine 16S rRNA gene sequencing datasets to identify robust microbial and metabolic responses to CTX exposure. Using a bioinformatic pipeline for taxonomic annotation and functional inference, we evaluated microbial diversity, community composition, and predicted functional pathways across studies.
RESULTS: CTX treatment consistently reduced gut microbial diversity and altered community composition relative to controls, with only partial recovery over time. Predicted microbial functions were extensively remodeled, with CTX-exposed communities showing enrichment in pathways related to aromatic compound and amino acid metabolism, amine metabolism, and stress response, whereas control communities retained higher biosynthetic potential.
DISCUSSION: These findings demonstrate that CTX exposure induces persistent, system-level restructuring of the gut microbiome, with potential detriment to host physiology.
Additional Links: PMID-42601985
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Citation:
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@article {pmid42601985,
year = {2026},
author = {Winters, AD and Rudagi, E and Koka, O and Angoa-Perez, M},
title = {Persistent gut microbiota dysbiosis and metabolic remodeling after ceftriaxone exposure in mice: a cross-study re-analysis.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1822390},
pmid = {42601985},
issn = {2235-2988},
mesh = {Animals ; *Ceftriaxone/adverse effects/pharmacology/administration & dosage ; *Dysbiosis/chemically induced/microbiology ; Mice ; *Gastrointestinal Microbiome/drug effects ; *Anti-Bacterial Agents/adverse effects/administration & dosage/pharmacology ; RNA, Ribosomal, 16S/genetics ; Bacteria/classification/genetics/drug effects ; },
abstract = {INTRODUCTION: Broad-spectrum antibiotics are known to disrupt the gut microbial environment, which can lead to sustained physiological consequences. Ceftriaxone (CTX) is a β-lactam antibiotic widely used in neuroscience research to enhance expression of the glutamate transporter GLT-1, a key regulator of excitatory neurotransmission in the brain. However, CTX also induces marked alterations in gut microbial composition, yet the consistency and functional consequences of these changes across studies remain poorly defined.
METHODS: Here, we conducted a cross-study re-analysis of four independent, publicly available murine 16S rRNA gene sequencing datasets to identify robust microbial and metabolic responses to CTX exposure. Using a bioinformatic pipeline for taxonomic annotation and functional inference, we evaluated microbial diversity, community composition, and predicted functional pathways across studies.
RESULTS: CTX treatment consistently reduced gut microbial diversity and altered community composition relative to controls, with only partial recovery over time. Predicted microbial functions were extensively remodeled, with CTX-exposed communities showing enrichment in pathways related to aromatic compound and amino acid metabolism, amine metabolism, and stress response, whereas control communities retained higher biosynthetic potential.
DISCUSSION: These findings demonstrate that CTX exposure induces persistent, system-level restructuring of the gut microbiome, with potential detriment to host physiology.},
}
MeSH Terms:
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Animals
*Ceftriaxone/adverse effects/pharmacology/administration & dosage
*Dysbiosis/chemically induced/microbiology
Mice
*Gastrointestinal Microbiome/drug effects
*Anti-Bacterial Agents/adverse effects/administration & dosage/pharmacology
RNA, Ribosomal, 16S/genetics
Bacteria/classification/genetics/drug effects
RevDate: 2026-08-15
Microbial neuroscience: The gut microbiota as a cognitive layer.
Trends open, 1(2):109-121.
Cognition is traditionally viewed as a brain-centred process, with gut microbes treated primarily as modulators of physiology and behaviour. Recent advances in microbiome research suggest that microbial communities can exhibit history-dependent functional states, adapt their outputs, and dynamically interact with neural systems. This opinion article proposes a distributed model of cognition in which the gut microbiota acts as an intermediate information-processing layer that may influence cognitive states through memory-like persistence and closed-loop feedback with the brain. By integrating concepts from systems neuroscience, microbiology, and cognitive theory, this framework reframes the microbiota as a potential functional contributor to cognition and outlines experimental approaches for testing causal microbiota-gut-brain interactions in behaviour and decision-making.
Additional Links: PMID-42602100
PubMed:
Citation:
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@article {pmid42602100,
year = {2026},
author = {Burnet, PWJ},
title = {Microbial neuroscience: The gut microbiota as a cognitive layer.},
journal = {Trends open},
volume = {1},
number = {2},
pages = {109-121},
pmid = {42602100},
issn = {3117-3470},
abstract = {Cognition is traditionally viewed as a brain-centred process, with gut microbes treated primarily as modulators of physiology and behaviour. Recent advances in microbiome research suggest that microbial communities can exhibit history-dependent functional states, adapt their outputs, and dynamically interact with neural systems. This opinion article proposes a distributed model of cognition in which the gut microbiota acts as an intermediate information-processing layer that may influence cognitive states through memory-like persistence and closed-loop feedback with the brain. By integrating concepts from systems neuroscience, microbiology, and cognitive theory, this framework reframes the microbiota as a potential functional contributor to cognition and outlines experimental approaches for testing causal microbiota-gut-brain interactions in behaviour and decision-making.},
}
RevDate: 2026-08-15
CmpDate: 2026-08-15
From natural assemblages to synthetic communities in the Lupinus microbiome.
Frontiers in plant science, 17:1891479.
INTRODUCTION: Plant roots harbour complex microbial communities that enhance nutrient acquisition, stress tolerance, and pathogen defence, yet their assembly and functional dynamics remain incompletely understood.
RESULTS: In this work, we isolated over 700 bacterial strains from wild Lupinus angustifolius across multiple compartments and soil types, capturing both dominant and rare bacterial taxa. Using co-occurrence network analysis, we selected representative strains to assemble synthetic communities (SynComs) of varying complexity, which were inoculated under sterile and non-sterile conditions. Plants were inoculated with SynComs of increasing complexity under both non-sterile soil and gnotobiotic conditions. SynCom inoculation reshaped root-associated microbiota, moderately influenced the rhizosphere, and had limited impact on bulk soil communities. Increasing SynCom complexity enhanced plant growth and triggered host transcriptional responses involving hormone signaling, defence pathways, and metabolic reprogramming.
DISCUSSION: These findings indicate that soil-driven filtering and microbial interactions govern microbiome assembly and plant responses. Incorporating taxa with distinct ecological roles, including low-abundance members, improves SynCom functionality and advances understanding of plant-microbe interactions in natural and agricultural systems.
Additional Links: PMID-42602126
PubMed:
Citation:
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@article {pmid42602126,
year = {2026},
author = {Ortúzar, M and Formariz, V and Suescún-Sepúlveda, JA and González-Hernández, M and Riesco, R and Garrido-Oter, R and Trujillo, ME},
title = {From natural assemblages to synthetic communities in the Lupinus microbiome.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1891479},
pmid = {42602126},
issn = {1664-462X},
abstract = {INTRODUCTION: Plant roots harbour complex microbial communities that enhance nutrient acquisition, stress tolerance, and pathogen defence, yet their assembly and functional dynamics remain incompletely understood.
RESULTS: In this work, we isolated over 700 bacterial strains from wild Lupinus angustifolius across multiple compartments and soil types, capturing both dominant and rare bacterial taxa. Using co-occurrence network analysis, we selected representative strains to assemble synthetic communities (SynComs) of varying complexity, which were inoculated under sterile and non-sterile conditions. Plants were inoculated with SynComs of increasing complexity under both non-sterile soil and gnotobiotic conditions. SynCom inoculation reshaped root-associated microbiota, moderately influenced the rhizosphere, and had limited impact on bulk soil communities. Increasing SynCom complexity enhanced plant growth and triggered host transcriptional responses involving hormone signaling, defence pathways, and metabolic reprogramming.
DISCUSSION: These findings indicate that soil-driven filtering and microbial interactions govern microbiome assembly and plant responses. Incorporating taxa with distinct ecological roles, including low-abundance members, improves SynCom functionality and advances understanding of plant-microbe interactions in natural and agricultural systems.},
}
RevDate: 2026-08-15
CmpDate: 2026-08-15
The Gut-Brain Axis in Neurodegeneration: Mechanistic Links Between Dysbiosis and Neuropathology.
Iranian journal of pathology, 21(4):507-522.
BACKGROUND & OBJECTIVE: The gut-brain axis is essentially a two-way communication system that physically connects the brain and the intestinal tract. The connection is mediated through a series of pathways, including neural, endocrine, and immune pathways. Gut dysbiosis, which is explained as an imbalance in the microbial community, has been linked to the causation of various neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. However, the pathological mechanisms in the brain are only partially known. The present review outlines the process of gut dysbiosis and neurodegeneration, detailing the roles of protein aggregation, neuroinflammation, barrier disruption, and neuroglial dysfunction. Then, extending the comparison to a range of neurodegenerative diseases, we discuss the possibility of common pathway therapeutics and actual microbiome-based treatment options planning from the standpoint of microbiome-directed interventions.
CONTENT/FINDINGS: Gut dysbiosis triggers a definable cascade, starting with the disruption of the intestinal barrier and increased permeability (leaky gut), which allows bacterial products (lipopolysaccharides, bacterial amyloids) and pro-inflammatory cytokines to enter systemic circulation. Such peripheral changes weaken the blood-brain barrier and thus allow these factors to access the CNS, where they lead to neuroglial dysfunction (microglial priming, astrocytic reactivity, and oligodendrocyte injury) by disruption of glial homeostasis. CNS glial cell malfunction leads to the development of proteinopathies characteristic of each disease: amyloid and tau hyperphosphorylation in Alzheimer's disease through BACE1 upregulation and kinase activation; synuclein in Parkinson's disease via molecular mimicry, oxidative stress, and impaired clearance; and demyelination in multiple sclerosis through oligodendrocyte apoptosis. Oral bacteria such as Porphyromonas gingivalis aggravate this inflammatory loop through the direct invasion of the CNS and proteolytic cleavage of amyloid and tau. The vagus nerve is yet another pathway through which gut-derived inflammatory signals and pathological synuclein can be transmitted to the brain.
CONCLUSION: The gut microbiome is more than just a correlate of neurodegeneration; it actively promotes neurodegenerative diseases through pathways that can be mechanistically defined. Microbiome-targeted interventions such as dietary changes, precision probiotics, fecal microbiota transplantation, and anti-inflammatory agents offer a measure of hope for changing these pathological processes. Future studies need to be directed at determining the time sequence of cause and effect, finding dependable microbiota-based biomarkers, and formulating tailored strategies that can account for individual microbial composition variability, genetic susceptibility, and environmental exposures. A deeper understanding of the gut-brain axis from this mechanistic perspective could eventually lead to the prevention or postponement of neurodegeneration.
Additional Links: PMID-42602177
PubMed:
Citation:
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@article {pmid42602177,
year = {2026},
author = {Azimzadeh, M and Ababzadeh, S and Kahaki, AG and Babaei, SMH and Seyedebrahimi, R and Farsani, ME},
title = {The Gut-Brain Axis in Neurodegeneration: Mechanistic Links Between Dysbiosis and Neuropathology.},
journal = {Iranian journal of pathology},
volume = {21},
number = {4},
pages = {507-522},
pmid = {42602177},
issn = {1735-5303},
abstract = {BACKGROUND & OBJECTIVE: The gut-brain axis is essentially a two-way communication system that physically connects the brain and the intestinal tract. The connection is mediated through a series of pathways, including neural, endocrine, and immune pathways. Gut dysbiosis, which is explained as an imbalance in the microbial community, has been linked to the causation of various neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. However, the pathological mechanisms in the brain are only partially known. The present review outlines the process of gut dysbiosis and neurodegeneration, detailing the roles of protein aggregation, neuroinflammation, barrier disruption, and neuroglial dysfunction. Then, extending the comparison to a range of neurodegenerative diseases, we discuss the possibility of common pathway therapeutics and actual microbiome-based treatment options planning from the standpoint of microbiome-directed interventions.
CONTENT/FINDINGS: Gut dysbiosis triggers a definable cascade, starting with the disruption of the intestinal barrier and increased permeability (leaky gut), which allows bacterial products (lipopolysaccharides, bacterial amyloids) and pro-inflammatory cytokines to enter systemic circulation. Such peripheral changes weaken the blood-brain barrier and thus allow these factors to access the CNS, where they lead to neuroglial dysfunction (microglial priming, astrocytic reactivity, and oligodendrocyte injury) by disruption of glial homeostasis. CNS glial cell malfunction leads to the development of proteinopathies characteristic of each disease: amyloid and tau hyperphosphorylation in Alzheimer's disease through BACE1 upregulation and kinase activation; synuclein in Parkinson's disease via molecular mimicry, oxidative stress, and impaired clearance; and demyelination in multiple sclerosis through oligodendrocyte apoptosis. Oral bacteria such as Porphyromonas gingivalis aggravate this inflammatory loop through the direct invasion of the CNS and proteolytic cleavage of amyloid and tau. The vagus nerve is yet another pathway through which gut-derived inflammatory signals and pathological synuclein can be transmitted to the brain.
CONCLUSION: The gut microbiome is more than just a correlate of neurodegeneration; it actively promotes neurodegenerative diseases through pathways that can be mechanistically defined. Microbiome-targeted interventions such as dietary changes, precision probiotics, fecal microbiota transplantation, and anti-inflammatory agents offer a measure of hope for changing these pathological processes. Future studies need to be directed at determining the time sequence of cause and effect, finding dependable microbiota-based biomarkers, and formulating tailored strategies that can account for individual microbial composition variability, genetic susceptibility, and environmental exposures. A deeper understanding of the gut-brain axis from this mechanistic perspective could eventually lead to the prevention or postponement of neurodegeneration.},
}
RevDate: 2026-08-15
CmpDate: 2026-08-15
Leveraging soil microbiome diversity for the management of highly virulent Fusarium wilt (FOV4) in cotton.
Frontiers in microbiology, 17:1856023.
INTRODUCTION: Cotton (Gossypium spp.) is a globally important crop increasingly threatened by Fusarium oxysporum f. sp. vasinfectum race 4 (FOV4), a soil-borne pathogen responsible for Fusarium wilt. FOV4 has negatively affected cotton production in California and was confirmed in the far west Texas region of El Paso, TX in 2017, where it has caused similar disruptions. Thus, there is an urgent need for improved disease management and the development of resistant commercial cotton cultivars to maintain agricultural productivity.
METHODS: To understand the relationships among soil properties, fungal communities, and disease incidence, we examined the elemental composition and fungal microbiome of five cotton fields in the lower valley of El Paso, Texas region, having varying levels of Fusarium wilt incidence. Comparisons between high Fusarium wilt incidence fields (F1, F2, and F5) and low Fusarium wilt incidence fields (F3 and F4) were performed. Metabarcoding analyses identified marked differences in fungal community composition and diversity between the fields.
RESULTS: Alpha diversity metrics indicated higher fungal diversity and evenness in the low Fusarium wilt incidence field F4, suggesting that high fungal diversity contributes to decreased disease incidence. In contrast, high Fusarium wilt incidence fields (F1, F2, and F5) exhibited lower diversity, indicative of a less resilient fungal ecosystem. Beta diversity analyses further confirmed the distinct fungal community composition between soils with contrasting Fusarium wilt incidence. Taxonomic profiling showed that the low Fusarium wilt incidence field F4 harbored beneficial fungal taxa, including Actinomucor, Fusarium (potentially non-pathogenic species), Penicillium, Preussia, and Pseudeurotium, generally recognized for their contributions to soil health and potential to suppress pathogenic organisms. In contrast, the high Fusarium wilt incidence fields were dominated by genera associated with plant pathogenicity, such as Alternaria, Cladosporium, and Stachybotrys, contributing to the higher disease prevalence observed.
DISCUSSION: These findings underscore the crucial role of fungal diversity and soil chemical composition in influencing the incidence of Fusarium wilt in cotton. Soils with low Fusarium wilt incidence, characterized by diverse and complex fungal communities, may suppress the establishment and proliferation of pathogens. Our results provide insights for developing targeted soil management practices and enhancing cotton resilience, essential for developing sustainable disease management strategies and breeding resistant cultivars.
Additional Links: PMID-42602225
PubMed:
Citation:
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@article {pmid42602225,
year = {2026},
author = {Laadsi, I and Abdelrahman, M and Ulloa, M and Fokar, M and Jobe, TO},
title = {Leveraging soil microbiome diversity for the management of highly virulent Fusarium wilt (FOV4) in cotton.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1856023},
pmid = {42602225},
issn = {1664-302X},
abstract = {INTRODUCTION: Cotton (Gossypium spp.) is a globally important crop increasingly threatened by Fusarium oxysporum f. sp. vasinfectum race 4 (FOV4), a soil-borne pathogen responsible for Fusarium wilt. FOV4 has negatively affected cotton production in California and was confirmed in the far west Texas region of El Paso, TX in 2017, where it has caused similar disruptions. Thus, there is an urgent need for improved disease management and the development of resistant commercial cotton cultivars to maintain agricultural productivity.
METHODS: To understand the relationships among soil properties, fungal communities, and disease incidence, we examined the elemental composition and fungal microbiome of five cotton fields in the lower valley of El Paso, Texas region, having varying levels of Fusarium wilt incidence. Comparisons between high Fusarium wilt incidence fields (F1, F2, and F5) and low Fusarium wilt incidence fields (F3 and F4) were performed. Metabarcoding analyses identified marked differences in fungal community composition and diversity between the fields.
RESULTS: Alpha diversity metrics indicated higher fungal diversity and evenness in the low Fusarium wilt incidence field F4, suggesting that high fungal diversity contributes to decreased disease incidence. In contrast, high Fusarium wilt incidence fields (F1, F2, and F5) exhibited lower diversity, indicative of a less resilient fungal ecosystem. Beta diversity analyses further confirmed the distinct fungal community composition between soils with contrasting Fusarium wilt incidence. Taxonomic profiling showed that the low Fusarium wilt incidence field F4 harbored beneficial fungal taxa, including Actinomucor, Fusarium (potentially non-pathogenic species), Penicillium, Preussia, and Pseudeurotium, generally recognized for their contributions to soil health and potential to suppress pathogenic organisms. In contrast, the high Fusarium wilt incidence fields were dominated by genera associated with plant pathogenicity, such as Alternaria, Cladosporium, and Stachybotrys, contributing to the higher disease prevalence observed.
DISCUSSION: These findings underscore the crucial role of fungal diversity and soil chemical composition in influencing the incidence of Fusarium wilt in cotton. Soils with low Fusarium wilt incidence, characterized by diverse and complex fungal communities, may suppress the establishment and proliferation of pathogens. Our results provide insights for developing targeted soil management practices and enhancing cotton resilience, essential for developing sustainable disease management strategies and breeding resistant cultivars.},
}
RevDate: 2026-08-15
CmpDate: 2026-08-15
From cooperation to collapse: the diet-microbiota-host gene triad in disease and aging.
Frontiers in microbiomes, 5:1872481.
Symbiotic relationships are the basis of biological complexity. It can be traced back from ancient mitochondrial acquisition to modern host-microbiota interactions. In this review, we explore aging and disease susceptibility through the lens of a diet-microbiota-host gene triad, a dynamic symbiotic network in which dietary inputs, the gut microbiota, and the host genome co-regulate physiological equilibrium. The symbiotic triad evolved as nutrition was outsourced, with dietary and microbial components internalized by the host. Dietary components modulate microbial composition and metabolic activity. In contrast, microbial fermentation of nutrients produces short-chain fatty acids, vitamins, bile acids, and neuroactive compounds, which, in turn, influence host gene expression, immune responses, barrier integrity, nutrient preferences, and health. Host genes have also co-evolved as critical modulators of this triad, encoding nutrient sensors, immune effectors, and proteins that maintain microbial balance and prevent dysbiosis. Polymorphisms in key metabolic and immune genes fine-tune responses to dietary and microbial adaptations, building resilience across different contexts. As organisms age, this triadic equilibrium destabilizes, leading to reduced microbial diversity, compromised barrier integrity and function, and chronic inflammation that accelerates age-related pathologies. Therefore, understanding dietary, microbial, and genetic interdependencies and viewing aging and disease from this perspective offers a blueprint for developing personalized nutrition- and microbiome-targeted therapies to combat age-associated diseases and promote health and longevity.
Additional Links: PMID-42602462
PubMed:
Citation:
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@article {pmid42602462,
year = {2026},
author = {Bhattacharjee, S and Mukhopadhyay, A},
title = {From cooperation to collapse: the diet-microbiota-host gene triad in disease and aging.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1872481},
pmid = {42602462},
issn = {2813-4338},
abstract = {Symbiotic relationships are the basis of biological complexity. It can be traced back from ancient mitochondrial acquisition to modern host-microbiota interactions. In this review, we explore aging and disease susceptibility through the lens of a diet-microbiota-host gene triad, a dynamic symbiotic network in which dietary inputs, the gut microbiota, and the host genome co-regulate physiological equilibrium. The symbiotic triad evolved as nutrition was outsourced, with dietary and microbial components internalized by the host. Dietary components modulate microbial composition and metabolic activity. In contrast, microbial fermentation of nutrients produces short-chain fatty acids, vitamins, bile acids, and neuroactive compounds, which, in turn, influence host gene expression, immune responses, barrier integrity, nutrient preferences, and health. Host genes have also co-evolved as critical modulators of this triad, encoding nutrient sensors, immune effectors, and proteins that maintain microbial balance and prevent dysbiosis. Polymorphisms in key metabolic and immune genes fine-tune responses to dietary and microbial adaptations, building resilience across different contexts. As organisms age, this triadic equilibrium destabilizes, leading to reduced microbial diversity, compromised barrier integrity and function, and chronic inflammation that accelerates age-related pathologies. Therefore, understanding dietary, microbial, and genetic interdependencies and viewing aging and disease from this perspective offers a blueprint for developing personalized nutrition- and microbiome-targeted therapies to combat age-associated diseases and promote health and longevity.},
}
RevDate: 2026-08-15
CmpDate: 2026-08-15
Longitudinal multi-omic dynamics in hospitalized COVID-19 patients based on disease severity.
Gut microbes reports, 3(1):2712728.
Despite a decline in global COVID-19 cases, severe disease requiring hospitalization remains a significant health burden. Microbial dysbiosis and microbial translocation have been implicated in COVID-19 severity through their contributions to systemic inflammation, yet the temporal dynamics of the microbiome and related metabolites across disease severity are not well defined. To address this, we conducted a longitudinal study of 22 hospitalized COVID-19 patients in Milan, Italy, classified as moderate, severe, or critical by the WHO criteria. Rectal and nasal microbiomes, plasma cytokines, bile acids, fatty acids, and gut barrier damage markers were measured at up to three timepoints over an average of 9 d. Critically ill patients exhibited sustained elevations in pro-inflammatory cytokines (IL-6, IL-8, and TNFα), increased gut barrier damage markers (LBP, zonulin, and sCD14), early depletion of beneficial commensals (including Faecalibacterium prausnitzii), and expansion of opportunistic pathogens such as Hungatella hathewayi and Erysipelatoclostridium ramosum. These microbial shifts were accompanied by the progressive loss of secondary and conjugated bile acids and increased levels of branched- and medium-chain fatty acids. Correlation analyses linked commensal taxa to reduced gut barrier damage and opportunistic pathogens to IL-6. Together, these findings define distinct trajectories associated with COVID-19 severity and highlight the importance of early interventions targeting microbial dysbiosis.
Additional Links: PMID-42602616
PubMed:
Citation:
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@article {pmid42602616,
year = {2026},
author = {Basting, CM and Schroeder, TA and Shields-Cutler, R and Swanson, E and Guerrero, C and Hemmila, CR and Broedlow, CA and Chakrawarti, A and Velez, A and Cromarty, R and Riva, A and Torre, A and Lai, A and Schifanella, L and Klatt, NR},
title = {Longitudinal multi-omic dynamics in hospitalized COVID-19 patients based on disease severity.},
journal = {Gut microbes reports},
volume = {3},
number = {1},
pages = {2712728},
pmid = {42602616},
issn = {2993-3935},
abstract = {Despite a decline in global COVID-19 cases, severe disease requiring hospitalization remains a significant health burden. Microbial dysbiosis and microbial translocation have been implicated in COVID-19 severity through their contributions to systemic inflammation, yet the temporal dynamics of the microbiome and related metabolites across disease severity are not well defined. To address this, we conducted a longitudinal study of 22 hospitalized COVID-19 patients in Milan, Italy, classified as moderate, severe, or critical by the WHO criteria. Rectal and nasal microbiomes, plasma cytokines, bile acids, fatty acids, and gut barrier damage markers were measured at up to three timepoints over an average of 9 d. Critically ill patients exhibited sustained elevations in pro-inflammatory cytokines (IL-6, IL-8, and TNFα), increased gut barrier damage markers (LBP, zonulin, and sCD14), early depletion of beneficial commensals (including Faecalibacterium prausnitzii), and expansion of opportunistic pathogens such as Hungatella hathewayi and Erysipelatoclostridium ramosum. These microbial shifts were accompanied by the progressive loss of secondary and conjugated bile acids and increased levels of branched- and medium-chain fatty acids. Correlation analyses linked commensal taxa to reduced gut barrier damage and opportunistic pathogens to IL-6. Together, these findings define distinct trajectories associated with COVID-19 severity and highlight the importance of early interventions targeting microbial dysbiosis.},
}
RevDate: 2026-08-15
CmpDate: 2026-08-15
Mechanically activated zinc oxide enhances growth performance and protects against diarrhea with potentially regulating gut microbiota in weaned piglets.
Animal nutrition (Zhongguo xu mu shou yi xue hui), 26:652-664.
High pharmacological doses of zinc oxide (ZnO) are widely used to control post-weaning diarrhea, but environmental pollution and potential adverse effects necessitate the search for effective low-dose alternatives. This study aimed to investigate the effects of dietary level of mechanically activated zinc oxide on growth performance and diarrhea in weaned piglets. A total of 1152 healthy weaned piglets (6.72 ± 0.63 kg) at 21 d of age were randomly assigned to six treatment groups with six replicates of 32 pigs per pen. Piglets received either a basal diet (BD), the BD supplemented with 100, 200, 400, or 600 mg Zn/kg mechanically activated zinc oxide (100 Zn, 200 Zn, 400 Zn, and 600 Zn), or the BD supplemented with 1600 mg Zn/kg conventional ZnO (1600 Zn) over a 28-d feeding period. Compared with the BD group, dietary 400 Zn supplementation significantly increased average daily gain during d 1 to 14, and decreased the feed/gain ratio during d 1 to 14 and d 1 to 28 (P < 0.05). Additionally, dietary 400 Zn supplementation consistently decreased the diarrhea rate regardless of the experimental period (P = 0.001). Notably, these effects are comparable to those observed with 1600 Zn treatment. Moreover, compared to 1600 Zn group, 400 or 600 Zn supplementation significantly reduced interleukin-6 (IL-6) content and diamine oxidase (DAO) activity, as well as significantly increased superoxide dismutase (SOD) activity (P < 0.05) in serum at d 28. Conversely, no significant differences were observed in serum malondialdehyde (MDA) and interleukin-1β (IL-1β) concentrations between the 400 or 600 Zn groups and the 1600 Zn group throughout the experimental period (P > 0.05). Further gut microbiome and serum metabolomic analysis found that the abundances of Lactobacillus, Ligilactobacillus, and Roseburia increased and tryptophan metabolism pathway was enriched by 400 Zn supplementation. Furthermore, the differential metabolites involved in tryptophan metabolism significantly correlated with most of differential genera. In conclusion, dietary supplementation with mechanically activated zinc oxide at 400 mg Zn/kg could exerted a certain positive effect on the growth performance of weaned piglets, which was comparable to or even superior to that of 1600 mg Zn/kg ZnO, indicating that mechanically activated zinc oxide could serve as an effective alternative to high-dose ZnO used in weaned piglets.
Additional Links: PMID-42602773
PubMed:
Citation:
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@article {pmid42602773,
year = {2026},
author = {Yuan, Z and Huang, J and Guo, J and Zhang, B and Bei, W and Wang, Y and Li, Y and Xin, H and Xing, W and Huang, Y and Sun, L and Deng, Z},
title = {Mechanically activated zinc oxide enhances growth performance and protects against diarrhea with potentially regulating gut microbiota in weaned piglets.},
journal = {Animal nutrition (Zhongguo xu mu shou yi xue hui)},
volume = {26},
number = {},
pages = {652-664},
pmid = {42602773},
issn = {2405-6383},
abstract = {High pharmacological doses of zinc oxide (ZnO) are widely used to control post-weaning diarrhea, but environmental pollution and potential adverse effects necessitate the search for effective low-dose alternatives. This study aimed to investigate the effects of dietary level of mechanically activated zinc oxide on growth performance and diarrhea in weaned piglets. A total of 1152 healthy weaned piglets (6.72 ± 0.63 kg) at 21 d of age were randomly assigned to six treatment groups with six replicates of 32 pigs per pen. Piglets received either a basal diet (BD), the BD supplemented with 100, 200, 400, or 600 mg Zn/kg mechanically activated zinc oxide (100 Zn, 200 Zn, 400 Zn, and 600 Zn), or the BD supplemented with 1600 mg Zn/kg conventional ZnO (1600 Zn) over a 28-d feeding period. Compared with the BD group, dietary 400 Zn supplementation significantly increased average daily gain during d 1 to 14, and decreased the feed/gain ratio during d 1 to 14 and d 1 to 28 (P < 0.05). Additionally, dietary 400 Zn supplementation consistently decreased the diarrhea rate regardless of the experimental period (P = 0.001). Notably, these effects are comparable to those observed with 1600 Zn treatment. Moreover, compared to 1600 Zn group, 400 or 600 Zn supplementation significantly reduced interleukin-6 (IL-6) content and diamine oxidase (DAO) activity, as well as significantly increased superoxide dismutase (SOD) activity (P < 0.05) in serum at d 28. Conversely, no significant differences were observed in serum malondialdehyde (MDA) and interleukin-1β (IL-1β) concentrations between the 400 or 600 Zn groups and the 1600 Zn group throughout the experimental period (P > 0.05). Further gut microbiome and serum metabolomic analysis found that the abundances of Lactobacillus, Ligilactobacillus, and Roseburia increased and tryptophan metabolism pathway was enriched by 400 Zn supplementation. Furthermore, the differential metabolites involved in tryptophan metabolism significantly correlated with most of differential genera. In conclusion, dietary supplementation with mechanically activated zinc oxide at 400 mg Zn/kg could exerted a certain positive effect on the growth performance of weaned piglets, which was comparable to or even superior to that of 1600 mg Zn/kg ZnO, indicating that mechanically activated zinc oxide could serve as an effective alternative to high-dose ZnO used in weaned piglets.},
}
RevDate: 2026-08-15
CmpDate: 2026-08-15
Qing-Re-Qu-Shi formula improves clinical outcomes and is accompanied by gut microbiota and microbial metabolite remodeling in adults with moderate atopic dermatitis: a randomized placebo-controlled multi-omics trial.
Frontiers in medicine, 13:1847003.
BACKGROUND: The gut-skin axis is increasingly implicated in atopic dermatitis (AD), but randomized adult studies linking clinical response to paired gut microbiome and circulating metabolite profiling remain limited. We evaluated Qing-Re-Qu-Shi formula in adults with moderate AD and examined associated microbiome and serum metabolite changes.
METHODS: In this randomized, double-blind, placebo-controlled 12-week trial, 152 adults with moderate AD were assigned 1:1 to Qing-Re-Qu-Shi formula or placebo. Outcomes included Eczema Area and Severity Index (EASI), SCORAD, Patient-Oriented Eczema Measure (POEM), pruritus numerical rating scale (NRS), Dermatology Life Quality Index (DLQI), and responder rates. The primary clinical analysis followed the intention-to-treat principle. Paired fecal 16S rRNA sequencing and targeted serum metabolomics were performed in the biospecimen subset. Differential feature analyses adjusted for baseline level, age, and sex; β diversity was assessed using repeated-measures-aware PERMANOVA.
RESULTS: All randomized participants were included in clinical analyses; 124 contributed paired fecal and serum specimens, and 102 also had week-12 clinical data for cross-domain analyses. Compared with placebo, Qing-Re-Qu-Shi produced greater week-12 improvements in EASI (adjusted mean difference, -3.78; 95% CI, -4.54 to -3.01), SCORAD (-9.73; 95% CI, -11.54 to -7.93), POEM (-3.39; 95% CI, -4.06 to -2.73), pruritus NRS (-0.94; 95% CI, -1.15 to -0.72), and DLQI (-2.86; 95% CI, -3.47 to -2.26) (all p < 0.001). EASI-50 and EASI-75 responses were more frequent with Qing-Re-Qu-Shi. Shannon diversity changed little, whereas β diversity showed a small but significant group-by-time effect (p = 0.001, R [2] = 0.016). Full-feature CLR analyses identified higher Blautia, Bifidobacterium, Lactobacillus, and Agathobacter and lower Escherichia/Shigella, Enterococcus, Prevotella, and Collinsella after false-discovery-rate correction. Serum metabolomics showed higher short-chain fatty acid and indole-related signals and lower kynurenine-related signals. Cross-domain correlations aligned these changes with greater symptom improvement.
CONCLUSION: Qing-Re-Qu-Shi formula improved clinical severity and patient-reported outcomes in adults with moderate AD. These benefits were accompanied by selective gut microbial remodeling and circulating microbiota-related metabolite changes, supporting an associative link between clinical improvement and gut ecosystem remodeling rather than proving causality.
Additional Links: PMID-42602801
PubMed:
Citation:
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@article {pmid42602801,
year = {2026},
author = {Xiong, Y and Huang, P and Wang, J and Zhao, Y and Zhang, J and Wang, D and Zhang, H},
title = {Qing-Re-Qu-Shi formula improves clinical outcomes and is accompanied by gut microbiota and microbial metabolite remodeling in adults with moderate atopic dermatitis: a randomized placebo-controlled multi-omics trial.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1847003},
pmid = {42602801},
issn = {2296-858X},
abstract = {BACKGROUND: The gut-skin axis is increasingly implicated in atopic dermatitis (AD), but randomized adult studies linking clinical response to paired gut microbiome and circulating metabolite profiling remain limited. We evaluated Qing-Re-Qu-Shi formula in adults with moderate AD and examined associated microbiome and serum metabolite changes.
METHODS: In this randomized, double-blind, placebo-controlled 12-week trial, 152 adults with moderate AD were assigned 1:1 to Qing-Re-Qu-Shi formula or placebo. Outcomes included Eczema Area and Severity Index (EASI), SCORAD, Patient-Oriented Eczema Measure (POEM), pruritus numerical rating scale (NRS), Dermatology Life Quality Index (DLQI), and responder rates. The primary clinical analysis followed the intention-to-treat principle. Paired fecal 16S rRNA sequencing and targeted serum metabolomics were performed in the biospecimen subset. Differential feature analyses adjusted for baseline level, age, and sex; β diversity was assessed using repeated-measures-aware PERMANOVA.
RESULTS: All randomized participants were included in clinical analyses; 124 contributed paired fecal and serum specimens, and 102 also had week-12 clinical data for cross-domain analyses. Compared with placebo, Qing-Re-Qu-Shi produced greater week-12 improvements in EASI (adjusted mean difference, -3.78; 95% CI, -4.54 to -3.01), SCORAD (-9.73; 95% CI, -11.54 to -7.93), POEM (-3.39; 95% CI, -4.06 to -2.73), pruritus NRS (-0.94; 95% CI, -1.15 to -0.72), and DLQI (-2.86; 95% CI, -3.47 to -2.26) (all p < 0.001). EASI-50 and EASI-75 responses were more frequent with Qing-Re-Qu-Shi. Shannon diversity changed little, whereas β diversity showed a small but significant group-by-time effect (p = 0.001, R [2] = 0.016). Full-feature CLR analyses identified higher Blautia, Bifidobacterium, Lactobacillus, and Agathobacter and lower Escherichia/Shigella, Enterococcus, Prevotella, and Collinsella after false-discovery-rate correction. Serum metabolomics showed higher short-chain fatty acid and indole-related signals and lower kynurenine-related signals. Cross-domain correlations aligned these changes with greater symptom improvement.
CONCLUSION: Qing-Re-Qu-Shi formula improved clinical severity and patient-reported outcomes in adults with moderate AD. These benefits were accompanied by selective gut microbial remodeling and circulating microbiota-related metabolite changes, supporting an associative link between clinical improvement and gut ecosystem remodeling rather than proving causality.},
}
RevDate: 2026-08-15
CmpDate: 2026-08-15
Correction: Moderate organic-inorganic fertilization optimizes soybean productivity by reshaping rhizosphere microbiome-metabolite networks.
Frontiers in plant science, 17:1902091.
[This corrects the article DOI: 10.3389/fpls.2026.1823609.].
Additional Links: PMID-42602867
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@article {pmid42602867,
year = {2026},
author = {Zhang, J and Liu, Q and Chen, J and Zhou, Y and Zhang, B and Yuan, Z and Li, P and Pang, Z},
title = {Correction: Moderate organic-inorganic fertilization optimizes soybean productivity by reshaping rhizosphere microbiome-metabolite networks.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1902091},
doi = {10.3389/fpls.2026.1902091},
pmid = {42602867},
issn = {1664-462X},
abstract = {[This corrects the article DOI: 10.3389/fpls.2026.1823609.].},
}
RevDate: 2026-08-15
The microbiome in human skin aging.
FEBS letters [Epub ahead of print].
Microbiome dysbiosis correlates with aging-associated pathological skin conditions, and our understanding of how the microbiome regulates skin aging at a molecular level is rapidly advancing. Classical hallmarks of skin aging, including genomic instability and telomere attrition, loss of proteostasis, epigenetic alterations, and altered intercellular communication, are critically regulated by the microbiome. Oxidative stress represents a key factor implicated in virtually all hallmarks of skin aging. Meanwhile, recent data underscore the role of metabolism in intercellular communication and aging. Here, we examine current evidence linking the skin microbiome to such molecular events in the aging skin.
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@article {pmid42603099,
year = {2026},
author = {Huerta Arana, M and Wiegand, C and Omrani, O and Fabri, M},
title = {The microbiome in human skin aging.},
journal = {FEBS letters},
volume = {},
number = {},
pages = {},
doi = {10.1002/1873-3468.70435},
pmid = {42603099},
issn = {1873-3468},
abstract = {Microbiome dysbiosis correlates with aging-associated pathological skin conditions, and our understanding of how the microbiome regulates skin aging at a molecular level is rapidly advancing. Classical hallmarks of skin aging, including genomic instability and telomere attrition, loss of proteostasis, epigenetic alterations, and altered intercellular communication, are critically regulated by the microbiome. Oxidative stress represents a key factor implicated in virtually all hallmarks of skin aging. Meanwhile, recent data underscore the role of metabolism in intercellular communication and aging. Here, we examine current evidence linking the skin microbiome to such molecular events in the aging skin.},
}
RevDate: 2026-08-13
Molecular Mechanisms and Therapeutic Targeting of the Macrophage Metabolic-Epigenetic Interaction Network in Chronic Obstructive Pulmonary Disease.
Cell biochemistry and biophysics [Epub ahead of print].
Pulmonary macrophages serve as one of the primary mediators of the complex and persistent inflammation in chronic obstructive pulmonary disease (COPD). While driven by multiple mechanisms-including oxidative stress pathways, macrophage heterogeneity, microbiome interactions, and the dynamics of acute exacerbations-the intrinsic drivers promoting continuous inflammatory amplification remain incompletely defined. Recent findings point to a bidirectional relationship between cellular metabolism and epigenetic regulation as a driver of this abnormal activation. This review outlines the biochemical components of this crosstalk, linking shifts in glucose, lipid, and glutamine metabolism to chromatin remodeling events. We detail four major molecular axes: α-ketoglutarate-dependent DNA methylation, NAD[+]/SIRT1-mediated deacetylation, the acetyl-CoA-fueled histone acetylation feedback loop, and the regulatory influence of non-coding RNAs (ncRNAs). Together, these pathways create a self-sustaining cycle where altered metabolic fluxes reshape the epigenetic landscape, which subsequently reinforces the initial metabolic abnormalities. This loop helps establish a stable "functional memory" in macrophages, accelerating alveolar damage. Finally, we discuss current gaps, including the need for spatial mapping and multi-omics integration, and evaluate how emerging targeted therapies-such as dual-inhibitors, PROTACs, and RNA-based treatments-could disrupt this pathogenic loop to provide novel preclinical strategies for COPD management.
