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ESP: PubMed Auto Bibliography 02 Jul 2026 at 01:58 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: 2026-06-29
CmpDate: 2026-06-29
Genome-based reclassification of Desulfovibrio sp. G11 (DSM 7057) as Desulfovibrio falkowii with an emended description of the species.
International journal of systematic and evolutionary microbiology, 76(6):.
Desulfovibrio sp. G11, originally isolated from bovine rumen fluid, has served as a model organism in many studies. Our analyses suggest its reassignment to Desulfovibrio falkowii, a species recently described from the human gut microbiome. Here, we present a genome-based reclassification of strain G11 using digital DNA-DNA hybridization (dDDH), average nucleotide identity (ANI) and phylogenomic inference. Our results show dDDH values ranging from 74.5 to 92.7% and an ANI of 98.73% between strain G11 and the D. falkowii type strain 13CB8C (DSM 116810T), supporting their relation. In addition, we expand the phenotypic description of D. falkowii by demonstrating catalase and desulfoviridin positivity and confirming motility in multiple strains, including the type strain previously described as non-motile.
Additional Links: PMID-42371689
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@article {pmid42371689,
year = {2026},
author = {Kolsi, A and Mohammadi, K and Hakovirta, J and Saris, PEJ},
title = {Genome-based reclassification of Desulfovibrio sp. G11 (DSM 7057) as Desulfovibrio falkowii with an emended description of the species.},
journal = {International journal of systematic and evolutionary microbiology},
volume = {76},
number = {6},
pages = {},
pmid = {42371689},
issn = {1466-5034},
mesh = {*Desulfovibrio/classification/genetics/isolation & purification ; *Phylogeny ; *Genome, Bacterial ; DNA, Bacterial/genetics ; Animals ; Sequence Analysis, DNA ; RNA, Ribosomal, 16S/genetics ; Cattle ; Bacterial Typing Techniques ; Nucleic Acid Hybridization ; Rumen/microbiology ; },
abstract = {Desulfovibrio sp. G11, originally isolated from bovine rumen fluid, has served as a model organism in many studies. Our analyses suggest its reassignment to Desulfovibrio falkowii, a species recently described from the human gut microbiome. Here, we present a genome-based reclassification of strain G11 using digital DNA-DNA hybridization (dDDH), average nucleotide identity (ANI) and phylogenomic inference. Our results show dDDH values ranging from 74.5 to 92.7% and an ANI of 98.73% between strain G11 and the D. falkowii type strain 13CB8C (DSM 116810T), supporting their relation. In addition, we expand the phenotypic description of D. falkowii by demonstrating catalase and desulfoviridin positivity and confirming motility in multiple strains, including the type strain previously described as non-motile.},
}
MeSH Terms:
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*Desulfovibrio/classification/genetics/isolation & purification
*Phylogeny
*Genome, Bacterial
DNA, Bacterial/genetics
Animals
Sequence Analysis, DNA
RNA, Ribosomal, 16S/genetics
Cattle
Bacterial Typing Techniques
Nucleic Acid Hybridization
Rumen/microbiology
RevDate: 2026-06-29
Microbiome-Targeted Antibiotics Provide No Additional Microbiologic or Inflammatory Benefit during Cystic Fibrosis Pulmonary Exacerbations: Results from the CFMATTERS Trial.
American journal of respiratory and critical care medicine pii:8721555 [Epub ahead of print].
Additional Links: PMID-42371757
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@article {pmid42371757,
year = {2026},
author = {Einarsson, GG and Lee, AJ and Alfahl, Z and Kerrigan, L and Eustace, JA and Weldon, S and Plant, BJ and Elborn, JS and Taggart, CC and Mall, MA and Tunney, MM},
title = {Microbiome-Targeted Antibiotics Provide No Additional Microbiologic or Inflammatory Benefit during Cystic Fibrosis Pulmonary Exacerbations: Results from the CFMATTERS Trial.},
journal = {American journal of respiratory and critical care medicine},
volume = {},
number = {},
pages = {},
doi = {10.1093/ajrccm/aamag336},
pmid = {42371757},
issn = {1535-4970},
}
RevDate: 2026-06-29
CmpDate: 2026-06-29
Seasonal dynamics in sheep fecal microbiome and soil bacterial communities under grazing management.
PloS one, 21(6):e0352436.
The gut microbiome plays a key role in animal health, productivity, and environmental sustainability. As it represents a valuable proxy for animal welfare, its investigation has become increasingly important in livestock studies. With the growing focus on promoting sustainable livestock, supporting rural areas at risk of abandonment is receiving particular attention. Indeed, sheep grazing offers a promising strategy for improving sustainability, biodiversity, and land management. This study focuses on the interconnected dynamics between the sheep gut and soil microbiomes, assessing how seasonal changes and grazing activity shape microbial diversity and community structure across the animal-soil interface. Fecal and soil samples were collected throughout 2024 in a commercial farm in Tuscany, Italy: 215 fecal and 46 soil samples (23 pasture and 23 meadow - i.e., not grazed) were stored. Alpha and Beta diversity were assessed using the Kruskal-Wallis test and PERMANOVA, respectively, and the differential abundance analysis was also performed. The relative abundance analysis at the family and genus level revealed an increase in the number of taxa from winter to autumn in both fecal and soil samples. When the Chao1 index was considered, alpha diversity was higher in fecal samples, followed by soils. Principal Coordinate Analysis revealed distinct clustering between animal and soil microbiota, with slightly reduced differentiation in Summer. In fecal samples, the five most abundant bacterial families were Ruminococcaceae, Spirochaetaceae, Porphyromonadaceae, Lachnospiraceae, and Rikenellaceae, whose abundance varied seasonally. Ruminococcaceae, Lachnospiraceae, and Rikenellaceae decreased in Summer, while Spirochaetaceae and Porphyromonadaceae increased. The increased abundance of these families during Summer may reflect heat stress in animals. Differential abundance analysis also suggested potential microbial transfer from animals to soil: Peptostreptococcaceae and Erysipelotrichaceae were enriched in grazed soils across multiple seasons. Repeated cross-sectional studies like this are essential for understanding microbiome dynamics and animal-soil interactions in grazing systems.
Additional Links: PMID-42371924
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Citation:
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@article {pmid42371924,
year = {2026},
author = {Fabbri, MC and Biada, I and Ceccherini, MT and Maltecca, C and Fiore, B and Sirtori, F and Pulido-Rodríguez, L and Mastrolonardo, G and Bozzi, R and Tiezzi, F},
title = {Seasonal dynamics in sheep fecal microbiome and soil bacterial communities under grazing management.},
journal = {PloS one},
volume = {21},
number = {6},
pages = {e0352436},
pmid = {42371924},
issn = {1932-6203},
mesh = {Animals ; Seasons ; *Soil Microbiology ; *Feces/microbiology ; Sheep/microbiology ; *Bacteria/classification/genetics/isolation & purification ; Biodiversity ; Italy ; *Gastrointestinal Microbiome ; *Microbiota ; },
abstract = {The gut microbiome plays a key role in animal health, productivity, and environmental sustainability. As it represents a valuable proxy for animal welfare, its investigation has become increasingly important in livestock studies. With the growing focus on promoting sustainable livestock, supporting rural areas at risk of abandonment is receiving particular attention. Indeed, sheep grazing offers a promising strategy for improving sustainability, biodiversity, and land management. This study focuses on the interconnected dynamics between the sheep gut and soil microbiomes, assessing how seasonal changes and grazing activity shape microbial diversity and community structure across the animal-soil interface. Fecal and soil samples were collected throughout 2024 in a commercial farm in Tuscany, Italy: 215 fecal and 46 soil samples (23 pasture and 23 meadow - i.e., not grazed) were stored. Alpha and Beta diversity were assessed using the Kruskal-Wallis test and PERMANOVA, respectively, and the differential abundance analysis was also performed. The relative abundance analysis at the family and genus level revealed an increase in the number of taxa from winter to autumn in both fecal and soil samples. When the Chao1 index was considered, alpha diversity was higher in fecal samples, followed by soils. Principal Coordinate Analysis revealed distinct clustering between animal and soil microbiota, with slightly reduced differentiation in Summer. In fecal samples, the five most abundant bacterial families were Ruminococcaceae, Spirochaetaceae, Porphyromonadaceae, Lachnospiraceae, and Rikenellaceae, whose abundance varied seasonally. Ruminococcaceae, Lachnospiraceae, and Rikenellaceae decreased in Summer, while Spirochaetaceae and Porphyromonadaceae increased. The increased abundance of these families during Summer may reflect heat stress in animals. Differential abundance analysis also suggested potential microbial transfer from animals to soil: Peptostreptococcaceae and Erysipelotrichaceae were enriched in grazed soils across multiple seasons. Repeated cross-sectional studies like this are essential for understanding microbiome dynamics and animal-soil interactions in grazing systems.},
}
MeSH Terms:
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hide MeSH Terms
Animals
Seasons
*Soil Microbiology
*Feces/microbiology
Sheep/microbiology
*Bacteria/classification/genetics/isolation & purification
Biodiversity
Italy
*Gastrointestinal Microbiome
*Microbiota
RevDate: 2026-06-29
Trichoderma enriches Burkholderia via cross-feeding of degradation intermediates to enhance atrazine degradation and alleviate soybean phytotoxicity.
The ISME journal pii:8721683 [Epub ahead of print].