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@article {pmid42593569,
year = {2026},
author = {Liu, Q and Liu, W},
title = {Molecular Mechanisms and Therapeutic Targeting of the Macrophage Metabolic-Epigenetic Interaction Network in Chronic Obstructive Pulmonary Disease.},
journal = {Cell biochemistry and biophysics},
volume = {},
number = {},
pages = {},
pmid = {42593569},
issn = {1559-0283},
support = {No.82560013//National Natural Science Foundation of China/ ; },
abstract = {Pulmonary macrophages serve as one of the primary mediators of the complex and persistent inflammation in chronic obstructive pulmonary disease (COPD). While driven by multiple mechanisms-including oxidative stress pathways, macrophage heterogeneity, microbiome interactions, and the dynamics of acute exacerbations-the intrinsic drivers promoting continuous inflammatory amplification remain incompletely defined. Recent findings point to a bidirectional relationship between cellular metabolism and epigenetic regulation as a driver of this abnormal activation. This review outlines the biochemical components of this crosstalk, linking shifts in glucose, lipid, and glutamine metabolism to chromatin remodeling events. We detail four major molecular axes: α-ketoglutarate-dependent DNA methylation, NAD[+]/SIRT1-mediated deacetylation, the acetyl-CoA-fueled histone acetylation feedback loop, and the regulatory influence of non-coding RNAs (ncRNAs). Together, these pathways create a self-sustaining cycle where altered metabolic fluxes reshape the epigenetic landscape, which subsequently reinforces the initial metabolic abnormalities. This loop helps establish a stable "functional memory" in macrophages, accelerating alveolar damage. Finally, we discuss current gaps, including the need for spatial mapping and multi-omics integration, and evaluate how emerging targeted therapies-such as dual-inhibitors, PROTACs, and RNA-based treatments-could disrupt this pathogenic loop to provide novel preclinical strategies for COPD management.},
}
RevDate: 2026-08-13
CmpDate: 2026-08-13
Association Between Gut Microbiota Dysbiosis and Bilirubin Metabolism Dysregulation in Children with Heart Failure.
Journal of cardiovascular translational research, 19(1):.
Patients with heart failure (HF) demonstrate dysregulation in bilirubin metabolism. The specific characteristics of intestinal bilirubin metabolism in HF remain unclear. This study involved metagenomic sequencing and metabolomic profiling of fecal samples from 45 children with HF and 32 healthy children. Serum total bilirubin levels were 11.3umol/L, 19.4umol/L and 5.0umol/L in HF New York Heart Association (NYHA) I-II, NYHA III-IV and control group (p < 0.001), and the median gut microbiome health index (GMHI) were - 0.78, -1.53 and 0.09 in each (p < 0.001). The abundance of 2 bacteria species containing bilirubin reductase, Ruminococcus gnavus (p = 0.028) and Clostridium sp.M62/1 (p = 0.002) significantly decreased in NYHA III-IV group. The gut downstream bilirubin products, urobilinogen and stercobilin were decreased in the HF group; while the upstream bilirubin products, unconjugated and conjugated bilirubin increased. Dysbiosis of the gut microbiome and the decrease of bilirubin reductase containing bacteria in pediatric HF patients related to a reduction in gut bilirubin metabolism.
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@article {pmid42593705,
year = {2026},
author = {Wei, W and Zhou, L and Huang, Y and Lu, Z and Zhang, R and Zeng, M and Wang, X},
title = {Association Between Gut Microbiota Dysbiosis and Bilirubin Metabolism Dysregulation in Children with Heart Failure.},
journal = {Journal of cardiovascular translational research},
volume = {19},
number = {1},
pages = {},
pmid = {42593705},
issn = {1937-5395},
mesh = {Humans ; *Heart Failure/microbiology/diagnosis/blood ; *Bilirubin/blood ; *Dysbiosis ; *Gastrointestinal Microbiome ; Female ; Child, Preschool ; Male ; Child ; Case-Control Studies ; Biomarkers/blood ; Feces/microbiology ; Age Factors ; Metabolomics ; Infant ; Ribotyping ; Clostridium/genetics ; Adolescent ; Eubacteriales ; },
abstract = {Patients with heart failure (HF) demonstrate dysregulation in bilirubin metabolism. The specific characteristics of intestinal bilirubin metabolism in HF remain unclear. This study involved metagenomic sequencing and metabolomic profiling of fecal samples from 45 children with HF and 32 healthy children. Serum total bilirubin levels were 11.3umol/L, 19.4umol/L and 5.0umol/L in HF New York Heart Association (NYHA) I-II, NYHA III-IV and control group (p < 0.001), and the median gut microbiome health index (GMHI) were - 0.78, -1.53 and 0.09 in each (p < 0.001). The abundance of 2 bacteria species containing bilirubin reductase, Ruminococcus gnavus (p = 0.028) and Clostridium sp.M62/1 (p = 0.002) significantly decreased in NYHA III-IV group. The gut downstream bilirubin products, urobilinogen and stercobilin were decreased in the HF group; while the upstream bilirubin products, unconjugated and conjugated bilirubin increased. Dysbiosis of the gut microbiome and the decrease of bilirubin reductase containing bacteria in pediatric HF patients related to a reduction in gut bilirubin metabolism.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Heart Failure/microbiology/diagnosis/blood
*Bilirubin/blood
*Dysbiosis
*Gastrointestinal Microbiome
Female
Child, Preschool
Male
Child
Case-Control Studies
Biomarkers/blood
Feces/microbiology
Age Factors
Metabolomics
Infant
Ribotyping
Clostridium/genetics
Adolescent
Eubacteriales
RevDate: 2026-08-13
CmpDate: 2026-08-13
Integrated multi-omics reveals dysbiosis in hemodialysis patients: A multi-center study.
PloS one, 21(8):e0355698.
INTRODUCTION: The gut microbiome-metabolome interplay in hemodialysis (HD) patients remains poorly characterized. Using multi-omics approaches, we compared HD patients with healthy controls (HC) to identify microbial signatures, metabolic perturbations, and their integrated correlations.
METHODS: This case-control study included 192 participants (96 HD-HC pairs under identical dietary and living conditions). The gut microbiota composition was analyzed using 16S ribosomal RNA gene sequencing, and fecal metabolomes were analyzed using ultra-high-performance liquid chromatography and high-resolution mass spectrometry (UPLC-HRMS). A multi-omics analysis was conducted utilizing Spearman correlation analysis, Mantel test analysis, and differential functional pathway analysis.
RESULTS: We observed significant differences in gut microbiota composition between the HD and HC groups, such as Ruminococcus and Bifidobacterium. Comparative analysis revealed 497 significantly altered metabolites in the HD group versus HC, primarily associated with amino acid, vitamin, lipid, purine, and pyrimidine metabolisms. ROC analysis identified 4-pyridoxic acid, nudifloramide, imidazoleacetic acid, ascorbic acid, and tocopheronic acid as potential diagnostic biomarkers (AUC > 0.8, p < 0.01). Integrated multi-omics analysis revealed correlations between Ruminococcus and metabolites such as Docosapentoic acid (DPA), 13 - EPAHAAB (EPA), and tryptamine, with shared differential pathways in bile secretion, caffeine metabolism, gastric acid secretion, and vitamin B6 metabolism.
CONCLUSION: Hemodialysis patients exhibited significant alterations in gut microbiota composition and metabolic profiles (amino acid, vitamin, and lipid metabolism) compared with healthy controls, with demonstrated microbiome-metabolome interactions and shared functional pathways. The potential diagnostic and therapeutic value of these differential features warrants further exploration and external validation.
Additional Links: PMID-42594080
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@article {pmid42594080,
year = {2026},
author = {Zhang, X and Yu, D and Cui, Y and Chi, Y and Yan, Z and Song, Y and Hou, L and Qin, J and Zhang, J and Wang, Y and Wei, W and Di, H},
title = {Integrated multi-omics reveals dysbiosis in hemodialysis patients: A multi-center study.},
journal = {PloS one},
volume = {21},
number = {8},
pages = {e0355698},
pmid = {42594080},
issn = {1932-6203},
mesh = {Humans ; *Renal Dialysis/adverse effects ; Multiomics ; *Dysbiosis/metabolism/microbiology/etiology ; Case-Control Studies ; Female ; RNA, Ribosomal, 16S/genetics ; Male ; Middle Aged ; *Gastrointestinal Microbiome ; Metabolome ; Feces/microbiology ; Aged ; Metabolomics ; },
abstract = {INTRODUCTION: The gut microbiome-metabolome interplay in hemodialysis (HD) patients remains poorly characterized. Using multi-omics approaches, we compared HD patients with healthy controls (HC) to identify microbial signatures, metabolic perturbations, and their integrated correlations.
METHODS: This case-control study included 192 participants (96 HD-HC pairs under identical dietary and living conditions). The gut microbiota composition was analyzed using 16S ribosomal RNA gene sequencing, and fecal metabolomes were analyzed using ultra-high-performance liquid chromatography and high-resolution mass spectrometry (UPLC-HRMS). A multi-omics analysis was conducted utilizing Spearman correlation analysis, Mantel test analysis, and differential functional pathway analysis.
RESULTS: We observed significant differences in gut microbiota composition between the HD and HC groups, such as Ruminococcus and Bifidobacterium. Comparative analysis revealed 497 significantly altered metabolites in the HD group versus HC, primarily associated with amino acid, vitamin, lipid, purine, and pyrimidine metabolisms. ROC analysis identified 4-pyridoxic acid, nudifloramide, imidazoleacetic acid, ascorbic acid, and tocopheronic acid as potential diagnostic biomarkers (AUC > 0.8, p < 0.01). Integrated multi-omics analysis revealed correlations between Ruminococcus and metabolites such as Docosapentoic acid (DPA), 13 - EPAHAAB (EPA), and tryptamine, with shared differential pathways in bile secretion, caffeine metabolism, gastric acid secretion, and vitamin B6 metabolism.
CONCLUSION: Hemodialysis patients exhibited significant alterations in gut microbiota composition and metabolic profiles (amino acid, vitamin, and lipid metabolism) compared with healthy controls, with demonstrated microbiome-metabolome interactions and shared functional pathways. The potential diagnostic and therapeutic value of these differential features warrants further exploration and external validation.},
}
MeSH Terms:
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Humans
*Renal Dialysis/adverse effects
Multiomics
*Dysbiosis/metabolism/microbiology/etiology
Case-Control Studies
Female
RNA, Ribosomal, 16S/genetics
Male
Middle Aged
*Gastrointestinal Microbiome
Metabolome
Feces/microbiology
Aged
Metabolomics
RevDate: 2026-08-13
Gut microbiota-derived TMA/TMAO and IRAK4 signaling in type 2 diabetes: Current evidence, knowledge gaps and future therapeutic opportunities.
International immunopharmacology, 188:117240 pii:S1567-5769(26)01086-6 [Epub ahead of print].
Diabetes mellitus type 2 (T2DM) is now considered an immunometabolic condition with a long-term low-grade inflammatory state, insulin resistance, and host-microbiome interactions. Emerging evidence suggests that gut microbiota-derived trimethylamine (TMA), its hepatic metabolite trimethylamine N-oxide (TMAO), and IRAK4-mediated innate immune signaling may contribute to metabolic inflammation and insulin resistance. However, direct mechanistic evidence linking these components remains limited, and most available data originate from preclinical studies. Gut microbiota produces TMA based on the nutrients present in the diet, such as choline, betaine, and l-carnitine, which are then oxidized in the liver to trimethylamine N-oxide (TMAO), a metabolite linked to inflammation, metabolic maladaptation, and cardiovascular issues. IRAK4, a signaling mediator of Toll-like receptor and interleukin-1 receptor, may induce NF- kB and MAPK signaling, which may contribute to metaflammation and defective insulin signaling. This overview highlights existing evidence of the TMAIRAK4 axis in the pathogenesis and insulin resistance in T2DM. We discuss current evidence suggesting that TMA/TMAO may influence innate immune signaling and inflammatory pathways associated with insulin resistance. Special attention is given to the interference with the IRSPI3KAkt-pathway by inflammatory signaling mediated by IRAK4. We also consider new treatment approaches, such as IRAK4 inhibitors, control of microbial TMA synthesis, and FMO3-based interventions. Lastly, we underscore important translational issues, such as inconsistency in the evidence about TMAO biology, microbiome diversity, insufficient human validation, and the necessity of multi-omics-based precision methods in patient stratification and personalized treatment.
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@article {pmid42594838,
year = {2026},
author = {Sarma, AD and Devi, M and Kumar, D and Choudhary, N},
title = {Gut microbiota-derived TMA/TMAO and IRAK4 signaling in type 2 diabetes: Current evidence, knowledge gaps and future therapeutic opportunities.},
journal = {International immunopharmacology},
volume = {188},
number = {},
pages = {117240},
doi = {10.1016/j.intimp.2026.117240},
pmid = {42594838},
issn = {1878-1705},
abstract = {Diabetes mellitus type 2 (T2DM) is now considered an immunometabolic condition with a long-term low-grade inflammatory state, insulin resistance, and host-microbiome interactions. Emerging evidence suggests that gut microbiota-derived trimethylamine (TMA), its hepatic metabolite trimethylamine N-oxide (TMAO), and IRAK4-mediated innate immune signaling may contribute to metabolic inflammation and insulin resistance. However, direct mechanistic evidence linking these components remains limited, and most available data originate from preclinical studies. Gut microbiota produces TMA based on the nutrients present in the diet, such as choline, betaine, and l-carnitine, which are then oxidized in the liver to trimethylamine N-oxide (TMAO), a metabolite linked to inflammation, metabolic maladaptation, and cardiovascular issues. IRAK4, a signaling mediator of Toll-like receptor and interleukin-1 receptor, may induce NF- kB and MAPK signaling, which may contribute to metaflammation and defective insulin signaling. This overview highlights existing evidence of the TMAIRAK4 axis in the pathogenesis and insulin resistance in T2DM. We discuss current evidence suggesting that TMA/TMAO may influence innate immune signaling and inflammatory pathways associated with insulin resistance. Special attention is given to the interference with the IRSPI3KAkt-pathway by inflammatory signaling mediated by IRAK4. We also consider new treatment approaches, such as IRAK4 inhibitors, control of microbial TMA synthesis, and FMO3-based interventions. Lastly, we underscore important translational issues, such as inconsistency in the evidence about TMAO biology, microbiome diversity, insufficient human validation, and the necessity of multi-omics-based precision methods in patient stratification and personalized treatment.},
}
RevDate: 2026-08-13
CmpDate: 2026-08-13
More Than Skin Deep: Understanding the Skin-Bone Axis.
Skin therapy letter, 31(4):1-5.
The skin's role as a mirror of internal disease has long been established, with clear associations to several internal organs. However, its relationship with bone is less well known. There are clear physiological links between the two organ systems, with their shared factors crucial to maintain structural integrity and homeostasis. Collagen, vitamin D homeostasis, aging, medications, and the gut microbiome are all factors that impact both skin and bone. It is of utmost importance that the skin-bone axis be adequately understood to support a healthy aging process. In this review, we discuss the multiple facets related to skin and bone health, their interconnectivity, as well as the importance of promoting whole body health.
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@article {pmid42594848,
year = {2026},
author = {Conte, S and Le, V and Li, MK},
title = {More Than Skin Deep: Understanding the Skin-Bone Axis.},
journal = {Skin therapy letter},
volume = {31},
number = {4},
pages = {1-5},
pmid = {42594848},
issn = {1201-5989},
mesh = {Humans ; *Bone and Bones/physiology ; Vitamin D/metabolism ; Aging/physiology ; Homeostasis/physiology ; *Skin Aging/physiology ; Collagen/metabolism/physiology ; *Skin/metabolism ; *Skin Physiological Phenomena ; Gastrointestinal Microbiome/physiology ; },
abstract = {The skin's role as a mirror of internal disease has long been established, with clear associations to several internal organs. However, its relationship with bone is less well known. There are clear physiological links between the two organ systems, with their shared factors crucial to maintain structural integrity and homeostasis. Collagen, vitamin D homeostasis, aging, medications, and the gut microbiome are all factors that impact both skin and bone. It is of utmost importance that the skin-bone axis be adequately understood to support a healthy aging process. In this review, we discuss the multiple facets related to skin and bone health, their interconnectivity, as well as the importance of promoting whole body health.},
}
MeSH Terms:
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Humans
*Bone and Bones/physiology
Vitamin D/metabolism
Aging/physiology
Homeostasis/physiology
*Skin Aging/physiology
Collagen/metabolism/physiology
*Skin/metabolism
*Skin Physiological Phenomena
Gastrointestinal Microbiome/physiology
RevDate: 2026-08-13
Modeling microbiome modulation of tumor metabolic networks to predict synergistic therapies.
Cell reports methods pii:S2667-2375(26)00250-X [Epub ahead of print].
Differences in microbiome composition profoundly influence drug response, yet methods to model the metabolic impact of microbes on host cells and therapeutics remain limited. We present a microbiome-aware computational framework combining machine learning and genome-scale metabolic models to predict combination therapies for colorectal cancer (CRC) in the presence of Fusobacterium nucleatum (Fn) and other pathogenic, probiotic, and commensal microbes. The model learned predictive metabolic flux signatures from 6,514 drug combination profiles in CRC cell lines and predicted synergistic drug combinations across both microbe-free and microbe-associated contexts. Model performance was supported through prospective comparison with newly reported drug combinations, in vitro drug synergy assays, microbiome co-culture experiments, and targeted metabolic perturbations of predicted pathway dependencies. Pharmacological perturbations in asymmetric co-cultures revealed phosphoinositol metabolism and cysteine transport as key determinants of Fn-dependent drug synergy. Together, this work introduces a scalable strategy for discovering microbiome-dependent combination therapies, including chemotherapies, immunotherapy, and probiotics.
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@article {pmid42594868,
year = {2026},
author = {Badenoch, AJ and Pang, Z and Chung, CH and Robida, A and Badenoch, B and Natesan, R and Kakish, L and Li, J and Chandrasekaran, S},
title = {Modeling microbiome modulation of tumor metabolic networks to predict synergistic therapies.},
journal = {Cell reports methods},
volume = {},
number = {},
pages = {101549},
doi = {10.1016/j.crmeth.2026.101549},
pmid = {42594868},
issn = {2667-2375},
abstract = {Differences in microbiome composition profoundly influence drug response, yet methods to model the metabolic impact of microbes on host cells and therapeutics remain limited. We present a microbiome-aware computational framework combining machine learning and genome-scale metabolic models to predict combination therapies for colorectal cancer (CRC) in the presence of Fusobacterium nucleatum (Fn) and other pathogenic, probiotic, and commensal microbes. The model learned predictive metabolic flux signatures from 6,514 drug combination profiles in CRC cell lines and predicted synergistic drug combinations across both microbe-free and microbe-associated contexts. Model performance was supported through prospective comparison with newly reported drug combinations, in vitro drug synergy assays, microbiome co-culture experiments, and targeted metabolic perturbations of predicted pathway dependencies. Pharmacological perturbations in asymmetric co-cultures revealed phosphoinositol metabolism and cysteine transport as key determinants of Fn-dependent drug synergy. Together, this work introduces a scalable strategy for discovering microbiome-dependent combination therapies, including chemotherapies, immunotherapy, and probiotics.},
}
RevDate: 2026-08-13
The association of gut microbiome composition with musculoskeletal features in middle-aged and older adults: A two-cohort joint study.
Bone pii:S8756-3282(26)00277-2 [Epub ahead of print].
BACKGROUND: Bones and muscles are connected chemically, anatomically, and functionally. While animal studies suggest the gut microbiome influences musculoskeletal aging, human evidence remains limited. We assessed associations between musculoskeletal phenotypes and gut microbiome composition in community-dwelling middle-aged and older adults.
METHODS: We analyzed DXA-derived phenotypes from two population-based cohorts: the Rotterdam Study (mean age 62.7 years; n = 1249) and the Framingham Heart Study (mean age 55.2 years; n = 1227). Phenotypes included appendicular lean mass (ALM), femoral neck bone mineral density (FN-BMD), and trabecular bone score (TBS). Gut microbiome composition was assessed via 16S rRNA sequencing, and functional potential predicted using PICRUSt2. Multivariate linear regression analyses were adjusted for demographic, lifestyle, and clinical covariates.
RESULTS: Alpha diversity was not associated with any musculoskeletal phenotype after multiple testing, whereas beta diversity was associated with ALM in the combined and female analyses. Four genera associated with ALM: lower abundance of Oscillibacter (β = -0.51, 95%CI [-0.74,-0.29]), Anaerotruncus (β = -0.41, 95%CI[-0.61,-0.21]), Eisenbergiella (β = -0.39, 95%CI[-0.59,-0.19]) and higher abundance of Agathobacter (β = 0.40, 95%CI [0.20,0.60]) were associated with higher ALM. In females, lower abundance of Anaerotruncus (β = -0.32, 95%CI[-0.45,-0.19]), Hungatella (β = -0.26, 95%CI[-0.38,-0.15]), and Clostridiales bacterium DTU089 (β = -0.37, 95%CI[-0.55,-0.19]), and higher biotin biosynthesis II pathway (β = 0.44, 95%CI[0.24,0.64]) associated with higher ALM. No robust associations were observed for bone traits.
CONCLUSION: Although no associations were identified between gut microbial features and bone measures, several microbial genera were associated with appendicular lean mass in middle-aged and older adults, with evidence of sex-specific effects. Larger studies are needed to confirm these findings and clarify underlying mechanisms.
Additional Links: PMID-42595281
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PubMed:
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@article {pmid42595281,
year = {2026},
author = {Li, R and Okoro, PC and Zillikens, MC and Vasan, RS and Sahni, S and Rivadeneira, F and Kiel, DP and Medina-Gomez, C},
title = {The association of gut microbiome composition with musculoskeletal features in middle-aged and older adults: A two-cohort joint study.},
journal = {Bone},
volume = {},
number = {},
pages = {118051},
doi = {10.1016/j.bone.2026.118051},
pmid = {42595281},
issn = {1873-2763},
abstract = {BACKGROUND: Bones and muscles are connected chemically, anatomically, and functionally. While animal studies suggest the gut microbiome influences musculoskeletal aging, human evidence remains limited. We assessed associations between musculoskeletal phenotypes and gut microbiome composition in community-dwelling middle-aged and older adults.
METHODS: We analyzed DXA-derived phenotypes from two population-based cohorts: the Rotterdam Study (mean age 62.7 years; n = 1249) and the Framingham Heart Study (mean age 55.2 years; n = 1227). Phenotypes included appendicular lean mass (ALM), femoral neck bone mineral density (FN-BMD), and trabecular bone score (TBS). Gut microbiome composition was assessed via 16S rRNA sequencing, and functional potential predicted using PICRUSt2. Multivariate linear regression analyses were adjusted for demographic, lifestyle, and clinical covariates.
RESULTS: Alpha diversity was not associated with any musculoskeletal phenotype after multiple testing, whereas beta diversity was associated with ALM in the combined and female analyses. Four genera associated with ALM: lower abundance of Oscillibacter (β = -0.51, 95%CI [-0.74,-0.29]), Anaerotruncus (β = -0.41, 95%CI[-0.61,-0.21]), Eisenbergiella (β = -0.39, 95%CI[-0.59,-0.19]) and higher abundance of Agathobacter (β = 0.40, 95%CI [0.20,0.60]) were associated with higher ALM. In females, lower abundance of Anaerotruncus (β = -0.32, 95%CI[-0.45,-0.19]), Hungatella (β = -0.26, 95%CI[-0.38,-0.15]), and Clostridiales bacterium DTU089 (β = -0.37, 95%CI[-0.55,-0.19]), and higher biotin biosynthesis II pathway (β = 0.44, 95%CI[0.24,0.64]) associated with higher ALM. No robust associations were observed for bone traits.
CONCLUSION: Although no associations were identified between gut microbial features and bone measures, several microbial genera were associated with appendicular lean mass in middle-aged and older adults, with evidence of sex-specific effects. Larger studies are needed to confirm these findings and clarify underlying mechanisms.},
}
RevDate: 2026-08-13
CmpDate: 2026-08-13
Optimized Controlled-Release Fertilization Improves Productivity and Reshapes the Rhizosphere Microbiome in Lei Bamboo: A Metagenomic Assessment.
Environmental microbiology, 28(8):e70401.
Intensive nitrogen fertilization in Lei bamboo (Phyllostachys praecox) plantations has increased productivity but has also reduced nitrogen-use efficiency (NUE), accelerated nutrient losses, and contributed to soil degradation. How nutrient-release strategies influence rhizosphere microbiome assembly and ecosystem functioning remains poorly understood. Here, we developed a bamboo shoot-specific controlled-release fertilizer (CRF) and evaluated different urea-CRF blending ratios to identify sustainable fertilization strategy for Lei bamboo production. Mixed CRF-urea treatments outperformed both sole-fertilizer applications and the unfertilized control. T2 (30% urea + 70% CRF) achieved the highest shoot yield, whereas T3 (50% urea + 50% CRF) enhanced NUE. Optimized fertilization improved soil nutrient availability and organic matter accumulation without significantly affecting soil pH. Metagenomic analysis revealed the enrichment of taxa associated with nutrient transformation, organic matter turnover, and plant growth. However, pathway-level analysis revealed shifts in carbon, nitrogen, and sulfur cycling activities under optimized nutrient-release regimes. Our results demonstrate that synchronizing nitrogen release with plant and microbial demand enhances rhizosphere function, productivity and NUE. T2 delivered the strongest overall agronomic performance by maximizing shoot yield while maintaining improved nutrient retention and ecological stability. These findings provide a mechanistic link between fertilization strategy, rhizosphere microbial dynamics, and ecosystem function, supporting sustainable Lei bamboo production.
Additional Links: PMID-42595349
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Citation:
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@article {pmid42595349,
year = {2026},
author = {Yang, Z and Ramakrishnan, M and Wang, B and Wei, Q and Ahmad, Z},
title = {Optimized Controlled-Release Fertilization Improves Productivity and Reshapes the Rhizosphere Microbiome in Lei Bamboo: A Metagenomic Assessment.},
journal = {Environmental microbiology},
volume = {28},
number = {8},
pages = {e70401},
pmid = {42595349},
issn = {1462-2920},
support = {2018YFD060010403//National Key Research and Development Program of China/ ; 2021F1065-10//Special Project of Zhejiang Provincial Scientific Research Institutes/ ; },
mesh = {*Fertilizers/analysis ; *Rhizosphere ; *Microbiota ; *Soil Microbiology ; *Poaceae/microbiology/growth & development ; Nitrogen/metabolism ; Metagenomics ; Bacteria/classification/genetics/isolation & purification/metabolism ; Soil/chemistry ; Urea/metabolism ; },
abstract = {Intensive nitrogen fertilization in Lei bamboo (Phyllostachys praecox) plantations has increased productivity but has also reduced nitrogen-use efficiency (NUE), accelerated nutrient losses, and contributed to soil degradation. How nutrient-release strategies influence rhizosphere microbiome assembly and ecosystem functioning remains poorly understood. Here, we developed a bamboo shoot-specific controlled-release fertilizer (CRF) and evaluated different urea-CRF blending ratios to identify sustainable fertilization strategy for Lei bamboo production. Mixed CRF-urea treatments outperformed both sole-fertilizer applications and the unfertilized control. T2 (30% urea + 70% CRF) achieved the highest shoot yield, whereas T3 (50% urea + 50% CRF) enhanced NUE. Optimized fertilization improved soil nutrient availability and organic matter accumulation without significantly affecting soil pH. Metagenomic analysis revealed the enrichment of taxa associated with nutrient transformation, organic matter turnover, and plant growth. However, pathway-level analysis revealed shifts in carbon, nitrogen, and sulfur cycling activities under optimized nutrient-release regimes. Our results demonstrate that synchronizing nitrogen release with plant and microbial demand enhances rhizosphere function, productivity and NUE. T2 delivered the strongest overall agronomic performance by maximizing shoot yield while maintaining improved nutrient retention and ecological stability. These findings provide a mechanistic link between fertilization strategy, rhizosphere microbial dynamics, and ecosystem function, supporting sustainable Lei bamboo production.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Fertilizers/analysis
*Rhizosphere
*Microbiota
*Soil Microbiology
*Poaceae/microbiology/growth & development
Nitrogen/metabolism
Metagenomics
Bacteria/classification/genetics/isolation & purification/metabolism
Soil/chemistry
Urea/metabolism
RevDate: 2026-08-13
Nasal Corynebacterium depletion is associated with polysensitization to inhalant allergens in adults.
Allergology international : official journal of the Japanese Society of Allergology pii:S1323-8930(26)00088-2 [Epub ahead of print].
BACKGROUND: Polysensitization to inhalant allergens is an important determinant of disease progression and severity in allergic conditions. Although microbial dysbiosis has been implicated in various allergic conditions, the association between nasal microbiome composition and polysensitization remains unclear. This study aimed to investigate the association between the nasal microbiome and airborne allergen sensitization burden in adults.
METHODS: In this cross-sectional observational study, 278 adults were categorized into four groups based on the number of sensitizations (range: 0-9): zero, mono (1), oligo (2-3), and poly (≥4). Allergen-specific IgE levels were measured in blood samples. Nasal swabs were analyzed using 16S rRNA gene sequencing to characterize microbial composition and predict functional pathways.
RESULTS: Age was inversely correlated with the number of sensitizations, while both total IgE levels and allergic rhinitis prevalence increased across groups. Corynebacterium, a dominant commensal genus in the nasal microbiome, was significantly reduced in the polysensitized group and was inversely correlated with sensitization burden. Although overall microbial diversity remained stable, the abundance and co-occurrence patterns of key genera, including Corynebacterium, were altered in polysensitized individuals. Functional predictions revealed reduced activity in pathways related to carbohydrate metabolism (e.g., d-galactose degradation), cofactor biosynthesis (e.g., biotin and folate), and amino acid metabolism, all essential for epithelial integrity and repair.
CONCLUSIONS: Polysensitized individuals exhibit Corynebacterium depletion along with altered microbial interactions and metabolic potential. Thus, nasal microbiome dysbiosis may impair epithelial barrier function and contribute to allergen sensitization, serving as a potential target for preventive strategies.
Additional Links: PMID-42595650
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@article {pmid42595650,
year = {2026},
author = {Koyama, K and Kidoguchi, M and Adachi, N and Ii, R and Nakamura, T and Yoshida, K and Tsutsumiuchi, T and Kimura, Y and Kato, Y and Ogi, K and Imoto, Y and Sakashita, M and Takabayashi, T and Noguchi, E and Fujieda, S},
title = {Nasal Corynebacterium depletion is associated with polysensitization to inhalant allergens in adults.},
journal = {Allergology international : official journal of the Japanese Society of Allergology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.alit.2026.08.001},
pmid = {42595650},
issn = {1440-1592},
abstract = {BACKGROUND: Polysensitization to inhalant allergens is an important determinant of disease progression and severity in allergic conditions. Although microbial dysbiosis has been implicated in various allergic conditions, the association between nasal microbiome composition and polysensitization remains unclear. This study aimed to investigate the association between the nasal microbiome and airborne allergen sensitization burden in adults.
METHODS: In this cross-sectional observational study, 278 adults were categorized into four groups based on the number of sensitizations (range: 0-9): zero, mono (1), oligo (2-3), and poly (≥4). Allergen-specific IgE levels were measured in blood samples. Nasal swabs were analyzed using 16S rRNA gene sequencing to characterize microbial composition and predict functional pathways.
RESULTS: Age was inversely correlated with the number of sensitizations, while both total IgE levels and allergic rhinitis prevalence increased across groups. Corynebacterium, a dominant commensal genus in the nasal microbiome, was significantly reduced in the polysensitized group and was inversely correlated with sensitization burden. Although overall microbial diversity remained stable, the abundance and co-occurrence patterns of key genera, including Corynebacterium, were altered in polysensitized individuals. Functional predictions revealed reduced activity in pathways related to carbohydrate metabolism (e.g., d-galactose degradation), cofactor biosynthesis (e.g., biotin and folate), and amino acid metabolism, all essential for epithelial integrity and repair.
CONCLUSIONS: Polysensitized individuals exhibit Corynebacterium depletion along with altered microbial interactions and metabolic potential. Thus, nasal microbiome dysbiosis may impair epithelial barrier function and contribute to allergen sensitization, serving as a potential target for preventive strategies.},
}
RevDate: 2026-08-14
Beneath the surface: non-target effects of multiple pesticides on the soil microbiome in organic and conventional agricultural European fields.
Environmental science and pollution research international [Epub ahead of print].
Previous studies have shown that diverse cocktails of pesticide mixtures are omnipresent in agricultural soils yet miss a clear link to the effects on the soil microbiome. In this study, we linked the occurrence of pesticides in conventional and organic agricultural soils of the SPRINT (Sustainable plant protection transition) projects' Case Study Sites to the composition and function of soil microbial communities. Metagenomic sequencing, phospholipid fatty acids analysis and enzyme activity measurements were used to characterize the soil microbiome and effects of site-specific parameters such as pH and SOC, and pesticide residues. Differences in the soil microbiome were strongly influenced by the geographic origin of the samples, with the pH value as dominant driver. Against our hypothesis, effects of the investigated management systems were limited, yet significant at the European level. Notably, an association between some pesticides could still be observed after accounting for the variation explained by the environmental factors. Among these, especially fungicides, with modes of action that aim to interfere with processes in microorganisms, seemed to affect the soil microbiome. This might occur either by directly affecting these processes in non-target organisms or by changing co-dependencies between fungi and bacteria. Next to fungicides, aminomethylphosphonic acid showed a significant effect on the soil microbial composition and an interactive, possibly synergistic effect with the persistent pesticide hexachlorobenzene. The latter raises concerns about a possible interaction of recently applied pesticides and persistent "legacy" pesticides. This work highlights that even though environmental parameters can overshadow the effects of pesticides, especially the identity of the pesticides present, can have an influence on the soil microbiome.
Additional Links: PMID-42595876
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Citation:
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@article {pmid42595876,
year = {2026},
author = {Knuth, D and Mäder, P and Boekhorst, J and Poll, C and Kandeler, E and Alaoui, A and Pasković, I and Polić Pasković, M and Baldi, I and Bureau, M and Alcon, F and Contreras, J and Glavan, M and Abrantes, N and Campos, I and Norgaard, T and Huerta Lwanga, E and Geissen, V and Harkes, P},
title = {Beneath the surface: non-target effects of multiple pesticides on the soil microbiome in organic and conventional agricultural European fields.},
journal = {Environmental science and pollution research international},
volume = {},
number = {},
pages = {},
pmid = {42595876},
issn = {1614-7499},
support = {862568//HORIZON EUROPE Framework Programme/ ; },
abstract = {Previous studies have shown that diverse cocktails of pesticide mixtures are omnipresent in agricultural soils yet miss a clear link to the effects on the soil microbiome. In this study, we linked the occurrence of pesticides in conventional and organic agricultural soils of the SPRINT (Sustainable plant protection transition) projects' Case Study Sites to the composition and function of soil microbial communities. Metagenomic sequencing, phospholipid fatty acids analysis and enzyme activity measurements were used to characterize the soil microbiome and effects of site-specific parameters such as pH and SOC, and pesticide residues. Differences in the soil microbiome were strongly influenced by the geographic origin of the samples, with the pH value as dominant driver. Against our hypothesis, effects of the investigated management systems were limited, yet significant at the European level. Notably, an association between some pesticides could still be observed after accounting for the variation explained by the environmental factors. Among these, especially fungicides, with modes of action that aim to interfere with processes in microorganisms, seemed to affect the soil microbiome. This might occur either by directly affecting these processes in non-target organisms or by changing co-dependencies between fungi and bacteria. Next to fungicides, aminomethylphosphonic acid showed a significant effect on the soil microbial composition and an interactive, possibly synergistic effect with the persistent pesticide hexachlorobenzene. The latter raises concerns about a possible interaction of recently applied pesticides and persistent "legacy" pesticides. This work highlights that even though environmental parameters can overshadow the effects of pesticides, especially the identity of the pesticides present, can have an influence on the soil microbiome.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Dietary tryptophan mitigates lung ischemia-reperfusion injury in association with increased indole-3-propionate and aryl hydrocarbon receptor signaling.
Gut microbes, 18(1):2715839.
BACKGROUND: Lung ischemia-reperfusion (IR) injury drives early morbidity after lung transplantation and cardiothoracic surgery, yet targeted preventive therapies are lacking. The gut-lung axis and microbiota-derived tryptophan metabolites, including indole-3-propionate (IPA), may regulate pulmonary immunity and inflammation. We investigated whether a tryptophan-rich (Trp-Rich) diet attenuates sterile lung IR injury by increasing microbiota-derived indole metabolites and reprogramming alveolar macrophage (AM) inflammatory responses.
METHODS: C57BL/6 mice receiving isocaloric tryptophan-standard (Trp-Std) or tryptophan-rich (Trp-Rich) diets underwent lung IR injury. Oxygen saturation, lung cytokines, and aryl hydrocarbon receptor (AhR) signaling readouts were evaluated. Gut microbiota was profiled by 16S rRNA sequencing, and targeted metabolomics quantified tryptophan metabolites in feces, portal vein (PV) plasma, and lung tissue. To further assess inflammatory priming in vivo, mice were additionally challenged with intratracheal lipopolysaccharide (LPS). Mechanistic studies compared IPA with related indoles in cell lines and primary human AMs, including ex vivo nutritional IR, LPS stimulation, and AhR stimulation and blockade using synthetic agonists and antagonists.
RESULTS: Trp-Rich feeding improved post-IR oxygenation, reduced lung IL-1β, and increased pulmonary AhR-downstream gene expression. Trp-Rich diet remodeled gut microbiota, enriching for Bifidobacterium and Lactobacillus, and increasing IPA levels across feces, PV plasma, and lung tissue. In the LPS intratracheal challenge, Trp-Rich feeding reduced IL-6 levels in lung tissue and systemic plasma. Primary AMs isolated from Trp-Rich mice also showed reduced IL-1β and IL-6 release in an ex vivo nutritional IR model. Among the tested indole metabolites, IPA showed the strongest dose-dependent suppression of LPS-induced cytokines and chemokines, suppressed ex vivo nutritional IR injury, and its effects were attenuated by pharmacologic AhR blockade.
CONCLUSIONS: A Trp-Rich diet attenuated sterile lung IR injury, coinciding with gut microbiota remodeling, increased systemic and pulmonary IPA, reduced inflammatory priming, and reprogrammed AM responses. These data support diet- or microbiome-directed strategies targeting IPA-AhR signaling to mitigate perioperative lung IR injury.
Additional Links: PMID-42596535
Publisher:
PubMed:
Citation:
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@article {pmid42596535,
year = {2026},
author = {Chaki, T and Maruyama, D and Doan, TNM and Tian, X and Prakash, A},
title = {Dietary tryptophan mitigates lung ischemia-reperfusion injury in association with increased indole-3-propionate and aryl hydrocarbon receptor signaling.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2715839},
doi = {10.1080/19490976.2026.2715839},
pmid = {42596535},
issn = {1949-0984},
mesh = {Animals ; *Receptors, Aryl Hydrocarbon/metabolism/genetics ; *Tryptophan/metabolism/administration & dosage ; *Reperfusion Injury/metabolism/diet therapy/microbiology ; *Indoles/metabolism ; Mice, Inbred C57BL ; Mice ; Signal Transduction ; Humans ; Male ; Gastrointestinal Microbiome ; Lung/metabolism ; Diet ; Macrophages, Alveolar/immunology/metabolism ; *Lung Injury/metabolism ; Cytokines/metabolism ; },
abstract = {BACKGROUND: Lung ischemia-reperfusion (IR) injury drives early morbidity after lung transplantation and cardiothoracic surgery, yet targeted preventive therapies are lacking. The gut-lung axis and microbiota-derived tryptophan metabolites, including indole-3-propionate (IPA), may regulate pulmonary immunity and inflammation. We investigated whether a tryptophan-rich (Trp-Rich) diet attenuates sterile lung IR injury by increasing microbiota-derived indole metabolites and reprogramming alveolar macrophage (AM) inflammatory responses.
METHODS: C57BL/6 mice receiving isocaloric tryptophan-standard (Trp-Std) or tryptophan-rich (Trp-Rich) diets underwent lung IR injury. Oxygen saturation, lung cytokines, and aryl hydrocarbon receptor (AhR) signaling readouts were evaluated. Gut microbiota was profiled by 16S rRNA sequencing, and targeted metabolomics quantified tryptophan metabolites in feces, portal vein (PV) plasma, and lung tissue. To further assess inflammatory priming in vivo, mice were additionally challenged with intratracheal lipopolysaccharide (LPS). Mechanistic studies compared IPA with related indoles in cell lines and primary human AMs, including ex vivo nutritional IR, LPS stimulation, and AhR stimulation and blockade using synthetic agonists and antagonists.
RESULTS: Trp-Rich feeding improved post-IR oxygenation, reduced lung IL-1β, and increased pulmonary AhR-downstream gene expression. Trp-Rich diet remodeled gut microbiota, enriching for Bifidobacterium and Lactobacillus, and increasing IPA levels across feces, PV plasma, and lung tissue. In the LPS intratracheal challenge, Trp-Rich feeding reduced IL-6 levels in lung tissue and systemic plasma. Primary AMs isolated from Trp-Rich mice also showed reduced IL-1β and IL-6 release in an ex vivo nutritional IR model. Among the tested indole metabolites, IPA showed the strongest dose-dependent suppression of LPS-induced cytokines and chemokines, suppressed ex vivo nutritional IR injury, and its effects were attenuated by pharmacologic AhR blockade.
CONCLUSIONS: A Trp-Rich diet attenuated sterile lung IR injury, coinciding with gut microbiota remodeling, increased systemic and pulmonary IPA, reduced inflammatory priming, and reprogrammed AM responses. These data support diet- or microbiome-directed strategies targeting IPA-AhR signaling to mitigate perioperative lung IR injury.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Receptors, Aryl Hydrocarbon/metabolism/genetics
*Tryptophan/metabolism/administration & dosage
*Reperfusion Injury/metabolism/diet therapy/microbiology
*Indoles/metabolism
Mice, Inbred C57BL
Mice
Signal Transduction
Humans
Male
Gastrointestinal Microbiome
Lung/metabolism
Diet
Macrophages, Alveolar/immunology/metabolism
*Lung Injury/metabolism
Cytokines/metabolism
RevDate: 2026-08-14
Beyond the root: microbial partners extend plant metabolic pathways to mobilize iron.
Molecular plant pii:S1674-2052(26)00265-0 [Epub ahead of print].
Under iron (Fe)-limiting conditions, Arabidopsis thaliana roots secrete coumarins, phenylpropanoid-derived secondary metabolites that can mobilize sparingly available Fe and shape the composition of the root-associated microbiome. Recent studies show that microbial partners can act on root-secreted coumarins to produce forms with higher Fe-mobilization capacity. Besides providing a mechanistic understanding of the positive interaction of soil microbiota to improved plant Fe nutrition, these findings provide new evidence that the functional boundaries of plant metabolic pathways extend into the rhizosphere.
Additional Links: PMID-42596544
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@article {pmid42596544,
year = {2026},
author = {Shalmani, A and Giehl, RFH},
title = {Beyond the root: microbial partners extend plant metabolic pathways to mobilize iron.},
journal = {Molecular plant},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.molp.2026.08.007},
pmid = {42596544},
issn = {1752-9867},
abstract = {Under iron (Fe)-limiting conditions, Arabidopsis thaliana roots secrete coumarins, phenylpropanoid-derived secondary metabolites that can mobilize sparingly available Fe and shape the composition of the root-associated microbiome. Recent studies show that microbial partners can act on root-secreted coumarins to produce forms with higher Fe-mobilization capacity. Besides providing a mechanistic understanding of the positive interaction of soil microbiota to improved plant Fe nutrition, these findings provide new evidence that the functional boundaries of plant metabolic pathways extend into the rhizosphere.},
}
RevDate: 2026-08-14
DC vaccine loaded with Bacteroides fragilis elicits functional cross-reactivity and enhances anti-PD-1 immunotherapy.
Molecular therapy : the journal of the American Society of Gene Therapy pii:S1525-0016(26)00702-1 [Epub ahead of print].
The gut microbiome profoundly influences the clinical benefits of antitumor immunotherapy. Although various gut microbiota have been shown to enhance immunotherapy, their clinical application remains unexplored. In this study, a dendritic cell (DC) vaccine loaded with the gut commensal Bacteroides fragilis (DC-Bf) was used as a therapeutic cancer vaccine. DC-Bf elicited T-cell responses that recognize both B.fragilis and tumor cells, primarily via major histocompatibility complex-I-mediated cross-presentation of B.fragilis antigens to prime CD8[+] T cells. DC-Bf treatment increased CD8[+] T cell infiltration and activation, expanded the diversity of the T-cell receptor repertoire, and reduced the proportion of regulatory T cells and M2-type tumor-associated macrophages, thereby improving the immunosuppressive tumor microenvironment. In multiple tumor-bearing models, DC-Bf enhanced the therapeutic activity of programmed cell death protein 1 inhibitors by inducing interleukin-12-driven, CD8[+] T-cell-dependent antitumor immune responses. This study confirms the potential of using bacteria-loaded DCs to augment immunotherapy efficacy and provides a new perspective for the clinical application of the gut microbiome. Targeting the gut microbiota holds promise as a novel avenue for developing antitumor vaccines.
Additional Links: PMID-42596550
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PubMed:
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@article {pmid42596550,
year = {2026},
author = {Hu, S and Shi, G and Zhao, J and Long, X and Tang, L and Qi, Z and Xu, X and Cheng, P and Liu, J},
title = {DC vaccine loaded with Bacteroides fragilis elicits functional cross-reactivity and enhances anti-PD-1 immunotherapy.},
journal = {Molecular therapy : the journal of the American Society of Gene Therapy},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ymthe.2026.08.021},
pmid = {42596550},
issn = {1525-0024},
abstract = {The gut microbiome profoundly influences the clinical benefits of antitumor immunotherapy. Although various gut microbiota have been shown to enhance immunotherapy, their clinical application remains unexplored. In this study, a dendritic cell (DC) vaccine loaded with the gut commensal Bacteroides fragilis (DC-Bf) was used as a therapeutic cancer vaccine. DC-Bf elicited T-cell responses that recognize both B.fragilis and tumor cells, primarily via major histocompatibility complex-I-mediated cross-presentation of B.fragilis antigens to prime CD8[+] T cells. DC-Bf treatment increased CD8[+] T cell infiltration and activation, expanded the diversity of the T-cell receptor repertoire, and reduced the proportion of regulatory T cells and M2-type tumor-associated macrophages, thereby improving the immunosuppressive tumor microenvironment. In multiple tumor-bearing models, DC-Bf enhanced the therapeutic activity of programmed cell death protein 1 inhibitors by inducing interleukin-12-driven, CD8[+] T-cell-dependent antitumor immune responses. This study confirms the potential of using bacteria-loaded DCs to augment immunotherapy efficacy and provides a new perspective for the clinical application of the gut microbiome. Targeting the gut microbiota holds promise as a novel avenue for developing antitumor vaccines.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Effects of single and synthetic microbial community inoculants on the rhizosphere soil and root microbiomes of rice (Oryza sativa).
Functional plant biology : FPB, 53(8):.
This study compared the effects of a single-strain microbial inoculant, Brevundimonas diminuta NH1, and a synthetic microbial community (FSQN) composed of Bacillus amyloliquefaciens FH1, Ochrobactrum tritici S112, Gluconacetobacter liquefaciens QZR14, and B. diminuta NH1 on the rhizosphere soil and root microbiomes of rice (Oryza sativa) to investigate how these inoculation strategies differ in microbiome regulation and growth promotion. High-throughput sequencing was used to assess microbial α- and β-diversity, community composition, predicted bacterial and fungal functions, and correlations between microbiome shifts and rice growth traits. We found that neither inoculant significantly affected microbial α-diversity, but both significantly altered β-diversity in rhizosphere soil and roots. Compared with the control, the single-strain treatment mainly enriched Mortierella, Glaciozyma, and Bovista in rhizosphere soil, and Clostridium sensu stricto, Cronobacter, Exiguobacterium, Kosakonia, and Pseudomonas in roots. The synthetic community mainly enriched Mortierella, Tausonia, Fusarium, and Glomerella in rhizosphere soil, and Exiguobacterium, Pseudomonas, and Rhodotorula in roots. Functional prediction indicated that the single-strain inoculant enhanced sulfur respiration, ureolysis, xylanolysis, and denitrification-related functions, whereas the synthetic community enhanced ectomycorrhizal, endomycorrhizal, and plant-saprotrophic functions. Shoot height and dry weight were may positively associated with enriched taxa and functions, particularly Mortierella, Exiguobacterium, and endophytic functions.
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@article {pmid42596554,
year = {2026},
author = {Kossalbayev, BD and Wang, J and Wei, M and Sadvakasova, AK and Zaletova, DE and Bauenova, MO and Kelden, D and Zhang, X and Huang, Z},
title = {Effects of single and synthetic microbial community inoculants on the rhizosphere soil and root microbiomes of rice (Oryza sativa).},
journal = {Functional plant biology : FPB},
volume = {53},
number = {8},
pages = {},
doi = {10.1071/FP26125},
pmid = {42596554},
issn = {1445-4416},
mesh = {*Oryza/microbiology/growth & development ; *Rhizosphere ; *Soil Microbiology ; *Microbiota ; *Plant Roots/microbiology ; Bacteria/genetics ; },
abstract = {This study compared the effects of a single-strain microbial inoculant, Brevundimonas diminuta NH1, and a synthetic microbial community (FSQN) composed of Bacillus amyloliquefaciens FH1, Ochrobactrum tritici S112, Gluconacetobacter liquefaciens QZR14, and B. diminuta NH1 on the rhizosphere soil and root microbiomes of rice (Oryza sativa) to investigate how these inoculation strategies differ in microbiome regulation and growth promotion. High-throughput sequencing was used to assess microbial α- and β-diversity, community composition, predicted bacterial and fungal functions, and correlations between microbiome shifts and rice growth traits. We found that neither inoculant significantly affected microbial α-diversity, but both significantly altered β-diversity in rhizosphere soil and roots. Compared with the control, the single-strain treatment mainly enriched Mortierella, Glaciozyma, and Bovista in rhizosphere soil, and Clostridium sensu stricto, Cronobacter, Exiguobacterium, Kosakonia, and Pseudomonas in roots. The synthetic community mainly enriched Mortierella, Tausonia, Fusarium, and Glomerella in rhizosphere soil, and Exiguobacterium, Pseudomonas, and Rhodotorula in roots. Functional prediction indicated that the single-strain inoculant enhanced sulfur respiration, ureolysis, xylanolysis, and denitrification-related functions, whereas the synthetic community enhanced ectomycorrhizal, endomycorrhizal, and plant-saprotrophic functions. Shoot height and dry weight were may positively associated with enriched taxa and functions, particularly Mortierella, Exiguobacterium, and endophytic functions.},
}
MeSH Terms:
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*Oryza/microbiology/growth & development
*Rhizosphere
*Soil Microbiology
*Microbiota
*Plant Roots/microbiology
Bacteria/genetics
RevDate: 2026-08-14
The Dual Face of Fusobacterium nucleatum in Cancer: Foe, Friend or Both?.
Journal of periodontal research [Epub ahead of print].
Fusobacterium is a genus of anaerobic Gram-negative bacteria that has been increasingly implicated in a range of diseases, including periodontitis and cancer. This review critically evaluates the reported role of Fusobacterium nucleatum in cancer, highlighting new findings that suggest a more nuanced cross-talk with the disease. We contextualise current evidence on the interactions with the wider tumour micro-environment, including the roles of polymicrobial communities, microbial metabolites and taxonomic heterogeneity. Collectively, the evidence suggests that Fusobacterium nucleatum should not be regarded as universally pathogenic or oncogenic. Rather, its behaviour is likely context-dependent and shaped by its surrounding microenvironment. Notably, opposing pro- and anti-tumoural mechanisms can coexist within the same cancer type. For example, in colorectal cancer, F. nucleatum is predominantly associated with poorer outcomes by promoting immune evasion (e.g., suppression of cytotoxic T cell responses) and oncogenic signalling (e.g., via the E-cadherin/β-catenin pathway), yet it also displays oncosuppressive activity through promotion of neutrophil-mediated anti-tumoural cytotoxicity and butyrate-driven cytotoxic T cell activation and potentiation of immunotherapy. In head and neck cancer, by contrast, F. nucleatum detection is associated with improved survival across independent cohorts, potentially reflecting a different balance of these same competing mechanisms. We suggest implications for its proposed use as a biomarker and as a target in cancer therapy. Lingering questions are also laid out to help investigators shape future research to better capture the complexity of the TME and elucidate the overall impact of Fusobacterium nucleatum in cancer.
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@article {pmid42596786,
year = {2026},
author = {Chander, A and Lim, H and Bachrach, G and Ferreira, MR},
title = {The Dual Face of Fusobacterium nucleatum in Cancer: Foe, Friend or Both?.},
journal = {Journal of periodontal research},
volume = {},
number = {},
pages = {},
doi = {10.1111/jre.70165},
pmid = {42596786},
issn = {1600-0765},
support = {CTRQQR-2021\100004//CRUK City of London Cancer Centre Award/ ; //Guy's Charity/ ; //Wilson + Olegario Philanthropy/ ; },
abstract = {Fusobacterium is a genus of anaerobic Gram-negative bacteria that has been increasingly implicated in a range of diseases, including periodontitis and cancer. This review critically evaluates the reported role of Fusobacterium nucleatum in cancer, highlighting new findings that suggest a more nuanced cross-talk with the disease. We contextualise current evidence on the interactions with the wider tumour micro-environment, including the roles of polymicrobial communities, microbial metabolites and taxonomic heterogeneity. Collectively, the evidence suggests that Fusobacterium nucleatum should not be regarded as universally pathogenic or oncogenic. Rather, its behaviour is likely context-dependent and shaped by its surrounding microenvironment. Notably, opposing pro- and anti-tumoural mechanisms can coexist within the same cancer type. For example, in colorectal cancer, F. nucleatum is predominantly associated with poorer outcomes by promoting immune evasion (e.g., suppression of cytotoxic T cell responses) and oncogenic signalling (e.g., via the E-cadherin/β-catenin pathway), yet it also displays oncosuppressive activity through promotion of neutrophil-mediated anti-tumoural cytotoxicity and butyrate-driven cytotoxic T cell activation and potentiation of immunotherapy. In head and neck cancer, by contrast, F. nucleatum detection is associated with improved survival across independent cohorts, potentially reflecting a different balance of these same competing mechanisms. We suggest implications for its proposed use as a biomarker and as a target in cancer therapy. Lingering questions are also laid out to help investigators shape future research to better capture the complexity of the TME and elucidate the overall impact of Fusobacterium nucleatum in cancer.},
}
RevDate: 2026-08-14
Making dietary modification in the immunotherapy Era: from mechanistic evidence to practical implementation.
Additional Links: PMID-42596801
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@article {pmid42596801,
year = {2026},
author = {Habibzadeh, P and Hurd, D and Davar, D},
title = {Making dietary modification in the immunotherapy Era: from mechanistic evidence to practical implementation.},
journal = {Immunotherapy},
volume = {},
number = {},
pages = {1-4},
doi = {10.1080/1750743X.2026.2717073},
pmid = {42596801},
issn = {1750-7448},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Polyphenol‑based interventions in breast cancer: Signaling pathways, molecular mechanisms and translational therapeutic strategies (Review).
Oncology reports, 56(4):.
Breast cancer (BC) comprises multiple molecular subtypes with distinct epidemiological, biological and therapeutic features. Although advances in diagnosis and systemic therapy have improved patient outcomes, therapeutic resistance, treatment‑related toxicity and disease recurrence remain major clinical challenges. Growing evidence suggests that plant‑derived polyphenols may influence BC progression through multiple biological mechanisms. These compounds can inhibit tumor‑cell proliferation, migration, angiogenesis, inflammation, epithelial‑mesenchymal transition and metastasis, while promoting apoptosis, autophagy, cell‑cycle arrest and tumor‑suppressive responses. Mechanistically, polyphenols may regulate several interconnected signaling pathways involved in BC development and progression, including PI3K/AKT/mTOR, p53, NF‑κB, STAT3, Wnt/β‑catenin and MAPK signaling. In addition to their direct effects on tumor cells, polyphenols may interact with the gut microbiome, which in turn influences polyphenol metabolism, estrogen homeostasis, immune regulation, inflammation and bioavailability. Probiotics, prebiotics and microbiota‑derived metabolites may further influence this polyphenol‑gut microbiome‑BC axis. Polyphenols have also been explored as adjuvant or supportive agents in combination with chemotherapy, endocrine therapy and radiotherapy, as well as in novel delivery systems designed to improve their bioavailability and therapeutic efficacy. However, most current evidence remains preclinical. Well‑designed clinical trials are therefore needed to define the optimal formulations, doses, safety profiles, pharmacokinetics and therapeutic relevance of polyphenol‑based interventions in BC.
Additional Links: PMID-42596834
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@article {pmid42596834,
year = {2026},
author = {Zeng, J and Hu, J and Ma, Z and Zhu, S and Lv, X and Zhang, L and Shen, M and Li, T},
title = {Polyphenol‑based interventions in breast cancer: Signaling pathways, molecular mechanisms and translational therapeutic strategies (Review).},
journal = {Oncology reports},
volume = {56},
number = {4},
pages = {},
doi = {10.3892/or.2026.9176},
pmid = {42596834},
issn = {1791-2431},
mesh = {Humans ; Female ; *Polyphenols/therapeutic use/pharmacology ; *Breast Neoplasms/drug therapy/pathology ; Signal Transduction/drug effects ; Animals ; Translational Research, Biomedical ; },
abstract = {Breast cancer (BC) comprises multiple molecular subtypes with distinct epidemiological, biological and therapeutic features. Although advances in diagnosis and systemic therapy have improved patient outcomes, therapeutic resistance, treatment‑related toxicity and disease recurrence remain major clinical challenges. Growing evidence suggests that plant‑derived polyphenols may influence BC progression through multiple biological mechanisms. These compounds can inhibit tumor‑cell proliferation, migration, angiogenesis, inflammation, epithelial‑mesenchymal transition and metastasis, while promoting apoptosis, autophagy, cell‑cycle arrest and tumor‑suppressive responses. Mechanistically, polyphenols may regulate several interconnected signaling pathways involved in BC development and progression, including PI3K/AKT/mTOR, p53, NF‑κB, STAT3, Wnt/β‑catenin and MAPK signaling. In addition to their direct effects on tumor cells, polyphenols may interact with the gut microbiome, which in turn influences polyphenol metabolism, estrogen homeostasis, immune regulation, inflammation and bioavailability. Probiotics, prebiotics and microbiota‑derived metabolites may further influence this polyphenol‑gut microbiome‑BC axis. Polyphenols have also been explored as adjuvant or supportive agents in combination with chemotherapy, endocrine therapy and radiotherapy, as well as in novel delivery systems designed to improve their bioavailability and therapeutic efficacy. However, most current evidence remains preclinical. Well‑designed clinical trials are therefore needed to define the optimal formulations, doses, safety profiles, pharmacokinetics and therapeutic relevance of polyphenol‑based interventions in BC.},
}
MeSH Terms:
show MeSH Terms
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Humans
Female
*Polyphenols/therapeutic use/pharmacology
*Breast Neoplasms/drug therapy/pathology
Signal Transduction/drug effects
Animals
Translational Research, Biomedical
RevDate: 2026-08-14
CmpDate: 2026-08-14
Microbiota-gut-brain axis in cerebral palsy: from mechanisms to interventions.
Frontiers in medicine, 13:1911417.
Cerebral palsy (CP) is the most common cause of chronic motor disability in childhood and arises from non-progressive injury to the developing brain. Despite the static nature of the primary lesion, children with CP frequently experience evolving gastrointestinal, nutritional, inflammatory, sleep, cognitive, and seizure-related comorbidities that substantially influence functional recovery and caregiver burden. The microbiota-gut-brain axis (MGBA) provides a biologically plausible framework linking these multisystem manifestations. Emerging evidence suggests that children with CP may exhibit reduced gut microbial diversity, depletion of short-chain fatty acid (SCFA)-producing taxa, enrichment of opportunistic bacteria, and microbiome remodeling related to diet, constipation, antiepileptic drug exposure, oral inflammation, and care patterns. Dysbiosis may interact with CP through epithelial barrier disruption, lipopolysaccharide translocation, systemic immune activation, altered tryptophan-kynurenine metabolism, abnormal bile acid and SCFA signaling, vagal and enteric nervous system pathways, hypothalamic-pituitary-adrenal axis dysregulation, and microglial priming. These mechanisms may create a self-reinforcing cycle in which early brain injury promotes gut dysfunction, gut dysfunction reshapes the microbiome, and dysbiotic immune-metabolic signals further amplify symptom burden. Current interventions, including nutritional optimization, constipation protocols, dietary fiber, probiotics, prebiotics, synbiotics, oral health management, and family-centered care, show promise for improving bowel symptoms and selected microbial or inflammatory indices. However, most clinical studies remain small, short-term, and focused on constipation rather than long-term neurodevelopmental outcomes. All CP-specific human evidence currently demonstrates association rather than causation; no study has established that dysbiosis initiates CP or causally drives its neurological phenotype. Accordingly, mechanistic pathways are presented as testable hypotheses, not validated causal mechanisms in CP. This review synthesizes current evidence on the MGBA in CP, outlines mechanistic pathways, evaluates therapeutic opportunities, and proposes future directions for biomarker-driven and stratified intervention trials.
Additional Links: PMID-42597189
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Citation:
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@article {pmid42597189,
year = {2026},
author = {Xie, F and Bai, C and Xu, J and Luan, X},
title = {Microbiota-gut-brain axis in cerebral palsy: from mechanisms to interventions.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1911417},
pmid = {42597189},
issn = {2296-858X},
abstract = {Cerebral palsy (CP) is the most common cause of chronic motor disability in childhood and arises from non-progressive injury to the developing brain. Despite the static nature of the primary lesion, children with CP frequently experience evolving gastrointestinal, nutritional, inflammatory, sleep, cognitive, and seizure-related comorbidities that substantially influence functional recovery and caregiver burden. The microbiota-gut-brain axis (MGBA) provides a biologically plausible framework linking these multisystem manifestations. Emerging evidence suggests that children with CP may exhibit reduced gut microbial diversity, depletion of short-chain fatty acid (SCFA)-producing taxa, enrichment of opportunistic bacteria, and microbiome remodeling related to diet, constipation, antiepileptic drug exposure, oral inflammation, and care patterns. Dysbiosis may interact with CP through epithelial barrier disruption, lipopolysaccharide translocation, systemic immune activation, altered tryptophan-kynurenine metabolism, abnormal bile acid and SCFA signaling, vagal and enteric nervous system pathways, hypothalamic-pituitary-adrenal axis dysregulation, and microglial priming. These mechanisms may create a self-reinforcing cycle in which early brain injury promotes gut dysfunction, gut dysfunction reshapes the microbiome, and dysbiotic immune-metabolic signals further amplify symptom burden. Current interventions, including nutritional optimization, constipation protocols, dietary fiber, probiotics, prebiotics, synbiotics, oral health management, and family-centered care, show promise for improving bowel symptoms and selected microbial or inflammatory indices. However, most clinical studies remain small, short-term, and focused on constipation rather than long-term neurodevelopmental outcomes. All CP-specific human evidence currently demonstrates association rather than causation; no study has established that dysbiosis initiates CP or causally drives its neurological phenotype. Accordingly, mechanistic pathways are presented as testable hypotheses, not validated causal mechanisms in CP. This review synthesizes current evidence on the MGBA in CP, outlines mechanistic pathways, evaluates therapeutic opportunities, and proposes future directions for biomarker-driven and stratified intervention trials.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Gut dysbiosis and vitamin-dependent immune regulation in degenerative musculoskeletal and bone diseases.
Frontiers in immunology, 17:1920962.
Degenerative musculoskeletal and metabolic bone diseases are increasingly recognized as conditions sustained not only by endocrine and mechanical factors, but also by chronic low-grade immune activation and osteo-immune imbalance. This Perspective proposes a mechanistic framework in which gut dysbiosis may contribute to skeletal degeneration through alterations in vitamin-dependent immune regulation, with particular attention to the interaction between vitamin D signaling and microbiota-derived menaquinones. Dysbiosis may impair intestinal barrier integrity and increase exposure to microbial-associated molecular patterns, thereby sustaining innate and adaptive immune activation and promoting a pro-inflammatory cytokine milieu involving IL-6, TNF-α, IL-17, and IL-1β. These pathways may promote osteoclastogenesis and disrupt bone remodeling through the RANKL/RANK/OPG axis. While the immunomodulatory role of vitamin D is well established, microbiota-derived menaquinones may represent a less explored but biologically plausible interface between microbial metabolism, inflammatory signaling, and skeletal homeostasis . However, the extent to which microbiota-derived menaquinones significantly contribute to systemic vitamin K status in humans remains controversial and incompletely characterized. Within this framework, dietary patterns are conceptualized as modulators of microbial ecology and immune activation, while microbiota-modulating strategies may indirectly influence osteo-immune balance through immune-mediated mechanisms. This Perspective integrates microbial, immunological, and vitamin-dependent pathways into an immunology-centered model of skeletal degeneration and highlights the need for studies combining microbiome profiling, immune phenotyping, vitamin-dependent signaling, and bone remodeling outcomes.
Additional Links: PMID-42597253
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@article {pmid42597253,
year = {2026},
author = {Stefanelli, N},
title = {Gut dysbiosis and vitamin-dependent immune regulation in degenerative musculoskeletal and bone diseases.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1920962},
pmid = {42597253},
issn = {1664-3224},
mesh = {Humans ; *Dysbiosis/immunology ; Animals ; *Gastrointestinal Microbiome/immunology ; *Bone Diseases/immunology/metabolism ; Vitamin D/metabolism ; *Immunomodulation ; *Vitamins/metabolism ; },
abstract = {Degenerative musculoskeletal and metabolic bone diseases are increasingly recognized as conditions sustained not only by endocrine and mechanical factors, but also by chronic low-grade immune activation and osteo-immune imbalance. This Perspective proposes a mechanistic framework in which gut dysbiosis may contribute to skeletal degeneration through alterations in vitamin-dependent immune regulation, with particular attention to the interaction between vitamin D signaling and microbiota-derived menaquinones. Dysbiosis may impair intestinal barrier integrity and increase exposure to microbial-associated molecular patterns, thereby sustaining innate and adaptive immune activation and promoting a pro-inflammatory cytokine milieu involving IL-6, TNF-α, IL-17, and IL-1β. These pathways may promote osteoclastogenesis and disrupt bone remodeling through the RANKL/RANK/OPG axis. While the immunomodulatory role of vitamin D is well established, microbiota-derived menaquinones may represent a less explored but biologically plausible interface between microbial metabolism, inflammatory signaling, and skeletal homeostasis . However, the extent to which microbiota-derived menaquinones significantly contribute to systemic vitamin K status in humans remains controversial and incompletely characterized. Within this framework, dietary patterns are conceptualized as modulators of microbial ecology and immune activation, while microbiota-modulating strategies may indirectly influence osteo-immune balance through immune-mediated mechanisms. This Perspective integrates microbial, immunological, and vitamin-dependent pathways into an immunology-centered model of skeletal degeneration and highlights the need for studies combining microbiome profiling, immune phenotyping, vitamin-dependent signaling, and bone remodeling outcomes.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Dysbiosis/immunology
Animals
*Gastrointestinal Microbiome/immunology
*Bone Diseases/immunology/metabolism
Vitamin D/metabolism
*Immunomodulation
*Vitamins/metabolism
RevDate: 2026-08-14
CmpDate: 2026-08-14
Precision diagnostics in bronchiectasis: current advances in imaging, microbiology, biomarkers, and digital health.
Frontiers in medicine, 13:1907636.
Bronchiectasis is a complex, chronic airway syndrome driven by a vicious cycle of irreversible bronchial dilatation, impaired mucociliary clearance, recurrent infection, and tissue-destructive inflammation. Reflecting its profound clinical heterogeneity, patients with identical structural damage on high-resolution computed tomography (HRCT) often exhibit divergent profiles in airway microbiology, inflammatory endotypes, exacerbation frequencies, and therapeutic responses, indicating that static anatomical classification fails to capture disease complexity. Sole reliance on visual CT inspection, standard sputum cultures, and subjective symptom tracking misses the driving mechanisms of individual disease progression. Emerging modalities-artificial intelligence (AI)-driven quantitative imaging, molecular microbiology, high-throughput biomarker profiling, and digital remote monitoring-aim to address these gaps. Our analysis shows that while these tools cannot substitute for bedside clinical acumen, they clarify obscure phenotypes, expose actionable treatable traits, and enable earlier, preemptive strategies. This review evaluates these contemporary diagnostic frameworks in non-cystic fibrosis bronchiectasis, dissecting their clinical utility, evidentiary maturity, and the economic and logistical barriers to routine adoption. Given that current evidence remains fragmented, advancing the field demands standardized imaging protocols, transparent algorithmic pipelines, clinically actionable metagenomic reporting, and robust validation in underrepresented Asian and Chinese cohorts. The real challenge lies not in generating more data, but in integrating these heterogeneous, high-dimensional datasets into pragmatic, point-of-care decision pathways that improve patient outcomes without widening disparities in global healthcare delivery.
Additional Links: PMID-42597328
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@article {pmid42597328,
year = {2026},
author = {Wu, B and Lu, S and Liu, H},
title = {Precision diagnostics in bronchiectasis: current advances in imaging, microbiology, biomarkers, and digital health.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1907636},
pmid = {42597328},
issn = {2296-858X},
abstract = {Bronchiectasis is a complex, chronic airway syndrome driven by a vicious cycle of irreversible bronchial dilatation, impaired mucociliary clearance, recurrent infection, and tissue-destructive inflammation. Reflecting its profound clinical heterogeneity, patients with identical structural damage on high-resolution computed tomography (HRCT) often exhibit divergent profiles in airway microbiology, inflammatory endotypes, exacerbation frequencies, and therapeutic responses, indicating that static anatomical classification fails to capture disease complexity. Sole reliance on visual CT inspection, standard sputum cultures, and subjective symptom tracking misses the driving mechanisms of individual disease progression. Emerging modalities-artificial intelligence (AI)-driven quantitative imaging, molecular microbiology, high-throughput biomarker profiling, and digital remote monitoring-aim to address these gaps. Our analysis shows that while these tools cannot substitute for bedside clinical acumen, they clarify obscure phenotypes, expose actionable treatable traits, and enable earlier, preemptive strategies. This review evaluates these contemporary diagnostic frameworks in non-cystic fibrosis bronchiectasis, dissecting their clinical utility, evidentiary maturity, and the economic and logistical barriers to routine adoption. Given that current evidence remains fragmented, advancing the field demands standardized imaging protocols, transparent algorithmic pipelines, clinically actionable metagenomic reporting, and robust validation in underrepresented Asian and Chinese cohorts. The real challenge lies not in generating more data, but in integrating these heterogeneous, high-dimensional datasets into pragmatic, point-of-care decision pathways that improve patient outcomes without widening disparities in global healthcare delivery.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Methodological bias shapes the interpretation of the urinary microbiome in low-biomass systems.
Frontiers in microbiology, 17:1851926.
The recognition of the urinary microbiome (urobiome) has challenged the long-standing paradigm of urinary tract sterility, revealing diverse microbial communities associated with both urinary health and disease. However, the characterization of the urobiome remains highly variable across studies, particularly due to the low-biomass nature of urine samples and the strong influence of methodological bias. In this Mini Review, we examine how factors such as sample collection methods, contamination dynamics, DNA extraction protocols, sequencing approaches, and bioinformatic pipelines shape microbial profiles and contribute to inconsistencies in microbiome-disease associations. We further discuss the limitations of traditional culture-based diagnostics, which fail to detect many microorganisms identified through sequencing-based approaches, and highlight the need for standardized, contamination-aware, and function-oriented frameworks. Finally, we explore the potential of integrated multi-omics strategies to improve the reliability, reproducibility, and clinical relevance of urobiome research in urinary tract health and disease.
Additional Links: PMID-42597333
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@article {pmid42597333,
year = {2026},
author = {Méndez-Sacta, V and Agreda Orellana, S and Ayavaca-Tapia, LM and Gutiérrez León, YY and Calero-Cáceres, W},
title = {Methodological bias shapes the interpretation of the urinary microbiome in low-biomass systems.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1851926},
pmid = {42597333},
issn = {1664-302X},
abstract = {The recognition of the urinary microbiome (urobiome) has challenged the long-standing paradigm of urinary tract sterility, revealing diverse microbial communities associated with both urinary health and disease. However, the characterization of the urobiome remains highly variable across studies, particularly due to the low-biomass nature of urine samples and the strong influence of methodological bias. In this Mini Review, we examine how factors such as sample collection methods, contamination dynamics, DNA extraction protocols, sequencing approaches, and bioinformatic pipelines shape microbial profiles and contribute to inconsistencies in microbiome-disease associations. We further discuss the limitations of traditional culture-based diagnostics, which fail to detect many microorganisms identified through sequencing-based approaches, and highlight the need for standardized, contamination-aware, and function-oriented frameworks. Finally, we explore the potential of integrated multi-omics strategies to improve the reliability, reproducibility, and clinical relevance of urobiome research in urinary tract health and disease.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Natural flavonoids in multiple sclerosis: molecular insights and emerging therapeutic strategies.
Frontiers in immunology, 17:1888423.
Multiple sclerosis is a chronic immune mediated disease in which current disease modifying therapies reduce inflammatory relapses but incompletely address neurodegeneration and remyelination. Natural flavonoids are pleiotropic polyphenols that can modulate immune and glial signaling, oxidative stress, and mitochondrial function. This review synthesizes evidence from experimental models and human studies on flavonoids relevant to multiple sclerosis, emphasizing mechanisms involving NF-κB, Nrf2, inflammasome signaling, and microglia and macrophage polarization that shape oligodendrocyte precursor cell differentiation and remyelination permissiveness. We highlight structure activity features, metabolism and glycosylation that govern exposure, and discuss translational barriers including low and variable bioavailability, limited blood brain barrier penetration, standardization, and potential interactions with approved therapies. Emerging enabling strategies are reviewed, including lipid and polymeric nanocarriers, stimuli responsive delivery, systems biology and multi omics target discovery, network pharmacology for multi target prioritization, microbiome informed approaches, and synthetic biology for scalable production and derivative optimization. Overall, preclinical studies consistently support anti-inflammatory and neuroprotective effects, while clinical evidence remains early and mixed, underscoring the need for well powered trials with pharmacokinetic and pharmacodynamic endpoints.
Additional Links: PMID-42597552
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@article {pmid42597552,
year = {2026},
author = {Abusaliya, A and Al Shamsi, M and Orsud, H and Al Rasbi, Z and Zoughbor, S and Joher, N},
title = {Natural flavonoids in multiple sclerosis: molecular insights and emerging therapeutic strategies.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1888423},
pmid = {42597552},
issn = {1664-3224},
mesh = {Humans ; *Multiple Sclerosis/drug therapy/metabolism/immunology ; *Flavonoids/therapeutic use/pharmacology/chemistry ; Animals ; Signal Transduction/drug effects ; Neuroprotective Agents/therapeutic use ; Anti-Inflammatory Agents/therapeutic use/pharmacology ; Remyelination/drug effects ; },
abstract = {Multiple sclerosis is a chronic immune mediated disease in which current disease modifying therapies reduce inflammatory relapses but incompletely address neurodegeneration and remyelination. Natural flavonoids are pleiotropic polyphenols that can modulate immune and glial signaling, oxidative stress, and mitochondrial function. This review synthesizes evidence from experimental models and human studies on flavonoids relevant to multiple sclerosis, emphasizing mechanisms involving NF-κB, Nrf2, inflammasome signaling, and microglia and macrophage polarization that shape oligodendrocyte precursor cell differentiation and remyelination permissiveness. We highlight structure activity features, metabolism and glycosylation that govern exposure, and discuss translational barriers including low and variable bioavailability, limited blood brain barrier penetration, standardization, and potential interactions with approved therapies. Emerging enabling strategies are reviewed, including lipid and polymeric nanocarriers, stimuli responsive delivery, systems biology and multi omics target discovery, network pharmacology for multi target prioritization, microbiome informed approaches, and synthetic biology for scalable production and derivative optimization. Overall, preclinical studies consistently support anti-inflammatory and neuroprotective effects, while clinical evidence remains early and mixed, underscoring the need for well powered trials with pharmacokinetic and pharmacodynamic endpoints.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Multiple Sclerosis/drug therapy/metabolism/immunology
*Flavonoids/therapeutic use/pharmacology/chemistry
Animals
Signal Transduction/drug effects
Neuroprotective Agents/therapeutic use
Anti-Inflammatory Agents/therapeutic use/pharmacology
Remyelination/drug effects
RevDate: 2026-08-14
CmpDate: 2026-08-14
The gut microbiome as a plausible but unproven moderator of cinnamon trial outcomes in type 2 diabetes: toward phytochemical standardization and precision nutraceuticals.
Frontiers in nutrition, 13:1874182.
Cinnamon (Cinnamomum spp.) has been widely investigated as an adjunctive nutraceutical for glycemic management in type 2 diabetes mellitus, yet clinical findings remain inconsistent. This variability is commonly attributed to differences in cinnamon species, dosage, intervention duration, baseline glycemic status and phytochemical standardization, alongside methodological factors such as trial quality, dietary patterns, medication use, adherence and endpoint selection. One potential contributor that has received limited attention is the gut microbiome. We propose a testable hypothesis that a substantial proportion of the marked inter-trial heterogeneity observed in cinnamon meta-analyses (I[2] > 75%) may reflect underlying gut-microbial metabotypes differing in their ability to convert cinnamon polyphenols and procyanidins into bioactive metabolites. Type 2 diabetes is associated with altered microbial composition, reduced butyrate-producing taxa and disrupted metabolic pathways. Cinnamon phytochemicals, including polyphenols, cinnamaldehyde, procyanidins and coumarin, undergo microbial biotransformation that may influence their bioavailability and metabolic effects. Because cinnamaldehyde is rapidly absorbed in the proximal gastrointestinal tract, colon-targeted delivery systems may be required to rigorously evaluate microbiome-mediated mechanisms. No randomized controlled trial has directly examined whether microbiome composition modifies cinnamon's glycemic effects in type 2 diabetes. Future studies should therefore incorporate microbiome-informed designs, including phytochemical fingerprinting, safety monitoring and, where feasible, metagenomic and metabolomic profiling, to distinguish true biological non-response from intervention heterogeneity and advance precision nutraceutical approaches for diabetes management.
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Citation:
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@article {pmid42597565,
year = {2026},
author = {Okonta, EO and Nnadi, CO and Paul-Chima, UO},
title = {The gut microbiome as a plausible but unproven moderator of cinnamon trial outcomes in type 2 diabetes: toward phytochemical standardization and precision nutraceuticals.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1874182},
pmid = {42597565},
issn = {2296-861X},
abstract = {Cinnamon (Cinnamomum spp.) has been widely investigated as an adjunctive nutraceutical for glycemic management in type 2 diabetes mellitus, yet clinical findings remain inconsistent. This variability is commonly attributed to differences in cinnamon species, dosage, intervention duration, baseline glycemic status and phytochemical standardization, alongside methodological factors such as trial quality, dietary patterns, medication use, adherence and endpoint selection. One potential contributor that has received limited attention is the gut microbiome. We propose a testable hypothesis that a substantial proportion of the marked inter-trial heterogeneity observed in cinnamon meta-analyses (I[2] > 75%) may reflect underlying gut-microbial metabotypes differing in their ability to convert cinnamon polyphenols and procyanidins into bioactive metabolites. Type 2 diabetes is associated with altered microbial composition, reduced butyrate-producing taxa and disrupted metabolic pathways. Cinnamon phytochemicals, including polyphenols, cinnamaldehyde, procyanidins and coumarin, undergo microbial biotransformation that may influence their bioavailability and metabolic effects. Because cinnamaldehyde is rapidly absorbed in the proximal gastrointestinal tract, colon-targeted delivery systems may be required to rigorously evaluate microbiome-mediated mechanisms. No randomized controlled trial has directly examined whether microbiome composition modifies cinnamon's glycemic effects in type 2 diabetes. Future studies should therefore incorporate microbiome-informed designs, including phytochemical fingerprinting, safety monitoring and, where feasible, metagenomic and metabolomic profiling, to distinguish true biological non-response from intervention heterogeneity and advance precision nutraceutical approaches for diabetes management.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Dual zeitgeber axes in psoriasis: a chronobiological framework for immune jet lag.
Frontiers in immunology, 17:1848727.
Psoriasis is primarily characterized by interleukin-23/T helper 17 (IL-23/Th17)-related inflammation, but clinical and epidemiological observations also suggest recurrent temporal features, including seasonal fluctuation, nocturnal symptom exacerbation, sleep-wake disturbance, and circadian-related risk contexts. Here, we propose the Dual Zeitgeber Model as a hypothesis-generating and testable chronobiological framework for organizing these observations. The central hypothesis is that persistent misalignment between the light-suprachiasmatic nucleus (SCN)-neuroendocrine axis (Axis I) and the feeding-metabolism-microbiome axis (Axis II) may contribute to immune temporal desynchronization. Within this framework, immune jet lag is reserved for this hypothesized state of immune temporal desynchronization. This concept describes a condition in which neuroendocrine immune gating and metabolic-microbial immune signals may become temporally misaligned. This hypothesis raises several testable questions: whether Axis I-Axis II temporal relationships are associated with disease activity, whether abnormal immune temporal organization persists over time, and whether adjunctive circadian-oriented strategies may provide mechanistic insight or potential clinical value alongside established therapies. More broadly, this framework reframes time as a measurable, stratifiable, and testable research dimension, thereby providing new directions for circadian phenotype-based stratification, longitudinal tracking of disease trajectories and treatment responses, and the design of time-controlled intervention studies.