The widespread agricultural use of atrazine threatens soil health, and residual phytotoxicity in corn-soybean rotation systems necessitates sustainable remediation strategies. By leveraging the atrazine-degrading fungus Trichoderma lentiforme HN154, we achieved an 80.3% removal of atrazine (500 mg/kg) in non-sterilized soils from a corn planting system within 14 days, 22.1% higher degradation than in sterilized soil, while concurrently alleviating phytotoxic symptoms in soybean plants. Metagenomic analysis revealed that colonization by T. lentiforme HN154 drove restructuring of microbial networks, enriching the keystone family Burkholderiaceae, which was strongly associated with atrazine catabolism and four key catabolic enzymes (EC 3.5.4.43 (atzB), EC 3.5.1.131 (atzE), EC 3.5.1.54 (atzF), EC 3.5.4.42 (atzC)). Among 23 rhizosphere isolates, the Burkholderia strains Bur-4, Bur-5, and Bur-14 showed the highest atrazine degradation rates (26.3% - 29.4%) within 72 h. A Trichoderma-Burkholderia synthetic consortium further enhanced remediation by boosting plant antioxidant defenses (SOD, POD, CAT) and reducing oxidative damage (MDA). Mechanistically, intermediates (hydroxyatrazine and biuret) generated during T. lentiforme HN154-mediated degradation stimulated Burkholderia chemotaxis, swarming and swimming motility, while cross-feeding on these metabolites synergistically accelerated bioaugmentation (the Trichoderma-Burkholderia synthetic consortium achieved rapid atrazine degradation of 86.3% within 168 h). This study reveals tripartite interactions among exogenous microbial degraders, pollutant metabolites, and indigenous microbiota, offering a strategic foundation for microbiome-guided, precision bioaugmentation to restore soil ecological health and crop resilience.
Additional Links: PMID-42372060
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@article {pmid42372060,
year = {2026},
author = {Jiang, H and Zhang, M and Khan, RAA and Zhao, J and Hou, J and Liu, T},
title = {Trichoderma enriches Burkholderia via cross-feeding of degradation intermediates to enhance atrazine degradation and alleviate soybean phytotoxicity.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag152},
pmid = {42372060},
issn = {1751-7370},
abstract = {The widespread agricultural use of atrazine threatens soil health, and residual phytotoxicity in corn-soybean rotation systems necessitates sustainable remediation strategies. By leveraging the atrazine-degrading fungus Trichoderma lentiforme HN154, we achieved an 80.3% removal of atrazine (500 mg/kg) in non-sterilized soils from a corn planting system within 14 days, 22.1% higher degradation than in sterilized soil, while concurrently alleviating phytotoxic symptoms in soybean plants. Metagenomic analysis revealed that colonization by T. lentiforme HN154 drove restructuring of microbial networks, enriching the keystone family Burkholderiaceae, which was strongly associated with atrazine catabolism and four key catabolic enzymes (EC 3.5.4.43 (atzB), EC 3.5.1.131 (atzE), EC 3.5.1.54 (atzF), EC 3.5.4.42 (atzC)). Among 23 rhizosphere isolates, the Burkholderia strains Bur-4, Bur-5, and Bur-14 showed the highest atrazine degradation rates (26.3% - 29.4%) within 72 h. A Trichoderma-Burkholderia synthetic consortium further enhanced remediation by boosting plant antioxidant defenses (SOD, POD, CAT) and reducing oxidative damage (MDA). Mechanistically, intermediates (hydroxyatrazine and biuret) generated during T. lentiforme HN154-mediated degradation stimulated Burkholderia chemotaxis, swarming and swimming motility, while cross-feeding on these metabolites synergistically accelerated bioaugmentation (the Trichoderma-Burkholderia synthetic consortium achieved rapid atrazine degradation of 86.3% within 168 h). This study reveals tripartite interactions among exogenous microbial degraders, pollutant metabolites, and indigenous microbiota, offering a strategic foundation for microbiome-guided, precision bioaugmentation to restore soil ecological health and crop resilience.},
}
RevDate: 2026-06-29
Selenium nanoparticles alleviate chromium stress in wheat (Triticum aestivum L.) by inhibiting root uptake, enhancing antioxidant capacity, and regulating the rhizosphere microbiome.
Journal of environmental management, 413:130214 pii:S0301-4797(26)01674-9 [Epub ahead of print].
Chromium (Cr) pollution poses a severe threat to crop production, while the detoxification mechanisms of selenium nanoparticles (SeNPs) in the Triticum aestivum L rhizosphere microbiome remain unclear. This study investigated the mitigation effects of SeNPs on Cr toxicity in wheat seedlings through pot experiments. Results showed that SeNPs significantly reduced Cr accumulation in wheat roots and aboveground parts by 21.87% and 35.19%, respectively and inhibited Cr transport from roots to aboveground parts by 17.05%. SeNPs promoted seedling growth, enhanced root vitality, reduced malondialdehyde (MDA) content, and increased antioxidant enzyme activities such as superoxide dismutase (SOD) and peroxidase (POD), thereby mitigating oxidative damage. Metabolomics analysis revealed that SeNPs upregulated levels of rhizosphere metabolites including xanthine, L-proline, and betaine, synergistically enhancing the rhizosphere's reactive oxygen species (ROS) scavenging capacity. Microbiome analysis further indicates that SeNPs enrich beneficial microbial communities involved in carbon cycling (Gemmatimonas), nitrogen cycling (Actinobacteria), phosphorus cycling (Proteobacteria), and chromium fixation (Firmicutes), thereby reshaping the rhizosphere microbial community structure. Concurrently, they enhance the activity of key enzymes such as soil urease (S-UE) and sucrase (S-SC), thereby improving carbon, nitrogen, and phosphorus nutrient cycling and reducing Cr bioavailability. Collectively, this study reveals a multidimensional mechanism by which Se nanoparticles mitigate chromium toxicity through root barrier reinforcement, antioxidant activation, and microbiome remodeling, offering a nano-enabled strategy for safe crop production in contaminated soils.
Additional Links: PMID-42372448
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@article {pmid42372448,
year = {2026},
author = {Qu, L and Liu, H and Li, J and Li, X and Chen, R and Liang, X and Jia, X and Wu, P and Qiao, X and Xu, C},
title = {Selenium nanoparticles alleviate chromium stress in wheat (Triticum aestivum L.) by inhibiting root uptake, enhancing antioxidant capacity, and regulating the rhizosphere microbiome.},
journal = {Journal of environmental management},
volume = {413},
number = {},
pages = {130214},
doi = {10.1016/j.jenvman.2026.130214},
pmid = {42372448},
issn = {1095-8630},
abstract = {Chromium (Cr) pollution poses a severe threat to crop production, while the detoxification mechanisms of selenium nanoparticles (SeNPs) in the Triticum aestivum L rhizosphere microbiome remain unclear. This study investigated the mitigation effects of SeNPs on Cr toxicity in wheat seedlings through pot experiments. Results showed that SeNPs significantly reduced Cr accumulation in wheat roots and aboveground parts by 21.87% and 35.19%, respectively and inhibited Cr transport from roots to aboveground parts by 17.05%. SeNPs promoted seedling growth, enhanced root vitality, reduced malondialdehyde (MDA) content, and increased antioxidant enzyme activities such as superoxide dismutase (SOD) and peroxidase (POD), thereby mitigating oxidative damage. Metabolomics analysis revealed that SeNPs upregulated levels of rhizosphere metabolites including xanthine, L-proline, and betaine, synergistically enhancing the rhizosphere's reactive oxygen species (ROS) scavenging capacity. Microbiome analysis further indicates that SeNPs enrich beneficial microbial communities involved in carbon cycling (Gemmatimonas), nitrogen cycling (Actinobacteria), phosphorus cycling (Proteobacteria), and chromium fixation (Firmicutes), thereby reshaping the rhizosphere microbial community structure. Concurrently, they enhance the activity of key enzymes such as soil urease (S-UE) and sucrase (S-SC), thereby improving carbon, nitrogen, and phosphorus nutrient cycling and reducing Cr bioavailability. Collectively, this study reveals a multidimensional mechanism by which Se nanoparticles mitigate chromium toxicity through root barrier reinforcement, antioxidant activation, and microbiome remodeling, offering a nano-enabled strategy for safe crop production in contaminated soils.},
}
RevDate: 2026-06-29
Targeted genomic editing of human gut Bacteroides species based on CRISPR-associated transposases.
Cell systems pii:S2405-4712(26)00132-8 [Epub ahead of print].
Gut Bacteroides are abundant and critical to human health, yet most are genetically cumbersome, non-model microbes. A widely applicable editing tool for Bacteroides is essential for gut microbiome manipulation. Here, we develop STIB (ShCAST-based transient insertion system for Bacteroides), an efficient genome-editing tool derived from CRISPR-associated transposases that enables rapid and site-specific insertions independent of homologous recombination. By fusing a nicking homing endonuclease to the transposase and an ATPase to Cas12k, we systematically optimize STIB to minimize plasmid cointegration and achieve >97% on-target insertion. STIB exhibits broad applicability across different genomic loci in diverse Bacteroides species, including non-model species. Finally, we apply STIB to achieve species- and site-specific editing of distinct Bacteroides species within a complex synthetic gut microbiota. Overall, STIB expands the toolbox for the functional investigation and engineering of the human microbiome. A record of this paper's transparent peer review process is included in the supplemental information.