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@article {pmid42597665,
year = {2026},
author = {Lv, H and Ling, G and Mo, H and Lu, M and Yao, D and Lu, C},
title = {Dual zeitgeber axes in psoriasis: a chronobiological framework for immune jet lag.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1848727},
pmid = {42597665},
issn = {1664-3224},
mesh = {Humans ; *Psoriasis/immunology/metabolism/physiopathology ; *Circadian Rhythm/immunology ; Animals ; *Jet Lag Syndrome/immunology/physiopathology ; Suprachiasmatic Nucleus/metabolism/immunology ; },
abstract = {Psoriasis is primarily characterized by interleukin-23/T helper 17 (IL-23/Th17)-related inflammation, but clinical and epidemiological observations also suggest recurrent temporal features, including seasonal fluctuation, nocturnal symptom exacerbation, sleep-wake disturbance, and circadian-related risk contexts. Here, we propose the Dual Zeitgeber Model as a hypothesis-generating and testable chronobiological framework for organizing these observations. The central hypothesis is that persistent misalignment between the light-suprachiasmatic nucleus (SCN)-neuroendocrine axis (Axis I) and the feeding-metabolism-microbiome axis (Axis II) may contribute to immune temporal desynchronization. Within this framework, immune jet lag is reserved for this hypothesized state of immune temporal desynchronization. This concept describes a condition in which neuroendocrine immune gating and metabolic-microbial immune signals may become temporally misaligned. This hypothesis raises several testable questions: whether Axis I-Axis II temporal relationships are associated with disease activity, whether abnormal immune temporal organization persists over time, and whether adjunctive circadian-oriented strategies may provide mechanistic insight or potential clinical value alongside established therapies. More broadly, this framework reframes time as a measurable, stratifiable, and testable research dimension, thereby providing new directions for circadian phenotype-based stratification, longitudinal tracking of disease trajectories and treatment responses, and the design of time-controlled intervention studies.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Psoriasis/immunology/metabolism/physiopathology
*Circadian Rhythm/immunology
Animals
*Jet Lag Syndrome/immunology/physiopathology
Suprachiasmatic Nucleus/metabolism/immunology
RevDate: 2026-08-14
CmpDate: 2026-08-14
The Microbiome of Nurdles: Life on the Primary Microplastics of the Texas Gulf Coast.
microPublication biology, 2026:.
Nurdles are small, pre-production plastic pellets. Globally, nurdles are the second largest source of microplastic pollution due to release during manufacture and transport. As these nurdles persist in the environment, they undergo weathering-a process that significantly increases surface area and colonization by microbes. To gain an understanding of the composition of the microbiome found on nurdles, full-length 16S targeted metagenomic sequencing was performed on DNA extracted from nurdles collected from the Texas Gulf Coast. Sequencing data showed a greater amount and diversity of microbes found to be associated with nurdles than with the sand from which the nurdles were collected.
Additional Links: PMID-42597686
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@article {pmid42597686,
year = {2026},
author = {Annaswamy, V and Mikesh, M and Dinkeloo, K},
title = {The Microbiome of Nurdles: Life on the Primary Microplastics of the Texas Gulf Coast.},
journal = {microPublication biology},
volume = {2026},
number = {},
pages = {},
pmid = {42597686},
issn = {2578-9430},
abstract = {Nurdles are small, pre-production plastic pellets. Globally, nurdles are the second largest source of microplastic pollution due to release during manufacture and transport. As these nurdles persist in the environment, they undergo weathering-a process that significantly increases surface area and colonization by microbes. To gain an understanding of the composition of the microbiome found on nurdles, full-length 16S targeted metagenomic sequencing was performed on DNA extracted from nurdles collected from the Texas Gulf Coast. Sequencing data showed a greater amount and diversity of microbes found to be associated with nurdles than with the sand from which the nurdles were collected.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Mental health and gut-brain crosstalk: implications for depression and Alzheimer's disease.
Neuroscience applied, 5:107023.
Brain health and mental health disorders are increasingly becoming an essential priority for modern societies as they affect different parameters of life, such as brain health, quality of life, and productivity with a heavy societal and economic burden. Among mental health disorders, depression and Alzheimer disease (AD) have the higher impact on mental health globally as they are highly prevalent, cause long-term cognitive and mood deficits while they are deeply interconnected, with chronic stress raising as a risk factor and potential link between both disorders. This review focuses on the gut-brain axis, a bidirectional communication network that links the gut microbiome with the central nervous system, and its role in brain malfunction and pathology related to stress, depression and AD. This intricate gut-brain crosstalk is orchestrated through top-down and bottom-up mechanisms implicating the HPA axis, the enteric nervous system as well as gut microbiota-derived metabolites, neurotransmitters, epigenetic processes and extracellular vesicles/exosomes that can contribute to depression and AD. The current work provides a comprehensive summary of evidence linking gut microbial alterations to these brain pathologies, with particular focus on lifestyle and nutrition (e.g. food, water) as critical regulators. Lastly, we explore the therapeutic potential of microbiome-targeted interventions including pro/pre/post-biotics, and trace elements (e.g. lithium and silicon). Overall, this review highlights the potential of microbiome-centered strategies as novel interventions to support mental health and wellbeing.
Additional Links: PMID-42597739
PubMed:
Citation:
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@article {pmid42597739,
year = {2026},
author = {Skourti, K and Katsaitis, F and Pavlidi, P and Anesti, M and Balla, J and Emvalomatis, A and Kokras, N and Dalla, C and Sotiropoulos, I},
title = {Mental health and gut-brain crosstalk: implications for depression and Alzheimer's disease.},
journal = {Neuroscience applied},
volume = {5},
number = {},
pages = {107023},
pmid = {42597739},
issn = {2772-4085},
abstract = {Brain health and mental health disorders are increasingly becoming an essential priority for modern societies as they affect different parameters of life, such as brain health, quality of life, and productivity with a heavy societal and economic burden. Among mental health disorders, depression and Alzheimer disease (AD) have the higher impact on mental health globally as they are highly prevalent, cause long-term cognitive and mood deficits while they are deeply interconnected, with chronic stress raising as a risk factor and potential link between both disorders. This review focuses on the gut-brain axis, a bidirectional communication network that links the gut microbiome with the central nervous system, and its role in brain malfunction and pathology related to stress, depression and AD. This intricate gut-brain crosstalk is orchestrated through top-down and bottom-up mechanisms implicating the HPA axis, the enteric nervous system as well as gut microbiota-derived metabolites, neurotransmitters, epigenetic processes and extracellular vesicles/exosomes that can contribute to depression and AD. The current work provides a comprehensive summary of evidence linking gut microbial alterations to these brain pathologies, with particular focus on lifestyle and nutrition (e.g. food, water) as critical regulators. Lastly, we explore the therapeutic potential of microbiome-targeted interventions including pro/pre/post-biotics, and trace elements (e.g. lithium and silicon). Overall, this review highlights the potential of microbiome-centered strategies as novel interventions to support mental health and wellbeing.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
D-serine supplementation is associated with mucosal-prioritized rumen development and propionate-enriched fermentation with selective microbial shifts in pre-weaning Hu lambs.
Frontiers in microbiology, 17:1899537.
This study evaluated whether dietary D-serine (D-Ser) could modulate rumen development, fermentation, microbiota, and metabolomic profiles in pre-weaning Hu lambs. Twenty healthy male lambs were assigned to a control group or a D-Ser group (n = 10/group); D-Ser was supplied at 2 g·kg[-1] BW·d[-1] from 7 to 48 days of age. Growth and starter intake were recorded, and rumen morphology, volatile fatty acids, 16S rRNA profiles, and untargeted LC-MS metabolomes were analyzed in slaughtered lambs (n = 6/group). D-Ser increased average daily starter intake during the 30-d starter-intake recording period by 25.96% (p = 0.036) and tended to advance first voluntary starter intake, whereas final body weight and average daily gain were numerically but not significantly higher. Rumen weight, rumen weight-to-body weight ratio, and rumen volume were significantly increased. Papillae length, width, density, and epithelial thickness were also enhanced, while muscle layer thickness was unchanged, indicating mucosa-prioritized morphological development. D-Ser increased total volatile fatty acids, acetate, propionate, and butyrate concentrations; propionate molar proportion rose from 21.41 to 25.11%, and the acetate-to-propionate ratio decreased from 2.90 to 2.44. Microbial diversity was not significantly altered, but Bacteroidota abundance increased, with enrichment of Shuttleworthia, Erysipelotrichaceae_UCG-006/UCG-009, Corynebacterium, and Sutterella. Metabolomics identified 248 differential metabolites enriched in amino acid, carbohydrate, and secondary bile acid pathways. The upregulation of L-N-carboxymethylserine and isodeoxycholic acid was consistent with possible microbial processing of D-Ser, but direct transformation was not experimentally verified. Overall, D-Ser improved starter intake and was associated with propionate-enriched fermentation and mucosal morphological development, whereas its growth-promoting effect and causal microbial mechanisms require further validation.
Additional Links: PMID-42597796
PubMed:
Citation:
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@article {pmid42597796,
year = {2026},
author = {Zhang, S and Tang, Z and Ding, Y and Xu, P and Yimamu, M and Chen, K},
title = {D-serine supplementation is associated with mucosal-prioritized rumen development and propionate-enriched fermentation with selective microbial shifts in pre-weaning Hu lambs.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1899537},
pmid = {42597796},
issn = {1664-302X},
abstract = {This study evaluated whether dietary D-serine (D-Ser) could modulate rumen development, fermentation, microbiota, and metabolomic profiles in pre-weaning Hu lambs. Twenty healthy male lambs were assigned to a control group or a D-Ser group (n = 10/group); D-Ser was supplied at 2 g·kg[-1] BW·d[-1] from 7 to 48 days of age. Growth and starter intake were recorded, and rumen morphology, volatile fatty acids, 16S rRNA profiles, and untargeted LC-MS metabolomes were analyzed in slaughtered lambs (n = 6/group). D-Ser increased average daily starter intake during the 30-d starter-intake recording period by 25.96% (p = 0.036) and tended to advance first voluntary starter intake, whereas final body weight and average daily gain were numerically but not significantly higher. Rumen weight, rumen weight-to-body weight ratio, and rumen volume were significantly increased. Papillae length, width, density, and epithelial thickness were also enhanced, while muscle layer thickness was unchanged, indicating mucosa-prioritized morphological development. D-Ser increased total volatile fatty acids, acetate, propionate, and butyrate concentrations; propionate molar proportion rose from 21.41 to 25.11%, and the acetate-to-propionate ratio decreased from 2.90 to 2.44. Microbial diversity was not significantly altered, but Bacteroidota abundance increased, with enrichment of Shuttleworthia, Erysipelotrichaceae_UCG-006/UCG-009, Corynebacterium, and Sutterella. Metabolomics identified 248 differential metabolites enriched in amino acid, carbohydrate, and secondary bile acid pathways. The upregulation of L-N-carboxymethylserine and isodeoxycholic acid was consistent with possible microbial processing of D-Ser, but direct transformation was not experimentally verified. Overall, D-Ser improved starter intake and was associated with propionate-enriched fermentation and mucosal morphological development, whereas its growth-promoting effect and causal microbial mechanisms require further validation.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Gut-brain axis dysregulation in Parkinson's disease: Mechanisms linking microbiota to neuroinflammation and α-synuclein pathology.
Journal of pharmaceutical analysis, 16(8):101521.
Parkinson's disease (PD) is increasingly understood as a multisystem disorder originating not only in the central nervous system (CNS) but also involving the gut-brain axis (GBA). A key driver of PD pathogenesis is gut microbiota dysbiosis, which contributes to disease progression by inducing intestinal inflammation, altered microbial metabolite production, and compromised gut barrier integrity. These alterations can initiate the misfolding and aggregation of α-synuclein in the enteric nervous system (ENS), facilitating its spread to the CNS via vagal pathways. Furthermore, microbiota-derived molecules, including short-chain fatty acids (SCFAs) and lipopolysaccharides (LPS), are implicated in triggering systemic and neuroinflammatory cascades that exacerbate the degeneration of dopaminergic neurons. This review consolidates current evidence on the mechanistic connections between gut microbiota dysregulation, neuroinflammation, and α-synuclein pathology in PD. We also discuss the translational potential of microbiota-focused biomarkers and innovative therapeutic strategies, providing new perspectives for early diagnosis and disease modification. Elucidating the GBA in PD paves the way for personalized medicine and microbiome-targeted therapies.
Additional Links: PMID-42598050
PubMed:
Citation:
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@article {pmid42598050,
year = {2026},
author = {Zhao, Z and Dong, M and Mu, Z and Zheng, Z and Zhang, Z},
title = {Gut-brain axis dysregulation in Parkinson's disease: Mechanisms linking microbiota to neuroinflammation and α-synuclein pathology.},
journal = {Journal of pharmaceutical analysis},
volume = {16},
number = {8},
pages = {101521},
pmid = {42598050},
issn = {2214-0883},
abstract = {Parkinson's disease (PD) is increasingly understood as a multisystem disorder originating not only in the central nervous system (CNS) but also involving the gut-brain axis (GBA). A key driver of PD pathogenesis is gut microbiota dysbiosis, which contributes to disease progression by inducing intestinal inflammation, altered microbial metabolite production, and compromised gut barrier integrity. These alterations can initiate the misfolding and aggregation of α-synuclein in the enteric nervous system (ENS), facilitating its spread to the CNS via vagal pathways. Furthermore, microbiota-derived molecules, including short-chain fatty acids (SCFAs) and lipopolysaccharides (LPS), are implicated in triggering systemic and neuroinflammatory cascades that exacerbate the degeneration of dopaminergic neurons. This review consolidates current evidence on the mechanistic connections between gut microbiota dysregulation, neuroinflammation, and α-synuclein pathology in PD. We also discuss the translational potential of microbiota-focused biomarkers and innovative therapeutic strategies, providing new perspectives for early diagnosis and disease modification. Elucidating the GBA in PD paves the way for personalized medicine and microbiome-targeted therapies.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Gut microbial diversity and candidate keystone taxa in Indian tribes: Insights across lifestyle-ecological continuum and health associations.
Current research in microbial sciences, 11:100650.
Despite the critical role of the gut microbiome in host physiology and health, it remains poorly characterized in Indigenous populations undergoing rapid acculturation. This study presents high-resolution, whole-genome metagenomic profiling of gut microbiota from five Particularly Vulnerable Tribal Groups (PVTGs) of Southern India, Irula, Jenu Kuruba, Kurumba, Chenchu, and Konda Savara, spanning distinct ecological zones and cultural transitions. Using an ecology-lifestyle continuum framework, we investigated taxonomic and functional diversity with a focus on identifying computationally inferred candidate keystone taxa, defined by their association with variation in community ordination structure. A leave-one-taxon-out ordination framework identified 121 candidate keystone taxa, many of which were population-specific and have not been widely reported. Functional analyses revealed a conserved core of metabolic pathways, including glycolysis and folate biosynthesis, alongside group-specific enrichment in xenobiotic degradation, amino acid biosynthesis, mucin metabolism, and lipid processing, associated with differences in dietary and environmental exposures across populations. Large-scale disease-association mapping (n = 5,625) linked 50 candidate keystone taxa to 14 conditions, with 44 associated with health and 6 with disease. While Fusicatenibacter saccharivorans and Alistipes shahii were enriched in healthy states, Ruminococcus gnavus, Bifidobacterium longum, Flavonifractor plautii, and Blautia wexlerae were enriched in disease-associated profiles. Cross-cohort validation against an independent set of traditional metagenomes (n = 119) further showed that a subset of Indian tribal core candidate keystone taxa was consistently identified across geographically distinct populations, with partial conservation of community associations and health associations, indicating reproducible context-dependent microbial association patterns across traditional populations. Alpha diversity was highest in minimally acculturated groups, with higher degrees of acculturation associated with reduced microbial diversity and greater enrichment of disease-associated taxa. Overall, this study provides a context-aware framework for understanding gut microbiome dynamics in culturally transitioning populations, emphasizing the conservation of microbial heritage and informing population-specific microbiome-based interventions.
Additional Links: PMID-42598143
PubMed:
Citation:
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@article {pmid42598143,
year = {2026},
author = {Mollick, SA and Khual, GK and Ghosh, A and Patel, SK and Bhattacharyya, S and Roy, CS and Maile, A and Nagarajaram, HA and Longkumer, M and Babu, MN and Kundapur, AR and Uniyal, S and Chattterjee, A and Mitra, M and Sikdar, M and Urade, BP and Pulamaghatta, VN},
title = {Gut microbial diversity and candidate keystone taxa in Indian tribes: Insights across lifestyle-ecological continuum and health associations.},
journal = {Current research in microbial sciences},
volume = {11},
number = {},
pages = {100650},
pmid = {42598143},
issn = {2666-5174},
abstract = {Despite the critical role of the gut microbiome in host physiology and health, it remains poorly characterized in Indigenous populations undergoing rapid acculturation. This study presents high-resolution, whole-genome metagenomic profiling of gut microbiota from five Particularly Vulnerable Tribal Groups (PVTGs) of Southern India, Irula, Jenu Kuruba, Kurumba, Chenchu, and Konda Savara, spanning distinct ecological zones and cultural transitions. Using an ecology-lifestyle continuum framework, we investigated taxonomic and functional diversity with a focus on identifying computationally inferred candidate keystone taxa, defined by their association with variation in community ordination structure. A leave-one-taxon-out ordination framework identified 121 candidate keystone taxa, many of which were population-specific and have not been widely reported. Functional analyses revealed a conserved core of metabolic pathways, including glycolysis and folate biosynthesis, alongside group-specific enrichment in xenobiotic degradation, amino acid biosynthesis, mucin metabolism, and lipid processing, associated with differences in dietary and environmental exposures across populations. Large-scale disease-association mapping (n = 5,625) linked 50 candidate keystone taxa to 14 conditions, with 44 associated with health and 6 with disease. While Fusicatenibacter saccharivorans and Alistipes shahii were enriched in healthy states, Ruminococcus gnavus, Bifidobacterium longum, Flavonifractor plautii, and Blautia wexlerae were enriched in disease-associated profiles. Cross-cohort validation against an independent set of traditional metagenomes (n = 119) further showed that a subset of Indian tribal core candidate keystone taxa was consistently identified across geographically distinct populations, with partial conservation of community associations and health associations, indicating reproducible context-dependent microbial association patterns across traditional populations. Alpha diversity was highest in minimally acculturated groups, with higher degrees of acculturation associated with reduced microbial diversity and greater enrichment of disease-associated taxa. Overall, this study provides a context-aware framework for understanding gut microbiome dynamics in culturally transitioning populations, emphasizing the conservation of microbial heritage and informing population-specific microbiome-based interventions.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Precision synbiotic intervention with 2'-fucosyllactose and infant-derived Bifidobacterium modulates gut-immune axis and reduces disease risk in toddlers: a randomized controlled trial.
Frontiers in nutrition, 13:1856180.
BACKGROUND: Early childhood represents a critical window for nutritional programming of immune function and microbiome establishment. While human milk oligosaccharides (HMOs) and probiotics individually demonstrate health benefits, their synergistic integration as synbiotics remains underexplored in toddler populations. This study aimed to evaluate whether a precision synbiotic combining 2'-fucosyllactose (2'-FL) with infant-adapted Bifidobacterium strains provides superior protection against common pediatric conditions compared with probiotics alone or placebo, and to elucidate underlying gut-immune mechanisms.
AIM: To determine the efficacy of a 2'-FL-containing synbiotic on infectious and atopic disease incidence, gut microbiota composition, and intestinal immune markers in children aged 1-3 years.
METHODS: In this multicenter, double-blind, placebo-controlled, three-arm trial, 390 healthy toddlers were randomized (1:1:1) to receive: (1) synbiotic (2'-FL 1.0 g/day + B. infantis R0033 1.5 × 10[10] CFU + B. bifidum R0071 1.5 × 10[10] CFU); (2) probiotic (identical strains/doses); or (3) placebo (maltodextrin 1.5 g/day) for 12 weeks, with 12-week follow-up. Primary outcome was upper respiratory tract infections (URTIs) incidence over 24 weeks. Secondary outcomes included pneumonia, diarrhea, eczema, antibiotic use, gut microbiota (16S rRNA V3-V4 sequencing), and fecal immune biomarkers (calprotectin, sIgA, HBD-2, LL-37). Dietary intake was monitored to control nutritional confounders.
RESULT: Synbiotic vs. placebo: URTI incidence reduced from 85.4 to 55.4% (adjusted risk ratio (aRR) 0.64, 95% CI 0.43-0.95; ARR 30.0%, NNT = 3.3; p = 0.028); pneumonia from 17.7 to 7.7% (RR 0.40, 0.17-0.94; p = 0.034); diarrhea from 17.7 to 10.0% (aRR 0.54, 0.30-0.95; p = 0.032); and eczema from 13.1 to 1.5% (aRR 0.12, 0.04-0.35; ARR 11.6%, NNT = 2.9; p < 0.001). Probiotic alone reduced only eczema (aRR 0.10, 0.03-0.40; p = 0.001). The synbiotic significantly altered gut beta-diversity (Bray-Curtis, p = 0.042) and enriched Bifidobacterium catenulatum and B. kashiwanohense species with conserved HMO utilization pathways. At 24 weeks, synbiotic reduced fecal calprotectin (62.7 ± 23.9 vs. 77.9 ± 24.6 μg/g; p = 0.004) and increased sIgA (1.37 ± 0.38 vs. 1.15 ± 0.49 mg/g; p = 0.014), indicating enhanced intestinal immune homeostasis.
CONCLUSION: A 12-week precision synbiotic intervention combining 2'-FL with infant-derived Bifidobacterium strains significantly reduced the burden of respiratory infections, diarrhea, and atopic dermatitis in toddlers, with effects exceeding probiotics alone. These benefits were mediated by targeted gut microbiota modulation and enhanced mucosal immune function. This study provides evidence for integrative nutritional strategies in early childhood disease prevention and supports the development of next-generation synbiotic formulations.
CLINICAL TRIAL REGISTRATION: This study was registered in the Chinese Clinical Trial Registry (ChiCTR2400088943) prior to enrollment (https://www.chictr.org.cn/showprojEN.html?proj=235745).
Additional Links: PMID-42598364
PubMed:
Citation:
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@article {pmid42598364,
year = {2026},
author = {Chen, K and Zhang, X and Jin, S and Zhong, J and Chen, H and Yue, G and Cheng, Y and Peng, R and Fang, Z and Liu, F and Lu, Z and Zhao, L and Hu, R and Tao, X and He, Q and Liu, C},
title = {Precision synbiotic intervention with 2'-fucosyllactose and infant-derived Bifidobacterium modulates gut-immune axis and reduces disease risk in toddlers: a randomized controlled trial.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1856180},
pmid = {42598364},
issn = {2296-861X},
abstract = {BACKGROUND: Early childhood represents a critical window for nutritional programming of immune function and microbiome establishment. While human milk oligosaccharides (HMOs) and probiotics individually demonstrate health benefits, their synergistic integration as synbiotics remains underexplored in toddler populations. This study aimed to evaluate whether a precision synbiotic combining 2'-fucosyllactose (2'-FL) with infant-adapted Bifidobacterium strains provides superior protection against common pediatric conditions compared with probiotics alone or placebo, and to elucidate underlying gut-immune mechanisms.
AIM: To determine the efficacy of a 2'-FL-containing synbiotic on infectious and atopic disease incidence, gut microbiota composition, and intestinal immune markers in children aged 1-3 years.
METHODS: In this multicenter, double-blind, placebo-controlled, three-arm trial, 390 healthy toddlers were randomized (1:1:1) to receive: (1) synbiotic (2'-FL 1.0 g/day + B. infantis R0033 1.5 × 10[10] CFU + B. bifidum R0071 1.5 × 10[10] CFU); (2) probiotic (identical strains/doses); or (3) placebo (maltodextrin 1.5 g/day) for 12 weeks, with 12-week follow-up. Primary outcome was upper respiratory tract infections (URTIs) incidence over 24 weeks. Secondary outcomes included pneumonia, diarrhea, eczema, antibiotic use, gut microbiota (16S rRNA V3-V4 sequencing), and fecal immune biomarkers (calprotectin, sIgA, HBD-2, LL-37). Dietary intake was monitored to control nutritional confounders.
RESULT: Synbiotic vs. placebo: URTI incidence reduced from 85.4 to 55.4% (adjusted risk ratio (aRR) 0.64, 95% CI 0.43-0.95; ARR 30.0%, NNT = 3.3; p = 0.028); pneumonia from 17.7 to 7.7% (RR 0.40, 0.17-0.94; p = 0.034); diarrhea from 17.7 to 10.0% (aRR 0.54, 0.30-0.95; p = 0.032); and eczema from 13.1 to 1.5% (aRR 0.12, 0.04-0.35; ARR 11.6%, NNT = 2.9; p < 0.001). Probiotic alone reduced only eczema (aRR 0.10, 0.03-0.40; p = 0.001). The synbiotic significantly altered gut beta-diversity (Bray-Curtis, p = 0.042) and enriched Bifidobacterium catenulatum and B. kashiwanohense species with conserved HMO utilization pathways. At 24 weeks, synbiotic reduced fecal calprotectin (62.7 ± 23.9 vs. 77.9 ± 24.6 μg/g; p = 0.004) and increased sIgA (1.37 ± 0.38 vs. 1.15 ± 0.49 mg/g; p = 0.014), indicating enhanced intestinal immune homeostasis.
CONCLUSION: A 12-week precision synbiotic intervention combining 2'-FL with infant-derived Bifidobacterium strains significantly reduced the burden of respiratory infections, diarrhea, and atopic dermatitis in toddlers, with effects exceeding probiotics alone. These benefits were mediated by targeted gut microbiota modulation and enhanced mucosal immune function. This study provides evidence for integrative nutritional strategies in early childhood disease prevention and supports the development of next-generation synbiotic formulations.
CLINICAL TRIAL REGISTRATION: This study was registered in the Chinese Clinical Trial Registry (ChiCTR2400088943) prior to enrollment (https://www.chictr.org.cn/showprojEN.html?proj=235745).},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Multi-omics uncovers the critical role of ceramide-mediated Acinetobacter growth suppression in pressure injury healing under aging and malnutrition.
Journal of pharmaceutical analysis, 16(8):101587.
The epidemiology of tolerance and susceptibility in an individual suggests that aging and malnutrition (MN) should be critically regarded as a common clinical combination in the pathomechanism of pressure ulcer/injury (PU). However, the influence of these two factors on wound healing has not been fully elucidated. In this study, we used a random forest (RF) to screen macro and laboratory indicators to compare the characteristic variables of single versus dual interventions for aging or MN. The 16S ribosomal RNA (16S rRNA) microbiome sequencing as well as serum and skin metabolomics studies were conducted, along with the integration of bulk and single-cell RNA sequencing (scRNA-seq) data using bioinformatics. MetOrigin, MIMOSA2, and MetaNet were used to identify the molecular driving factors. The main findings demonstrated that the dual intervention played an essential role in inflammatory infiltration, promoting Acinetobacter colonization, affecting the activity of arachidonic acid (AA) and sphingolipid metabolic pathways, and simulating the metabolic profile of natural skin aging. The results of multi-omics association analysis, molecular biology, and antibacterial experiments in vitro indicated that the dual intervention affected keratinocytes through the cascading changes of the ceramide-Acinetobacter-AA-autophagy/wingless/integrated (WNT) axis to influence the healing process of PU wounds. In summary, this study has identified previously unknown links among skin microbiota, metabolites, and genomics in MN and aging, demonstrating that ceramide supplementation promotes wound healing in the older adults.
Additional Links: PMID-42598458
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Citation:
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@article {pmid42598458,
year = {2026},
author = {Wang, Z and Zhang, Y and Hou, J and Lv, B and Li, X and Gao, L and Qin, X and Liu, Y},
title = {Multi-omics uncovers the critical role of ceramide-mediated Acinetobacter growth suppression in pressure injury healing under aging and malnutrition.},
journal = {Journal of pharmaceutical analysis},
volume = {16},
number = {8},
pages = {101587},
pmid = {42598458},
issn = {2214-0883},
abstract = {The epidemiology of tolerance and susceptibility in an individual suggests that aging and malnutrition (MN) should be critically regarded as a common clinical combination in the pathomechanism of pressure ulcer/injury (PU). However, the influence of these two factors on wound healing has not been fully elucidated. In this study, we used a random forest (RF) to screen macro and laboratory indicators to compare the characteristic variables of single versus dual interventions for aging or MN. The 16S ribosomal RNA (16S rRNA) microbiome sequencing as well as serum and skin metabolomics studies were conducted, along with the integration of bulk and single-cell RNA sequencing (scRNA-seq) data using bioinformatics. MetOrigin, MIMOSA2, and MetaNet were used to identify the molecular driving factors. The main findings demonstrated that the dual intervention played an essential role in inflammatory infiltration, promoting Acinetobacter colonization, affecting the activity of arachidonic acid (AA) and sphingolipid metabolic pathways, and simulating the metabolic profile of natural skin aging. The results of multi-omics association analysis, molecular biology, and antibacterial experiments in vitro indicated that the dual intervention affected keratinocytes through the cascading changes of the ceramide-Acinetobacter-AA-autophagy/wingless/integrated (WNT) axis to influence the healing process of PU wounds. In summary, this study has identified previously unknown links among skin microbiota, metabolites, and genomics in MN and aging, demonstrating that ceramide supplementation promotes wound healing in the older adults.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Precision periodontology through periodontal endophenotyping: A narrative review.
Journal of Indian Society of Periodontology, 30(2):193-198.
Periodontal disease is a chronic inflammatory disease that is influenced by microbial, immunological, genetic, and systemic factors. The 2017 World Workshop staging and grading framework has improved clinical categorization. However, it does not consider underlying biological diversity among patients with similar clinical presentations. In psychiatry, endocrinology, and pulmonology, the concept of endophenotypes connects genotype, environmental factors, and clinical outcome. Evidence from periodontology suggests that genetic and epigenetic variation, local microbiology, immunoinflammatory responses, chronic systemic conditions, and behavioral factors form biologically distinct subgroups. This review aims to provide current evidence that supports the concept of periodontal endophenotypes and discusses their role in diagnostics, risk assessment, and precision therapy. Standardized markers are yet to be established. This paper seeks to identify current gaps in understanding and outline future directions for research in precision periodontology. The findings could pave the way for more personalized treatment strategies tailored to individual patient profiles. By addressing these gaps, researchers may enhance the effectiveness of interventions and improve overall patient outcomes in periodontal care.
Additional Links: PMID-42598638
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@article {pmid42598638,
year = {2026},
author = {Khanna, T and Bansal, RK and Gupta, S and Gupta, SD and Bogra, P and Kapoor, A},
title = {Precision periodontology through periodontal endophenotyping: A narrative review.},
journal = {Journal of Indian Society of Periodontology},
volume = {30},
number = {2},
pages = {193-198},
pmid = {42598638},
issn = {0972-124X},
abstract = {Periodontal disease is a chronic inflammatory disease that is influenced by microbial, immunological, genetic, and systemic factors. The 2017 World Workshop staging and grading framework has improved clinical categorization. However, it does not consider underlying biological diversity among patients with similar clinical presentations. In psychiatry, endocrinology, and pulmonology, the concept of endophenotypes connects genotype, environmental factors, and clinical outcome. Evidence from periodontology suggests that genetic and epigenetic variation, local microbiology, immunoinflammatory responses, chronic systemic conditions, and behavioral factors form biologically distinct subgroups. This review aims to provide current evidence that supports the concept of periodontal endophenotypes and discusses their role in diagnostics, risk assessment, and precision therapy. Standardized markers are yet to be established. This paper seeks to identify current gaps in understanding and outline future directions for research in precision periodontology. The findings could pave the way for more personalized treatment strategies tailored to individual patient profiles. By addressing these gaps, researchers may enhance the effectiveness of interventions and improve overall patient outcomes in periodontal care.},
}
RevDate: 2026-08-14
Growth, signals, and survival: the evolutionary divergence of terpenoid metabolism in terrestrial plants.
Natural product reports [Epub ahead of print].
Covering: primarily from 2011 to 2026Terpenoids are an ancient and immensely diverse class of natural products. Since their emergence more than two billion years ago alongside early biological membranes, terpenoid metabolism has undergone a vast expansion in both structure and function, which directly contributed to the ecological success of terrestrial plants. Biosynthetically derived from two isomeric five-carbon isoprenoid precursors, plant terpenoids include hemi-, mono-, sesqui-, di-, sester-, tri-, tetra-, and poly-, and mero-terpenoids, that exhibit extensive variation in chain length, structural scaffolds, and functional decoration. This large chemical space is generated via dynamic metabolic networks, in which functionally versatile enzymes - most notably scaffold-forming terpene synthases and tailoring cytochrome P450 monooxygenases - are assembled into combinatorial pathway modules to yield complex bioactive terpenoid structures. Lineage-specific expansion of the underlying gene families, driven by recurrent genome and gene duplications followed by functional divergence, have facilitated the evolution of both conserved and specialized metabolic branches and natural products. Functionally, conserved terpenoids act as phytohormones, signaling molecules, and pigments governing plant growth and development, whereas typically species-specific specialized terpenoids mediate dynamic plant-environment interactions, including pest and pathogen defenses, allelopathy, pollinator attraction, root-microbiome communication, and abiotic stress tolerance. Advances in genomics, metabolomics, and synthetic biology continue to accelerate the discovery of terpenoid structures, pathways, and functions at an ever-increasing pace. Elucidating the mechanisms that generate this diversity, and the multifaceted roles that terpenoids play in plant ecology and physiology not only deepens our understanding of the evolutionary history of terrestrial plants, but also unlocks new opportunities for biotechnological innovation, spanning terpenoid-derived therapeutics, biofuels, fragrances, polymers, agrochemicals, and many other bioproducts.
Additional Links: PMID-42598787
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@article {pmid42598787,
year = {2026},
author = {Wyatt, G and Yasmin, F and Donaldson, AR and Schumaker, SL and Gueorguieva, GA and Zerbe, P},
title = {Growth, signals, and survival: the evolutionary divergence of terpenoid metabolism in terrestrial plants.},
journal = {Natural product reports},
volume = {},
number = {},
pages = {},
doi = {10.1039/d6np00035e},
pmid = {42598787},
issn = {1460-4752},
abstract = {Covering: primarily from 2011 to 2026Terpenoids are an ancient and immensely diverse class of natural products. Since their emergence more than two billion years ago alongside early biological membranes, terpenoid metabolism has undergone a vast expansion in both structure and function, which directly contributed to the ecological success of terrestrial plants. Biosynthetically derived from two isomeric five-carbon isoprenoid precursors, plant terpenoids include hemi-, mono-, sesqui-, di-, sester-, tri-, tetra-, and poly-, and mero-terpenoids, that exhibit extensive variation in chain length, structural scaffolds, and functional decoration. This large chemical space is generated via dynamic metabolic networks, in which functionally versatile enzymes - most notably scaffold-forming terpene synthases and tailoring cytochrome P450 monooxygenases - are assembled into combinatorial pathway modules to yield complex bioactive terpenoid structures. Lineage-specific expansion of the underlying gene families, driven by recurrent genome and gene duplications followed by functional divergence, have facilitated the evolution of both conserved and specialized metabolic branches and natural products. Functionally, conserved terpenoids act as phytohormones, signaling molecules, and pigments governing plant growth and development, whereas typically species-specific specialized terpenoids mediate dynamic plant-environment interactions, including pest and pathogen defenses, allelopathy, pollinator attraction, root-microbiome communication, and abiotic stress tolerance. Advances in genomics, metabolomics, and synthetic biology continue to accelerate the discovery of terpenoid structures, pathways, and functions at an ever-increasing pace. Elucidating the mechanisms that generate this diversity, and the multifaceted roles that terpenoids play in plant ecology and physiology not only deepens our understanding of the evolutionary history of terrestrial plants, but also unlocks new opportunities for biotechnological innovation, spanning terpenoid-derived therapeutics, biofuels, fragrances, polymers, agrochemicals, and many other bioproducts.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Cathepsin B, Airway Pathogens, and Inflammation in the Lower Airways of Children With Cystic Fibrosis.
Pediatric pulmonology, 61(8):e71793.
INTRODUCTION: Dysregulated protease activity contributes to airway inflammation and tissue remodeling in cystic fibrosis (CF); however, the role of the lysosomal cysteine protease Cathepsin B (CTSB) remains incompletely defined. This cross-sectional study investigates relationships between pro-CTSB and mature CTSB activity with CF-specific pathogens and airway inflammation in children with and without CF.
METHODS: Bronchoalveolar lavage fluid (BALF) was collected from clinically indicated bronchoscopies in children (N = 52 CF, N = 161 non-CF). CTSB was interrogated using ELISA, fluorogenic activity assay, and Western blot analysis to distinguish pro- and mature CTSB. Total bacterial and total fungal load (TFL) were quantified by quantitative polymerase chain reaction, and community composition was determined by 16S bacterial and 18S fungal sequencing. Concentrations of proinflammatory cytokines and neutrophil elastase (NE) were measured via Luminex multiplatform and a spectrophotometric assay, respectively. Analyses included Spearman's rank correlations and Wilcoxon rank-based tests.
RESULTS: Pro-CTSB and CTSB activity were significantly (p < 0.01) elevated in CF BALF and in samples with a positive Staphylococcus aureus airway culture. Pro-CTSB concentrations correlated with staphylococcal relative abundance (RA, ρ = 0.25, p < 0.02) and reduced bacterial diversity (ρ = -0.41, p < 0.01). Mature CTSB activity correlated with TFL (ρ = 0.50, p < 0.05) and Aspergillus spp. RA (ρ = 0.36, p < 0.04). Western blot analysis confirmed pro-CTSB expression and mature CTSB in BALF with measurable activity. Both CTSB measures correlated strongly with NE and proinflammatory cytokines (ρ ≥ 0.47, p < 0.001). Pro-CTSB concentrations negatively correlated with FEV1/FVC measurements in CF (ρ = -0.32, p = 0.05).
CONCLUSIONS: BALF CTSB concentration may serve as a CF-specific biomarker of infection-related inflammation and obstructive lung disease driven by specific pathogen interactions.
Additional Links: PMID-42598879
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@article {pmid42598879,
year = {2026},
author = {Fought, MK and O'Connor, JB and Wagner, BD and Quinn, AC and Kirk Harris, J and Laguna, TA},
title = {Cathepsin B, Airway Pathogens, and Inflammation in the Lower Airways of Children With Cystic Fibrosis.},
journal = {Pediatric pulmonology},
volume = {61},
number = {8},
pages = {e71793},
doi = {10.1002/ppul.71793},
pmid = {42598879},
issn = {1099-0496},
support = {NIH R01HL136499/NH/NIH HHS/United States ; CFF LAGUNA17A0//Cystic Fibrosis Foundation/ ; },
mesh = {Humans ; *Cystic Fibrosis/microbiology/metabolism ; Cross-Sectional Studies ; *Cathepsin B/metabolism/analysis ; Female ; Male ; Child ; *Bronchoalveolar Lavage Fluid/microbiology/chemistry ; Adolescent ; Leukocyte Elastase/metabolism ; Cytokines/metabolism ; Child, Preschool ; Staphylococcus aureus/isolation & purification ; Inflammation/microbiology ; },
abstract = {INTRODUCTION: Dysregulated protease activity contributes to airway inflammation and tissue remodeling in cystic fibrosis (CF); however, the role of the lysosomal cysteine protease Cathepsin B (CTSB) remains incompletely defined. This cross-sectional study investigates relationships between pro-CTSB and mature CTSB activity with CF-specific pathogens and airway inflammation in children with and without CF.
METHODS: Bronchoalveolar lavage fluid (BALF) was collected from clinically indicated bronchoscopies in children (N = 52 CF, N = 161 non-CF). CTSB was interrogated using ELISA, fluorogenic activity assay, and Western blot analysis to distinguish pro- and mature CTSB. Total bacterial and total fungal load (TFL) were quantified by quantitative polymerase chain reaction, and community composition was determined by 16S bacterial and 18S fungal sequencing. Concentrations of proinflammatory cytokines and neutrophil elastase (NE) were measured via Luminex multiplatform and a spectrophotometric assay, respectively. Analyses included Spearman's rank correlations and Wilcoxon rank-based tests.
RESULTS: Pro-CTSB and CTSB activity were significantly (p < 0.01) elevated in CF BALF and in samples with a positive Staphylococcus aureus airway culture. Pro-CTSB concentrations correlated with staphylococcal relative abundance (RA, ρ = 0.25, p < 0.02) and reduced bacterial diversity (ρ = -0.41, p < 0.01). Mature CTSB activity correlated with TFL (ρ = 0.50, p < 0.05) and Aspergillus spp. RA (ρ = 0.36, p < 0.04). Western blot analysis confirmed pro-CTSB expression and mature CTSB in BALF with measurable activity. Both CTSB measures correlated strongly with NE and proinflammatory cytokines (ρ ≥ 0.47, p < 0.001). Pro-CTSB concentrations negatively correlated with FEV1/FVC measurements in CF (ρ = -0.32, p = 0.05).
CONCLUSIONS: BALF CTSB concentration may serve as a CF-specific biomarker of infection-related inflammation and obstructive lung disease driven by specific pathogen interactions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Cystic Fibrosis/microbiology/metabolism
Cross-Sectional Studies
*Cathepsin B/metabolism/analysis
Female
Male
Child
*Bronchoalveolar Lavage Fluid/microbiology/chemistry
Adolescent
Leukocyte Elastase/metabolism
Cytokines/metabolism
Child, Preschool
Staphylococcus aureus/isolation & purification
Inflammation/microbiology
RevDate: 2026-08-14
Serum-Cecal Metabolome Integration Predicts Gut Microbial Communities and Reveals Pathway-Level Host-Microbe Crosstalk Under Disease-Induced Dysbiosis.
Omics : a journal of integrative biology [Epub ahead of print].
The gut microbiome shapes systemic physiology through metabolites that enter circulation, yet most computational approaches focus on predicting metabolite profiles from microbial features rather than inferring microbial composition from host metabolomes. Here, we investigate whether host-derived metabolomic profiles can be leveraged to predict gut microbial community structure and to determine how disease-associated dysbiosis reshapes metabolite-microbe interactions and gut-to-systemic metabolic communication. We developed an integrative multi-omics framework combining serum and cecal metabolomics with 16S rRNA-based microbiome profiling. Supervised learning models demonstrated that cecal metabolites carry predictive signals for microbial abundances across conditions. Regularized canonical correlation analysis (rCCA) revealed cross-compartment metabolite-microbe networks. These analyses showed both conserved and condition-specific interaction patterns, indicating substantial network reorganization under disease-associated dysbiosis. Pathway-level integration further identified metabolic pathways linking the gut microbiome, the cecal environment, and the systemic circulation, representing coordinated gut-to-systemic communication axes. Together, our results establish a multi-omics strategy for predictive inference of gut microbial composition from host metabolomes and provide a framework for identifying pathway-level mechanisms underlying host-microbe metabolic crosstalk.
Additional Links: PMID-42598885
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PubMed:
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@article {pmid42598885,
year = {2026},
author = {Baidya, AK and Aich, P},
title = {Serum-Cecal Metabolome Integration Predicts Gut Microbial Communities and Reveals Pathway-Level Host-Microbe Crosstalk Under Disease-Induced Dysbiosis.},
journal = {Omics : a journal of integrative biology},
volume = {},
number = {},
pages = {15578100261479266},
doi = {10.1177/15578100261479266},
pmid = {42598885},
issn = {1557-8100},
abstract = {The gut microbiome shapes systemic physiology through metabolites that enter circulation, yet most computational approaches focus on predicting metabolite profiles from microbial features rather than inferring microbial composition from host metabolomes. Here, we investigate whether host-derived metabolomic profiles can be leveraged to predict gut microbial community structure and to determine how disease-associated dysbiosis reshapes metabolite-microbe interactions and gut-to-systemic metabolic communication. We developed an integrative multi-omics framework combining serum and cecal metabolomics with 16S rRNA-based microbiome profiling. Supervised learning models demonstrated that cecal metabolites carry predictive signals for microbial abundances across conditions. Regularized canonical correlation analysis (rCCA) revealed cross-compartment metabolite-microbe networks. These analyses showed both conserved and condition-specific interaction patterns, indicating substantial network reorganization under disease-associated dysbiosis. Pathway-level integration further identified metabolic pathways linking the gut microbiome, the cecal environment, and the systemic circulation, representing coordinated gut-to-systemic communication axes. Together, our results establish a multi-omics strategy for predictive inference of gut microbial composition from host metabolomes and provide a framework for identifying pathway-level mechanisms underlying host-microbe metabolic crosstalk.},
}
RevDate: 2026-08-14
Microbiome symbiosis, host-pathogen dynamics, and the search for new therapeutics: highlights from the Theobald Smith Society Spring 2026 Symposium.
mSphere [Epub ahead of print].
The annual Theobald Smith Society (TSS) spring meeting was convened at Rutgers University in New Brunswick, New Jersey, on 8 May 2026. TSS is the New Jersey branch of ASM and holds two annual meetings, in the fall and spring. These meetings bring together microbiologists, trainees at all levels, and professionals from both academia and industry to share their research, to network, and to engage in discussions on a wide array of topics that fall under ASM's three main units: health, mechanism discovery, and applied and environmental microbiology. The TSS spring meeting brought together more than 140 attendees from institutions across New Jersey. This report highlights the vision and work of TSS and ASM, the breadth of research presented at the meeting through invited talks and posters, and the two keynote lectures on nutritional immunity and the modern decline of human microbiome diversity.
Additional Links: PMID-42599078
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PubMed:
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@article {pmid42599078,
year = {2026},
author = {Battaje, RR and Skalenko, KS and Han, A and Abdujabbarova, K and Boyd, JM and Carabetta, VJ and Yang, JH and Yadavalli, SS},
title = {Microbiome symbiosis, host-pathogen dynamics, and the search for new therapeutics: highlights from the Theobald Smith Society Spring 2026 Symposium.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0036626},
doi = {10.1128/msphere.00366-26},
pmid = {42599078},
issn = {2379-5042},
abstract = {The annual Theobald Smith Society (TSS) spring meeting was convened at Rutgers University in New Brunswick, New Jersey, on 8 May 2026. TSS is the New Jersey branch of ASM and holds two annual meetings, in the fall and spring. These meetings bring together microbiologists, trainees at all levels, and professionals from both academia and industry to share their research, to network, and to engage in discussions on a wide array of topics that fall under ASM's three main units: health, mechanism discovery, and applied and environmental microbiology. The TSS spring meeting brought together more than 140 attendees from institutions across New Jersey. This report highlights the vision and work of TSS and ASM, the breadth of research presented at the meeting through invited talks and posters, and the two keynote lectures on nutritional immunity and the modern decline of human microbiome diversity.},
}
RevDate: 2026-08-14
Shotgun metagenomic sequence data from milk and fecal samples of dairy cattle in Thailand.
Microbiology resource announcements [Epub ahead of print].
We report shotgun metagenomic sequence data from milk and fecal samples of dairy cattle in Thailand. This data set captures microbial genetic profiles from mammary- and gut-associated sample types and provides a resource for future comparative microbiome, functional, and antimicrobial resistance gene analyses in dairy cattle.
Additional Links: PMID-42599081
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PubMed:
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@article {pmid42599081,
year = {2026},
author = {Buddhasiri, S and Singhla, T and Pengpanun, S and Eiamsam-Ang, T and Thiennimitr, P},
title = {Shotgun metagenomic sequence data from milk and fecal samples of dairy cattle in Thailand.},
journal = {Microbiology resource announcements},
volume = {},
number = {},
pages = {e0056426},
doi = {10.1128/mra.00564-26},
pmid = {42599081},
issn = {2576-098X},
abstract = {We report shotgun metagenomic sequence data from milk and fecal samples of dairy cattle in Thailand. This data set captures microbial genetic profiles from mammary- and gut-associated sample types and provides a resource for future comparative microbiome, functional, and antimicrobial resistance gene analyses in dairy cattle.},
}
RevDate: 2026-08-14
Precision Lipid Management in the Era of Biotechnology and Artificial Intelligence: From Gene Editing to Smart Drug Delivery.
Therapeutic innovation & regulatory science [Epub ahead of print].
BACKGROUND: Hyperlipidemia is a major modifiable contributor to atherosclerotic cardiovascular disease (ASCVD). Despite statins as first-line therapy, residual cardiovascular risk, treatment intolerance, and genetic dyslipidemias highlight the need for innovative strategies.
OBJECTIVE: This narrative review critically evaluates emerging biotechnology- and artificial intelligence (AI)-enhanced approaches for hyperlipidemia, emphasizing translational maturity, clinical applicability, and regulatory implications.
METHODS AND SCOPE: A structured literature search of PubMed/MEDLINE, Scopus, and Web of Science Core Collection was conducted to identify relevant evidence published primarily between January 2015 and February 2025. The review methodology, including the approximate literature search yield, is described in the Methods section. Evidence was synthesized across three developmental tiers: preclinical and early clinical gene-editing strategies; clinically established or late-stage therapies, including PCSK9 monoclonal antibodies and inclisiran; and early translational or conceptual platforms involving nanotechnology, microbiome modulation, and AI-assisted treatment optimization.
RESULTS AND IMPLICATIONS: PCSK9 monoclonal antibodies provide substantial LDL-C reduction and established cardiovascular outcome benefits, whereas inclisiran offers durable LDL-C lowering with infrequent dosing, although definitive cardiovascular outcomes evidence remains pending. CRISPR-based approaches may enable durable lipid regulation but remain constrained by delivery efficiency, off-target effects, immunogenicity, and long-term safety concerns. Nanoparticle-based delivery, microbiome-targeted interventions, and AI-driven prediction and treatment optimization are promising, but clinical translation is limited by biological variability, standardization challenges, insufficient external validation, algorithmic bias, data-governance concerns, and workflow integration barriers.
CONCLUSION: Biotechnology and AI are reshaping precision lipid management. Successful translation will require long-term safety and outcomes validation, reproducible delivery platforms, cost-effectiveness, equitable implementation, and adaptive regulatory frameworks.
Additional Links: PMID-42599575
PubMed:
Citation:
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@article {pmid42599575,
year = {2026},
author = {Palabiyik, E},
title = {Precision Lipid Management in the Era of Biotechnology and Artificial Intelligence: From Gene Editing to Smart Drug Delivery.},
journal = {Therapeutic innovation & regulatory science},
volume = {},
number = {},
pages = {},
pmid = {42599575},
issn = {2168-4804},
abstract = {BACKGROUND: Hyperlipidemia is a major modifiable contributor to atherosclerotic cardiovascular disease (ASCVD). Despite statins as first-line therapy, residual cardiovascular risk, treatment intolerance, and genetic dyslipidemias highlight the need for innovative strategies.
OBJECTIVE: This narrative review critically evaluates emerging biotechnology- and artificial intelligence (AI)-enhanced approaches for hyperlipidemia, emphasizing translational maturity, clinical applicability, and regulatory implications.
METHODS AND SCOPE: A structured literature search of PubMed/MEDLINE, Scopus, and Web of Science Core Collection was conducted to identify relevant evidence published primarily between January 2015 and February 2025. The review methodology, including the approximate literature search yield, is described in the Methods section. Evidence was synthesized across three developmental tiers: preclinical and early clinical gene-editing strategies; clinically established or late-stage therapies, including PCSK9 monoclonal antibodies and inclisiran; and early translational or conceptual platforms involving nanotechnology, microbiome modulation, and AI-assisted treatment optimization.
RESULTS AND IMPLICATIONS: PCSK9 monoclonal antibodies provide substantial LDL-C reduction and established cardiovascular outcome benefits, whereas inclisiran offers durable LDL-C lowering with infrequent dosing, although definitive cardiovascular outcomes evidence remains pending. CRISPR-based approaches may enable durable lipid regulation but remain constrained by delivery efficiency, off-target effects, immunogenicity, and long-term safety concerns. Nanoparticle-based delivery, microbiome-targeted interventions, and AI-driven prediction and treatment optimization are promising, but clinical translation is limited by biological variability, standardization challenges, insufficient external validation, algorithmic bias, data-governance concerns, and workflow integration barriers.
CONCLUSION: Biotechnology and AI are reshaping precision lipid management. Successful translation will require long-term safety and outcomes validation, reproducible delivery platforms, cost-effectiveness, equitable implementation, and adaptive regulatory frameworks.},
}
RevDate: 2026-08-14
Seasonal Dynamics of Community and Function of Gut Microbiome in Taihangshan Macaque (Macaca mulatta tcheliensis): Inferred From Metagenomic Data.
Integrative zoology [Epub ahead of print].
The gut microbiome is a key regulator of host nutritional intake, growth, and health, playing an essential role in mediating host adaptation to environmental changes. The northernmost population of rhesus macaque, Taihangshan macaque (Macaca mulatta tcheliensis), faces severe survival challenges, such as food shortages and harsh temperatures during winter and early spring. Previous studies have shown that they cope with seasonal changes through behavioral adaptations, such as adjusting food resources and flexibly regulating macronutrient intake. However, the role of the gut microbiome in supporting the seasonal adaptation of Taihangshan macaques remains unclear. Herein, we investigated seasonal variations in gut microbiome alpha diversity, composition, and functions from fecal samples of Taihangshan macaques using metagenomic analysis. The results showed that: (1) totally 435 non-redundant metagenome assembled genomes (MAGs) were generated; (2) alpha diversity was significantly higher in spring and winter than in summer and autumn; and (3) in winter, pathways of fatty acid biosynthesis and essential amino acid (EAA) biosynthesis, as well as CAZymes (GH3 and GH5) involved in cellulose and hemicellulose degradation, were significantly enriched. In contrast, pathways related to carbohydrate, energy, and glycan biosynthesis and metabolism, along with CAZymes (GT8 and GH23) potentially facilitating fat synthesis and storage, were enriched in summer. These functional adjustments likely help the host cope with seasonal variations in food availability and environmental conditions. Overall, this study provides new insights into how the gut microbiome responds to seasonal changes in diet and environmental factors in mammals inhabiting temperate forests.
Additional Links: PMID-42599752
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PubMed:
Citation:
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@article {pmid42599752,
year = {2026},
author = {Zhou, Y and Shao, Q and Liu, C and Tian, J and Guan, X and Zhang, X and Lu, J},
title = {Seasonal Dynamics of Community and Function of Gut Microbiome in Taihangshan Macaque (Macaca mulatta tcheliensis): Inferred From Metagenomic Data.},
journal = {Integrative zoology},
volume = {},
number = {},
pages = {},
doi = {10.1111/1749-4877.70163},
pmid = {42599752},
issn = {1749-4877},
support = {No.31672302;No.32070446//National Natural Science Foundation of China/ ; },
abstract = {The gut microbiome is a key regulator of host nutritional intake, growth, and health, playing an essential role in mediating host adaptation to environmental changes. The northernmost population of rhesus macaque, Taihangshan macaque (Macaca mulatta tcheliensis), faces severe survival challenges, such as food shortages and harsh temperatures during winter and early spring. Previous studies have shown that they cope with seasonal changes through behavioral adaptations, such as adjusting food resources and flexibly regulating macronutrient intake. However, the role of the gut microbiome in supporting the seasonal adaptation of Taihangshan macaques remains unclear. Herein, we investigated seasonal variations in gut microbiome alpha diversity, composition, and functions from fecal samples of Taihangshan macaques using metagenomic analysis. The results showed that: (1) totally 435 non-redundant metagenome assembled genomes (MAGs) were generated; (2) alpha diversity was significantly higher in spring and winter than in summer and autumn; and (3) in winter, pathways of fatty acid biosynthesis and essential amino acid (EAA) biosynthesis, as well as CAZymes (GH3 and GH5) involved in cellulose and hemicellulose degradation, were significantly enriched. In contrast, pathways related to carbohydrate, energy, and glycan biosynthesis and metabolism, along with CAZymes (GT8 and GH23) potentially facilitating fat synthesis and storage, were enriched in summer. These functional adjustments likely help the host cope with seasonal variations in food availability and environmental conditions. Overall, this study provides new insights into how the gut microbiome responds to seasonal changes in diet and environmental factors in mammals inhabiting temperate forests.},
}
RevDate: 2026-08-14
CmpDate: 2026-08-14
Sex differences in the effects of shift work-like schedules on gut microbiome and intestinal barrier in relation to stroke survival.
PloS one, 21(8):e0355842 pii:PONE-D-26-20020.
Disturbances of 24-hour or circadian rhythms imposed by everyday irregular work and/or social schedules have been linked to vascular disease, including ischemic stroke. Using an established shift work-like paradigm and preclinical model for ischemic stroke, we have shown that environment-induced circadian dysregulation exacerbates stroke outcomes differentially to a greater extent in male than female rats. Because more severe stroke outcomes and circadian rhythm disturbances have been linked to gut pathophysiology, the present study examined the effects of chronic shifts in the LD cycle on gut cytoarchitecture, microbiota composition, metabolites, and inflammatory mediators for evidence of corresponding sex differences. Two independent cohorts of adult (5-7mo) rats exposed for 50d to fixed or shifted (12hr advance/5d) LD 12:12 cycles were used to examine the effects of circadian dysregulation on: fecal microbiome composition in relation to stroke survival (Cohort 1); and gut morphology, metabolites and inflammatory mediators (Cohort 2). Circadian entrainment of activity rhythms was stable during exposure to fixed LD cycles but was severely disrupted in shifted LD rats. Relative to fixed LD controls, male but not female rats exposed to shifted LD cycles were distinguished by significant alterations in the composition of the gut microbiome including reduced alpha diversity, shifts in beta diversity and correlations between the abundance of beneficial gut bacteria and stroke survival. The effects of circadian dysregulation on gut microbiota were accompanied by evidence of pathologic gut morphology (i.e., shorter and blunted villi, crypt hyperplasia, disruption of tight junction proteins and gut barrier integrity), decreased circulating levels of the neuroprotective short-chain fatty acid butyrate, and elevated serum concentrations of endotoxin and proinflammatory cytokine IL-17A in shifted LD male rats. These results suggest that alterations in gut cytoarchitecture, microbiota, metabolites and inflammatory mediators may contribute to sex differences in the effects of circadian dysregulation on ischemic stroke outcomes.
Additional Links: PMID-42599922
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PubMed:
Citation:
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@article {pmid42599922,
year = {2026},
author = {Barnum, E and Turck, JL and Souza, KA and Mani, KK and Pilla, R and Selvamani, A and Sohrabji, F and Earnest, DJ},
title = {Sex differences in the effects of shift work-like schedules on gut microbiome and intestinal barrier in relation to stroke survival.},
journal = {PloS one},
volume = {21},
number = {8},
pages = {e0355842},
doi = {10.1371/journal.pone.0355842},
pmid = {42599922},
issn = {1932-6203},
mesh = {Animals ; Female ; Male ; Rats ; *Gastrointestinal Microbiome/physiology ; *Stroke/mortality/physiopathology/microbiology ; Circadian Rhythm/physiology ; *Shift Work Schedule/adverse effects ; Intestinal Barrier Function ; Sex Characteristics ; Sex Factors ; Feces/microbiology ; },
abstract = {Disturbances of 24-hour or circadian rhythms imposed by everyday irregular work and/or social schedules have been linked to vascular disease, including ischemic stroke. Using an established shift work-like paradigm and preclinical model for ischemic stroke, we have shown that environment-induced circadian dysregulation exacerbates stroke outcomes differentially to a greater extent in male than female rats. Because more severe stroke outcomes and circadian rhythm disturbances have been linked to gut pathophysiology, the present study examined the effects of chronic shifts in the LD cycle on gut cytoarchitecture, microbiota composition, metabolites, and inflammatory mediators for evidence of corresponding sex differences. Two independent cohorts of adult (5-7mo) rats exposed for 50d to fixed or shifted (12hr advance/5d) LD 12:12 cycles were used to examine the effects of circadian dysregulation on: fecal microbiome composition in relation to stroke survival (Cohort 1); and gut morphology, metabolites and inflammatory mediators (Cohort 2). Circadian entrainment of activity rhythms was stable during exposure to fixed LD cycles but was severely disrupted in shifted LD rats. Relative to fixed LD controls, male but not female rats exposed to shifted LD cycles were distinguished by significant alterations in the composition of the gut microbiome including reduced alpha diversity, shifts in beta diversity and correlations between the abundance of beneficial gut bacteria and stroke survival. The effects of circadian dysregulation on gut microbiota were accompanied by evidence of pathologic gut morphology (i.e., shorter and blunted villi, crypt hyperplasia, disruption of tight junction proteins and gut barrier integrity), decreased circulating levels of the neuroprotective short-chain fatty acid butyrate, and elevated serum concentrations of endotoxin and proinflammatory cytokine IL-17A in shifted LD male rats. These results suggest that alterations in gut cytoarchitecture, microbiota, metabolites and inflammatory mediators may contribute to sex differences in the effects of circadian dysregulation on ischemic stroke outcomes.},
}
MeSH Terms:
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Animals
Female
Male
Rats
*Gastrointestinal Microbiome/physiology
*Stroke/mortality/physiopathology/microbiology
Circadian Rhythm/physiology
*Shift Work Schedule/adverse effects
Intestinal Barrier Function
Sex Characteristics
Sex Factors
Feces/microbiology
RevDate: 2026-08-14
CmpDate: 2026-08-14
Ingestible probes for breath-based monitoring of drug-metabolizing activity from the microbiome.
Science advances, 12(33):eaee2632.
Due to their effects on drug activity and safety, drug-metabolizing enzymes (DMEs) from the gut microbiome are attractive drug targets, and noninvasive strategies are needed to measure their activities. Here, we report the development of ingestible probes that sense and produce breath signals for β-glucuronidase (GUS), a microbiome DME that causes drug toxicity. GUS probes comprise safe-to-ingest components and release volatile reporters upon cleavage by GUS. After oral administration, probes transit the gastrointestinal tract intact until they reach the microbiome in the large intestine. There, probes are cleaved by GUS and release volatile reporters, which are rapidly exhaled to provide a near real-time breath signal for GUS activity that can be measured via mass spectrometry. In mouse studies, breath signals were produced in naïve mice with GUS-expressing microbiome but absent in microbiome-depleted mice. Repeated probe dosing and breath analysis enabled monitoring of dynamic changes in GUS activities.
Additional Links: PMID-42600024
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PubMed:
Citation:
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@article {pmid42600024,
year = {2026},
author = {Manickam, VA and Kimpling, CE and Le, KN and Troussé, ME and Kang, A and Patel, AS and Chan, LW},
title = {Ingestible probes for breath-based monitoring of drug-metabolizing activity from the microbiome.},
journal = {Science advances},
volume = {12},
number = {33},
pages = {eaee2632},
doi = {10.1126/sciadv.aee2632},
pmid = {42600024},
issn = {2375-2548},
mesh = {Animals ; Breath Tests/methods ; Mice ; *Gastrointestinal Microbiome ; *Glucuronidase/metabolism ; *Microbiota ; Humans ; Administration, Oral ; },
abstract = {Due to their effects on drug activity and safety, drug-metabolizing enzymes (DMEs) from the gut microbiome are attractive drug targets, and noninvasive strategies are needed to measure their activities. Here, we report the development of ingestible probes that sense and produce breath signals for β-glucuronidase (GUS), a microbiome DME that causes drug toxicity. GUS probes comprise safe-to-ingest components and release volatile reporters upon cleavage by GUS. After oral administration, probes transit the gastrointestinal tract intact until they reach the microbiome in the large intestine. There, probes are cleaved by GUS and release volatile reporters, which are rapidly exhaled to provide a near real-time breath signal for GUS activity that can be measured via mass spectrometry. In mouse studies, breath signals were produced in naïve mice with GUS-expressing microbiome but absent in microbiome-depleted mice. Repeated probe dosing and breath analysis enabled monitoring of dynamic changes in GUS activities.},
}
MeSH Terms:
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Animals
Breath Tests/methods
Mice
*Gastrointestinal Microbiome
*Glucuronidase/metabolism
*Microbiota
Humans
Administration, Oral
RevDate: 2026-08-14
Triphala ameliorates hyperuricemia-associated nephropathy by modulating the gut microbiota-glycerophospholipid-TLR4 axis.
Phytomedicine : international journal of phytotherapy and phytopharmacology, 160:158694 pii:S0944-7113(26)00926-8 [Epub ahead of print].
BACKGROUND: Hyperuricemia (HUA) is a metabolic disorder with an escalating global prevalence, and its progression to HUA-associated nephropathy represents an important contributor to chronic kidney injury. Emerging evidence highlights a bidirectional relationship between uric acid and lipid metabolism, with dyslipidemia contributing to the pathological progression of HUA-related complications. Triphala (TRP), a classic Tibetan herbal formula with broad metabolic regulatory properties, was selected as a potential intervention for the complex metabolic disturbances associated with HUA. However, its therapeutic efficacy and the precise molecular mechanisms underlying its effects in HUA remain to be fully elucidated.
PURPOSE: This study aimed to investigate the protective effects of TRP on hyperuricemia-associated nephropathy and to elucidate the underlying mechanisms.
METHODS: High-performance liquid chromatography (HPLC) was first employed to identify and quantify seven representative constituents in the TRP aqueous extract. To evaluate the efficacy of TRP, an HUA mouse model was established through the combined administration of intraperitoneal potassium oxonate injections and a yeast-containing diet. A multi-omics strategy integrating 16S rRNA sequencing, metabolomics and lipidomics elucidated TRP's impact on the gut microbiota and host metabolism. Critically, fecal microbiota transplantation (FMT), TLR4 blockade experiments, and in vitro assays were employed to evaluate the contribution of TRP-modulated microbiota and the LPC-TLR4 pathway to the protective effects of TRP.
RESULTS: HPLC identified chebulic acid, gallic acid, and corilagin as the major representative constituents of TRP aqueous extract. TRP dose-dependently reduced serum uric acid, improved renal function by lowering serum creatinine (Cr) and blood urea nitrogen (BUN) levels, increased the fractional excretion of uric acid (FEUA), and alleviated tubular injury and fibrosis. These improvements were accompanied by normalized urate transporters (downregulated URAT1/GLUT9; restored OAT1/OAT3) and suppressed renal inflammatory cytokines. Multi-omics analysis revealed that TRP reversed HUA-induced dysbiosis by suppressing opportunistic pathogens (e.g., Parasutterella, Allobaculum) and enriching beneficial genera (e.g., Bifidobacterium, Akkermansia), specifically reducing pro-inflammatory LPC (e.g., LPC16:0, LPC18:1). TRP and FMT effectively inhibited the TLR4/MyD88/NF-κB signaling axis and reduced LPC accumulation within the kidney. In vitro experiments validated that these specific LPC directly trigger TLR4 expression and TNF-α release, confirming the potential role of the microbiota-driven lysophospholipid-TLR4 pathway in HUA-associated chronic renal inflammation.
CONCLUSION: TRP ameliorates HUA and renal inflammation by remodeling the gut microbiota to suppress the aberrant accumulation of pro-inflammatory lysophospholipids, thereby deactivating the TLR4-mediated inflammatory cascade. These findings establish the gut microbiota-glycerophospholipid metabolism-renal inflammation axis as a potential therapeutic target and validate TRP as a relevant strategy for targeting the gut microbiome to treat systemic metabolic disease.
Additional Links: PMID-42600364
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PubMed:
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@article {pmid42600364,
year = {2026},
author = {Liu, C and Zhang, H and Zhang, H and Zhao, Y and Wu, C and Lin, Q and Luo, Y and Wei, L and Chen, J and Rao, X and Xiong, S and Shen, H and Hong, S and Shi, Z and Yin, S and Lan, Z and Chen, L},
title = {Triphala ameliorates hyperuricemia-associated nephropathy by modulating the gut microbiota-glycerophospholipid-TLR4 axis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {160},
number = {},
pages = {158694},
doi = {10.1016/j.phymed.2026.158694},
pmid = {42600364},
issn = {1618-095X},
abstract = {BACKGROUND: Hyperuricemia (HUA) is a metabolic disorder with an escalating global prevalence, and its progression to HUA-associated nephropathy represents an important contributor to chronic kidney injury. Emerging evidence highlights a bidirectional relationship between uric acid and lipid metabolism, with dyslipidemia contributing to the pathological progression of HUA-related complications. Triphala (TRP), a classic Tibetan herbal formula with broad metabolic regulatory properties, was selected as a potential intervention for the complex metabolic disturbances associated with HUA. However, its therapeutic efficacy and the precise molecular mechanisms underlying its effects in HUA remain to be fully elucidated.
PURPOSE: This study aimed to investigate the protective effects of TRP on hyperuricemia-associated nephropathy and to elucidate the underlying mechanisms.
METHODS: High-performance liquid chromatography (HPLC) was first employed to identify and quantify seven representative constituents in the TRP aqueous extract. To evaluate the efficacy of TRP, an HUA mouse model was established through the combined administration of intraperitoneal potassium oxonate injections and a yeast-containing diet. A multi-omics strategy integrating 16S rRNA sequencing, metabolomics and lipidomics elucidated TRP's impact on the gut microbiota and host metabolism. Critically, fecal microbiota transplantation (FMT), TLR4 blockade experiments, and in vitro assays were employed to evaluate the contribution of TRP-modulated microbiota and the LPC-TLR4 pathway to the protective effects of TRP.
RESULTS: HPLC identified chebulic acid, gallic acid, and corilagin as the major representative constituents of TRP aqueous extract. TRP dose-dependently reduced serum uric acid, improved renal function by lowering serum creatinine (Cr) and blood urea nitrogen (BUN) levels, increased the fractional excretion of uric acid (FEUA), and alleviated tubular injury and fibrosis. These improvements were accompanied by normalized urate transporters (downregulated URAT1/GLUT9; restored OAT1/OAT3) and suppressed renal inflammatory cytokines. Multi-omics analysis revealed that TRP reversed HUA-induced dysbiosis by suppressing opportunistic pathogens (e.g., Parasutterella, Allobaculum) and enriching beneficial genera (e.g., Bifidobacterium, Akkermansia), specifically reducing pro-inflammatory LPC (e.g., LPC16:0, LPC18:1). TRP and FMT effectively inhibited the TLR4/MyD88/NF-κB signaling axis and reduced LPC accumulation within the kidney. In vitro experiments validated that these specific LPC directly trigger TLR4 expression and TNF-α release, confirming the potential role of the microbiota-driven lysophospholipid-TLR4 pathway in HUA-associated chronic renal inflammation.
CONCLUSION: TRP ameliorates HUA and renal inflammation by remodeling the gut microbiota to suppress the aberrant accumulation of pro-inflammatory lysophospholipids, thereby deactivating the TLR4-mediated inflammatory cascade. These findings establish the gut microbiota-glycerophospholipid metabolism-renal inflammation axis as a potential therapeutic target and validate TRP as a relevant strategy for targeting the gut microbiome to treat systemic metabolic disease.},
}
RevDate: 2026-08-14
Metabolic and endocrine modulation of the gut-adipose tissue axis via pro-, pre-, and postbiotics in overweight dogs: A systematic review.
Domestic animal endocrinology, 97:107044 pii:S0739-7240(26)00051-2 [Epub ahead of print].
Canine obesity is a complex metabolic disorder driven by luminal dysbiosis, impaired gut barrier function, and metaflammation. Following PRISMA 2020 guidelines, this systematic review evaluated the efficacy of pro-, pre-, and postbiotics in modulating the gut-adipose tissue axis in overweight dogs (BCS ≥ 6/9) or diet-induced obesity models. Searches across PubMed and Dimensions (April 2026) identified seven eligible experimental trials. Results suggest that postbiotic Bifidobacterium animalis subsp. lactis CECT 8145 reduced postprandial glucose AUC by 6 % strictly during energy restriction. Pasteurized Akkermansia muciniphila postbiotics limited diet-induced weight gain, though glucoregulatory impacts were highly strain-specific (AKK2 reduced fasting glucose and insulin resistance indexes, whereas EB-AMDK19 exerted no significant effect). Specific probiotics (including Enterococcus faecium, Bifidobacterium lactis, Lactiplantibacillus plantarum and Bifidobacterium breve) attenuated fasting hyperinsulinemia and preserved circulating adiponectin, but lipid profile improvements (triglycerides and total cholesterol) were inconsistent across trials. In dogs, increased luminal short-chain fatty acids are not consistently mirrored by endocrine responses, so the coupling between microbial metabolites and incretin signaling remains incomplete. A critical lack of standardized reporting for species-validated insulin sensitivity metrics was identified. In conclusion, microbiome-targeted therapies, particularly inanimate postbiotics, may represent useful adjunctive strategies to mitigate metabolic dysregulation in obesogenic environments. However, clinical efficacy remains strictly strain-specific and dependent on host energy balance. Given the scarcity of high-certainty evidence, future trials must integrate dynamic physiological assessments with species-validated surrogate indexes alongside standardized dietary controls.
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PubMed:
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@article {pmid42600415,
year = {2026},
author = {Southwell, M and Faraco, M and Ruíz, MJ and Romanelli, A and Sagües, MF},
title = {Metabolic and endocrine modulation of the gut-adipose tissue axis via pro-, pre-, and postbiotics in overweight dogs: A systematic review.},
journal = {Domestic animal endocrinology},
volume = {97},
number = {},
pages = {107044},
doi = {10.1016/j.domaniend.2026.107044},
pmid = {42600415},
issn = {1879-0054},
abstract = {Canine obesity is a complex metabolic disorder driven by luminal dysbiosis, impaired gut barrier function, and metaflammation. Following PRISMA 2020 guidelines, this systematic review evaluated the efficacy of pro-, pre-, and postbiotics in modulating the gut-adipose tissue axis in overweight dogs (BCS ≥ 6/9) or diet-induced obesity models. Searches across PubMed and Dimensions (April 2026) identified seven eligible experimental trials. Results suggest that postbiotic Bifidobacterium animalis subsp. lactis CECT 8145 reduced postprandial glucose AUC by 6 % strictly during energy restriction. Pasteurized Akkermansia muciniphila postbiotics limited diet-induced weight gain, though glucoregulatory impacts were highly strain-specific (AKK2 reduced fasting glucose and insulin resistance indexes, whereas EB-AMDK19 exerted no significant effect). Specific probiotics (including Enterococcus faecium, Bifidobacterium lactis, Lactiplantibacillus plantarum and Bifidobacterium breve) attenuated fasting hyperinsulinemia and preserved circulating adiponectin, but lipid profile improvements (triglycerides and total cholesterol) were inconsistent across trials. In dogs, increased luminal short-chain fatty acids are not consistently mirrored by endocrine responses, so the coupling between microbial metabolites and incretin signaling remains incomplete. A critical lack of standardized reporting for species-validated insulin sensitivity metrics was identified. In conclusion, microbiome-targeted therapies, particularly inanimate postbiotics, may represent useful adjunctive strategies to mitigate metabolic dysregulation in obesogenic environments. However, clinical efficacy remains strictly strain-specific and dependent on host energy balance. Given the scarcity of high-certainty evidence, future trials must integrate dynamic physiological assessments with species-validated surrogate indexes alongside standardized dietary controls.},
}
RevDate: 2026-08-14
Physio-informatics linking rumen biology, systemic metabolism and meat quality in Japanese black cattle.
Meat science, 242:110130 pii:S0309-1740(26)00100-2 [Epub ahead of print].
Japanese Black cattle (Wagyu) are raised under a distinctive long-term fattening system designed to enhance intramuscular fat (marbling) and carcass value. Because most metabolizable energy and many metabolic signals in ruminants derive from rumen fermentation products, variation in rumen microbial ecology and fermentation chemistry can extend to systemic metabolism and ultimately influence meat quality traits. Recent work in Japanese Black steers has provided a structured, multi-layered dataset spanning rumen fermentation characteristics, blood metabolites and hormones, liver transcriptome profiles, and rumen microbiome composition and predicted function across fattening stages and metabolic phenotypes. This review integrates these findings with established concepts in ruminant physiology to propose a physio-informatic framework linking rumen microbiota to hepatic metabolic regulation and adipose tissue development via the rumen-liver-adipose axis, with potential relevance to broader meat quality traits. We highlight (i) microbial succession across the three-stage feeding program, (ii) fermentation-derived short-chain fatty acids and their absorption and metabolic fates, and (iii) endocrine and transcriptional regulation of energy partitioning during fattening as an interpretable systems signal rather than a single downstream endpoint. Finally, we discuss potential analytic strategies, including longitudinal modeling, network inference, and machine learning approaches, that may support the future development of predictive biomarkers of carcass traits and intervention strategies potentially applicable to improving marbling consistency and metabolic efficiency.
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PubMed:
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@article {pmid42600416,
year = {2026},
author = {Lee, H and Haga, S and Roh, S},
title = {Physio-informatics linking rumen biology, systemic metabolism and meat quality in Japanese black cattle.},
journal = {Meat science},
volume = {242},
number = {},
pages = {110130},
doi = {10.1016/j.meatsci.2026.110130},
pmid = {42600416},
issn = {1873-4138},
abstract = {Japanese Black cattle (Wagyu) are raised under a distinctive long-term fattening system designed to enhance intramuscular fat (marbling) and carcass value. Because most metabolizable energy and many metabolic signals in ruminants derive from rumen fermentation products, variation in rumen microbial ecology and fermentation chemistry can extend to systemic metabolism and ultimately influence meat quality traits. Recent work in Japanese Black steers has provided a structured, multi-layered dataset spanning rumen fermentation characteristics, blood metabolites and hormones, liver transcriptome profiles, and rumen microbiome composition and predicted function across fattening stages and metabolic phenotypes. This review integrates these findings with established concepts in ruminant physiology to propose a physio-informatic framework linking rumen microbiota to hepatic metabolic regulation and adipose tissue development via the rumen-liver-adipose axis, with potential relevance to broader meat quality traits. We highlight (i) microbial succession across the three-stage feeding program, (ii) fermentation-derived short-chain fatty acids and their absorption and metabolic fates, and (iii) endocrine and transcriptional regulation of energy partitioning during fattening as an interpretable systems signal rather than a single downstream endpoint. Finally, we discuss potential analytic strategies, including longitudinal modeling, network inference, and machine learning approaches, that may support the future development of predictive biomarkers of carcass traits and intervention strategies potentially applicable to improving marbling consistency and metabolic efficiency.},
}
RevDate: 2026-08-12
Oropharyngeal Microbiome Signatures Associated with Meningococcal Carriage in Healthy Young AdultsRunning title: Oropharyngeal microbiome and meningococcal carriage.
The Journal of infection pii:S0163-4453(26)00156-8 [Epub ahead of print].
BACKGROUND: Neisseria meningitidis (Nm) colonizes the oropharynx of healthy individuals, yet the relationship between the oropharyngeal microbiome and meningococcal carriage remains poorly characterized. We studied the oropharyngeal microbiome in relation to Nm carriage and capsular phenotype in a cohort of healthy young adults.
METHODS: We enrolled 202 Nm carriers (of whom 101 harbored invasive capsular strains (B, C, W, X, Y)) and 202 matched non-carriers for microbiome analysis using 16S rRNA gene amplicon sequencing of oropharyngeal swabs. We compared the microbiome between carriers and non-carriers, carriers of invasive and non-invasive strains, and smokers and non-smokers, using alpha and beta diversity and differential abundance analyses. Isolate genomes were analyzed for the prp locus.
RESULTS: Carriers exhibited significantly higher Simpson diversity (p≤0.01) and distinct community composition (p=0.0002) compared to non-carriers. Differentially abundant taxa included Stomatobaculum, Lachnoanaerobaculum, Granulicatella, and Atopobium (enriched in carriers), and Epsilonbacteraeota and Patescibacteriota (enriched in non-carriers). Among carriers, invasive capsular strain carriers demonstrated significantly higher alpha diversity across all metrics and distinct beta diversity compared to non-capsular carriers. Notably, Campylobacter (Epsilonbacteraeota), Rothia, and Leptotrichia were enriched in capsular carriers, a pattern directionally opposite to that observed in the carrier vs. non-carrier comparison. Whole genome sequencing of Nm isolates revealed that the intact propionate utilization pathway (prp gene cluster) was far more prevalent in invasive capsular (62%) than in non-invasive isolates (10.5%, p<0.0001). Whether a metabolic relationship exists between the Campylobacter-enriched capsular carrier microbiome and propionate-utilizing Nm strains cannot be established from these genus-level data. Differences in diversity between carriers and non-carriers remained after stratification by smoking status.
CONCLUSIONS: Nm carriage was associated with a distinct oropharyngeal microbiome, characterized by community reorganization rather than diversity loss, with divergent profiles between capsular and non-capsular carriers and a notable enrichment of Campylobacter alongside an intact prp locus in invasive capsular strains. Taken together, these findings identify microbial features that may shape meningococcal colonization and warrant longitudinal, species-level investigations to define their mechanistic and translational relevance.
Additional Links: PMID-42586443
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PubMed:
Citation:
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@article {pmid42586443,
year = {2026},
author = {Roif-Kaminsky, D and Grupel, D and Sofer-Sali, N and Motro, Y and Moran-Gilad, J},
title = {Oropharyngeal Microbiome Signatures Associated with Meningococcal Carriage in Healthy Young AdultsRunning title: Oropharyngeal microbiome and meningococcal carriage.},
journal = {The Journal of infection},
volume = {},
number = {},
pages = {106830},
doi = {10.1016/j.jinf.2026.106830},
pmid = {42586443},
issn = {1532-2742},
abstract = {BACKGROUND: Neisseria meningitidis (Nm) colonizes the oropharynx of healthy individuals, yet the relationship between the oropharyngeal microbiome and meningococcal carriage remains poorly characterized. We studied the oropharyngeal microbiome in relation to Nm carriage and capsular phenotype in a cohort of healthy young adults.
METHODS: We enrolled 202 Nm carriers (of whom 101 harbored invasive capsular strains (B, C, W, X, Y)) and 202 matched non-carriers for microbiome analysis using 16S rRNA gene amplicon sequencing of oropharyngeal swabs. We compared the microbiome between carriers and non-carriers, carriers of invasive and non-invasive strains, and smokers and non-smokers, using alpha and beta diversity and differential abundance analyses. Isolate genomes were analyzed for the prp locus.