Additional Links: PMID-42372725
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PubMed:
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@article {pmid42372725,
year = {2026},
author = {Hu, Y and Li, Q and Li, Y and Zeng, Y and Zheng, L and Shen, J and Gao, X and Zhao, GP and Zhao, W and Dai, L},
title = {Targeted genomic editing of human gut Bacteroides species based on CRISPR-associated transposases.},
journal = {Cell systems},
volume = {},
number = {},
pages = {101650},
doi = {10.1016/j.cels.2026.101650},
pmid = {42372725},
issn = {2405-4720},
abstract = {Gut Bacteroides are abundant and critical to human health, yet most are genetically cumbersome, non-model microbes. A widely applicable editing tool for Bacteroides is essential for gut microbiome manipulation. Here, we develop STIB (ShCAST-based transient insertion system for Bacteroides), an efficient genome-editing tool derived from CRISPR-associated transposases that enables rapid and site-specific insertions independent of homologous recombination. By fusing a nicking homing endonuclease to the transposase and an ATPase to Cas12k, we systematically optimize STIB to minimize plasmid cointegration and achieve >97% on-target insertion. STIB exhibits broad applicability across different genomic loci in diverse Bacteroides species, including non-model species. Finally, we apply STIB to achieve species- and site-specific editing of distinct Bacteroides species within a complex synthetic gut microbiota. Overall, STIB expands the toolbox for the functional investigation and engineering of the human microbiome. A record of this paper's transparent peer review process is included in the supplemental information.},
}
RevDate: 2026-06-29
The interplay between the microbiome and immune cells in metabolic homeostasis and disease.
Cell metabolism pii:S1550-4131(26)00230-5 [Epub ahead of print].
Microbiome-derived metabolites, including short-chain fatty acids, bile acids, indoles, and lipopolysaccharides, among other bioactives, modulate mammalian immune cells through a variety of molecular processes, including epigenetic remodeling, mitochondrial metabolic reprogramming, and regulation of mTOR and AMPK signaling pathways. These diverse signals shape inflammatory programs that influence metabolic outcomes in a context-dependent manner, which may sustain metabolic health or drive chronic inflammation impacting obesity, type 2 diabetes, metabolic dysfunction-associated steatotic liver disease, and cardiovascular diseases. Here, we review these metabolite-driven immune-metabolic influences and highlight innovative directions in their exploration, including integration of spatial and single-cell multi-omics to deconvolute microbiome-derived signaling networks within metabolic tissues. We further outline emerging microbiome-based therapeutic strategies targeting immune pathways in cardiometabolic disease, ranging from personalized nutrition, precision probiotics, and microbial consortium transplantation to metabolite-based postbiotics. Collectively, advancing our understanding of host immune-microbiome-metabolic interactions may support the development of targeted interventions for the prevention and treatment of cardiometabolic diseases.
Additional Links: PMID-42372727
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PubMed:
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@article {pmid42372727,
year = {2026},
author = {Shapiro, H and Jickeli, B and Niv, I and Ernan, B and Elinav, E},
title = {The interplay between the microbiome and immune cells in metabolic homeostasis and disease.},
journal = {Cell metabolism},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmet.2026.06.004},
pmid = {42372727},
issn = {1932-7420},
abstract = {Microbiome-derived metabolites, including short-chain fatty acids, bile acids, indoles, and lipopolysaccharides, among other bioactives, modulate mammalian immune cells through a variety of molecular processes, including epigenetic remodeling, mitochondrial metabolic reprogramming, and regulation of mTOR and AMPK signaling pathways. These diverse signals shape inflammatory programs that influence metabolic outcomes in a context-dependent manner, which may sustain metabolic health or drive chronic inflammation impacting obesity, type 2 diabetes, metabolic dysfunction-associated steatotic liver disease, and cardiovascular diseases. Here, we review these metabolite-driven immune-metabolic influences and highlight innovative directions in their exploration, including integration of spatial and single-cell multi-omics to deconvolute microbiome-derived signaling networks within metabolic tissues. We further outline emerging microbiome-based therapeutic strategies targeting immune pathways in cardiometabolic disease, ranging from personalized nutrition, precision probiotics, and microbial consortium transplantation to metabolite-based postbiotics. Collectively, advancing our understanding of host immune-microbiome-metabolic interactions may support the development of targeted interventions for the prevention and treatment of cardiometabolic diseases.},
}
RevDate: 2026-06-29
Maternal antibiotic exposure alters the newborn metabolomic profile and increases the risk of respiratory infections in offspring: a 13-year longitudinal birth cohort study.
The Journal of allergy and clinical immunology pii:S0091-6749(26)00448-3 [Epub ahead of print].
BACKGROUND: Maternal antibiotic exposure during pregnancy has been associated with early childhood infection proneness, but the underlying mechanisms remain unknown. Longitudinal birth cohort studies with long follow-up and multi-omics data are lacking.
OBJECTIVE: To 1) investigate the association between prenatal antibiotics and offspring infection risk 2) investigate the potential mechanisms.
METHODS: The Danish population-based COPSAC2010 cohort with 663 mother-child pairs were followed from pregnancy until age 13 years. Detailed infection diaries age 0-3 years for common infections (cold, tonsillitis, otitis media, fever, gastrointestinal infections, and pneumonia) and moderate-to-severe (hospital diagnoses) infections were registered until age 13 years. We analyzed maternal antibiotic exposure vs risk of offspring infection risk with assessments of newborn child blood metabolome, gut and airway (age 1 week and 1 month) microbiome, and airway cytokine profiles (age 1 month). We adjusted for genetic, environmental, and socioeconomic factors.
RESULTS: Children whose mothers were exposed to antibiotic treatment during pregnancy had a higher risk of infections until age 13 years: adjusted incidence rate ratio (aIRR): 1.75 (1.19-2.57), p=0.005) and pneumonia (aIRR: 1.81 (1.10-2.99), p=0.015). Maternal antibiotic exposure related changes in the newborn child metabolome profile associated with increased child pneumonia, tonsilitis and fever risk. Both number and types of maternal antibiotic treatments had an impact on offspring infection risk. There were no noticeable findings for microbiome, genetics and airway cytokine profiling.
CONCLUSION: Maternal antibiotics during pregnancy increased long-term risk of childhood respiratory infection risk following a dose-response pattern, which was linked to newborn metabolomic alterations.
Additional Links: PMID-42372831
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PubMed:
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@article {pmid42372831,
year = {2026},
author = {Hauerslev, M and Wang, T and Kjellberg, A and Luo, Y and Thorsen, J and Brix, S and Sultan, T and Sørensen, S and Ernst, M and Stokholm, J and Bønnelykke, K and Chawes, B and Brustad, N},
title = {Maternal antibiotic exposure alters the newborn metabolomic profile and increases the risk of respiratory infections in offspring: a 13-year longitudinal birth cohort study.},
journal = {The Journal of allergy and clinical immunology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaci.2026.05.034},
pmid = {42372831},
issn = {1097-6825},
abstract = {BACKGROUND: Maternal antibiotic exposure during pregnancy has been associated with early childhood infection proneness, but the underlying mechanisms remain unknown. Longitudinal birth cohort studies with long follow-up and multi-omics data are lacking.
OBJECTIVE: To 1) investigate the association between prenatal antibiotics and offspring infection risk 2) investigate the potential mechanisms.
METHODS: The Danish population-based COPSAC2010 cohort with 663 mother-child pairs were followed from pregnancy until age 13 years. Detailed infection diaries age 0-3 years for common infections (cold, tonsillitis, otitis media, fever, gastrointestinal infections, and pneumonia) and moderate-to-severe (hospital diagnoses) infections were registered until age 13 years. We analyzed maternal antibiotic exposure vs risk of offspring infection risk with assessments of newborn child blood metabolome, gut and airway (age 1 week and 1 month) microbiome, and airway cytokine profiles (age 1 month). We adjusted for genetic, environmental, and socioeconomic factors.
RESULTS: Children whose mothers were exposed to antibiotic treatment during pregnancy had a higher risk of infections until age 13 years: adjusted incidence rate ratio (aIRR): 1.75 (1.19-2.57), p=0.005) and pneumonia (aIRR: 1.81 (1.10-2.99), p=0.015). Maternal antibiotic exposure related changes in the newborn child metabolome profile associated with increased child pneumonia, tonsilitis and fever risk. Both number and types of maternal antibiotic treatments had an impact on offspring infection risk. There were no noticeable findings for microbiome, genetics and airway cytokine profiling.
CONCLUSION: Maternal antibiotics during pregnancy increased long-term risk of childhood respiratory infection risk following a dose-response pattern, which was linked to newborn metabolomic alterations.},
}
RevDate: 2026-07-01
Root exudates recruit beneficial microbes to promote anammox-driven nitrogen cycling in wetland.
Environmental research, 306(Pt 1):125149 pii:S0013-9351(26)01480-5 [Epub ahead of print].