RESULTS: Carriers exhibited significantly higher Simpson diversity (p≤0.01) and distinct community composition (p=0.0002) compared to non-carriers. Differentially abundant taxa included Stomatobaculum, Lachnoanaerobaculum, Granulicatella, and Atopobium (enriched in carriers), and Epsilonbacteraeota and Patescibacteriota (enriched in non-carriers). Among carriers, invasive capsular strain carriers demonstrated significantly higher alpha diversity across all metrics and distinct beta diversity compared to non-capsular carriers. Notably, Campylobacter (Epsilonbacteraeota), Rothia, and Leptotrichia were enriched in capsular carriers, a pattern directionally opposite to that observed in the carrier vs. non-carrier comparison. Whole genome sequencing of Nm isolates revealed that the intact propionate utilization pathway (prp gene cluster) was far more prevalent in invasive capsular (62%) than in non-invasive isolates (10.5%, p<0.0001). Whether a metabolic relationship exists between the Campylobacter-enriched capsular carrier microbiome and propionate-utilizing Nm strains cannot be established from these genus-level data. Differences in diversity between carriers and non-carriers remained after stratification by smoking status.
CONCLUSIONS: Nm carriage was associated with a distinct oropharyngeal microbiome, characterized by community reorganization rather than diversity loss, with divergent profiles between capsular and non-capsular carriers and a notable enrichment of Campylobacter alongside an intact prp locus in invasive capsular strains. Taken together, these findings identify microbial features that may shape meningococcal colonization and warrant longitudinal, species-level investigations to define their mechanistic and translational relevance.},
}
RevDate: 2026-08-12
Oral and gut microbiota features associated with weight-loss outcomes after metabolic and bariatric surgery: a pilot study.
Clinical nutrition ESPEN pii:S2405-4577(26)02122-4 [Epub ahead of print].
BACKGROUND: Metabolic and bariatric surgery (MBS) is an effective treatment for severe obesity, yet postoperative weight loss outcomes vary considerably between patients. With the relevance of the gut microbiome for obesity, it is of interest to understand the potential role of the oral and gut microbiota for the outcome of MBS. This pilot, hypothesis-generating study aimed to investigate associations between microbiota features and postoperative weight loss outcomes after MBS, assessed by percentage excess weight loss (EWL).
METHODS: In this pilot study, microbiota profiles from multiple body sites were analyzed in 33 patients undergoing MBS. Stool, oral swab, serum, and adipose tissue samples were collected at the time of surgery; stool and oral samples were collected again six months postoperatively. Microbiota diversity and composition were assessed using 16S rRNA gene sequencing and related to EWL and metabolic outcomes. Bacterial DNA in adipose tissue and serum was explored as an indirect marker of microbial translocation.
RESULTS: Higher diversity of the oral microbiota before surgery was associated with greater postoperative EWL. Stool microbiota diversity increased after surgery and was positively associated with EWL, suggesting postoperative recovery of the gut microbiota in patients with better weight loss outcomes. At the taxonomic level, higher postoperative abundance of Alistipes was observed in stool of patients achieving the greatest EWL, while for the oral cavity at time of operation, Veillonella, a bacteria considered largely beneficial in the oral cavity, was found to be positively associated with response. Community-level analyses of bacterial profiles in subcutaneous fat samples taken at time of MBS showed associations with both EWL (R[2] = 0.097, p = 0.006) and BMI (R[2] = 0.055, p = 0.017), whereas no associations were observed for visceral fat or serum. Findings related to individual bacterial taxa and extraintestinal compartments should be interpreted cautiously due to the exploratory nature of the analyses.
CONCLUSIONS: This exploratory pilot study suggests that oral and gut microbiota features may be associated with weight loss outcomes after metabolic and bariatric surgery. Future studies are required for validation in larger, procedure-specific cohorts with adjustment for clinical confounders.
Additional Links: PMID-42586481
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PubMed:
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@article {pmid42586481,
year = {2026},
author = {Alwali, A and Thingholm, LB and Bang, C and Beckmann, JH and Sebens, S and Rühlemann, M and Laudes, M and Schafmayer, C and Franke, A and Philipp, M and von Schönfels, W},
title = {Oral and gut microbiota features associated with weight-loss outcomes after metabolic and bariatric surgery: a pilot study.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {105025},
doi = {10.1016/j.clnesp.2026.105025},
pmid = {42586481},
issn = {2405-4577},
abstract = {BACKGROUND: Metabolic and bariatric surgery (MBS) is an effective treatment for severe obesity, yet postoperative weight loss outcomes vary considerably between patients. With the relevance of the gut microbiome for obesity, it is of interest to understand the potential role of the oral and gut microbiota for the outcome of MBS. This pilot, hypothesis-generating study aimed to investigate associations between microbiota features and postoperative weight loss outcomes after MBS, assessed by percentage excess weight loss (EWL).
METHODS: In this pilot study, microbiota profiles from multiple body sites were analyzed in 33 patients undergoing MBS. Stool, oral swab, serum, and adipose tissue samples were collected at the time of surgery; stool and oral samples were collected again six months postoperatively. Microbiota diversity and composition were assessed using 16S rRNA gene sequencing and related to EWL and metabolic outcomes. Bacterial DNA in adipose tissue and serum was explored as an indirect marker of microbial translocation.
RESULTS: Higher diversity of the oral microbiota before surgery was associated with greater postoperative EWL. Stool microbiota diversity increased after surgery and was positively associated with EWL, suggesting postoperative recovery of the gut microbiota in patients with better weight loss outcomes. At the taxonomic level, higher postoperative abundance of Alistipes was observed in stool of patients achieving the greatest EWL, while for the oral cavity at time of operation, Veillonella, a bacteria considered largely beneficial in the oral cavity, was found to be positively associated with response. Community-level analyses of bacterial profiles in subcutaneous fat samples taken at time of MBS showed associations with both EWL (R[2] = 0.097, p = 0.006) and BMI (R[2] = 0.055, p = 0.017), whereas no associations were observed for visceral fat or serum. Findings related to individual bacterial taxa and extraintestinal compartments should be interpreted cautiously due to the exploratory nature of the analyses.
CONCLUSIONS: This exploratory pilot study suggests that oral and gut microbiota features may be associated with weight loss outcomes after metabolic and bariatric surgery. Future studies are required for validation in larger, procedure-specific cohorts with adjustment for clinical confounders.},
}
RevDate: 2026-08-12
Ozone Hydrotherapy Improves Seborrheic Dermatitis by Regulating Scalp Microbiome and Mitochondrial Lactate Shuttle in Keratinocytes.
The Journal of infectious diseases pii:8759866 [Epub ahead of print].
BACKGROUND: Seborrheic dermatitis (SD) is characterized by limited therapeutic options and high recurrence rates, and the efficacy and mechanism of ozone hydrotherapy for SD remain unclear, especially its potential role in regulating metabolic pathways of keratinocytes.
METHODS: We performed a single-arm, open-label, self-controlled before-and-after study of ozone hydrotherapy in 24 SD patients, evaluating clinical symptoms and analyzing scalp microbiome. A Malassezia-induced guinea pig model of SD-like lesions and a Malassezia-infected HaCaT cell model were used to explore barrier repair, anti-inflammatory effects and the potential involvement of mitochondrial lactate shuttle.
RESULTS: Ozone hydrotherapy significantly alleviated erythema, scaling and pruritus during the 3-week treatment period in SD patients. Treatment was well tolerated with no serious adverse events observed. It decreased the abundance of Malassezia and Staphylococcus, increased skin microbial Shannon diversity, and reshaped the structure of scalp fungal and bacterial communities. In guinea pigs, ozone water upregulated barrier-related genes and suppressed inflammatory cytokines. In HaCaT cells, ozone water restored mitochondrial lactate shuttle function, reversed the abnormal expression and localization of MCT1, MCT4 and LDHB, reduced lactate accumulation and pro-inflammatory factor release.
CONCLUSION: Ozone hydrotherapy may improve SD symptoms by regulating scalp microbial homeostasis, mechanistic studies further suggest that it may alleviate inflammation by reversing Malassezia-induced mitochondrial lactate shuttle abnormalities in keratinocytes. Ozone hydrotherapy represents a promising candidate intervention for SD symptom management, pending validation in controlled clinical trials.
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@article {pmid42586552,
year = {2026},
author = {Xu, S and Lu, J and Wang, D},
title = {Ozone Hydrotherapy Improves Seborrheic Dermatitis by Regulating Scalp Microbiome and Mitochondrial Lactate Shuttle in Keratinocytes.},
journal = {The Journal of infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/infdis/jiag420},
pmid = {42586552},
issn = {1537-6613},
abstract = {BACKGROUND: Seborrheic dermatitis (SD) is characterized by limited therapeutic options and high recurrence rates, and the efficacy and mechanism of ozone hydrotherapy for SD remain unclear, especially its potential role in regulating metabolic pathways of keratinocytes.
METHODS: We performed a single-arm, open-label, self-controlled before-and-after study of ozone hydrotherapy in 24 SD patients, evaluating clinical symptoms and analyzing scalp microbiome. A Malassezia-induced guinea pig model of SD-like lesions and a Malassezia-infected HaCaT cell model were used to explore barrier repair, anti-inflammatory effects and the potential involvement of mitochondrial lactate shuttle.
RESULTS: Ozone hydrotherapy significantly alleviated erythema, scaling and pruritus during the 3-week treatment period in SD patients. Treatment was well tolerated with no serious adverse events observed. It decreased the abundance of Malassezia and Staphylococcus, increased skin microbial Shannon diversity, and reshaped the structure of scalp fungal and bacterial communities. In guinea pigs, ozone water upregulated barrier-related genes and suppressed inflammatory cytokines. In HaCaT cells, ozone water restored mitochondrial lactate shuttle function, reversed the abnormal expression and localization of MCT1, MCT4 and LDHB, reduced lactate accumulation and pro-inflammatory factor release.
CONCLUSION: Ozone hydrotherapy may improve SD symptoms by regulating scalp microbial homeostasis, mechanistic studies further suggest that it may alleviate inflammation by reversing Malassezia-induced mitochondrial lactate shuttle abnormalities in keratinocytes. Ozone hydrotherapy represents a promising candidate intervention for SD symptom management, pending validation in controlled clinical trials.},
}
RevDate: 2026-08-12
Gut-Meningeal Immunity: A Missing Link in Neuroinflammatory Disorders.
Immunology [Epub ahead of print].
Traditionally considered immune-privileged, the central nervous system (CNS) is now recognised as immunologically dynamic, with the meninges serving as a key interface for immune surveillance and neuroimmune communication. Recent advances support the emerging concept of a gut-meningeal immune axis, wherein the gut microbiota may influence meningeal immunity, through the recruitment of gut-educated immune cells and other microbiota-dependent signals, although the mechanisms involved remain incompletely understood. Notably, the neonatal period represents a critical window of immune and microbial development, during which dysbiosis can disrupt microglia maturation, cytokine balance, and long-term neuroimmune resilience. Here, we review the structural and immunological properties of the meninges, the mechanisms potentially linking the gut microbiota to meningeal immunity, and the role of this emerging axis in neuroinflammatory diseases. We further explore the developmental implications of early-life microbial disturbances and discuss the therapeutic potential of microbiota-targeted interventions to modulate meningeal immunity and mitigate CNS pathology.
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@article {pmid42586607,
year = {2026},
author = {Ribeiro, N and Andrade, EB},
title = {Gut-Meningeal Immunity: A Missing Link in Neuroinflammatory Disorders.},
journal = {Immunology},
volume = {},
number = {},
pages = {},
doi = {10.1111/imm.70190},
pmid = {42586607},
issn = {1365-2567},
support = {CEECIND/03675/2018//Fundação para a Ciência e a Tecnologia/ ; 2024.04517.BD//Fundação para a Ciência e a Tecnologia/ ; },
abstract = {Traditionally considered immune-privileged, the central nervous system (CNS) is now recognised as immunologically dynamic, with the meninges serving as a key interface for immune surveillance and neuroimmune communication. Recent advances support the emerging concept of a gut-meningeal immune axis, wherein the gut microbiota may influence meningeal immunity, through the recruitment of gut-educated immune cells and other microbiota-dependent signals, although the mechanisms involved remain incompletely understood. Notably, the neonatal period represents a critical window of immune and microbial development, during which dysbiosis can disrupt microglia maturation, cytokine balance, and long-term neuroimmune resilience. Here, we review the structural and immunological properties of the meninges, the mechanisms potentially linking the gut microbiota to meningeal immunity, and the role of this emerging axis in neuroinflammatory diseases. We further explore the developmental implications of early-life microbial disturbances and discuss the therapeutic potential of microbiota-targeted interventions to modulate meningeal immunity and mitigate CNS pathology.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Natural polysaccharides modulate the microbiota-gut-brain axis through multiple targets: A new perspective on the pathogenesis and treatment of depression.
Carbohydrate polymers, 389:125640.
Depression is increasingly understood as a systemic disorder involving microbiota-gut-brain axis (MGBA) dysfunction rather than only central monoaminergic imbalance. Gut microbial dysbiosis, barrier disruption, immune inflammation, metabolic disturbance, oxidative stress, mitochondrial injury, and impaired neuroplasticity jointly drive depressive pathology. Natural polysaccharides offer a structurally diverse class of MGBA-oriented adjunctive candidates. Their effects are governed not simply by source or total sugar content, but by monosaccharide composition, glycosidic linkages, branching architecture, and molecular-weight distribution. These features determine microbial accessibility, fermentation kinetics, metabolite output, mucus and epithelial interactions, receptor recognition, and possible epithelial uptake, thereby defining distinct routes of MGBA regulation. Through these structure-dependent routes, natural polysaccharides may alleviate depression-related abnormalities by rebuilding gut microbial ecology, reprogramming short-chain fatty acids, tryptophan-derived indoles and bile acid metabolism, restoring intestinal and blood-brain barrier integrity, suppressing neuroimmune activation and oxidative injury, supporting mitochondrial homeostasis and promoting BDNF-TrkB-related neurogenesis and synaptic plasticity. This Review highlights structure-guided MGBA modulation and discusses translational challenges, including activity attribution, quality control, pharmacokinetics, and microbiome-dependent response variability for stratified, mechanism-guided adjunctive use.
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@article {pmid42586669,
year = {2026},
author = {Luo, Z and Fang, Y and Qi, H and Peng, X and Zang, X and Yi, L and Zeng, J and He, L and Zeng, N},
title = {Natural polysaccharides modulate the microbiota-gut-brain axis through multiple targets: A new perspective on the pathogenesis and treatment of depression.},
journal = {Carbohydrate polymers},
volume = {389},
number = {},
pages = {125640},
doi = {10.1016/j.carbpol.2026.125640},
pmid = {42586669},
issn = {1879-1344},
mesh = {Humans ; Animals ; *Polysaccharides/pharmacology/chemistry/therapeutic use ; *Depression/drug therapy/metabolism/microbiology ; *Gastrointestinal Microbiome/drug effects ; *Brain/drug effects/metabolism ; Blood-Brain Barrier/drug effects/metabolism ; },
abstract = {Depression is increasingly understood as a systemic disorder involving microbiota-gut-brain axis (MGBA) dysfunction rather than only central monoaminergic imbalance. Gut microbial dysbiosis, barrier disruption, immune inflammation, metabolic disturbance, oxidative stress, mitochondrial injury, and impaired neuroplasticity jointly drive depressive pathology. Natural polysaccharides offer a structurally diverse class of MGBA-oriented adjunctive candidates. Their effects are governed not simply by source or total sugar content, but by monosaccharide composition, glycosidic linkages, branching architecture, and molecular-weight distribution. These features determine microbial accessibility, fermentation kinetics, metabolite output, mucus and epithelial interactions, receptor recognition, and possible epithelial uptake, thereby defining distinct routes of MGBA regulation. Through these structure-dependent routes, natural polysaccharides may alleviate depression-related abnormalities by rebuilding gut microbial ecology, reprogramming short-chain fatty acids, tryptophan-derived indoles and bile acid metabolism, restoring intestinal and blood-brain barrier integrity, suppressing neuroimmune activation and oxidative injury, supporting mitochondrial homeostasis and promoting BDNF-TrkB-related neurogenesis and synaptic plasticity. This Review highlights structure-guided MGBA modulation and discusses translational challenges, including activity attribution, quality control, pharmacokinetics, and microbiome-dependent response variability for stratified, mechanism-guided adjunctive use.},
}
MeSH Terms:
show MeSH Terms
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Humans
Animals
*Polysaccharides/pharmacology/chemistry/therapeutic use
*Depression/drug therapy/metabolism/microbiology
*Gastrointestinal Microbiome/drug effects
*Brain/drug effects/metabolism
Blood-Brain Barrier/drug effects/metabolism
RevDate: 2026-08-12
CmpDate: 2026-08-12
Encapsulated faecal microbiota transfer to target immune activation in patients with cirrhosis and ascites (TransImmune): protocol for a randomised, double-blind, Phase IIa, placebo-controlled trial.
BMJ open, 16(8):e119299 pii:bmjopen-2026-119299.
INTRODUCTION: Bacterial translocation and gut dysbiosis are key drivers of systemic immune activation in decompensated cirrhosis, precipitating inflammatory complications such as acute-on-chronic liver failure (ACLF). Currently, no licensed therapies effectively restore intestinal barrier function or reverse dysbiosis in this vulnerable population. While previous studies have suggested benefits of faecal microbiota transfer (FMT) in hepatic encephalopathy or alcohol-associated hepatitis, data on its safety and immunomodulatory effects in decompensated cirrhosis with ascites are lacking. This Phase IIa trial (TransImmune) aims to evaluate the safety and tolerability of encapsulated FMT. Furthermore, it will assess feasibility, microbial engraftment and downstream effects on intestinal barrier integrity, as well as systemic and peritoneal inflammation.
METHODS AND ANALYSIS: This is a prospective, single-centre, randomised, double-blind, placebo-controlled Phase IIa pilot study. A total of 24 patients with decompensated cirrhosis and ascites will be randomised in a 1:1 ratio to receive either encapsulated FMT or placebo over three consecutive days. The investigational product, INTESTIFIX 001, is an encapsulated FMT preparation derived from rigorously screened healthy donors and manufactured under Good Manufacturing Practice (GMP) conditions with predefined release specifications, including minimum alpha-diversity QC criteria, manufactured by the Cologne Microbiota Bank (CMB). The primary endpoints are the occurrence of serious adverse events (SAE) up to the end of study (EOS) and the occurrence and severity of treatment-emergent adverse events (TEAE). Secondary endpoints evaluate signals of clinical efficacy, specifically: (1) systemic inflammation (white blood cell count, C-reactive protein, procalcitonin and IL-6); (2) gut inflammation (faecal calprotectin); (3) organ dysfunction (Child-Pugh, MELD and CLIF-SOFA scores); (4) quality of life (EQ-5D-5L and CLDQ) and (5) the number of antibiotic-free days. Patients will be monitored across five study visits up to 90 days.
ETHICS AND DISSEMINATION: The study was approved by ethics committee review and the German Federal Institute for Drugs and Medical Devices (BfArM). The trial is registered under EU CT no. 2023-5 07 790-18-00. The results of the study will be disseminated via peer-reviewed publications and at international conferences.
TRIAL REGISTRATION NUMBER: EU Clinical Trials Register: 2023-507790-18-00. Registered on 8 August 2024.
Additional Links: PMID-42586732
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PubMed:
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@article {pmid42586732,
year = {2026},
author = {Große, K and Haedge, F and Fera, C and Hecker, J and Wienstroer, J and Tsakmaklis, A and Fichtner, A and Treichel, NS and Clavel, T and Wirtz, TH and Pabst, O and Schuckelt, R and Vehreschild, MJ and Bruns, T},
title = {Encapsulated faecal microbiota transfer to target immune activation in patients with cirrhosis and ascites (TransImmune): protocol for a randomised, double-blind, Phase IIa, placebo-controlled trial.},
journal = {BMJ open},
volume = {16},
number = {8},
pages = {e119299},
doi = {10.1136/bmjopen-2026-119299},
pmid = {42586732},
issn = {2044-6055},
mesh = {Humans ; Double-Blind Method ; *Liver Cirrhosis/therapy/immunology/complications ; *Fecal Microbiota Transplantation/methods ; *Ascites/therapy/immunology ; Clinical Trials, Phase II as Topic ; Randomized Controlled Trials as Topic ; Prospective Studies ; Pilot Projects ; *Dysbiosis/therapy ; },
abstract = {INTRODUCTION: Bacterial translocation and gut dysbiosis are key drivers of systemic immune activation in decompensated cirrhosis, precipitating inflammatory complications such as acute-on-chronic liver failure (ACLF). Currently, no licensed therapies effectively restore intestinal barrier function or reverse dysbiosis in this vulnerable population. While previous studies have suggested benefits of faecal microbiota transfer (FMT) in hepatic encephalopathy or alcohol-associated hepatitis, data on its safety and immunomodulatory effects in decompensated cirrhosis with ascites are lacking. This Phase IIa trial (TransImmune) aims to evaluate the safety and tolerability of encapsulated FMT. Furthermore, it will assess feasibility, microbial engraftment and downstream effects on intestinal barrier integrity, as well as systemic and peritoneal inflammation.
METHODS AND ANALYSIS: This is a prospective, single-centre, randomised, double-blind, placebo-controlled Phase IIa pilot study. A total of 24 patients with decompensated cirrhosis and ascites will be randomised in a 1:1 ratio to receive either encapsulated FMT or placebo over three consecutive days. The investigational product, INTESTIFIX 001, is an encapsulated FMT preparation derived from rigorously screened healthy donors and manufactured under Good Manufacturing Practice (GMP) conditions with predefined release specifications, including minimum alpha-diversity QC criteria, manufactured by the Cologne Microbiota Bank (CMB). The primary endpoints are the occurrence of serious adverse events (SAE) up to the end of study (EOS) and the occurrence and severity of treatment-emergent adverse events (TEAE). Secondary endpoints evaluate signals of clinical efficacy, specifically: (1) systemic inflammation (white blood cell count, C-reactive protein, procalcitonin and IL-6); (2) gut inflammation (faecal calprotectin); (3) organ dysfunction (Child-Pugh, MELD and CLIF-SOFA scores); (4) quality of life (EQ-5D-5L and CLDQ) and (5) the number of antibiotic-free days. Patients will be monitored across five study visits up to 90 days.
ETHICS AND DISSEMINATION: The study was approved by ethics committee review and the German Federal Institute for Drugs and Medical Devices (BfArM). The trial is registered under EU CT no. 2023-5 07 790-18-00. The results of the study will be disseminated via peer-reviewed publications and at international conferences.
TRIAL REGISTRATION NUMBER: EU Clinical Trials Register: 2023-507790-18-00. Registered on 8 August 2024.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Double-Blind Method
*Liver Cirrhosis/therapy/immunology/complications
*Fecal Microbiota Transplantation/methods
*Ascites/therapy/immunology
Clinical Trials, Phase II as Topic
Randomized Controlled Trials as Topic
Prospective Studies
Pilot Projects
*Dysbiosis/therapy
RevDate: 2026-08-12
CmpDate: 2026-08-12
Soil Microbiome Predator Diversity Outperforms Nitrogen Addition in Boosting Plant Biomass via Bacterial Community Shifts.
Global change biology, 32(8):e71019.
Nitrogen (N) is crucial for plant growth, but its overuse harms biodiversity. Increasing soil biodiversity might provide the means to reduce N inputs, but experimental evidence for this paradigm shift is limited. Using microbiome predators (protists and nematodes) that shape microbiome composition and participate in N cycling, we examined how interactions between their diversity and N addition affect Cannabis sativa growth. The addition of microbiome predators increased plant biomass by up to 53%, irrespective of diversity level, with effects reaching up to 60% under higher microbiome predator diversity. This biomass increase was primarily associated with changes in bacterial community composition and enriching functions related to carbon and N cycling. In contrast, N input played a greater role in determining plant and soil nutrient content. These findings suggest that microbiome predators determine plant biomass in a diversity and N-specific manner, showing the pivotal role of soil biodiversity in enhancing plant performance and serving as promising tools to mitigate N inputs.
Additional Links: PMID-42586775
PubMed:
Citation:
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@article {pmid42586775,
year = {2026},
author = {Berlinches de Gea, A and Both, J and Haas, N and Wilschut, RA and Wichern, F and Geisen, S},
title = {Soil Microbiome Predator Diversity Outperforms Nitrogen Addition in Boosting Plant Biomass via Bacterial Community Shifts.},
journal = {Global change biology},
volume = {32},
number = {8},
pages = {e71019},
pmid = {42586775},
issn = {1365-2486},
mesh = {*Soil Microbiology ; *Nitrogen/metabolism ; Animals ; *Microbiota ; Biomass ; *Nematoda/physiology ; Biodiversity ; Soil/chemistry ; Bacteria ; },
abstract = {Nitrogen (N) is crucial for plant growth, but its overuse harms biodiversity. Increasing soil biodiversity might provide the means to reduce N inputs, but experimental evidence for this paradigm shift is limited. Using microbiome predators (protists and nematodes) that shape microbiome composition and participate in N cycling, we examined how interactions between their diversity and N addition affect Cannabis sativa growth. The addition of microbiome predators increased plant biomass by up to 53%, irrespective of diversity level, with effects reaching up to 60% under higher microbiome predator diversity. This biomass increase was primarily associated with changes in bacterial community composition and enriching functions related to carbon and N cycling. In contrast, N input played a greater role in determining plant and soil nutrient content. These findings suggest that microbiome predators determine plant biomass in a diversity and N-specific manner, showing the pivotal role of soil biodiversity in enhancing plant performance and serving as promising tools to mitigate N inputs.},
}
MeSH Terms:
show MeSH Terms
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*Soil Microbiology
*Nitrogen/metabolism
Animals
*Microbiota
Biomass
*Nematoda/physiology
Biodiversity
Soil/chemistry
Bacteria
RevDate: 2026-08-12
The role of pharmacomicrobiomics in colorectal cancer therapy.
Trends in molecular medicine pii:S1471-4914(26)00176-0 [Epub ahead of print].
Interindividual variability in response to cancer therapy is a major challenge in the management of colorectal cancer (CRC). The gut microbiome contributes to differential therapeutic efficacy and toxicity by modifying the pharmacokinetics and pharmacodynamics of anticancer drugs. Furthermore, bacterial products interact with tumor and immune cells, altering therapeutic outcomes. This review focuses on the impact of pharmacomicrobiomics on CRC therapy. We describe how gut microbiota affects drug metabolism on a mechanistic level and outline the interactions of specific microbes and their products with chemo-, targeted, and immunotherapies employed in CRC. Finally, we provide an overview of current strategies, including probiotics, engineered bacteria, and fecal microbiota transplantation, that exploit the gut microbiome to improve therapeutic efficacy and reduce toxicity.
Additional Links: PMID-42586870
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PubMed:
Citation:
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@article {pmid42586870,
year = {2026},
author = {Feng, X and Pora, M and Ebert, M and Zimmermann, M and Zhan, T},
title = {The role of pharmacomicrobiomics in colorectal cancer therapy.},
journal = {Trends in molecular medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.molmed.2026.07.006},
pmid = {42586870},
issn = {1471-499X},
abstract = {Interindividual variability in response to cancer therapy is a major challenge in the management of colorectal cancer (CRC). The gut microbiome contributes to differential therapeutic efficacy and toxicity by modifying the pharmacokinetics and pharmacodynamics of anticancer drugs. Furthermore, bacterial products interact with tumor and immune cells, altering therapeutic outcomes. This review focuses on the impact of pharmacomicrobiomics on CRC therapy. We describe how gut microbiota affects drug metabolism on a mechanistic level and outline the interactions of specific microbes and their products with chemo-, targeted, and immunotherapies employed in CRC. Finally, we provide an overview of current strategies, including probiotics, engineered bacteria, and fecal microbiota transplantation, that exploit the gut microbiome to improve therapeutic efficacy and reduce toxicity.},
}
RevDate: 2026-08-12
Intratumoral microbiota in pancreatic neuroendocrine tumors: Enriched bacterial biomass and diversity with association to dyslipidemia.
Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] pii:S1424-3903(26)00874-4 [Epub ahead of print].
BACKGROUND: Intratumoral microbiota have been implicated in several cancers, including pancreatic cancer, but data on pancreatic neuroendocrine tumors (PNETs) remain limited.
METHODS: We analyzed two complementary cohorts: a retrospective formalin-fixed paraffin-embedded cohort comprising 53 primary PNETs, 26 paired adjacent non-tumor tissues (ANTs), and 5 liver metastases assessed by fluorescence in situ hybridization (FISH); and a prospective subset of 25 paired fresh tumor-center and ANT samples analyzed by 16S rRNA gene sequencing. Taxonomic composition, alpha and beta diversity, differential abundance, predicted microbial functions, and associations with clinicopathological features and fasting serum lipids were evaluated.
RESULTS: PNETs showed a higher frequency of detectable bacterial signals and greater microbial richness and diversity than ANTs. LEfSe identified 38 nominally differentially abundant taxa (P < 0.05; LDA > 2.5), including enrichment of Blautia, Rothia, and Ferrovibrio in tumors. Their combined abundance differentiated PNETs from ANTs with an area under the curve of 0.843. Exploratory functional inference suggested enrichment of 15 pathways in PNETs, including fatty acid and short-chain fatty acid biosynthesis pathways. Serum high-density lipoprotein levels were inversely associated with intratumoral microbial richness (Ace index: r = -0.497, P = 0.049).
CONCLUSIONS: PNETs exhibited greater bacterial burden, microbial richness, and diversity than ANTs, with distinct taxonomic patterns and lipid-related associations. These exploratory findings warrant external validation in larger cohorts with rigorous low-biomass contamination control.
Additional Links: PMID-42586877
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PubMed:
Citation:
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@article {pmid42586877,
year = {2026},
author = {Meng, YF and Liu, LY and Fan, ZY and Zhan, HX},
title = {Intratumoral microbiota in pancreatic neuroendocrine tumors: Enriched bacterial biomass and diversity with association to dyslipidemia.},
journal = {Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.pan.2026.08.004},
pmid = {42586877},
issn = {1424-3911},
abstract = {BACKGROUND: Intratumoral microbiota have been implicated in several cancers, including pancreatic cancer, but data on pancreatic neuroendocrine tumors (PNETs) remain limited.
METHODS: We analyzed two complementary cohorts: a retrospective formalin-fixed paraffin-embedded cohort comprising 53 primary PNETs, 26 paired adjacent non-tumor tissues (ANTs), and 5 liver metastases assessed by fluorescence in situ hybridization (FISH); and a prospective subset of 25 paired fresh tumor-center and ANT samples analyzed by 16S rRNA gene sequencing. Taxonomic composition, alpha and beta diversity, differential abundance, predicted microbial functions, and associations with clinicopathological features and fasting serum lipids were evaluated.
RESULTS: PNETs showed a higher frequency of detectable bacterial signals and greater microbial richness and diversity than ANTs. LEfSe identified 38 nominally differentially abundant taxa (P < 0.05; LDA > 2.5), including enrichment of Blautia, Rothia, and Ferrovibrio in tumors. Their combined abundance differentiated PNETs from ANTs with an area under the curve of 0.843. Exploratory functional inference suggested enrichment of 15 pathways in PNETs, including fatty acid and short-chain fatty acid biosynthesis pathways. Serum high-density lipoprotein levels were inversely associated with intratumoral microbial richness (Ace index: r = -0.497, P = 0.049).
CONCLUSIONS: PNETs exhibited greater bacterial burden, microbial richness, and diversity than ANTs, with distinct taxonomic patterns and lipid-related associations. These exploratory findings warrant external validation in larger cohorts with rigorous low-biomass contamination control.},
}
RevDate: 2026-08-12
Safety, tolerability, and gastrointestinal effect of a Bifidobacterium-based synergistic synbiotic in infants and toddlers.
Pediatric research [Epub ahead of print].
BACKGROUND: Bifidobacterium are critical components of the infant gut microbiome, yet most infants in developed countries are deficient.
METHODS: The ARTEMIS trial is the first clinical study in the United States to evaluate a synergistic synbiotic supplement in infants. It enrolled 114 participants in a randomized, double-blind, placebo-controlled study conducted to evaluate the safety, tolerability, and gastrointestinal colonization of the supplement in infants (n = 58) and toddlers (n = 56). The synbiotic contains four proprietary strains of Bifidobacterium, four complementary human milk oligosaccharides and vitamin D.
RESULTS: Safety and tolerability were assessed, with no statistically significant differences in adverse events or gastrointestinal symptom burden relative to placebo. The administered Bifidobacterium strains were significantly more prevalent and abundant in the synbiotic group. After four weeks of dosing, at least one administered strain was detected in 72% of infants (2-12 months) and 67% of toddlers (12-24 months). Synbiotic supplementation was associated with a significant increase in Bifidobacterium infantis abundance at the species level and human milk oligosaccharide utilization genes. Strains persisted through the two-week washout period, supporting intestinal colonization beyond active supplementation unlike other transient probiotics like Lactobacillus.
CONCLUSIONS: This synbiotic was safe, well tolerated, and achieved sustained Bifidobacterium colonization in infants and toddlers.
IMPACT: The ARTEMIS trial is the first U.S. clinical study to evaluate a synergistic synbiotic in infants combining multiple Bifidobacterium strains with human milk oligosaccharides (HMOs). Safety and tolerability were evaluated in infants and toddlers, with no statistically significant differences in adverse events or gastrointestinal tolerance compared with placebo. Infants and toddlers receiving the synbiotic showed significantly greater prevalence and abundance of the administered strains, demonstrating successful gut colonization and shifts in overall Bifidobacterium populations, along with increased abundance of HMO-utilization genes. In toddlers, synbiotic supplementation was associated with a significant improvement in sleep relative to placebo.
Additional Links: PMID-42587033
PubMed:
Citation:
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@article {pmid42587033,
year = {2026},
author = {Jarman, JB and Torres, PJ and Baum, C and Tinoco, J and Sato, H and Rasteiro, CS and Selbrede, R and Insel, R and Culler, SJ and Van Dien, S},
title = {Safety, tolerability, and gastrointestinal effect of a Bifidobacterium-based synergistic synbiotic in infants and toddlers.},
journal = {Pediatric research},
volume = {},
number = {},
pages = {},
pmid = {42587033},
issn = {1530-0447},
abstract = {BACKGROUND: Bifidobacterium are critical components of the infant gut microbiome, yet most infants in developed countries are deficient.
METHODS: The ARTEMIS trial is the first clinical study in the United States to evaluate a synergistic synbiotic supplement in infants. It enrolled 114 participants in a randomized, double-blind, placebo-controlled study conducted to evaluate the safety, tolerability, and gastrointestinal colonization of the supplement in infants (n = 58) and toddlers (n = 56). The synbiotic contains four proprietary strains of Bifidobacterium, four complementary human milk oligosaccharides and vitamin D.
RESULTS: Safety and tolerability were assessed, with no statistically significant differences in adverse events or gastrointestinal symptom burden relative to placebo. The administered Bifidobacterium strains were significantly more prevalent and abundant in the synbiotic group. After four weeks of dosing, at least one administered strain was detected in 72% of infants (2-12 months) and 67% of toddlers (12-24 months). Synbiotic supplementation was associated with a significant increase in Bifidobacterium infantis abundance at the species level and human milk oligosaccharide utilization genes. Strains persisted through the two-week washout period, supporting intestinal colonization beyond active supplementation unlike other transient probiotics like Lactobacillus.
CONCLUSIONS: This synbiotic was safe, well tolerated, and achieved sustained Bifidobacterium colonization in infants and toddlers.
IMPACT: The ARTEMIS trial is the first U.S. clinical study to evaluate a synergistic synbiotic in infants combining multiple Bifidobacterium strains with human milk oligosaccharides (HMOs). Safety and tolerability were evaluated in infants and toddlers, with no statistically significant differences in adverse events or gastrointestinal tolerance compared with placebo. Infants and toddlers receiving the synbiotic showed significantly greater prevalence and abundance of the administered strains, demonstrating successful gut colonization and shifts in overall Bifidobacterium populations, along with increased abundance of HMO-utilization genes. In toddlers, synbiotic supplementation was associated with a significant improvement in sleep relative to placebo.},
}
RevDate: 2026-08-12
Maternal influences on infant gut microbiome and health.
Nature [Epub ahead of print].
The establishment of the infant gut microbiome is critical for later health[1,2], yet how it is shaped by maternal and early-life factors remains unclear. Here we metagenomically sequenced 4,526 longitudinal faecal samples from 714 mother-infant pairs in the Dutch birth cohort Lifelines NEXT, spanning 12 weeks of pregnancy to 1 year postpartum. We integrated these data with 474 clinical and exposure variables, and with ultra-deep sequencing of breast milk and vaginal microbiomes. We observe that the maternal gut microbiome undergoes only subtle changes during pregnancy and postpartum, influenced by diet, infections and pre-pregnancy smoking. The maternal gut microbiome is a major reservoir for infant gut strains, with only occasional transmission from vaginal and breast milk microbiomes. Mother-infant gut strain sharing is time dependent, and higher maternal gut species abundance increases the likelihood of strain transmission. We find that the maternal gut microbiome is a predictor of infant eczema. Mode of delivery and feeding mode primarily shaped the infant gut microbiome and its functional profiles, with maternal exposures also having a role. Of 585 vaginally delivered infants, 155 were born at home, but home delivery was only moderately associated with infant gut microbiome composition, similar to other birth parameters such as duration of pushing and ruptured membranes. Overall, we highlight the central role of the mother and her microbiome in shaping the infant gut ecosystem and early health outcomes.
Additional Links: PMID-42587158
PubMed:
Citation:
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@article {pmid42587158,
year = {2026},
author = {Sinha, T and Brushett, S and Fernández-Pato, A and Garmaeva, S and Andreu-Sánchez, S and Spreckels, JE and Mallon, CA and Kuzub, N and Gois, MB and Wu, J and Kruk, M and Jankipersadsing, SA and Dekens, JAM and Gacesa, R and Vila, AV and Bang, C and Perenboom, C and Franke, A and Tytgat, HLP and Mottaz, SC and Peters, L and de Jonge, A and Verkade, HJ and Swertz, MA and Wijmenga, C and Kuipers, F and Scherjon, S and Sikkema, J and Sprikkelman, AB and de Kroon, MLA and Prins, JR and Gordijn, SJ and Koppelman, GH and Reijneveld, SA and , and Fu, J and Yassour, M and Kurilshikov, A and Zhernakova, A},
title = {Maternal influences on infant gut microbiome and health.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {42587158},
issn = {1476-4687},
abstract = {The establishment of the infant gut microbiome is critical for later health[1,2], yet how it is shaped by maternal and early-life factors remains unclear. Here we metagenomically sequenced 4,526 longitudinal faecal samples from 714 mother-infant pairs in the Dutch birth cohort Lifelines NEXT, spanning 12 weeks of pregnancy to 1 year postpartum. We integrated these data with 474 clinical and exposure variables, and with ultra-deep sequencing of breast milk and vaginal microbiomes. We observe that the maternal gut microbiome undergoes only subtle changes during pregnancy and postpartum, influenced by diet, infections and pre-pregnancy smoking. The maternal gut microbiome is a major reservoir for infant gut strains, with only occasional transmission from vaginal and breast milk microbiomes. Mother-infant gut strain sharing is time dependent, and higher maternal gut species abundance increases the likelihood of strain transmission. We find that the maternal gut microbiome is a predictor of infant eczema. Mode of delivery and feeding mode primarily shaped the infant gut microbiome and its functional profiles, with maternal exposures also having a role. Of 585 vaginally delivered infants, 155 were born at home, but home delivery was only moderately associated with infant gut microbiome composition, similar to other birth parameters such as duration of pushing and ruptured membranes. Overall, we highlight the central role of the mother and her microbiome in shaping the infant gut ecosystem and early health outcomes.},
}
RevDate: 2026-08-13
CmpDate: 2026-08-13
Universal-Bac[3]Gel: A 3D Biofilm-Relevant Matrix That Supports In Vitro Growth and Biofilm Formation of ESKAPE Pathogens.
MicrobiologyOpen, 15(4):e70371.
Human microbiota is increasingly considered to shape health and disease, drawing interest of pharma and biotech industries in advanced models of in vitro human microbiome to streamline drug development. In this context, Universal-Bac[3]Gel represents a new generation of 3D biomaterials designed to mimic the properties of human mucus and biofilm features, including micro-gradients that replicate the heterogeneous environments colonized by microorganisms in the human body. To evaluate the suitability of Universal-Bac[3]Gel for studying clinically relevant species in antimicrobial resistance, the so-called ESKAPE pathogens (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter cloacae) were cultured within this 3D environment. Bacterial growth was monitored at 24- and 48-h post-inoculation via spot plating, while viability, spatial distribution, and organization were assessed by confocal laser scanning microscopy. All ESKAPE strains successfully grew throughout the structure of Universal-Bac[3]Gel. Distinct 3D biofilm architectures were observed across species, ranging from diffuse colonization to compact microcolony formation, in agreement with species-specific biofilm patterns. Ciprofloxacin susceptibility assays revealed reduced susceptibility of bacteria cultured within Universal-Bac[3]Gel compared with their planktonic counterparts, supporting the development of biofilm-associated tolerance phenotypes. Consistent with these findings, crystal violet staining confirmed the accumulation of biofilm-associated biomass within the hydrogel. Notably, the platform's ready-to-use 96-well format allowed direct comparison of these high-priority pathogens under standardized conditions, highlighting species-specific biofilm traits that would be difficult to discern in conventional two-dimensional culture systems. This work highlights the versatility of Universal-Bac[3]Gel as a biofilm-relevant in vitro platform for studying pathogen colonization, biofilm development and antimicrobial susceptibility under controlled conditions.