Anammox bacteria serve as a major biological sink in nitrogen (N) cycling within wetland, yet the hydrophyte root exudates-mediated microbial interplay mechanism that sustain their activity and ecosystem function remain unclear. To address this gap, we established flow-controlled microcosms planted with Iris pseudacorus, combined with [15]N stable isotope tracing and metagenome-assembled genomes (MAGs) analysis. Our findings revealed that root exudates significantly enhanced in-situ anammox rates (rhizosphere: 5.9 ± 2.0 mg N/(m[3]·d), non-rhizosphere: 0.4 ± 0.02 mg N/(m[3]·d), p < 0.001), leading to a remarkable enrichment of anammox bacteria in the rhizosphere (6.5 × 10[7] copies/g dry sludge, p < 0.001). We further uncovered a previously overlooked partial denitrification pathway that supplied nitrite, substantially increasing anammox contributions to rhizosphere N removal (16.6 ± 4.1%). Key bioactive components, flavonoids and amino acids, selectively recruited beneficial rhizobacteria affiliated to Pseudomonadota and Bacteroidota. MAGs-based analysis revealed that these microbial taxa encoded pathways for producing essential substrates (nitrite loop) and metabolites (cofactor, biotin) supporting anammox metabolism. The symbiotic interaction facilitated the survival and metabolic activity of anammox bacteria in the oligotrophic rhizosphere habitat. These findings unveil a natural plant-microbiota interaction that effectively enhances the sustainability of N cycling and provide new insights for optimizing nitrogen removal strategies in engineered wetland systems.
Additional Links: PMID-42372850
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@article {pmid42372850,
year = {2026},
author = {Gong, X and Zhang, L and Xu, A and Huang, Z and Wang, C and Yang, T and Liang, H and Zhang, M and Zhan, X and Peng, Y and Gao, D},
title = {Root exudates recruit beneficial microbes to promote anammox-driven nitrogen cycling in wetland.},
journal = {Environmental research},
volume = {306},
number = {Pt 1},
pages = {125149},
doi = {10.1016/j.envres.2026.125149},
pmid = {42372850},
issn = {1096-0953},
abstract = {Anammox bacteria serve as a major biological sink in nitrogen (N) cycling within wetland, yet the hydrophyte root exudates-mediated microbial interplay mechanism that sustain their activity and ecosystem function remain unclear. To address this gap, we established flow-controlled microcosms planted with Iris pseudacorus, combined with [15]N stable isotope tracing and metagenome-assembled genomes (MAGs) analysis. Our findings revealed that root exudates significantly enhanced in-situ anammox rates (rhizosphere: 5.9 ± 2.0 mg N/(m[3]·d), non-rhizosphere: 0.4 ± 0.02 mg N/(m[3]·d), p < 0.001), leading to a remarkable enrichment of anammox bacteria in the rhizosphere (6.5 × 10[7] copies/g dry sludge, p < 0.001). We further uncovered a previously overlooked partial denitrification pathway that supplied nitrite, substantially increasing anammox contributions to rhizosphere N removal (16.6 ± 4.1%). Key bioactive components, flavonoids and amino acids, selectively recruited beneficial rhizobacteria affiliated to Pseudomonadota and Bacteroidota. MAGs-based analysis revealed that these microbial taxa encoded pathways for producing essential substrates (nitrite loop) and metabolites (cofactor, biotin) supporting anammox metabolism. The symbiotic interaction facilitated the survival and metabolic activity of anammox bacteria in the oligotrophic rhizosphere habitat. These findings unveil a natural plant-microbiota interaction that effectively enhances the sustainability of N cycling and provide new insights for optimizing nitrogen removal strategies in engineered wetland systems.},
}
RevDate: 2026-06-30
Alginate-based biofilm-assisted encapsulation of a Co-culture of Bifidobacterium longum DSM20219 and Bacillus subtilis SOM8 enhances resistance to gastrointestinal stress.
International journal of biological macromolecules, 373:153262 pii:S0141-8130(26)03202-2 [Epub ahead of print].
Oral probiotic formulations are increasingly explored for supporting gastrointestinal health, restoring gut microbiome balance, and providing non-invasive alternatives to injections or transplants. However, delivering oxygen-sensitive probiotics orally remains challenging because gastric acidity, bile salts, digestive enzymes, and aerobic storage can substantially reduce bacterial viability. Sodium alginate is widely used for probiotic encapsulation because it forms mild, cell-compatible hydrogel beads, but alginate-only matrices often provide limited protection for highly sensitive anaerobes due to their hydrated and permeable network structure. Here, we developed an alginate-based, biofilm-assisted encapsulation system for the co-culture and co-delivery of Bacillus subtilis SOM8 and Bifidobacterium longum DSM20219. This strategy enhanced probiotic tolerance to simulated gastric fluids (SGF) and simulated intestinal fluids (SIF), and extended shelf life under aerobic conditions. Biofilm-assisted encapsulation improved B. longum DSM20219 viability, maintaining survival above 7-log CFU/g after 2 h in SGF and SIF, representing an approximately 3-log improvement over alginate-only encapsulation. It also maintained over 6-log CFU/g after 28 days of aerobic storage. Imaging and time-resolved co-culture analyses suggested that the enhanced protection was associated with biofilm formation, cell aggregation, extracellular matrix development, and dynamic interspecies interactions within the alginate system. While further in vivo and omics-based validation will be required, these findings support biofilm-assisted co-encapsulation as a promising biologically integrated strategy for polymer-based probiotic delivery.
Additional Links: PMID-42372892
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@article {pmid42372892,
year = {2026},
author = {Zhao, Z and Kok, NWH and Wong, ASW and Nataño, JHJ and Nolan, LM and Loo, SCJ},
title = {Alginate-based biofilm-assisted encapsulation of a Co-culture of Bifidobacterium longum DSM20219 and Bacillus subtilis SOM8 enhances resistance to gastrointestinal stress.},
journal = {International journal of biological macromolecules},
volume = {373},
number = {},
pages = {153262},
doi = {10.1016/j.ijbiomac.2026.153262},
pmid = {42372892},
issn = {1879-0003},
abstract = {Oral probiotic formulations are increasingly explored for supporting gastrointestinal health, restoring gut microbiome balance, and providing non-invasive alternatives to injections or transplants. However, delivering oxygen-sensitive probiotics orally remains challenging because gastric acidity, bile salts, digestive enzymes, and aerobic storage can substantially reduce bacterial viability. Sodium alginate is widely used for probiotic encapsulation because it forms mild, cell-compatible hydrogel beads, but alginate-only matrices often provide limited protection for highly sensitive anaerobes due to their hydrated and permeable network structure. Here, we developed an alginate-based, biofilm-assisted encapsulation system for the co-culture and co-delivery of Bacillus subtilis SOM8 and Bifidobacterium longum DSM20219. This strategy enhanced probiotic tolerance to simulated gastric fluids (SGF) and simulated intestinal fluids (SIF), and extended shelf life under aerobic conditions. Biofilm-assisted encapsulation improved B. longum DSM20219 viability, maintaining survival above 7-log CFU/g after 2 h in SGF and SIF, representing an approximately 3-log improvement over alginate-only encapsulation. It also maintained over 6-log CFU/g after 28 days of aerobic storage. Imaging and time-resolved co-culture analyses suggested that the enhanced protection was associated with biofilm formation, cell aggregation, extracellular matrix development, and dynamic interspecies interactions within the alginate system. While further in vivo and omics-based validation will be required, these findings support biofilm-assisted co-encapsulation as a promising biologically integrated strategy for polymer-based probiotic delivery.},
}
RevDate: 2026-06-30
Gut microbial signature for frailty discrimination: a metagenomic meta-analysis of 28 independent cohorts.
Experimental gerontology, 222:113223 pii:S0531-5565(26)00202-0 [Epub ahead of print].
Frailty, a clinical syndrome of multisystem decline and homeostatic vulnerability, is a critical public health priority. While the gut microbiome regulates immune and metabolic signaling, current evidence remains fragmented. We performed a metagenomic meta-analysis of 955 individuals from 28 independent cohorts across 24 countries to identify universal microbial signatures and develop a generalizable discriminative model. Frailty was determined using a Proxy Frailty Index based on the deficit accumulation model. Following refinement to isolate signatures from disease-specific dysbiosis, we used Firth's penalized regression for biomarker discovery and validated a Random Forest (RF) model via leave-one-study-out cross-validation. Shannon diversity exhibited a significant and sharp decline during the transition from robust to pre-frail states (p = 0.0006), manifesting at the earliest stages of physiological decline. We identified 16 microbial biomarkers characterized by the progressive attrition of core symbionts, such as Coprococcus eutactus, and the opportunistic expansion of pathobionts, including Enterococcus gallinarum. Sensitivity analysis in a healthy sub-cohort (n = 499) confirmed that these shifts occur independently of chronic clinical diagnoses and their associated confounding effects (p = 0.036). The 16-species RF model, predominantly driven by Collinsella massiliensis, achieved a corrected mean area under the receiver operating characteristic curve of 0.7572 across 5 eligible cohorts. Gut microbial restructuring is a sentinel biological hallmark of frailty that occurs independently of aging-related diseases. This study establishes a microbial signature broadly applicable across European and East Asian populations that serves as a high-fidelity, non-invasive metric for precision geriatric assessment.