Additional Links: PMID-42587415
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PubMed:
Citation:
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@article {pmid42587415,
year = {2026},
author = {Peluso, E and van Uden, S and Visentin, S and Petrini, P and Pacheco, DP and Visai, L},
title = {Universal-Bac[3]Gel: A 3D Biofilm-Relevant Matrix That Supports In Vitro Growth and Biofilm Formation of ESKAPE Pathogens.},
journal = {MicrobiologyOpen},
volume = {15},
number = {4},
pages = {e70371},
doi = {10.1002/mbo3.70371},
pmid = {42587415},
issn = {2045-8827},
support = {190135075//HORIZON-EIC-2023-ACCELERATOROPEN-01/ ; //Italian Ministry of University and Research (MUR)/ ; },
mesh = {*Biofilms/growth & development/drug effects ; Humans ; Anti-Bacterial Agents/pharmacology ; Microscopy, Confocal ; Staphylococcus aureus/growth & development/drug effects ; },
abstract = {Human microbiota is increasingly considered to shape health and disease, drawing interest of pharma and biotech industries in advanced models of in vitro human microbiome to streamline drug development. In this context, Universal-Bac[3]Gel represents a new generation of 3D biomaterials designed to mimic the properties of human mucus and biofilm features, including micro-gradients that replicate the heterogeneous environments colonized by microorganisms in the human body. To evaluate the suitability of Universal-Bac[3]Gel for studying clinically relevant species in antimicrobial resistance, the so-called ESKAPE pathogens (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter cloacae) were cultured within this 3D environment. Bacterial growth was monitored at 24- and 48-h post-inoculation via spot plating, while viability, spatial distribution, and organization were assessed by confocal laser scanning microscopy. All ESKAPE strains successfully grew throughout the structure of Universal-Bac[3]Gel. Distinct 3D biofilm architectures were observed across species, ranging from diffuse colonization to compact microcolony formation, in agreement with species-specific biofilm patterns. Ciprofloxacin susceptibility assays revealed reduced susceptibility of bacteria cultured within Universal-Bac[3]Gel compared with their planktonic counterparts, supporting the development of biofilm-associated tolerance phenotypes. Consistent with these findings, crystal violet staining confirmed the accumulation of biofilm-associated biomass within the hydrogel. Notably, the platform's ready-to-use 96-well format allowed direct comparison of these high-priority pathogens under standardized conditions, highlighting species-specific biofilm traits that would be difficult to discern in conventional two-dimensional culture systems. This work highlights the versatility of Universal-Bac[3]Gel as a biofilm-relevant in vitro platform for studying pathogen colonization, biofilm development and antimicrobial susceptibility under controlled conditions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Biofilms/growth & development/drug effects
Humans
Anti-Bacterial Agents/pharmacology
Microscopy, Confocal
Staphylococcus aureus/growth & development/drug effects
RevDate: 2026-08-13
CmpDate: 2026-08-13
Exploiting Bacterial Metabolism for Targeted Antimicrobial Release from Smart Nanocarriers.
ACS applied materials & interfaces, 18(31):42261-42272.
Acidogenic and aciduric bacteria acidify their local microenvironment through carbohydrate metabolism, contributing to pathological microenvironment acidification in diseases, including dental caries, infection, and inflammation. We present a mesoporous silica nanoparticle platform equipped with surface-bound, pH-responsive gatekeepers that remain sealed at physiological pH yet rapidly release a drug payload under acidic conditions. This system converts a broad-spectrum antimicrobial into a selectively activated antimicrobial system: release is suppressed under neutral conditions and triggered when bacteria generate acid. In a human oral microbiome model, the nanoparticles selectively eradicate acid-producing bacteria, with metabolic acidification directly activating their own killing, as evidenced by simultaneous single-cell-scale fluorescence imaging of pH and viability. Mechanistic studies using proton NMR and contact angle measurements show that the gating mechanism relies on synergistic molecular interactions and hydrophilicity-hydrophobicity transitions. This work establishes an on-site antimicrobial strategy triggered by metabolic acidification for targeting microbes with undesirable metabolic features, thus paving the way toward more controlled infection therapies.
Additional Links: PMID-42587528
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PubMed:
Citation:
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@article {pmid42587528,
year = {2026},
author = {Liu, J and Elias, J and Wang, X and Tian, J and Dong, PT and Cao, H and Cen, L and Zahedul Islam Nizami, M and He, X and Sun, J},
title = {Exploiting Bacterial Metabolism for Targeted Antimicrobial Release from Smart Nanocarriers.},
journal = {ACS applied materials & interfaces},
volume = {18},
number = {31},
pages = {42261-42272},
doi = {10.1021/acsami.6c05401},
pmid = {42587528},
issn = {1944-8252},
support = {1S10OD034405-01/DE/NIDCR NIH HHS/United States ; R01DE029479/DE/NIDCR NIH HHS/United States ; R01DE029479S/DE/NIDCR NIH HHS/United States ; },
mesh = {*Nanoparticles/chemistry ; Silicon Dioxide/chemistry ; Humans ; *Anti-Bacterial Agents/pharmacology/chemistry ; Hydrogen-Ion Concentration ; *Drug Carriers/chemistry ; *Bacteria/metabolism/drug effects ; Porosity ; },
abstract = {Acidogenic and aciduric bacteria acidify their local microenvironment through carbohydrate metabolism, contributing to pathological microenvironment acidification in diseases, including dental caries, infection, and inflammation. We present a mesoporous silica nanoparticle platform equipped with surface-bound, pH-responsive gatekeepers that remain sealed at physiological pH yet rapidly release a drug payload under acidic conditions. This system converts a broad-spectrum antimicrobial into a selectively activated antimicrobial system: release is suppressed under neutral conditions and triggered when bacteria generate acid. In a human oral microbiome model, the nanoparticles selectively eradicate acid-producing bacteria, with metabolic acidification directly activating their own killing, as evidenced by simultaneous single-cell-scale fluorescence imaging of pH and viability. Mechanistic studies using proton NMR and contact angle measurements show that the gating mechanism relies on synergistic molecular interactions and hydrophilicity-hydrophobicity transitions. This work establishes an on-site antimicrobial strategy triggered by metabolic acidification for targeting microbes with undesirable metabolic features, thus paving the way toward more controlled infection therapies.},
}
MeSH Terms:
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*Nanoparticles/chemistry
Silicon Dioxide/chemistry
Humans
*Anti-Bacterial Agents/pharmacology/chemistry
Hydrogen-Ion Concentration
*Drug Carriers/chemistry
*Bacteria/metabolism/drug effects
Porosity
RevDate: 2026-08-13
CmpDate: 2026-08-13
Iron Homeostasis and Reproduction: Unveiling the Microbiome-Gut-Brain Axis Connection in the Mosquito Anopheles culicifacies.
Cells, 15(15): pii:cells15151315.
Our study investigated how adult female Anopheles culicifacies mosquitoes regulate systemic iron homeostasis after blood feeding, a process essential for reproduction, and revealed striking parallels to iron deficiency disorders in mammals. This study identifies that coordinated transcriptional regulation of ferritin and transferrin plays a crucial role in follicle development and egg maturation. Silencing of both genes using ribonucleic acid interference led to severe reproductive impairment, including ovarian arrest in 50% of females, a 40% reduction in oocyte number, and a decrease in first instar larval size. These outcomes correlate with increased reactive oxygen species and altered serotonin receptor expression in the brain, possibly driven by alterations in microbial gut-brain axis communication due to disrupted iron metabolism. In summary, our research provides the first molecular proof and a new conceptual understanding of how iron metabolism disorders may affect microbiome-gut-brain-axis communication and, in turn, reproductive outcomes.
Additional Links: PMID-42587725
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PubMed:
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@article {pmid42587725,
year = {2026},
author = {Yadav, P and Rani, J and Singh, T and Saini, V and Rohilla, P and Srivastava, V and Tandon, G and Sankhala, N and Sharma, G and Tyagi, S and Tevatiya, S and Kumari, S and Dixit, R},
title = {Iron Homeostasis and Reproduction: Unveiling the Microbiome-Gut-Brain Axis Connection in the Mosquito Anopheles culicifacies.},
journal = {Cells},
volume = {15},
number = {15},
pages = {},
doi = {10.3390/cells15151315},
pmid = {42587725},
issn = {2073-4409},
support = {Ref # VBD/NIMR/Intra/002-ECD-II//Indian Council of Medical Research/ ; Ref # 191620022266//University Grants Commission/ ; },
mesh = {Animals ; *Iron/metabolism ; Female ; *Homeostasis ; *Anopheles/microbiology/metabolism/physiology ; *Reproduction ; *Brain/metabolism ; *Gastrointestinal Microbiome ; Transferrin/metabolism/genetics ; Reactive Oxygen Species/metabolism ; Ferritins/metabolism/genetics ; },
abstract = {Our study investigated how adult female Anopheles culicifacies mosquitoes regulate systemic iron homeostasis after blood feeding, a process essential for reproduction, and revealed striking parallels to iron deficiency disorders in mammals. This study identifies that coordinated transcriptional regulation of ferritin and transferrin plays a crucial role in follicle development and egg maturation. Silencing of both genes using ribonucleic acid interference led to severe reproductive impairment, including ovarian arrest in 50% of females, a 40% reduction in oocyte number, and a decrease in first instar larval size. These outcomes correlate with increased reactive oxygen species and altered serotonin receptor expression in the brain, possibly driven by alterations in microbial gut-brain axis communication due to disrupted iron metabolism. In summary, our research provides the first molecular proof and a new conceptual understanding of how iron metabolism disorders may affect microbiome-gut-brain-axis communication and, in turn, reproductive outcomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Iron/metabolism
Female
*Homeostasis
*Anopheles/microbiology/metabolism/physiology
*Reproduction
*Brain/metabolism
*Gastrointestinal Microbiome
Transferrin/metabolism/genetics
Reactive Oxygen Species/metabolism
Ferritins/metabolism/genetics
RevDate: 2026-08-13
CmpDate: 2026-08-13
Microbiota-Derived Corisin Is Elevated in Early Cervical Neoplasia and Drives Pathogenic Cellular Programs.
Cells, 15(15): pii:cells15151358.
Cervical cancer remains a major global health challenge and a leading cause of gynecological cancer-related mortality, particularly in developing countries. Although persistent human papillomavirus infection is the primary driver of cervical carcinogenesis, host factors such as immune dysregulation and microbiome dysbiosis may contribute to disease progression. Corisin is a microbiota-derived peptide implicated in epithelial injury and fibrosis, but its role in cervical neoplasia is unknown. To investigate its potential involvement, circulating corisin levels were measured in 27 women with cervical intraepithelial neoplasia (CIN) or cervical cancer and compared with those in 15 healthy women. Corisin localization in cervical carcinoma tissues was examined by immunohistochemistry, and its biological effects were evaluated in HeLa cells. Circulating corisin levels were significantly elevated in patients with CIN and cervical cancer, with the highest levels observed in CIN3 and cervical squamous cell carcinoma. Corisin was detected within cervical carcinoma tissues in intracellular and extracellular compartments adjacent to tumor cells. In HeLa cells, corisin accumulated in mitochondria, impaired cell-cycle progression, induced apoptosis, increased p21 expression, and promoted epithelial-mesenchymal transition-like morphological changes. These findings suggest that corisin is elevated from the early stages of cervical neoplasia, is present within the cervical tumor microenvironment, and may contribute to pathogenic cellular processes associated with cervical cancer progression.
Additional Links: PMID-42587768
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PubMed:
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@article {pmid42587768,
year = {2026},
author = {Watashige, N and Kubo-Kaneda, M and Makino, M and Kato, M and Okamoto, K and Matsumoto, T and Kotaka, S and Toda, M and D'Alessandro-Gabazza, CN and Cann, I and Gabazza, EC and Yasuma, T and Yoshida, K and Kondo, E},
title = {Microbiota-Derived Corisin Is Elevated in Early Cervical Neoplasia and Drives Pathogenic Cellular Programs.},
journal = {Cells},
volume = {15},
number = {15},
pages = {},
doi = {10.3390/cells15151358},
pmid = {42587768},
issn = {2073-4409},
support = {1708442//Japan Society for the Promotion of Science/ ; 2022//Takeda Science Foundation/ ; 2023//Takeda Science Foundation/ ; 2025-2026//MSD Life Science Foundation/ ; 2025-2026//Terumo (Japan)/ ; },
mesh = {Humans ; Female ; *Uterine Cervical Neoplasms/pathology/microbiology/metabolism/blood ; HeLa Cells ; *Microbiota ; Adult ; *Uterine Cervical Dysplasia/pathology/microbiology/blood/metabolism ; Apoptosis ; Epithelial-Mesenchymal Transition ; Middle Aged ; Mitochondria/metabolism ; },
abstract = {Cervical cancer remains a major global health challenge and a leading cause of gynecological cancer-related mortality, particularly in developing countries. Although persistent human papillomavirus infection is the primary driver of cervical carcinogenesis, host factors such as immune dysregulation and microbiome dysbiosis may contribute to disease progression. Corisin is a microbiota-derived peptide implicated in epithelial injury and fibrosis, but its role in cervical neoplasia is unknown. To investigate its potential involvement, circulating corisin levels were measured in 27 women with cervical intraepithelial neoplasia (CIN) or cervical cancer and compared with those in 15 healthy women. Corisin localization in cervical carcinoma tissues was examined by immunohistochemistry, and its biological effects were evaluated in HeLa cells. Circulating corisin levels were significantly elevated in patients with CIN and cervical cancer, with the highest levels observed in CIN3 and cervical squamous cell carcinoma. Corisin was detected within cervical carcinoma tissues in intracellular and extracellular compartments adjacent to tumor cells. In HeLa cells, corisin accumulated in mitochondria, impaired cell-cycle progression, induced apoptosis, increased p21 expression, and promoted epithelial-mesenchymal transition-like morphological changes. These findings suggest that corisin is elevated from the early stages of cervical neoplasia, is present within the cervical tumor microenvironment, and may contribute to pathogenic cellular processes associated with cervical cancer progression.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
*Uterine Cervical Neoplasms/pathology/microbiology/metabolism/blood
HeLa Cells
*Microbiota
Adult
*Uterine Cervical Dysplasia/pathology/microbiology/blood/metabolism
Apoptosis
Epithelial-Mesenchymal Transition
Middle Aged
Mitochondria/metabolism
RevDate: 2026-08-13
CmpDate: 2026-08-13
Gut Microbial Functional Ecology and Microbiota-Derived Metabolites in Rheumatoid Arthritis Autoimmunity.
Cells, 15(15): pii:cells15151398.
The gut microbiota is a key regulatory hub linking environmental exposure, the mucosal barrier, and joint inflammation, and plays an important role in the pathogenesis and progression of rheumatoid arthritis (RA). Mechanistic studies in this field mainly address two interrelated questions: how RA-associated gut microbiota modulate mucosal immunity and systemic autoimmunity through strain-level variation, niche competition, and metabolic remodeling; and how disease stage, host immune status, and drug exposure reciprocally reshape gut microbial structure and function. Accordingly, this review follows the framework of "anti-inflammatory/pro-inflammatory microbial niches-microbiota-derived metabolites-immune cell homing and migration" to summarize recent advances in the role of gut microbiota and their derivatives in RA onset, progression, and therapeutic response. Focusing on disease-stage-specific remodeling of gut functional ecology, we discuss how short-chain fatty acids, tryptophan-derived indoles, bile acids, succinate, and other microbial effector molecules regulate RA immunopathology through regulatory T cells (Treg), regulatory B cells (Breg), type 17 T helper cells (Th17), and IL-17-producing T follicular helper cells (Tfh17), dendritic cells, fibroblast-like synoviocytes, and osteoclasts. We also highlight intestinal antigen sampling, autoantibody generation, immune cell trafficking, and synovial reactivation as key links in the gut-joint axis. This review aims to shift RA microbiome research from taxonomic profiling toward stage-specific functional ecological analysis, providing a basis for risk stratification, therapeutic response prediction, and microbiota-based adjunctive interventions.
Additional Links: PMID-42587806
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PubMed:
Citation:
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@article {pmid42587806,
year = {2026},
author = {Rong, X and Zhang, X and Tan, Y and Lu, C},
title = {Gut Microbial Functional Ecology and Microbiota-Derived Metabolites in Rheumatoid Arthritis Autoimmunity.},
journal = {Cells},
volume = {15},
number = {15},
pages = {},
doi = {10.3390/cells15151398},
pmid = {42587806},
issn = {2073-4409},
support = {No. 2025ZD1801002//National Science and Technology Major Projects of China/ ; },
mesh = {Humans ; *Arthritis, Rheumatoid/immunology/microbiology/metabolism ; *Gastrointestinal Microbiome/immunology ; *Autoimmunity/immunology ; Animals ; },
abstract = {The gut microbiota is a key regulatory hub linking environmental exposure, the mucosal barrier, and joint inflammation, and plays an important role in the pathogenesis and progression of rheumatoid arthritis (RA). Mechanistic studies in this field mainly address two interrelated questions: how RA-associated gut microbiota modulate mucosal immunity and systemic autoimmunity through strain-level variation, niche competition, and metabolic remodeling; and how disease stage, host immune status, and drug exposure reciprocally reshape gut microbial structure and function. Accordingly, this review follows the framework of "anti-inflammatory/pro-inflammatory microbial niches-microbiota-derived metabolites-immune cell homing and migration" to summarize recent advances in the role of gut microbiota and their derivatives in RA onset, progression, and therapeutic response. Focusing on disease-stage-specific remodeling of gut functional ecology, we discuss how short-chain fatty acids, tryptophan-derived indoles, bile acids, succinate, and other microbial effector molecules regulate RA immunopathology through regulatory T cells (Treg), regulatory B cells (Breg), type 17 T helper cells (Th17), and IL-17-producing T follicular helper cells (Tfh17), dendritic cells, fibroblast-like synoviocytes, and osteoclasts. We also highlight intestinal antigen sampling, autoantibody generation, immune cell trafficking, and synovial reactivation as key links in the gut-joint axis. This review aims to shift RA microbiome research from taxonomic profiling toward stage-specific functional ecological analysis, providing a basis for risk stratification, therapeutic response prediction, and microbiota-based adjunctive interventions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Arthritis, Rheumatoid/immunology/microbiology/metabolism
*Gastrointestinal Microbiome/immunology
*Autoimmunity/immunology
Animals
RevDate: 2026-08-13
CmpDate: 2026-08-13
Amaranth Seeds as Lactic Acid Bacteria Fermentation Substrates: Prospects for Metabiotic Foods and Functional Ingredients.
Foods (Basel, Switzerland), 15(15): pii:foods15152645.
Amaranth, a nutritionally dense pseudocereal, is an exceptional substrate for producing functional and metabiotic food products via lactic acid fermentation. This review provides a comprehensive analysis of both ungerminated and germinated amaranth seeds as fermentation matrices, assigning their nutritional profiles, bioactive constituents, and compatibility with microbial transformation. Central to this discussion are the synergistic interactions between amaranth's native compounds and lactic acid bacteria (LAB), with an emphasis on four key bioconversion mechanisms: protein hydrolysis, polyphenol activation, antinutrient reduction, and the biosynthesis of functional and metabiotic metabolites. Essential fermentation parameters, including substrate preparation, inoculation strategies, pH, temperature, and fermentation time, are systematically reviewed to guide optimization of bioactive compound yields. Post-fermentation processing approaches, such as freeze-drying, controlled drying, and product standardization, are assessed for their capacity to preserve product stability and ensure consistent functional performance. The review further explores the incorporation of fermented amaranth into diverse food systems, such as gluten-free bakery goods, functional beverages, and nutraceutical formulations, as well as its application in animal nutrition, where it supports improved digestibility and gut microbiome health. The review concludes by mapping current challenges, unresolved knowledge gaps, and priority research directions, positioning fermented amaranth systems as versatile, science-backed platforms for developing next-generation functional and metabiotic ingredients.
Additional Links: PMID-42587905
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PubMed:
Citation:
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@article {pmid42587905,
year = {2026},
author = {Vasile, AM and Pihurov Procop, M and Cotârleț, M and Bahrim, GE},
title = {Amaranth Seeds as Lactic Acid Bacteria Fermentation Substrates: Prospects for Metabiotic Foods and Functional Ingredients.},
journal = {Foods (Basel, Switzerland)},
volume = {15},
number = {15},
pages = {},
doi = {10.3390/foods15152645},
pmid = {42587905},
issn = {2304-8158},
abstract = {Amaranth, a nutritionally dense pseudocereal, is an exceptional substrate for producing functional and metabiotic food products via lactic acid fermentation. This review provides a comprehensive analysis of both ungerminated and germinated amaranth seeds as fermentation matrices, assigning their nutritional profiles, bioactive constituents, and compatibility with microbial transformation. Central to this discussion are the synergistic interactions between amaranth's native compounds and lactic acid bacteria (LAB), with an emphasis on four key bioconversion mechanisms: protein hydrolysis, polyphenol activation, antinutrient reduction, and the biosynthesis of functional and metabiotic metabolites. Essential fermentation parameters, including substrate preparation, inoculation strategies, pH, temperature, and fermentation time, are systematically reviewed to guide optimization of bioactive compound yields. Post-fermentation processing approaches, such as freeze-drying, controlled drying, and product standardization, are assessed for their capacity to preserve product stability and ensure consistent functional performance. The review further explores the incorporation of fermented amaranth into diverse food systems, such as gluten-free bakery goods, functional beverages, and nutraceutical formulations, as well as its application in animal nutrition, where it supports improved digestibility and gut microbiome health. The review concludes by mapping current challenges, unresolved knowledge gaps, and priority research directions, positioning fermented amaranth systems as versatile, science-backed platforms for developing next-generation functional and metabiotic ingredients.},
}
RevDate: 2026-08-13
CmpDate: 2026-08-13
Financialization, Food Sovereignty, and Oral Health: A Structured Narrative Review Within the One Health Framework for Sustainable Food Systems.
Foods (Basel, Switzerland), 15(15): pii:foods15152718.
Contemporary food systems are increasingly shaped by financialization, corporate concentration, and unequal distributions of power that influence food production, food environments, dietary exposures, and population health. However, the relationships among food-system financialization, food sovereignty, and oral health remain insufficiently integrated within food-security, sustainability, and One Health research. This structured narrative review critically synthesized interdisciplinary evidence from Scopus, Web of Science, PubMed/MEDLINE, Google Scholar, citation searching, and authoritative institutional sources to examine these relationships and develop an integrative conceptual framework. The synthesis indicates that financialization may influence health through market concentration, commodity dependence, corporate control of food environments, and the expansion of ultra-processed foods, whereas food sovereignty may modify these pathways by strengthening agency, equitable resource distribution, local governance, and ecological resilience. Dietary exposures and related biological mechanisms provide plausible pathways through which these structural processes may contribute to oral-health outcomes and inequalities. The proposed framework integrates food-system structures, governance, food environments, dietary exposures, biological pathways, oral health, and One Health implications within a common analytical model. Oral health is therefore proposed as a potential biological interface through which food-system transformations and inequalities may become measurable. Empirical research is required to test these pathways and evaluate the framework's applicability across populations and food-system contexts.
Additional Links: PMID-42587976
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PubMed:
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@article {pmid42587976,
year = {2026},
author = {Antoniadou, M and Varzakas, T and Caraher, M},
title = {Financialization, Food Sovereignty, and Oral Health: A Structured Narrative Review Within the One Health Framework for Sustainable Food Systems.},
journal = {Foods (Basel, Switzerland)},
volume = {15},
number = {15},
pages = {},
doi = {10.3390/foods15152718},
pmid = {42587976},
issn = {2304-8158},
abstract = {Contemporary food systems are increasingly shaped by financialization, corporate concentration, and unequal distributions of power that influence food production, food environments, dietary exposures, and population health. However, the relationships among food-system financialization, food sovereignty, and oral health remain insufficiently integrated within food-security, sustainability, and One Health research. This structured narrative review critically synthesized interdisciplinary evidence from Scopus, Web of Science, PubMed/MEDLINE, Google Scholar, citation searching, and authoritative institutional sources to examine these relationships and develop an integrative conceptual framework. The synthesis indicates that financialization may influence health through market concentration, commodity dependence, corporate control of food environments, and the expansion of ultra-processed foods, whereas food sovereignty may modify these pathways by strengthening agency, equitable resource distribution, local governance, and ecological resilience. Dietary exposures and related biological mechanisms provide plausible pathways through which these structural processes may contribute to oral-health outcomes and inequalities. The proposed framework integrates food-system structures, governance, food environments, dietary exposures, biological pathways, oral health, and One Health implications within a common analytical model. Oral health is therefore proposed as a potential biological interface through which food-system transformations and inequalities may become measurable. Empirical research is required to test these pathways and evaluate the framework's applicability across populations and food-system contexts.},
}
RevDate: 2026-08-13
CmpDate: 2026-08-13
Oxidative Stress in Alzheimer's Disease: Can Dietary Interventions Provide Neuroprotection?.
Nutrients, 18(15): pii:nu18152436.
Population aging is a growing problem. This process is driven not only by genetic factors but also by environmental factors, such as diet. Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia worldwide, characterized by cognitive decline, synaptic dysfunction, and neuronal loss. Despite extensive research, effective disease-modifying therapies remain limited. Increasing evidence indicates that oxidative stress plays a central role in AD pathogenesis, acting as a key link between β-amyloid accumulation, tau hyperphosphorylation, mitochondrial dysfunction, and neuroinflammation. Accordingly, dietary strategies have been proposed to mitigate these pathological processes and may represent an important component of Alzheimer's disease prevention. Moreover, emerging evidence on the gut-brain axis highlights the critical role of gut microbiota in regulating neuroinflammation and oxidative stress. Dysbiosis has been associated with increased permeability of the intestinal barrier, systemic inflammation, and accelerated neurodegeneration. Dietary patterns such as the Mediterranean, DASH, and MIND diets may exert beneficial effects by simultaneously influencing antioxidant status and microbial composition. This review aims to provide a comprehensive overview of the role of oxidative stress in Alzheimer's disease and evaluate the potential of dietary interventions in modulating mechanisms involved in Alzheimer's disease pathogenesis and supporting cognitive health. Particular attention is given to the neuroprotective effects of dietary antioxidants, including vitamins, polyphenols, and polyunsaturated fatty acids, which act through the reduction in reactive oxygen species, modulation of inflammatory pathways, and support of neuronal survival. Although current findings are promising, inconsistencies in clinical data indicate the need for further well-designed studies. Future research should focus on personalized nutritional strategies integrating dietary, genetic, and microbiome-related factors. Targeting oxidative stress through diet and microbiota modulation represents a promising complementary strategy for Alzheimer's disease prevention and supportive management, although further clinical studies are required to establish disease-modifying effects.
Additional Links: PMID-42588059
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PubMed:
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@article {pmid42588059,
year = {2026},
author = {Kupczyk, D and Bilski, R and Kozieł, I and Słota, A and Kurek, M and Stablewska, E and Baumgart, S and Słomka, A and Studzińska, R},
title = {Oxidative Stress in Alzheimer's Disease: Can Dietary Interventions Provide Neuroprotection?.},
journal = {Nutrients},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/nu18152436},
pmid = {42588059},
issn = {2072-6643},
mesh = {Humans ; *Alzheimer Disease/diet therapy/metabolism/prevention & control ; *Oxidative Stress/physiology ; Antioxidants ; Gastrointestinal Microbiome ; *Neuroprotection ; Animals ; Brain/metabolism ; *Diet ; Polyphenols ; *Neuroprotective Agents ; },
abstract = {Population aging is a growing problem. This process is driven not only by genetic factors but also by environmental factors, such as diet. Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia worldwide, characterized by cognitive decline, synaptic dysfunction, and neuronal loss. Despite extensive research, effective disease-modifying therapies remain limited. Increasing evidence indicates that oxidative stress plays a central role in AD pathogenesis, acting as a key link between β-amyloid accumulation, tau hyperphosphorylation, mitochondrial dysfunction, and neuroinflammation. Accordingly, dietary strategies have been proposed to mitigate these pathological processes and may represent an important component of Alzheimer's disease prevention. Moreover, emerging evidence on the gut-brain axis highlights the critical role of gut microbiota in regulating neuroinflammation and oxidative stress. Dysbiosis has been associated with increased permeability of the intestinal barrier, systemic inflammation, and accelerated neurodegeneration. Dietary patterns such as the Mediterranean, DASH, and MIND diets may exert beneficial effects by simultaneously influencing antioxidant status and microbial composition. This review aims to provide a comprehensive overview of the role of oxidative stress in Alzheimer's disease and evaluate the potential of dietary interventions in modulating mechanisms involved in Alzheimer's disease pathogenesis and supporting cognitive health. Particular attention is given to the neuroprotective effects of dietary antioxidants, including vitamins, polyphenols, and polyunsaturated fatty acids, which act through the reduction in reactive oxygen species, modulation of inflammatory pathways, and support of neuronal survival. Although current findings are promising, inconsistencies in clinical data indicate the need for further well-designed studies. Future research should focus on personalized nutritional strategies integrating dietary, genetic, and microbiome-related factors. Targeting oxidative stress through diet and microbiota modulation represents a promising complementary strategy for Alzheimer's disease prevention and supportive management, although further clinical studies are required to establish disease-modifying effects.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Alzheimer Disease/diet therapy/metabolism/prevention & control
*Oxidative Stress/physiology
Antioxidants
Gastrointestinal Microbiome
*Neuroprotection
Animals
Brain/metabolism
*Diet
Polyphenols
*Neuroprotective Agents
RevDate: 2026-08-13
CmpDate: 2026-08-13
Clinical Improvement and Taxonomic-Functional Gut Microbiome Remodeling After Six Months of Multi-Strain Synbiotic Supplementation in Mexican Children with Autism Spectrum Disorder.
Nutrients, 18(15): pii:nu18152441.
Background/Objectives: Gut dysbiosis in children with autism spectrum disorder (ASD) has been associated with alterations in microbial ecology and metabolic function that may contribute to gastrointestinal dysfunction and the severity of clinical manifestations. Synbiotic and probiotic supplementation has emerged as a promising microbiome-targeted strategy for ASD; however, its effects on gut microbiome composition, functional potential, and clinical outcomes remain incompletely understood. We conducted a longitudinal study of Mexican children diagnosed with ASD to analyze changes in the composition, diversity, and functional potential of the gut microbiome during six months of multi-strain synbiotic supplementation. Methods: Stool samples were collected from 25 children with ASD at baseline and after 3 and 6 months of multi-strain synbiotic supplementation. Gut microbiome composition and diversity were analyzed by 16S rRNA gene sequencing, whereas whole metagenome sequencing (WMS) was performed in a subset of samples to evaluate the functional potential of the fecal microbiome. Gastrointestinal symptoms were assessed using the Rome IV criteria, and ASD severity was evaluated with the Childhood Autism Rating Scale (CARS). Results: Twenty-five children with ASD completed the 6 months of synbiotic supplementation. Overall, ASD severity decreased, reflected by a reduction in total CARS score, and improvements in several CARS domains. Gastrointestinal symptoms also decreased significantly. Longitudinal microbiome profiling revealed significant taxonomic and diversity changes over the supplementation period, while WMS identified changes in microbial metabolic potential, including enrichment of tryptophan biosynthesis pathways and reduced L-rhamnose degradation. Conclusions: This exploratory research provides proof-of-concept evidence supporting multi-strain synbiotic supplementation in children with ASD. Larger controlled studies are needed to confirm these findings and clarify their relevance to microbiota-gut-brain axis interactions. The observed concordance between clinical improvements and microbiome remodeling supports further investigation of microbiome-targeted interventions according to ASD severity and duration of supplementation.
Additional Links: PMID-42588064
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PubMed:
Citation:
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@article {pmid42588064,
year = {2026},
author = {De Sales-Millan, A and Reyes-Ferreira, P and González-Cervantes, RM and Luna-Álvarez, M and Guillén-López, S and Cobo-Díaz, JF and Ramos, S and Aguirre-Garrido, JF and Velázquez-Aragón, JA},
title = {Clinical Improvement and Taxonomic-Functional Gut Microbiome Remodeling After Six Months of Multi-Strain Synbiotic Supplementation in Mexican Children with Autism Spectrum Disorder.},
journal = {Nutrients},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/nu18152441},
pmid = {42588064},
issn = {2072-6643},
support = {E022 Program Recursos Fiscales para la Investigación//Instituto Nacional de Pediatria/ ; },
mesh = {Humans ; *Autism Spectrum Disorder/microbiology/therapy ; Male ; *Gastrointestinal Microbiome/genetics ; Female ; Mexico ; Longitudinal Studies ; *Synbiotics/administration & dosage ; Child ; Feces/microbiology ; Child, Preschool ; Probiotics/administration & dosage ; Dietary Supplements ; Treatment Outcome ; RNA, Ribosomal, 16S/genetics ; Dysbiosis/microbiology ; },
abstract = {Background/Objectives: Gut dysbiosis in children with autism spectrum disorder (ASD) has been associated with alterations in microbial ecology and metabolic function that may contribute to gastrointestinal dysfunction and the severity of clinical manifestations. Synbiotic and probiotic supplementation has emerged as a promising microbiome-targeted strategy for ASD; however, its effects on gut microbiome composition, functional potential, and clinical outcomes remain incompletely understood. We conducted a longitudinal study of Mexican children diagnosed with ASD to analyze changes in the composition, diversity, and functional potential of the gut microbiome during six months of multi-strain synbiotic supplementation. Methods: Stool samples were collected from 25 children with ASD at baseline and after 3 and 6 months of multi-strain synbiotic supplementation. Gut microbiome composition and diversity were analyzed by 16S rRNA gene sequencing, whereas whole metagenome sequencing (WMS) was performed in a subset of samples to evaluate the functional potential of the fecal microbiome. Gastrointestinal symptoms were assessed using the Rome IV criteria, and ASD severity was evaluated with the Childhood Autism Rating Scale (CARS). Results: Twenty-five children with ASD completed the 6 months of synbiotic supplementation. Overall, ASD severity decreased, reflected by a reduction in total CARS score, and improvements in several CARS domains. Gastrointestinal symptoms also decreased significantly. Longitudinal microbiome profiling revealed significant taxonomic and diversity changes over the supplementation period, while WMS identified changes in microbial metabolic potential, including enrichment of tryptophan biosynthesis pathways and reduced L-rhamnose degradation. Conclusions: This exploratory research provides proof-of-concept evidence supporting multi-strain synbiotic supplementation in children with ASD. Larger controlled studies are needed to confirm these findings and clarify their relevance to microbiota-gut-brain axis interactions. The observed concordance between clinical improvements and microbiome remodeling supports further investigation of microbiome-targeted interventions according to ASD severity and duration of supplementation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Autism Spectrum Disorder/microbiology/therapy
Male
*Gastrointestinal Microbiome/genetics
Female
Mexico
Longitudinal Studies
*Synbiotics/administration & dosage
Child
Feces/microbiology
Child, Preschool
Probiotics/administration & dosage
Dietary Supplements
Treatment Outcome
RNA, Ribosomal, 16S/genetics
Dysbiosis/microbiology
RevDate: 2026-08-13
CmpDate: 2026-08-13
The Impact of Nutrition on DNA Methylation: Methodological Challenges in Understanding Cause and Effect.
Nutrients, 18(15): pii:nu18152453.
DNA methylation is a key epigenetic mechanism linking nutritional exposures to gene regulation and downstream phenotypes. Both undernutrition and overnutrition are associated with distinct methylation signatures, some of which persist beyond the initial exposure window and may relate to long-term metabolic, immune, and neurodevelopmental outcomes. However, the extent to which these associations reflect causal mechanisms, adaptive responses, or secondary effects remains unresolved. Here, we synthesize current evidence on how nutrition influences DNA methylation across the life course, integrating biochemical pathways, metabolic signaling, and microbiome-derived processes within a unified framework. We highlight how these diverse inputs converge on core regulatory axes, including methyl donor availability, enzyme activity, and chromatin context. We then evaluate emerging long-read sequencing, single-cell methylomics, deconvolution strategies, and multi-omic integration methodologies that are improving cellular resolution and enabling a more mechanistic interpretation of nutritional epigenetic variation. Despite these advances, major challenges remain, including tissue specificity, measurement limitations, and the difficulty of distinguishing causation from correlation in observational data. We argue that progress will depend on longitudinal and interventional study designs, improved causal inference frameworks, and integration of functional validation with high-resolution molecular profiling. Addressing these challenges will be critical for determining whether nutrition-associated methylation changes represent biomarkers, mediators, or causal drivers of disease, and for translating epigenetic insights into precision nutrition strategies.
Additional Links: PMID-42588079
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@article {pmid42588079,
year = {2026},
author = {Araf, Y and Portlock, T and O'Sullivan, JM},
title = {The Impact of Nutrition on DNA Methylation: Methodological Challenges in Understanding Cause and Effect.},
journal = {Nutrients},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/nu18152453},
pmid = {42588079},
issn = {2072-6643},
support = {//University of Auckland/ ; },
mesh = {Humans ; *DNA Methylation ; *Epigenesis, Genetic ; *Nutritional Status/genetics ; Animals ; *Nutritional Physiological Phenomena/genetics ; Epigenomics/methods ; Developmental Origins of Health and Disease ; },
abstract = {DNA methylation is a key epigenetic mechanism linking nutritional exposures to gene regulation and downstream phenotypes. Both undernutrition and overnutrition are associated with distinct methylation signatures, some of which persist beyond the initial exposure window and may relate to long-term metabolic, immune, and neurodevelopmental outcomes. However, the extent to which these associations reflect causal mechanisms, adaptive responses, or secondary effects remains unresolved. Here, we synthesize current evidence on how nutrition influences DNA methylation across the life course, integrating biochemical pathways, metabolic signaling, and microbiome-derived processes within a unified framework. We highlight how these diverse inputs converge on core regulatory axes, including methyl donor availability, enzyme activity, and chromatin context. We then evaluate emerging long-read sequencing, single-cell methylomics, deconvolution strategies, and multi-omic integration methodologies that are improving cellular resolution and enabling a more mechanistic interpretation of nutritional epigenetic variation. Despite these advances, major challenges remain, including tissue specificity, measurement limitations, and the difficulty of distinguishing causation from correlation in observational data. We argue that progress will depend on longitudinal and interventional study designs, improved causal inference frameworks, and integration of functional validation with high-resolution molecular profiling. Addressing these challenges will be critical for determining whether nutrition-associated methylation changes represent biomarkers, mediators, or causal drivers of disease, and for translating epigenetic insights into precision nutrition strategies.},
}
MeSH Terms:
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Humans
*DNA Methylation
*Epigenesis, Genetic
*Nutritional Status/genetics
Animals
*Nutritional Physiological Phenomena/genetics
Epigenomics/methods
Developmental Origins of Health and Disease
RevDate: 2026-08-13
CmpDate: 2026-08-13
Chinese Yam Polysaccharides Alleviate Myocardial Ischemia/Reperfusion Injury by Modulating Gut Microbiota, Restoring Mitochondrial Function, and Reducing Oxidative Stress.
Nutrients, 18(15): pii:nu18152464.
Background/Objectives: Myocardial ischemia/reperfusion (I/R) injury remains a critical challenge in cardiovascular disease management. Although Chinese yam polysaccharides (CYPs), the primary bioactive macromolecules isolated from Dioscorea opposita Thunb, exhibit well-documented antioxidant and anti-inflammatory properties, their cardioprotective efficacy against acute I/R injury and the underlying multiscale mechanisms remain unexplored. This study investigated the protective effects of CYPs using an in vivo mouse model of myocardial I/R injury. Methods: An in vivo mouse model of myocardial I/R injury was used to evaluate the effects of 7-day prophylactic CYPs treatment (400 mg/kg). Echocardiographic and histological analyses were performed, and serum myocardial injury biomarkers, oxidative stress indicators, pro-inflammatory cytokines, mitochondrial ultrastructure, ATP bioenergetics, mitochondrial respiratory chain gene expression, and gut microbiota composition were assessed. Results: Echocardiographic and histological analyses revealed that CYPs pretreatment significantly ameliorated cardiac dysfunction, as indicated by increased LVEF from 28.98% to 57.68% and reduced myocardial infarct size by 36.73% compared with the I/R group and decreased serum myocardial injury biomarkers, including CK-MB, LDH, and LDH-1. Mechanistically, CYPs exerted robust cardioprotection by mitigating oxidative damage, with MDA levels reduced by 28.83% and SOD activity increased to 1.76-fold that of the I/R group, and suppressing the release of pro-inflammatory cytokines, including Tnf-α, Il-6, and Il-1β. Crucially, CYPs intervention preserved mitochondrial ultrastructure and ATP bioenergetics, and levels increased to 1.51-fold that of the I/R group and upregulated the expression of essential mitochondrial respiratory chain genes, including mt-Nd1, mt-Nd4l, mt-Cyb, mt-CoII, and mt-Atp6. Furthermore, 16S rRNA sequencing showed that CYPs treatment reshaped gut microbiota and elevated the relative abundance of anti-inflammatory and antioxidant beneficial genus Akkermansia. Conclusions: Collectively, these findings provide novel evidence that CYPs confer profound protection against myocardial I/R injury through a multitargeted network involving the restoration of mitochondrial homeostasis, attenuation of oxidative inflammation, and modulation of the gut microbiome, highlighting CYPs as a promising functional food-derived candidate for adjunctive therapy in ischemic heart disease.
Additional Links: PMID-42588087
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@article {pmid42588087,
year = {2026},
author = {Zhang, Z and Zhang, Y and Shi, Y and Luo, X and Wei, Z and An, P and Luo, Y and Luo, J},
title = {Chinese Yam Polysaccharides Alleviate Myocardial Ischemia/Reperfusion Injury by Modulating Gut Microbiota, Restoring Mitochondrial Function, and Reducing Oxidative Stress.},
journal = {Nutrients},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/nu18152464},
pmid = {42588087},
issn = {2072-6643},
support = {32570908//National Natural Science Foundation of China/ ; 32571359//National Natural Science Foundation of China/ ; 32371229//National Natural Science Foundation of China/ ; 82470442//National Natural Science Foundation of China/ ; 82170429//National Natural Science Foundation of China/ ; 7262078//Beijing Natural Science Foundation/ ; 2024GZkf-05//State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Sciences/ ; PC2023B01014//Pinduoduo-China Agricultural University Research Fund/ ; B18053//111 project from the Education Ministry of China/ ; NA//2115 Talent Development Program of China Agricultural University/ ; },
mesh = {Animals ; *Oxidative Stress/drug effects ; *Polysaccharides/pharmacology ; *Myocardial Reperfusion Injury/drug therapy/prevention & control ; *Dioscorea/chemistry ; *Gastrointestinal Microbiome/drug effects ; Male ; Mice ; Disease Models, Animal ; Mice, Inbred C57BL ; *Mitochondria/drug effects/metabolism ; Antioxidants/pharmacology ; Cytokines/metabolism ; Biomarkers/blood ; *Mitochondria, Heart/drug effects/metabolism ; },
abstract = {Background/Objectives: Myocardial ischemia/reperfusion (I/R) injury remains a critical challenge in cardiovascular disease management. Although Chinese yam polysaccharides (CYPs), the primary bioactive macromolecules isolated from Dioscorea opposita Thunb, exhibit well-documented antioxidant and anti-inflammatory properties, their cardioprotective efficacy against acute I/R injury and the underlying multiscale mechanisms remain unexplored. This study investigated the protective effects of CYPs using an in vivo mouse model of myocardial I/R injury. Methods: An in vivo mouse model of myocardial I/R injury was used to evaluate the effects of 7-day prophylactic CYPs treatment (400 mg/kg). Echocardiographic and histological analyses were performed, and serum myocardial injury biomarkers, oxidative stress indicators, pro-inflammatory cytokines, mitochondrial ultrastructure, ATP bioenergetics, mitochondrial respiratory chain gene expression, and gut microbiota composition were assessed. Results: Echocardiographic and histological analyses revealed that CYPs pretreatment significantly ameliorated cardiac dysfunction, as indicated by increased LVEF from 28.98% to 57.68% and reduced myocardial infarct size by 36.73% compared with the I/R group and decreased serum myocardial injury biomarkers, including CK-MB, LDH, and LDH-1. Mechanistically, CYPs exerted robust cardioprotection by mitigating oxidative damage, with MDA levels reduced by 28.83% and SOD activity increased to 1.76-fold that of the I/R group, and suppressing the release of pro-inflammatory cytokines, including Tnf-α, Il-6, and Il-1β. Crucially, CYPs intervention preserved mitochondrial ultrastructure and ATP bioenergetics, and levels increased to 1.51-fold that of the I/R group and upregulated the expression of essential mitochondrial respiratory chain genes, including mt-Nd1, mt-Nd4l, mt-Cyb, mt-CoII, and mt-Atp6. Furthermore, 16S rRNA sequencing showed that CYPs treatment reshaped gut microbiota and elevated the relative abundance of anti-inflammatory and antioxidant beneficial genus Akkermansia. Conclusions: Collectively, these findings provide novel evidence that CYPs confer profound protection against myocardial I/R injury through a multitargeted network involving the restoration of mitochondrial homeostasis, attenuation of oxidative inflammation, and modulation of the gut microbiome, highlighting CYPs as a promising functional food-derived candidate for adjunctive therapy in ischemic heart disease.},
}
MeSH Terms:
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Animals
*Oxidative Stress/drug effects
*Polysaccharides/pharmacology
*Myocardial Reperfusion Injury/drug therapy/prevention & control
*Dioscorea/chemistry
*Gastrointestinal Microbiome/drug effects
Male
Mice
Disease Models, Animal
Mice, Inbred C57BL
*Mitochondria/drug effects/metabolism
Antioxidants/pharmacology
Cytokines/metabolism
Biomarkers/blood
*Mitochondria, Heart/drug effects/metabolism
RevDate: 2026-08-13
CmpDate: 2026-08-13
The Oral-Gut-Brain Axis in Pediatric Populations: The Implications of Oral Dysbiosis for Systemic Inflammation and Neuroinflammation.
Nutrients, 18(15): pii:nu18152465.
Background: The oral microbiome plays a fundamental role in maintaining local and systemic health during childhood, a developmental period characterized by dynamic microbial, immune, and neuroendocrine maturation. Increasing evidence suggests that oral dysbiosis may influence gut microbiota composition, systemic inflammation, and neuroinflammatory pathways through the oral-gut-brain axis. Aim: This narrative review aimed to summarize and critically evaluate current evidence regarding the relationship between oral dysbiosis, gut microbial alterations, systemic inflammation, and neurodevelopmental processes in pediatric populations. Methods: A search of the literature was conducted using PubMed, Scopus, and Web of Science, including studies published between January 2016 and April 2026. Eligible studies included randomized controlled trials, observational studies, and reviews investigating at least one component of the oral-gut-brain axis in children or adolescents. Results: Current evidence supports a biological interaction between oral and gut microbiota through microbial translocation and immune-mediated mechanisms. Oral dysbiosis may contribute to gut microbial imbalance, intestinal barrier dysfunction, and systemic low-grade inflammation. Altered gut microbiota has been associated with neuroinflammatory signaling, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, and adverse neurodevelopmental outcomes. Furthermore, pediatric randomized controlled trials suggest that probiotics and synbiotics can modulate oral and gut microbial composition, improve selected inflammatory and immune biomarkers, and reduce salivary cortisol levels. Conclusions: The oral-gut-brain axis represents a promising framework for understanding the systemic consequences of oral dysbiosis during childhood. However, direct evidence integrating oral, intestinal, immunological, and neurodevelopmental outcomes remains limited, highlighting the need for longitudinal and multidisciplinary pediatric studies.
Additional Links: PMID-42588088
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@article {pmid42588088,
year = {2026},
author = {Inchingolo, AM and Severino, M and Marinelli, G and Casamassima, L and Nardelli, P and Ciccarese, D and Palermo, A and Inchingolo, F and Inchingolo, AD and Dipalma, G},
title = {The Oral-Gut-Brain Axis in Pediatric Populations: The Implications of Oral Dysbiosis for Systemic Inflammation and Neuroinflammation.},
journal = {Nutrients},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/nu18152465},
pmid = {42588088},
issn = {2072-6643},
mesh = {Humans ; *Dysbiosis/microbiology ; *Gastrointestinal Microbiome/physiology ; *Inflammation/microbiology ; Child ; *Neuroinflammatory Diseases/microbiology ; *Brain ; *Mouth/microbiology ; Adolescent ; Probiotics ; Child, Preschool ; },
abstract = {Background: The oral microbiome plays a fundamental role in maintaining local and systemic health during childhood, a developmental period characterized by dynamic microbial, immune, and neuroendocrine maturation. Increasing evidence suggests that oral dysbiosis may influence gut microbiota composition, systemic inflammation, and neuroinflammatory pathways through the oral-gut-brain axis. Aim: This narrative review aimed to summarize and critically evaluate current evidence regarding the relationship between oral dysbiosis, gut microbial alterations, systemic inflammation, and neurodevelopmental processes in pediatric populations. Methods: A search of the literature was conducted using PubMed, Scopus, and Web of Science, including studies published between January 2016 and April 2026. Eligible studies included randomized controlled trials, observational studies, and reviews investigating at least one component of the oral-gut-brain axis in children or adolescents. Results: Current evidence supports a biological interaction between oral and gut microbiota through microbial translocation and immune-mediated mechanisms. Oral dysbiosis may contribute to gut microbial imbalance, intestinal barrier dysfunction, and systemic low-grade inflammation. Altered gut microbiota has been associated with neuroinflammatory signaling, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, and adverse neurodevelopmental outcomes. Furthermore, pediatric randomized controlled trials suggest that probiotics and synbiotics can modulate oral and gut microbial composition, improve selected inflammatory and immune biomarkers, and reduce salivary cortisol levels. Conclusions: The oral-gut-brain axis represents a promising framework for understanding the systemic consequences of oral dysbiosis during childhood. However, direct evidence integrating oral, intestinal, immunological, and neurodevelopmental outcomes remains limited, highlighting the need for longitudinal and multidisciplinary pediatric studies.},
}
MeSH Terms:
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Humans
*Dysbiosis/microbiology
*Gastrointestinal Microbiome/physiology
*Inflammation/microbiology
Child
*Neuroinflammatory Diseases/microbiology
*Brain
*Mouth/microbiology
Adolescent
Probiotics
Child, Preschool
RevDate: 2026-08-13
CmpDate: 2026-08-13
Heyndrickxia coagulans IDCC 1201 Alters Gut Microbiome and Metabolome in Patients with Functional Bowel Disorders.
Nutrients, 18(15): pii:nu18152466.
Background/Objectives: Functional bowel disorders (FBDs) are chronic gastrointestinal conditions that substantially impair quality of life. This randomized, double-blind, placebo-controlled trial investigated the effects of Heyndrickxia coagulans IDCC 1201 (COA 1201) in adults with FBD. Methods: Participants received COA 1201 or a placebo for 8 weeks, with outcomes assessed using the irritable bowel syndrome (IBS) Symptom Severity Score (IBS-SSS), IBS Quality of Life (IBS-QOL), and bowel activity measures. And Fecal microbiome and metabolomics were measured by 16S rRNA gene sequencing gas chromatography-mass spectrometry, respectively. Results: Both groups showed improvement from baseline, but COA 1201 produced greater symptom relief, particularly in abdominal bloating, post-defecation discomfort, and the body image domain of IBS-QOL. Fecal microbiome profiling revealed modest changes in global diversity, yet taxa linked to saccharolytic activity and short-chain fatty acid production-including Ruminococcus bromii, Agathobacter rectalis, and Bifidobacterium-were enriched in participants receiving COA 1201, whereas Clostridium leptum increased in those receiving a placebo. Untargeted metabolomics demonstrated distinct metabolic signatures between groups, confirmed by supervised partial least squares discriminant analysis. Exploratory metabolites were identified using variable importance in projection scores (>1.5), statistical significance (p < 0.05), and absolute log2 fold change (>1). Alanine and proline emerged as time-dependent metabolites, while tryptophan, lactic acid, and phytosphingosine were specifically associated with COA 1201 treatment. Conclusions: Collectively, these findings suggest that COA 1201 alleviates FBD symptoms by modulating the gut microbiome and metabolome.
Additional Links: PMID-42588089
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PubMed:
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@article {pmid42588089,
year = {2026},
author = {Jeon, HJ and Moon, JS and Jeong, HM and Bang, WY and Kim, H and Kim, D and Shin, M and Yang, J and Shin, J and Jung, YH},
title = {Heyndrickxia coagulans IDCC 1201 Alters Gut Microbiome and Metabolome in Patients with Functional Bowel Disorders.},
journal = {Nutrients},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/nu18152466},
pmid = {42588089},
issn = {2072-6643},
support = {RS-2025-02216704//Korea Institute of Planning and Evaluation for Technology in Food, Agriculture and Forestry/ ; 202400352752//National Research Foundation of Korea/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; Male ; *Metabolome/drug effects ; Adult ; Female ; Feces/microbiology ; Double-Blind Method ; *Irritable Bowel Syndrome/microbiology/metabolism/therapy/drug therapy ; Middle Aged ; Quality of Life ; *Probiotics/therapeutic use ; Treatment Outcome ; Metabolomics ; RNA, Ribosomal, 16S ; },
abstract = {Background/Objectives: Functional bowel disorders (FBDs) are chronic gastrointestinal conditions that substantially impair quality of life. This randomized, double-blind, placebo-controlled trial investigated the effects of Heyndrickxia coagulans IDCC 1201 (COA 1201) in adults with FBD. Methods: Participants received COA 1201 or a placebo for 8 weeks, with outcomes assessed using the irritable bowel syndrome (IBS) Symptom Severity Score (IBS-SSS), IBS Quality of Life (IBS-QOL), and bowel activity measures. And Fecal microbiome and metabolomics were measured by 16S rRNA gene sequencing gas chromatography-mass spectrometry, respectively. Results: Both groups showed improvement from baseline, but COA 1201 produced greater symptom relief, particularly in abdominal bloating, post-defecation discomfort, and the body image domain of IBS-QOL. Fecal microbiome profiling revealed modest changes in global diversity, yet taxa linked to saccharolytic activity and short-chain fatty acid production-including Ruminococcus bromii, Agathobacter rectalis, and Bifidobacterium-were enriched in participants receiving COA 1201, whereas Clostridium leptum increased in those receiving a placebo. Untargeted metabolomics demonstrated distinct metabolic signatures between groups, confirmed by supervised partial least squares discriminant analysis. Exploratory metabolites were identified using variable importance in projection scores (>1.5), statistical significance (p < 0.05), and absolute log2 fold change (>1). Alanine and proline emerged as time-dependent metabolites, while tryptophan, lactic acid, and phytosphingosine were specifically associated with COA 1201 treatment. Conclusions: Collectively, these findings suggest that COA 1201 alleviates FBD symptoms by modulating the gut microbiome and metabolome.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/drug effects
Male
*Metabolome/drug effects
Adult
Female
Feces/microbiology
Double-Blind Method
*Irritable Bowel Syndrome/microbiology/metabolism/therapy/drug therapy
Middle Aged
Quality of Life
*Probiotics/therapeutic use
Treatment Outcome
Metabolomics
RNA, Ribosomal, 16S
RevDate: 2026-08-13
CmpDate: 2026-08-13
Gut Microbiome Changes in Preclinical Alzheimer's Disease.
Nutrients, 18(15): pii:nu18152469.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that develops many years before clinical symptoms appear. The biological changes involved in the earliest stages remain poorly understood, particularly during the preclinical stage. Our previous work has identified gradual gut microbial and metabolic changes during this stage, suggesting these may represent early biological shifts that precede disease progression. Recent studies suggest that the gut microbiome may contribute to early AD processes through its effects on immune regulation, metabolism, and gut-brain communication. Changes in gut microbial composition, including reduced levels of short-chain fatty acid (SCFA)-producing bacteria, such as Faecalibacterium, Roseburia, and Eubacterium, have been reported in individuals with AD and mild cognitive impairment. These microbial alterations have also been linked to disrupted metabolic activity, impaired gut barrier function, and increased neuroinflammatory responses. Diet is an important factor influencing gut microbial composition and metabolic activity. Mediterranean, DASH, and prudent dietary patterns are generally associated with beneficial microbial profiles and increased SCFA production, whereas Western dietary patterns are linked to lower microbial diversity and increased pro-inflammatory taxa. This review summarises the current evidence linking gut microbiota, SCFAs, microbial metabolism, and dietary patterns with early AD pathology, while highlighting important gaps in the existing literature.
Additional Links: PMID-42588092
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@article {pmid42588092,
year = {2026},
author = {Dissanayaka, DMS and Rainey-Smith, SR and Sohrabi, HR and Jayasinghe, TN and Ho, V and Jayasena, V and Taddei, K and Masters, CL and Martins, RN and Fernando, WMADB},
title = {Gut Microbiome Changes in Preclinical Alzheimer's Disease.},
journal = {Nutrients},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/nu18152469},
pmid = {42588092},
issn = {2072-6643},
mesh = {*Alzheimer Disease/microbiology/metabolism ; Humans ; *Gastrointestinal Microbiome/physiology ; Fatty Acids, Volatile/metabolism ; Animals ; Diet ; Brain/metabolism ; },
abstract = {Alzheimer's disease (AD) is a progressive neurodegenerative disorder that develops many years before clinical symptoms appear. The biological changes involved in the earliest stages remain poorly understood, particularly during the preclinical stage. Our previous work has identified gradual gut microbial and metabolic changes during this stage, suggesting these may represent early biological shifts that precede disease progression. Recent studies suggest that the gut microbiome may contribute to early AD processes through its effects on immune regulation, metabolism, and gut-brain communication. Changes in gut microbial composition, including reduced levels of short-chain fatty acid (SCFA)-producing bacteria, such as Faecalibacterium, Roseburia, and Eubacterium, have been reported in individuals with AD and mild cognitive impairment. These microbial alterations have also been linked to disrupted metabolic activity, impaired gut barrier function, and increased neuroinflammatory responses. Diet is an important factor influencing gut microbial composition and metabolic activity. Mediterranean, DASH, and prudent dietary patterns are generally associated with beneficial microbial profiles and increased SCFA production, whereas Western dietary patterns are linked to lower microbial diversity and increased pro-inflammatory taxa. This review summarises the current evidence linking gut microbiota, SCFAs, microbial metabolism, and dietary patterns with early AD pathology, while highlighting important gaps in the existing literature.},
}
MeSH Terms:
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*Alzheimer Disease/microbiology/metabolism
Humans
*Gastrointestinal Microbiome/physiology
Fatty Acids, Volatile/metabolism
Animals
Diet
Brain/metabolism
RevDate: 2026-08-13
CmpDate: 2026-08-13
Gut Microbiota-Targeted Nutrition for Healthy Aging: Mechanistic Roles of Polyphenols and Dietary Fiber in Geroscience.
Nutrients, 18(15): pii:nu18152478.
Age-related alterations in the gut microbiota contribute to chronic low-grade inflammation, immune dysregulation, metabolic dysfunction, frailty, sarcopenia, and cognitive decline. Dietary polyphenols and fermentable fiber modulate microbial composition and metabolism, promoting the production of bioactive metabolites, including short-chain fatty acids, secondary bile acids, indole derivatives, and urolithins, which regulate intestinal barrier integrity, immune homeostasis, mitochondrial function, and gut-organ communication. This narrative review critically synthesizes evidence from experimental studies, observational cohorts, randomized controlled trials, systematic reviews, and meta-analyses to examine microbiota-mediated mechanisms linking these dietary components to healthy aging within the geroscience framework. Although mechanistic evidence is compelling, translation into clinically meaningful aging outcomes remains limited because most intervention studies are small and heterogeneous and primarily rely on surrogate biomarkers. Current evidence supports polyphenol- and fiber-rich dietary patterns as biologically plausible strategies for promoting healthy aging through modulation of the gut microbiota; however, establishing causal relationships will require standardized microbiome methodologies, validated microbiome-derived biomarkers, integrated multi-omics approaches, and adequately powered longitudinal studies and randomized controlled trials.
Additional Links: PMID-42588100
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PubMed:
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@article {pmid42588100,
year = {2026},
author = {Kryczyk-Poprawa, A and Rząsa-Duran, E and Varga, JT and Lehoczki, A and Zábó, V and Fazekas-Pongor, V and Major, D and Csípő, T and Szappanos, Á and Lipécz, Á and Fekete, M},
title = {Gut Microbiota-Targeted Nutrition for Healthy Aging: Mechanistic Roles of Polyphenols and Dietary Fiber in Geroscience.},
journal = {Nutrients},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/nu18152478},
pmid = {42588100},
issn = {2072-6643},
support = {TKP2021-NKTA-47//Ministry of Innovation and Technology/ ; RRF-2.3.1-21-2022-00003//Ministry of Innovation and Technology/ ; No. 101004093/EUniWell/EAC-A02-2019/EAC-A02-2019-1//European University for Well-Being (EUniWell) program/ ; the Cooperative Translational Research Program (KTKP)//the Faculty of Medicine, Semmelweis University/ ; },
mesh = {Humans ; *Polyphenols/pharmacology/administration & dosage ; *Dietary Fiber/administration & dosage/pharmacology ; *Gastrointestinal Microbiome/physiology/drug effects ; *Healthy Aging/physiology ; *Geroscience ; Aging ; Animals ; },
abstract = {Age-related alterations in the gut microbiota contribute to chronic low-grade inflammation, immune dysregulation, metabolic dysfunction, frailty, sarcopenia, and cognitive decline. Dietary polyphenols and fermentable fiber modulate microbial composition and metabolism, promoting the production of bioactive metabolites, including short-chain fatty acids, secondary bile acids, indole derivatives, and urolithins, which regulate intestinal barrier integrity, immune homeostasis, mitochondrial function, and gut-organ communication. This narrative review critically synthesizes evidence from experimental studies, observational cohorts, randomized controlled trials, systematic reviews, and meta-analyses to examine microbiota-mediated mechanisms linking these dietary components to healthy aging within the geroscience framework. Although mechanistic evidence is compelling, translation into clinically meaningful aging outcomes remains limited because most intervention studies are small and heterogeneous and primarily rely on surrogate biomarkers. Current evidence supports polyphenol- and fiber-rich dietary patterns as biologically plausible strategies for promoting healthy aging through modulation of the gut microbiota; however, establishing causal relationships will require standardized microbiome methodologies, validated microbiome-derived biomarkers, integrated multi-omics approaches, and adequately powered longitudinal studies and randomized controlled trials.},
}
MeSH Terms:
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Humans
*Polyphenols/pharmacology/administration & dosage
*Dietary Fiber/administration & dosage/pharmacology
*Gastrointestinal Microbiome/physiology/drug effects
*Healthy Aging/physiology
*Geroscience
Aging
Animals
RevDate: 2026-08-13
CmpDate: 2026-08-13
Multistrain Probiotic Supplementation Combined with a Standardized Diet Did Not Significantly Affect Exercise Performance or Inflammatory Responses in Male Endurance Runners: A Randomized Controlled Trial.
Nutrients, 18(15): pii:nu18152484.
Background: Gut microbiota may influence metabolic and inflammatory responses to exercise through the gut-muscle axis, and probiotic supplementation has been proposed to support adaptation and recovery in endurance athletes. However, evidence in trained populations is inconsistent and is confounded by variability in diet, probiotic strains, dose, and intervention duration. We tested whether a multistrain probiotic, administered against a fully standardized diet, would affect exercise performance and inflammatory, metabolic, and muscle-damage responses. Methods: In this randomized, double-blind, placebo-controlled trial, 30 trained male long-distance runners were randomized and 27 completed the study (probiotic [PRO], n = 13; placebo [PLA], n = 14). All participants followed a standardized, normocaloric meal-box diet for four weeks. Aerobic capacity (peak oxygen uptake, VO2peak; primary outcome) was assessed by an incremental treadmill test and anaerobic performance by a 30 s Wingate test, before (PRE) and after (POST) supplementation. Interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), creatine kinase (CK), and lactate (LA) were measured around exercise. Outcomes were analyzed with linear mixed-effects models; the primary estimand was the group × phase interaction. Results: VO2peak did not differ between groups over time (PLA 55.00 ± 7.60 → 57.33 ± 8.41; PRO 55.40 ± 7.85 → 53.14 ± 5.95 mL·kg[-1]·min[-1]; group × phase -3.5 mL·kg[-1]·min[-1], 95% CI -7.0 to -0.1; nominal p = 0.044, not significant after FDR correction, adjusted p = 0.707). No group × phase or group × phase × sampling-time interaction was significant for IL-6, TNF-α, LA, or CK (all interaction p > 0.15), indicating that supplementation did not modify the exercise-induced response of any biomarker; exercise itself robustly increased IL-6, TNF-α, and LA in both groups (p < 0.001). Conclusions: In trained male endurance runners consuming a standardized diet, four weeks of multistrain probiotic supplementation did not significantly affect aerobic or anaerobic performance, LA response, muscle-damage markers, or circulating inflammatory cytokines compared with placebo. Adequately powered trials with prespecified primary endpoints and direct microbiome assessment are needed.
Additional Links: PMID-42588107
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@article {pmid42588107,
year = {2026},
author = {Jagłowska, K and Folwarski, M and Chroboczek, M and Potrykus, M and Kaczmarczyk, M and Skonieczna-Żydecka, K and Kaczor, JJ},
title = {Multistrain Probiotic Supplementation Combined with a Standardized Diet Did Not Significantly Affect Exercise Performance or Inflammatory Responses in Male Endurance Runners: A Randomized Controlled Trial.},
journal = {Nutrients},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/nu18152484},
pmid = {42588107},
issn = {2072-6643},
support = {2021/41/N/NZ4/02364//National Science Centre, Poland (NCN)/ ; },
mesh = {Humans ; Male ; *Probiotics/administration & dosage ; Double-Blind Method ; *Running/physiology ; *Dietary Supplements ; Adult ; *Physical Endurance/physiology ; *Inflammation ; Tumor Necrosis Factor-alpha/blood ; Interleukin-6/blood ; Creatine Kinase/blood ; Oxygen Consumption ; *Diet ; *Athletic Performance/physiology ; Biomarkers/blood ; Gastrointestinal Microbiome ; },
abstract = {Background: Gut microbiota may influence metabolic and inflammatory responses to exercise through the gut-muscle axis, and probiotic supplementation has been proposed to support adaptation and recovery in endurance athletes. However, evidence in trained populations is inconsistent and is confounded by variability in diet, probiotic strains, dose, and intervention duration. We tested whether a multistrain probiotic, administered against a fully standardized diet, would affect exercise performance and inflammatory, metabolic, and muscle-damage responses. Methods: In this randomized, double-blind, placebo-controlled trial, 30 trained male long-distance runners were randomized and 27 completed the study (probiotic [PRO], n = 13; placebo [PLA], n = 14). All participants followed a standardized, normocaloric meal-box diet for four weeks. Aerobic capacity (peak oxygen uptake, VO2peak; primary outcome) was assessed by an incremental treadmill test and anaerobic performance by a 30 s Wingate test, before (PRE) and after (POST) supplementation. Interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), creatine kinase (CK), and lactate (LA) were measured around exercise. Outcomes were analyzed with linear mixed-effects models; the primary estimand was the group × phase interaction. Results: VO2peak did not differ between groups over time (PLA 55.00 ± 7.60 → 57.33 ± 8.41; PRO 55.40 ± 7.85 → 53.14 ± 5.95 mL·kg[-1]·min[-1]; group × phase -3.5 mL·kg[-1]·min[-1], 95% CI -7.0 to -0.1; nominal p = 0.044, not significant after FDR correction, adjusted p = 0.707). No group × phase or group × phase × sampling-time interaction was significant for IL-6, TNF-α, LA, or CK (all interaction p > 0.15), indicating that supplementation did not modify the exercise-induced response of any biomarker; exercise itself robustly increased IL-6, TNF-α, and LA in both groups (p < 0.001). Conclusions: In trained male endurance runners consuming a standardized diet, four weeks of multistrain probiotic supplementation did not significantly affect aerobic or anaerobic performance, LA response, muscle-damage markers, or circulating inflammatory cytokines compared with placebo. Adequately powered trials with prespecified primary endpoints and direct microbiome assessment are needed.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Male
*Probiotics/administration & dosage
Double-Blind Method
*Running/physiology
*Dietary Supplements
Adult
*Physical Endurance/physiology
*Inflammation
Tumor Necrosis Factor-alpha/blood
Interleukin-6/blood
Creatine Kinase/blood
Oxygen Consumption
*Diet
*Athletic Performance/physiology
Biomarkers/blood
Gastrointestinal Microbiome
RevDate: 2026-08-13
CmpDate: 2026-08-13
From Diet to Dysbiosis: How Nutritional Factors Shape Gut Microbiota and Drive Airway Inflammation in Pediatric Asthma.
Nutrients, 18(15): pii:nu18152496.
Asthma prevalence in school-age children varies widely by geography, from below 5% in some regions to above 20% in others, averaging 10-12% across industrialized countries, but genetic factors account for less than 40% of disease liability. Gut microbiota is increasingly recognized as a critical intermediary between early-life dietary exposure and immunological trajectories that determine asthma susceptibility. Through the production of short-chain fatty acids (SCFAs), particularly butyrate, propionate, and acetate, commensal bacteria regulate dendritic cell function, promote T-regulatory (Treg) cell differentiation, and attenuate Th2-polarized airway inflammation via the gut-lung axis. Epidemiological cohorts including CHILD, WHEALS, and PASTURE associate early-life dysbiosis and reduced Lactobacillus, Bifidobacterium, and Faecalibacterium prausnitzii with increased asthma risk, while dietary patterns rich in fermentable fibre, omega-3 polyunsaturated fatty acids, and diverse plant-based foods are associated with preserved microbial diversity and, in preclinical models, attenuated type-2 inflammatory signalling. This narrative review synthesizes mechanistic and epidemiological evidence on how nutritional exposures shape gut microbiota composition and influences asthma onset and severity in paediatric populations, including the distinct obesity-related asthma phenotype. Critical gaps, insufficient dietary intervention trials with microbiome endpoints, methodological heterogeneity across cohorts, and the paucity of data from non-Western populations are discussed, with implications for preventive nutritional counselling in paediatric allergology practice.
Additional Links: PMID-42588119
Publisher:
PubMed:
Citation:
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@article {pmid42588119,
year = {2026},
author = {Temneanu, OR and Mihai, A and Olariu, R and Oros, M and Ioniuc, I and Lupu, VV and Lupu, A and Grudnicki, A and Roșu, MF and Șerban, R and Avasiloaiei, AL and Popovici, P},
title = {From Diet to Dysbiosis: How Nutritional Factors Shape Gut Microbiota and Drive Airway Inflammation in Pediatric Asthma.},
journal = {Nutrients},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/nu18152496},
pmid = {42588119},
issn = {2072-6643},
mesh = {Humans ; *Dysbiosis/microbiology ; *Asthma/microbiology/epidemiology/immunology/etiology ; Child ; *Gastrointestinal Microbiome/physiology ; *Diet/adverse effects ; Inflammation ; },
abstract = {Asthma prevalence in school-age children varies widely by geography, from below 5% in some regions to above 20% in others, averaging 10-12% across industrialized countries, but genetic factors account for less than 40% of disease liability. Gut microbiota is increasingly recognized as a critical intermediary between early-life dietary exposure and immunological trajectories that determine asthma susceptibility. Through the production of short-chain fatty acids (SCFAs), particularly butyrate, propionate, and acetate, commensal bacteria regulate dendritic cell function, promote T-regulatory (Treg) cell differentiation, and attenuate Th2-polarized airway inflammation via the gut-lung axis. Epidemiological cohorts including CHILD, WHEALS, and PASTURE associate early-life dysbiosis and reduced Lactobacillus, Bifidobacterium, and Faecalibacterium prausnitzii with increased asthma risk, while dietary patterns rich in fermentable fibre, omega-3 polyunsaturated fatty acids, and diverse plant-based foods are associated with preserved microbial diversity and, in preclinical models, attenuated type-2 inflammatory signalling. This narrative review synthesizes mechanistic and epidemiological evidence on how nutritional exposures shape gut microbiota composition and influences asthma onset and severity in paediatric populations, including the distinct obesity-related asthma phenotype. Critical gaps, insufficient dietary intervention trials with microbiome endpoints, methodological heterogeneity across cohorts, and the paucity of data from non-Western populations are discussed, with implications for preventive nutritional counselling in paediatric allergology practice.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Dysbiosis/microbiology
*Asthma/microbiology/epidemiology/immunology/etiology
Child
*Gastrointestinal Microbiome/physiology
*Diet/adverse effects
Inflammation
RevDate: 2026-08-13
CmpDate: 2026-08-13
Natural Bioactive Compounds Targeting Key Hallmarks of Aging: Functional Food Potential of Spermidine, Fisetin, Berberine, and Urolithin A.
Nutrients, 18(15): pii:nu18152511.
Naturally derived bioactive compounds that modulate aging-associated mechanisms have attracted growing research interest, yet few reviews examine how such compounds might act together. This narrative review examines four mechanistically distinct compounds, namely spermidine, fisetin, berberine, and urolithin A, as emerging functional food ingredients with scientifically supported effects on key hallmarks of human aging. Spermidine, a dietary polyamine from wheat germ and fermented foods, induces autophagy through EP300 inhibition and is associated with reduced all-cause mortality in prospective studies. Fisetin, a flavonoid from strawberries and apples, exerts senolytic activity by selectively eliminating senescent cells via PI3K/AKT and Bcl-2/Bcl-xL inhibition, with emerging clinical evidence. Berberine, an isoquinoline alkaloid from Berberis species, modulates metabolic dysfunction via AMP-activated protein kinase (AMPK) activation and reshapes gut microbiota composition through direct high intraluminal exposure, with the most extensive clinical dataset of the four compounds. Urolithin A, a gut microbiome-derived postbiotic from ellagitannins in pomegranates and nuts, induces mitophagy via PINK1/Parkin and has been evaluated in a growing number of registered human clinical trials. Together, the four compounds primarily target distinct but complementary aging-associated pathways (autophagy, senolysis, metabolic regulation, mitophagy), suggesting rational potential for combined functional food formulations. Limited direct evidence for their combined use and the need for dedicated co-administration studies are discussed, alongside bioavailability, safety, and regulatory considerations.
Additional Links: PMID-42588134
Publisher:
PubMed:
Citation:
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@article {pmid42588134,
year = {2026},
author = {Rzeski, W and Rzeska, W},
title = {Natural Bioactive Compounds Targeting Key Hallmarks of Aging: Functional Food Potential of Spermidine, Fisetin, Berberine, and Urolithin A.},
journal = {Nutrients},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/nu18152511},
pmid = {42588134},
issn = {2072-6643},
mesh = {Humans ; *Coumarins/pharmacology ; *Aging/drug effects ; Flavonols/pharmacology ; *Spermidine/pharmacology ; *Berberine/pharmacology ; *Functional Food ; *Flavonoids/pharmacology ; Animals ; Autophagy/drug effects ; },
abstract = {Naturally derived bioactive compounds that modulate aging-associated mechanisms have attracted growing research interest, yet few reviews examine how such compounds might act together. This narrative review examines four mechanistically distinct compounds, namely spermidine, fisetin, berberine, and urolithin A, as emerging functional food ingredients with scientifically supported effects on key hallmarks of human aging. Spermidine, a dietary polyamine from wheat germ and fermented foods, induces autophagy through EP300 inhibition and is associated with reduced all-cause mortality in prospective studies. Fisetin, a flavonoid from strawberries and apples, exerts senolytic activity by selectively eliminating senescent cells via PI3K/AKT and Bcl-2/Bcl-xL inhibition, with emerging clinical evidence. Berberine, an isoquinoline alkaloid from Berberis species, modulates metabolic dysfunction via AMP-activated protein kinase (AMPK) activation and reshapes gut microbiota composition through direct high intraluminal exposure, with the most extensive clinical dataset of the four compounds. Urolithin A, a gut microbiome-derived postbiotic from ellagitannins in pomegranates and nuts, induces mitophagy via PINK1/Parkin and has been evaluated in a growing number of registered human clinical trials. Together, the four compounds primarily target distinct but complementary aging-associated pathways (autophagy, senolysis, metabolic regulation, mitophagy), suggesting rational potential for combined functional food formulations. Limited direct evidence for their combined use and the need for dedicated co-administration studies are discussed, alongside bioavailability, safety, and regulatory considerations.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Coumarins/pharmacology
*Aging/drug effects
Flavonols/pharmacology
*Spermidine/pharmacology
*Berberine/pharmacology
*Functional Food
*Flavonoids/pharmacology
Animals
Autophagy/drug effects
RevDate: 2026-08-13
CmpDate: 2026-08-13
Food Additive Mixtures, Glucose Metabolism, and Type 2 Diabetes Mellitus Risk: Mechanistic Insights from Epidemiology, Human Intervention Studies, and Experimental Models.
Nutrients, 18(15): pii:nu18152521.
Food additives are consumed as mixtures in ultra-processed foods, but their independent contribution to glucose dysregulation is difficult to separate from diet quality and food matrix. PubMed/MEDLINE, Embase, Web of Science Core Collection, Scopus, and CENTRAL were searched from inception to 30 April 2026, followed by a supplementary PubMed update on 26 July 2026. This critical narrative review integrates epidemiological, human-intervention, animal, ex vivo, and mechanistic evidence. Successive NutriNet-Santé analyses associate several additive co-exposure profiles, emulsifiers, preservatives, food colouring additives, and non-nutritive sweeteners with incident type 2 diabetes mellitus. However, these analyses use substantially overlapping participants, lack independent additive-specific cohort replication, and remain vulnerable to residual confounding. Experimental evidence is strongest for selected emulsifiers and sweeteners, which may alter gut microbiota, intestinal barrier function, inflammatory signalling, or short-term glycaemic responses. No human trial has demonstrated the complete pathway from additive exposure to clinically meaningful insulin resistance or diabetes, and null or compound-specific findings argue against a uniform class effect. Current evidence therefore supports biological plausibility, not causality or additive-specific clinical recommendations. Longer controlled feeding trials should test realistic mixtures while holding the food matrix constant and should incorporate exposure validation, repeated microbiome and metabolomic sampling, intestinal permeability measures, and validated insulin-sensitivity endpoints.
Additional Links: PMID-42588144
Publisher:
PubMed:
Citation:
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@article {pmid42588144,
year = {2026},
author = {Santic, R and Kumric, M and Pavlovic, N and Bozic, J},
title = {Food Additive Mixtures, Glucose Metabolism, and Type 2 Diabetes Mellitus Risk: Mechanistic Insights from Epidemiology, Human Intervention Studies, and Experimental Models.},
journal = {Nutrients},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/nu18152521},
pmid = {42588144},
issn = {2072-6643},
mesh = {Humans ; *Diabetes Mellitus, Type 2/epidemiology/etiology ; *Food Additives/adverse effects ; Animals ; *Blood Glucose/metabolism ; *Glucose/metabolism ; Risk Factors ; Gastrointestinal Microbiome/drug effects ; },
abstract = {Food additives are consumed as mixtures in ultra-processed foods, but their independent contribution to glucose dysregulation is difficult to separate from diet quality and food matrix. PubMed/MEDLINE, Embase, Web of Science Core Collection, Scopus, and CENTRAL were searched from inception to 30 April 2026, followed by a supplementary PubMed update on 26 July 2026. This critical narrative review integrates epidemiological, human-intervention, animal, ex vivo, and mechanistic evidence. Successive NutriNet-Santé analyses associate several additive co-exposure profiles, emulsifiers, preservatives, food colouring additives, and non-nutritive sweeteners with incident type 2 diabetes mellitus. However, these analyses use substantially overlapping participants, lack independent additive-specific cohort replication, and remain vulnerable to residual confounding. Experimental evidence is strongest for selected emulsifiers and sweeteners, which may alter gut microbiota, intestinal barrier function, inflammatory signalling, or short-term glycaemic responses. No human trial has demonstrated the complete pathway from additive exposure to clinically meaningful insulin resistance or diabetes, and null or compound-specific findings argue against a uniform class effect. Current evidence therefore supports biological plausibility, not causality or additive-specific clinical recommendations. Longer controlled feeding trials should test realistic mixtures while holding the food matrix constant and should incorporate exposure validation, repeated microbiome and metabolomic sampling, intestinal permeability measures, and validated insulin-sensitivity endpoints.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Diabetes Mellitus, Type 2/epidemiology/etiology
*Food Additives/adverse effects
Animals
*Blood Glucose/metabolism
*Glucose/metabolism
Risk Factors
Gastrointestinal Microbiome/drug effects
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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.
Technologist
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.
Publisher
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.
Speaker
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.
Facilitator
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.
RJR Picks from Around the Web (updated 11 MAY 2018 )
Old Science
Weird Science
Treating Disease with Fecal Transplantation
Fossils of miniature humans (hobbits) discovered in Indonesia
Paleontology
Dinosaur tail, complete with feathers, found preserved in amber.
Astronomy
Mysterious fast radio burst (FRB) detected in the distant universe.
Big Data & Informatics
Big Data: Buzzword or Big Deal?
Hacking the genome: Identifying anonymized human subjects using publicly available data.