Additional Links: PMID-42372926
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PubMed:
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@article {pmid42372926,
year = {2026},
author = {Kwon, CY and Choi, YH and Kim, H and Han, K and Jang, D and Hwangbo, H},
title = {Gut microbial signature for frailty discrimination: a metagenomic meta-analysis of 28 independent cohorts.},
journal = {Experimental gerontology},
volume = {222},
number = {},
pages = {113223},
doi = {10.1016/j.exger.2026.113223},
pmid = {42372926},
issn = {1873-6815},
abstract = {Frailty, a clinical syndrome of multisystem decline and homeostatic vulnerability, is a critical public health priority. While the gut microbiome regulates immune and metabolic signaling, current evidence remains fragmented. We performed a metagenomic meta-analysis of 955 individuals from 28 independent cohorts across 24 countries to identify universal microbial signatures and develop a generalizable discriminative model. Frailty was determined using a Proxy Frailty Index based on the deficit accumulation model. Following refinement to isolate signatures from disease-specific dysbiosis, we used Firth's penalized regression for biomarker discovery and validated a Random Forest (RF) model via leave-one-study-out cross-validation. Shannon diversity exhibited a significant and sharp decline during the transition from robust to pre-frail states (p = 0.0006), manifesting at the earliest stages of physiological decline. We identified 16 microbial biomarkers characterized by the progressive attrition of core symbionts, such as Coprococcus eutactus, and the opportunistic expansion of pathobionts, including Enterococcus gallinarum. Sensitivity analysis in a healthy sub-cohort (n = 499) confirmed that these shifts occur independently of chronic clinical diagnoses and their associated confounding effects (p = 0.036). The 16-species RF model, predominantly driven by Collinsella massiliensis, achieved a corrected mean area under the receiver operating characteristic curve of 0.7572 across 5 eligible cohorts. Gut microbial restructuring is a sentinel biological hallmark of frailty that occurs independently of aging-related diseases. This study establishes a microbial signature broadly applicable across European and East Asian populations that serves as a high-fidelity, non-invasive metric for precision geriatric assessment.},
}
RevDate: 2026-07-01
Biodegradable polylactic acid microplastics affect nutrient cycling during the entire crop growth cycle: Implications for soil ecosystem multifunctionality.
Environmental pollution (Barking, Essex : 1987), 406:128664 pii:S0269-7491(26)01034-1 [Epub ahead of print].
While microplastics (MPs) have been extensively studied for their effects on soil nutrient cycling, their influence on ecosystem multifunctionality (EMF) across the entire crop growth cycle remains poorly understood. This study systematically investigated the impacts of a model biodegradable MP, polylactic acid (PLA), on soil microbiomes and EMF across different maize incubation periods. Results of 16S rRNA amplicon sequencing and metagenomic analysis revealed that PLA-MPs decreased bacterial community α-diversity, co-occurrence network complexity, and stability throughout the 120-day incubation period. Particularly, PLA-MPs exerted more pronounced effects at early incubation stages (30 and 60 days), and these effects were intensified with increasing PLA-MP concentrations. PLA-MPs suppressed anaerobic carbon fixation (porA, porB, frda) and pyruvate metabolism (ppdk), while promoting fermentation (L-lactate dehydrogenase), nitrogen fixation (nifD, nifH, nifK, anfG), and microbial phosphorus (P) acquisition (phoD, phn cluster). Over the entire incubation period, PLA-MP-induced shifts in nutrient cycling enhanced soil carbon (C) function by 37.6-569%, while decreasing nitrogen (N) and P functions by 8.40-22.4% and 16.8-56.2%, respectively. Path analysis revealed that PLA-MPs altered soil properties and bacterial community diversity, which in turn regulated functional genes and these individual soil functions, thereby reducing EMF by 2.05-27.0% (R[2] = 0.923), with bacterial community diversity as the primary driver of EMF (standardized path coefficient of 0.978). These findings underscore the impacts of PLA-MPs on EMF in the soil-crop system throughout the entire maize growth cycle, advancing the understanding of the agroecological safety of biodegradable MPs.
Additional Links: PMID-42372963
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PubMed:
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@article {pmid42372963,
year = {2026},
author = {Cui, Q and Wang, F and Shan, X and Ding, L and Qiu, X and Zhang, B and Li, X and Liang, X and Guo, X},
title = {Biodegradable polylactic acid microplastics affect nutrient cycling during the entire crop growth cycle: Implications for soil ecosystem multifunctionality.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {406},
number = {},
pages = {128664},
doi = {10.1016/j.envpol.2026.128664},
pmid = {42372963},
issn = {1873-6424},
abstract = {While microplastics (MPs) have been extensively studied for their effects on soil nutrient cycling, their influence on ecosystem multifunctionality (EMF) across the entire crop growth cycle remains poorly understood. This study systematically investigated the impacts of a model biodegradable MP, polylactic acid (PLA), on soil microbiomes and EMF across different maize incubation periods. Results of 16S rRNA amplicon sequencing and metagenomic analysis revealed that PLA-MPs decreased bacterial community α-diversity, co-occurrence network complexity, and stability throughout the 120-day incubation period. Particularly, PLA-MPs exerted more pronounced effects at early incubation stages (30 and 60 days), and these effects were intensified with increasing PLA-MP concentrations. PLA-MPs suppressed anaerobic carbon fixation (porA, porB, frda) and pyruvate metabolism (ppdk), while promoting fermentation (L-lactate dehydrogenase), nitrogen fixation (nifD, nifH, nifK, anfG), and microbial phosphorus (P) acquisition (phoD, phn cluster). Over the entire incubation period, PLA-MP-induced shifts in nutrient cycling enhanced soil carbon (C) function by 37.6-569%, while decreasing nitrogen (N) and P functions by 8.40-22.4% and 16.8-56.2%, respectively. Path analysis revealed that PLA-MPs altered soil properties and bacterial community diversity, which in turn regulated functional genes and these individual soil functions, thereby reducing EMF by 2.05-27.0% (R[2] = 0.923), with bacterial community diversity as the primary driver of EMF (standardized path coefficient of 0.978). These findings underscore the impacts of PLA-MPs on EMF in the soil-crop system throughout the entire maize growth cycle, advancing the understanding of the agroecological safety of biodegradable MPs.},
}
RevDate: 2026-06-29
Plant-based prebiotics to modulate skin microbiota: a novel approach for next-generation cosmeceuticals.
Scientific reports pii:10.1038/s41598-026-58189-4 [Epub ahead of print].
The skin microbiome maintains cutaneous homeostasis through colonization resistance and immune modulation, targeted prebiotic interventions however remain largely unexplored. The present study addresses this lacuna effectively demonstrating the ability of plant-derived prebiotics to selectively modulate key skin commensals and pathogenic bacteria thereby unraveling a new dimension to use of prebiotics in skin care. Linum usitatissimum (flaxseed) and Allium sativum (garlic) extracts used herein exhibited complete growth inhibition of Staphylococcus aureus within 6 h, while Curcuma amada (mango ginger) rapidly halted the growth of Cutibacterium acnes within 15 min. Gas chromatography-mass spectrometry was carried out to unveil the bioactive constituents in plant-prebiotics as well as the exposed organisms. Field emission gun-scanning electron microscopy validated bacterial cell membrane disruption correlating with antimicrobial efficacy. Remarkably, Allium cepa (onion) and Tinospora cordifolia (guduchi) selectively enhanced the proliferation of Staphylococcus epidermidis while simultaneously inhibiting pathogenic species. Metabolomic profiling revealed that prebiotic-stimulated S.epidermidis produced elevated levels of butyric and succinic acids that are documented to have anti-bacterial activity. Plant-based prebiotics can thus be strategically reinforced to benefit skin microbiota with simultaneous inhibition of skin pathogens, providing a scientific foundation for microbiome-targeted cosmeceuticals.
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@article {pmid42373689,
year = {2026},
author = {Gourh, KA and Kelkar Mane, V},
title = {Plant-based prebiotics to modulate skin microbiota: a novel approach for next-generation cosmeceuticals.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-58189-4},
pmid = {42373689},
issn = {2045-2322},
abstract = {The skin microbiome maintains cutaneous homeostasis through colonization resistance and immune modulation, targeted prebiotic interventions however remain largely unexplored. The present study addresses this lacuna effectively demonstrating the ability of plant-derived prebiotics to selectively modulate key skin commensals and pathogenic bacteria thereby unraveling a new dimension to use of prebiotics in skin care. Linum usitatissimum (flaxseed) and Allium sativum (garlic) extracts used herein exhibited complete growth inhibition of Staphylococcus aureus within 6 h, while Curcuma amada (mango ginger) rapidly halted the growth of Cutibacterium acnes within 15 min. Gas chromatography-mass spectrometry was carried out to unveil the bioactive constituents in plant-prebiotics as well as the exposed organisms. Field emission gun-scanning electron microscopy validated bacterial cell membrane disruption correlating with antimicrobial efficacy. Remarkably, Allium cepa (onion) and Tinospora cordifolia (guduchi) selectively enhanced the proliferation of Staphylococcus epidermidis while simultaneously inhibiting pathogenic species. Metabolomic profiling revealed that prebiotic-stimulated S.epidermidis produced elevated levels of butyric and succinic acids that are documented to have anti-bacterial activity. Plant-based prebiotics can thus be strategically reinforced to benefit skin microbiota with simultaneous inhibition of skin pathogens, providing a scientific foundation for microbiome-targeted cosmeceuticals.},
}
RevDate: 2026-06-29
Ketogenic diet alleviates acute radiation-induced intestinal injury through JAK2/STAT3/RORγt/IL-17A signaling pathway via gut microbiome.
Communications biology pii:10.1038/s42003-026-10546-9 [Epub ahead of print].
Emerging evidence suggests dietary interventions regulate inflammatory signaling through gut microbiome modulation, yet their therapeutic potential in radiation-induced intestinal injury (RIII) remains underexplored. This study demonstrates that ketogenic diet (KD), a high-fat and low-carbohydrate dietary regimen, exerts protective effects against RIII through dual mechanisms involving microbial regulation and inflammatory pathway inhibition. Using high-salt diet (HSD) as a dietary control, KD significantly attenuated intestinal inflammation by downregulating pro-inflammatory cytokines while enhancing barrier integrity through tight junction protein upregulation in radiation-exposed murine model. 16S rDNA sequencing showed KD enriched Akkermansia and reduced Enterobacteriaceae, whereas HSD exhibited inverse patterns. Mechanistically, RNA sequencing revealed that KD uniquely suppressed the JAK2/STAT3 pathway in RIII mice. In vitro studies demonstrated that β-hydroxybutyrate, a key ketone metabolite, effectively suppressed RORγt expression and subsequent downregulation of IL-17A gene transcription via the inhibition of JAK2/STAT3 pathway, thus mitigate inflammatory damage. Fecal microbiota transplantation validated that KD-modified microbiome directly inhibited JAK2/STAT3 signaling activation, as well as the downregulation of RORγt and IL-17A. These findings establish KD as a promising dietary strategy mitigate acute RIII through synergistic modulation of gut microbiota and inflammatory signaling, providing novel insights into nutritional approaches targeting microbial-host crosstalk in radiation injury.
Additional Links: PMID-42373816
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PubMed:
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@article {pmid42373816,
year = {2026},
author = {Yang, J and Ling, Z and Zhou, M and Tao, M and Mao, J and Guo, H and Wang, J and Qu, X and Wang, Y and Zhu, Y and Zhang, K and Yan, X},
title = {Ketogenic diet alleviates acute radiation-induced intestinal injury through JAK2/STAT3/RORγt/IL-17A signaling pathway via gut microbiome.},
journal = {Communications biology},
volume = {},
number = {},
pages = {},
doi = {10.1038/s42003-026-10546-9},
pmid = {42373816},
issn = {2399-3642},
support = {81902422//National Natural Science Foundation of China (National Science Foundation of China)/ ; BK20250559//Natural Science Foundation of Jiangsu Province (Jiangsu Provincial Natural Science Foundation)/ ; },
abstract = {Emerging evidence suggests dietary interventions regulate inflammatory signaling through gut microbiome modulation, yet their therapeutic potential in radiation-induced intestinal injury (RIII) remains underexplored. This study demonstrates that ketogenic diet (KD), a high-fat and low-carbohydrate dietary regimen, exerts protective effects against RIII through dual mechanisms involving microbial regulation and inflammatory pathway inhibition. Using high-salt diet (HSD) as a dietary control, KD significantly attenuated intestinal inflammation by downregulating pro-inflammatory cytokines while enhancing barrier integrity through tight junction protein upregulation in radiation-exposed murine model. 16S rDNA sequencing showed KD enriched Akkermansia and reduced Enterobacteriaceae, whereas HSD exhibited inverse patterns. Mechanistically, RNA sequencing revealed that KD uniquely suppressed the JAK2/STAT3 pathway in RIII mice. In vitro studies demonstrated that β-hydroxybutyrate, a key ketone metabolite, effectively suppressed RORγt expression and subsequent downregulation of IL-17A gene transcription via the inhibition of JAK2/STAT3 pathway, thus mitigate inflammatory damage. Fecal microbiota transplantation validated that KD-modified microbiome directly inhibited JAK2/STAT3 signaling activation, as well as the downregulation of RORγt and IL-17A. These findings establish KD as a promising dietary strategy mitigate acute RIII through synergistic modulation of gut microbiota and inflammatory signaling, providing novel insights into nutritional approaches targeting microbial-host crosstalk in radiation injury.},
}
RevDate: 2026-06-29
Study protocol for FAXAge: a randomized, controlled clinical trial of fasting and exercise to slow aging in humans.
GeroScience [Epub ahead of print].
Biomarkers of aging, particularly DNA methylation-based clocks, have shown promise as tools to assess whether interventions may impact the rate of biological aging. Among possible interventions physical exercise has shown protective effects against many age-associated diseases, while time-restricted feeding (TRF) has shown metabolic benefits in preclinical models. The combined effect of exercise and TRF on aging biomarkers remains largely unexplored. In this 52-week four-armed, randomized, controlled trial (clinicaltrials.gov: NCT07207044) 240 healthy adults aged 65 and above will be allocated to four groups: combined cardio and strength training (EXE), TRF, combined EXE and TRF, or control. Participants will undergo assessments at baseline, 3, 6, and 12 months, with follow-ups at 2, 5, and 10 years. The primary outcome measure is Dunedin Pace of Aging DNA methylation age with secondary measures including RNA-sequencing, metabolomics, inflammatory markers, microbiome analysis, cognitive and physical measures. By deeply phenotyping participants, the Fasting And eXercise (FAXAge) study will provide novel insights into whether TRF, EXE, or a combination can slow or reverse biological aging in older adults.
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@article {pmid42373885,
year = {2026},
author = {Fals, EB and Springborg, EC and Berthelsen, AB and Nyeman-Nielsen, J and Larsen, S and Scheibye-Knudsen, M},
title = {Study protocol for FAXAge: a randomized, controlled clinical trial of fasting and exercise to slow aging in humans.},
journal = {GeroScience},
volume = {},
number = {},
pages = {},
pmid = {42373885},
issn = {2509-2723},
abstract = {Biomarkers of aging, particularly DNA methylation-based clocks, have shown promise as tools to assess whether interventions may impact the rate of biological aging. Among possible interventions physical exercise has shown protective effects against many age-associated diseases, while time-restricted feeding (TRF) has shown metabolic benefits in preclinical models. The combined effect of exercise and TRF on aging biomarkers remains largely unexplored. In this 52-week four-armed, randomized, controlled trial (clinicaltrials.gov: NCT07207044) 240 healthy adults aged 65 and above will be allocated to four groups: combined cardio and strength training (EXE), TRF, combined EXE and TRF, or control. Participants will undergo assessments at baseline, 3, 6, and 12 months, with follow-ups at 2, 5, and 10 years. The primary outcome measure is Dunedin Pace of Aging DNA methylation age with secondary measures including RNA-sequencing, metabolomics, inflammatory markers, microbiome analysis, cognitive and physical measures. By deeply phenotyping participants, the Fasting And eXercise (FAXAge) study will provide novel insights into whether TRF, EXE, or a combination can slow or reverse biological aging in older adults.},
}
RevDate: 2026-06-29
Bifidobacterium animalis reshapes the bile acid pool and prevents neonatal jaundice: a clinical microbiome study from correlation to causation.
NPJ biofilms and microbiomes pii:10.1038/s41522-026-01057-w [Epub ahead of print].
Neonatal jaundice (NJ) affects 60-80% of neonates, yet the underlying microbial mechanisms remain elucidated, despite known links between gut dysbiosis and bilirubin and bile acid (BA) metabolism. Through two-stage shotgun metagenomic-metabolomic analysis of 150 fecal samples from 120 neonates, we identified key taxa linked to bile acid (BA) metabolism in moderate-to-severe NJ. Furthermore, multi-omics integration revealed significant interkingdom correlations among gut phages, bacteria, and BAs. Dysbiosis featured enriched Streptococcus and Escherichia, depleted Bifidobacterium animalis, and group-specific phage signatures. In the independent clinical validation cohort, jaundice intervention normalized the dysbiotic profile, demonstrating significant suppression of pathogenic taxa concomitant with restoration of B. animalis abundance. In vitro, B. animalis subsp. lactis Y103-OTU5 remodeled BA via deconjugation. In a phenylhydrazine hydrochloride (PHZ)-induced murine model of hemolytic jaundice, oral administration of isolated B. animalis subsp. lactis Y103-OTU5 significantly attenuated hyperbilirubinemia and hepatic inflammation, likely via Cyp7a1/Cyp7b1-dependent modulation of BA synthesis and detoxification pathways. Structural equation modeling revealed a tripartite regulatory network: phages indirectly modulated BA through bacterial remodeling, while B. animalis directly regulated BA pathways, positioning it as a potential therapeutic candidate for hemolysis-associated neonatal jaundice. Collectively, these findings reveal a gut phage-bacteria-BA network in NJ, highlighting B. animalis as a therapeutic candidate with dual modulation of BA metabolism and phage-bacteria interactions.
Additional Links: PMID-42374042
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PubMed:
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@article {pmid42374042,
year = {2026},
author = {Chen, X and Chen, C and Zhang, P and OuYang, X and Ma, H and Chen, W and Li, T and Han, J and Wang, Y and Wang, H and Zhou, Q and Cheng, G and Zhou, W and Yu, Z and Zhou, W and Wang, M and Zeng, S},
title = {Bifidobacterium animalis reshapes the bile acid pool and prevents neonatal jaundice: a clinical microbiome study from correlation to causation.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-01057-w},
pmid = {42374042},
issn = {2055-5008},
support = {2024YFC2707700//National Key R&D Program of China, Key Special Project for "Reproductive Health and Maternal and Child Health Security"/ ; 82571963//the National Natural Science Foundation of China/ ; 2025A1515012162//Natural Science Foundation of Guangdong Province, China/ ; JCYJ20250604145739052//Shenzhen Science and Technology Innovation Bureau/ ; Y2024001//the Research Initiation Fund of Longgang District Maternity & Child Healthcare Hospital of Shenzhen City/ ; },
abstract = {Neonatal jaundice (NJ) affects 60-80% of neonates, yet the underlying microbial mechanisms remain elucidated, despite known links between gut dysbiosis and bilirubin and bile acid (BA) metabolism. Through two-stage shotgun metagenomic-metabolomic analysis of 150 fecal samples from 120 neonates, we identified key taxa linked to bile acid (BA) metabolism in moderate-to-severe NJ. Furthermore, multi-omics integration revealed significant interkingdom correlations among gut phages, bacteria, and BAs. Dysbiosis featured enriched Streptococcus and Escherichia, depleted Bifidobacterium animalis, and group-specific phage signatures. In the independent clinical validation cohort, jaundice intervention normalized the dysbiotic profile, demonstrating significant suppression of pathogenic taxa concomitant with restoration of B. animalis abundance. In vitro, B. animalis subsp. lactis Y103-OTU5 remodeled BA via deconjugation. In a phenylhydrazine hydrochloride (PHZ)-induced murine model of hemolytic jaundice, oral administration of isolated B. animalis subsp. lactis Y103-OTU5 significantly attenuated hyperbilirubinemia and hepatic inflammation, likely via Cyp7a1/Cyp7b1-dependent modulation of BA synthesis and detoxification pathways. Structural equation modeling revealed a tripartite regulatory network: phages indirectly modulated BA through bacterial remodeling, while B. animalis directly regulated BA pathways, positioning it as a potential therapeutic candidate for hemolysis-associated neonatal jaundice. Collectively, these findings reveal a gut phage-bacteria-BA network in NJ, highlighting B. animalis as a therapeutic candidate with dual modulation of BA metabolism and phage-bacteria interactions.},
}
RevDate: 2026-06-29
Long-term selection for extended lifespan reshapes host physiology and gut microbiome structure in an insect model.
Scientific reports pii:10.1038/s41598-026-59408-8 [Epub ahead of print].
Longevity results from complex interactions between genetic, physiological, and environmental factors, however, the contribution of the gut microbiome to lifespan evolution is still poorly understood, especially in insects. In the present study, we tested whether long-term selection for delayed reproduction and extended lifespan can be associated with restructuring of the gut microbiome in the house cricket (Acheta domesticus). We compared a wild-type strain with a long-lived strain - selected for more than 20 years (64 generations) - maintained under the same laboratory conditions. The long-lived strain showed a significantly longer lifespan and larger body size. At the same time, no reduction in food intake or energy assimilation, no disturbance of antioxidant capacity, and no increased DNA damage were observed. These results support the supposition that lifespan extension was not primarily driven by metabolic suppression. Microbiome analyses showed strain-specific differences in community structure. Although overall microbial richness remained unchanged, the taxonomic analysis revealed two alternative microbial configurations: one characterized by higher relative abundance of Firmicutes and Bacteroidota in the wild-type strain and another enriched in Gammaproteobacteria and lactic acid bacteria in the long-lived strain. Our findings demonstrate that long-term selection can be associated with the emergence of strain-specific gut microbiome configurations. These differences may represent components of the longevity-associated phenotype, although their causal relationship with lifespan extension remains unresolved. Our results highlight the potential importance of gut microbiome variation during long-term life-history evolution in insects.
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@article {pmid42374089,
year = {2026},
author = {Augustyniak, M and Malicka, M and Flasz, B and Napora-Rutkowski, Ł and Rensing, C and Ajay, AK and Babczyńska, A and Tarnawska, M and Rozpędek, K and Świerczek, E and Kędziorski, A},
title = {Long-term selection for extended lifespan reshapes host physiology and gut microbiome structure in an insect model.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-59408-8},
pmid = {42374089},
issn = {2045-2322},
support = {UMO-2020/37/B/NZ7/00570//Narodowe Centrum Nauki/ ; POB5//Research Excellence Initiative of the University of Silesia in Katowice/ ; },
abstract = {Longevity results from complex interactions between genetic, physiological, and environmental factors, however, the contribution of the gut microbiome to lifespan evolution is still poorly understood, especially in insects. In the present study, we tested whether long-term selection for delayed reproduction and extended lifespan can be associated with restructuring of the gut microbiome in the house cricket (Acheta domesticus). We compared a wild-type strain with a long-lived strain - selected for more than 20 years (64 generations) - maintained under the same laboratory conditions. The long-lived strain showed a significantly longer lifespan and larger body size. At the same time, no reduction in food intake or energy assimilation, no disturbance of antioxidant capacity, and no increased DNA damage were observed. These results support the supposition that lifespan extension was not primarily driven by metabolic suppression. Microbiome analyses showed strain-specific differences in community structure. Although overall microbial richness remained unchanged, the taxonomic analysis revealed two alternative microbial configurations: one characterized by higher relative abundance of Firmicutes and Bacteroidota in the wild-type strain and another enriched in Gammaproteobacteria and lactic acid bacteria in the long-lived strain. Our findings demonstrate that long-term selection can be associated with the emergence of strain-specific gut microbiome configurations. These differences may represent components of the longevity-associated phenotype, although their causal relationship with lifespan extension remains unresolved. Our results highlight the potential importance of gut microbiome variation during long-term life-history evolution in insects.},
}
RevDate: 2026-06-29
Diabetes exacerbates experimental peri-implantitis in mice with elevated IL-17A-associated inflammation and IL-17F upregulation.
Scientific reports pii:10.1038/s41598-026-58925-w [Epub ahead of print].
This study investigated the role of interleukin-17 (IL-17) and the oral microbiome in peri-implant inflammation and bone loss under hyperglycemic and normoglycemic conditions. Wild-type (WT) and diabetic (db/db) mice with maxillary implants underwent ligature placement with or without IL-17A neutralization. Bone loss, osteoclast activity, inflammatory cytokines, Th17/Treg balance, and expression of IL-17Family members were analyzed. The oral microbiota was profiled by 16S rRNA sequencing, and its inflammatory potential was evaluated by co-culture with immune cells. Diabetic db/db mice exhibited greater peri-implant bone loss, osteoclast numbers, and RANKL/OPG ratios than WT, accompanied by elevated Il17a expression, reduced anti-inflammatory cytokines, enhanced Th17-associated inflammatory features, and altered FOXP3[+] cell profiles. IL-17A neutralization significantly attenuated, but did not fully normalize, heightened inflammatory responses in db/db mice, whereas ligature-induced Il17f upregulation was observed only in db/db mice. Microbial alterations were partially shifted toward control profiles by IL-17A inhibition in WT mice, while diabetes-associated changes persisted regardless of ligation or anti-IL-17A. In vitro, peri-implant microbiota induced pro-inflammatory cytokine responses in splenocytes, with residual inflammatory responses remaining more evident in DB-derived microbiota after IL-17A inhibition. These findings suggest that peri-implantitis in diabetes is exacerbated by heightened IL-17-mediated inflammation and persistent microbial alterations, underscoring the need for more comprehensive therapeutic approaches to address the disease under diabetic conditions.
Additional Links: PMID-42374093
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@article {pmid42374093,
year = {2026},
author = {Memida, T and Jaar, JC and Chen, T and Cao, G and Kuriki, N and Abdolahinia, ED and Shindo, S and Yamashita, S and Ruiz, S and Meraji, A and Albu, A and Okamoto, M and He, X and Vardar, S and Suzuki, M and Lin, J and Kawai, T and Han, X},
title = {Diabetes exacerbates experimental peri-implantitis in mice with elevated IL-17A-associated inflammation and IL-17F upregulation.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-58925-w},
pmid = {42374093},
issn = {2045-2322},
support = {DE027648//National Institutes of Dental and Craniofacial Research (NIDCR)/ ; DE029709//National Institutes of Dental and Craniofacial Research (NIDCR)/ ; DE032156//National Institutes of Dental and Craniofacial Research (NIDCR)/ ; S10 OD032199-01A1/NH/NIH HHS/United States ; },
abstract = {This study investigated the role of interleukin-17 (IL-17) and the oral microbiome in peri-implant inflammation and bone loss under hyperglycemic and normoglycemic conditions. Wild-type (WT) and diabetic (db/db) mice with maxillary implants underwent ligature placement with or without IL-17A neutralization. Bone loss, osteoclast activity, inflammatory cytokines, Th17/Treg balance, and expression of IL-17Family members were analyzed. The oral microbiota was profiled by 16S rRNA sequencing, and its inflammatory potential was evaluated by co-culture with immune cells. Diabetic db/db mice exhibited greater peri-implant bone loss, osteoclast numbers, and RANKL/OPG ratios than WT, accompanied by elevated Il17a expression, reduced anti-inflammatory cytokines, enhanced Th17-associated inflammatory features, and altered FOXP3[+] cell profiles. IL-17A neutralization significantly attenuated, but did not fully normalize, heightened inflammatory responses in db/db mice, whereas ligature-induced Il17f upregulation was observed only in db/db mice. Microbial alterations were partially shifted toward control profiles by IL-17A inhibition in WT mice, while diabetes-associated changes persisted regardless of ligation or anti-IL-17A. In vitro, peri-implant microbiota induced pro-inflammatory cytokine responses in splenocytes, with residual inflammatory responses remaining more evident in DB-derived microbiota after IL-17A inhibition. These findings suggest that peri-implantitis in diabetes is exacerbated by heightened IL-17-mediated inflammation and persistent microbial alterations, underscoring the need for more comprehensive therapeutic approaches to address the disease under diabetic conditions.},
}
RevDate: 2026-06-29
NAP: an open source pipeline for cross-domain microbiome profiling using Nanopore sequencing-derived amplicon data.
BMC bioinformatics pii:10.1186/s12859-026-06544-7 [Epub ahead of print].
BACKGROUND: Nanopore sequencing offers a cost-effective and portable platform for microbiome analysis, but amplicon-based approaches remain limited by higher sequencing error rates and a lack of workflows tailored to mixed domain ribosomal RNA profiling. While short-read technologies dominate microbial community analysis, their portability and flexibility are constrained. There is therefore a need for robust pipelines designed specifically for cross-domain Nanopore amplicon data.
RESULTS: We introduce the Nanopore sequencing-based Amplicon Pipeline (NAP; https://github.com/Luke-B-Jones/NAP), an open source workflow optimised for flexible mixed domain primer sets such as 515Y/926R. NAP combines dynamic quality filtering and base muting, chimera removal, centroid generation, BLAST-based taxonomic classification, hierarchical consensus correction, RAW-read reassignment, blank-informed decontamination, and domain-aware post-processing to produce curated genus level and species level abundance tables. Validation against logarithmic and gut commercial mock communities showed strongest performance at genus level, with reliable recovery above ca. 1% relative abundance and reproducible community reconstruction under Bray-Curtis, Jaccard, agreement plot, and Bland-Altman analyses. Internal benchmarking showed that dynamic filtering and base muting provided the most defensible balance between read quality, retained depth, and taxonomic fidelity across heterogeneous inputs, avoiding the sensitivity loss of fixed filtering approaches, and the reduced fidelity of overly permissive or aggressively masked alternatives. The consensus step substantially reduced raw centroid-based false positive burden in biological mocks by 82.9% at genus level and 78.8% at species level, while decontamination removed 7.00 ± 2.68 species level contaminant hits per replicate and adjusted a further 9.83 ± 6.49 abundances. Direct benchmarking against QIIME2 and Kraken2/Bracken showed that NAP best preserved expected community structure, with markedly fewer unexpected genera and stronger species level behaviour under the tested conditions. Synthetic ground truth benchmarking across richness/evenness panels, high similarity marker conflicts, and low abundance titrations further supported robustness: NAP produced no unsupported genus level calls, achieved genus level precision, recall, and F1-score of 1.000, 0.939, and 0.967 across community structure panels, and showed complete detection from ca. 1% relative abundance under default filtering. Residual species level errors were concentrated in high identity marker conflicts rather than arbitrary taxonomic assignments.
CONCLUSIONS: NAP provides a reproducible, flexible, domain-aware consensus workflow for cross-domain Nanopore amplicon profiling, with strongest support at genus level and competitive species level performance for well resolved taxa.
Additional Links: PMID-42374176
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@article {pmid42374176,
year = {2026},
author = {Jones, LB and Bagby, S},
title = {NAP: an open source pipeline for cross-domain microbiome profiling using Nanopore sequencing-derived amplicon data.},
journal = {BMC bioinformatics},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12859-026-06544-7},
pmid = {42374176},
issn = {1471-2105},
abstract = {BACKGROUND: Nanopore sequencing offers a cost-effective and portable platform for microbiome analysis, but amplicon-based approaches remain limited by higher sequencing error rates and a lack of workflows tailored to mixed domain ribosomal RNA profiling. While short-read technologies dominate microbial community analysis, their portability and flexibility are constrained. There is therefore a need for robust pipelines designed specifically for cross-domain Nanopore amplicon data.
RESULTS: We introduce the Nanopore sequencing-based Amplicon Pipeline (NAP; https://github.com/Luke-B-Jones/NAP), an open source workflow optimised for flexible mixed domain primer sets such as 515Y/926R. NAP combines dynamic quality filtering and base muting, chimera removal, centroid generation, BLAST-based taxonomic classification, hierarchical consensus correction, RAW-read reassignment, blank-informed decontamination, and domain-aware post-processing to produce curated genus level and species level abundance tables. Validation against logarithmic and gut commercial mock communities showed strongest performance at genus level, with reliable recovery above ca. 1% relative abundance and reproducible community reconstruction under Bray-Curtis, Jaccard, agreement plot, and Bland-Altman analyses. Internal benchmarking showed that dynamic filtering and base muting provided the most defensible balance between read quality, retained depth, and taxonomic fidelity across heterogeneous inputs, avoiding the sensitivity loss of fixed filtering approaches, and the reduced fidelity of overly permissive or aggressively masked alternatives. The consensus step substantially reduced raw centroid-based false positive burden in biological mocks by 82.9% at genus level and 78.8% at species level, while decontamination removed 7.00 ± 2.68 species level contaminant hits per replicate and adjusted a further 9.83 ± 6.49 abundances. Direct benchmarking against QIIME2 and Kraken2/Bracken showed that NAP best preserved expected community structure, with markedly fewer unexpected genera and stronger species level behaviour under the tested conditions. Synthetic ground truth benchmarking across richness/evenness panels, high similarity marker conflicts, and low abundance titrations further supported robustness: NAP produced no unsupported genus level calls, achieved genus level precision, recall, and F1-score of 1.000, 0.939, and 0.967 across community structure panels, and showed complete detection from ca. 1% relative abundance under default filtering. Residual species level errors were concentrated in high identity marker conflicts rather than arbitrary taxonomic assignments.
CONCLUSIONS: NAP provides a reproducible, flexible, domain-aware consensus workflow for cross-domain Nanopore amplicon profiling, with strongest support at genus level and competitive species level performance for well resolved taxa.},
}
RevDate: 2026-06-29
The gut microbiome in the Lebanese population and its alterations in metastatic colorectal cancer: benchmarking and application.
BMC microbiology pii:10.1186/s12866-026-05325-9 [Epub ahead of print].
BACKGROUND: Colorectal cancer (CRC) is a rising health concern in Lebanon and across the Arab world, concomitant with dietary and lifestyle transitions. The gut microbiome may contribute to CRC progression and treatment response, and it remains understudied in Arab populations. This pilot study investigates gut microbiome dynamics in a cohort of stage IV CRC patients and cancer-free individuals from Lebanon, benchmarking computational tools for 16S rRNA sequencing and analyzing microbial and functional shifts associated with cancer development and therapy.
METHODS: Stool samples were collected from cancer-free individuals (n = 32) and newly diagnosed stage IV CRC patients before therapy (n = 17). A subset of CRC patients (n = 10) provided follow-up samples 3-6 months after therapy. 16S rRNA microbial profiling was conducted using the Illumina MiSeq platform. Computational tools were benchmarked using a mock community, with a defined microbial composition. Microbiome and functional analyses included diversity metrics, differential abundance testing, and pathway prediction, with adjustments for age and sex, followed by sensitivity analyses accounting for antibiotic use and immunotherapy.
RESULTS: Among the evaluated computational tools, USEARCH was selected for downstream CRC microbiome analyses based on its performance. CRC patients exhibited progressive dysbiosis, characterised by distinct beta diversity profiles, reduced alpha diversity and a declining Firmicutes/Bacteroidota ratio from cancer-free controls to baseline CRC and post-therapy samples. Differential abundance analysis identified taxa associated with CRC development and therapy response, including Fusobacterium, Muribaculaceae, Intestinimonas, Intestinimonas butyriciproducens and Lactobacillus fermentum. Notably, some potentially beneficial taxa increased progressively across the disease and treatment continuum, suggesting that therapy may promote specific favorable microorganisms while coinciding with broader microbiome dysregulation. Functional pathway analysis revealed widespread alterations in microbial functional capacity, including potential therapy-associated shifts.
CONCLUSION: This study represents a pioneering effort in gut microbiome profiling of Lebanese population with advanced CRC, establishing a molecular reference map during a period of rising CRC incidence and dietary transition. Computational benchmarking using a mock community supported the robustness of the analytical workflow. The results may facilitate the discovery of microbial signatures associated with CRC development and therapy response, providing insights into cancer prevention and clinical intervention.
Additional Links: PMID-42374179
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PubMed:
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@article {pmid42374179,
year = {2026},
author = {Temraz, S and Nassar, FJ and Bertrand, P and Al Tartir, R and Mezher, M and Hadla, R and Msheik, ZS and Chamandi, G and Cahais, V and Cuenin, C and Al Shoukari, A and Shamseddine, A and Shatila, H and Naja, F and Zheng, Y and Hou, L and Nasr, R and Ghantous, A},
title = {The gut microbiome in the Lebanese population and its alterations in metastatic colorectal cancer: benchmarking and application.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05325-9},
pmid = {42374179},
issn = {1471-2180},
abstract = {BACKGROUND: Colorectal cancer (CRC) is a rising health concern in Lebanon and across the Arab world, concomitant with dietary and lifestyle transitions. The gut microbiome may contribute to CRC progression and treatment response, and it remains understudied in Arab populations. This pilot study investigates gut microbiome dynamics in a cohort of stage IV CRC patients and cancer-free individuals from Lebanon, benchmarking computational tools for 16S rRNA sequencing and analyzing microbial and functional shifts associated with cancer development and therapy.
METHODS: Stool samples were collected from cancer-free individuals (n = 32) and newly diagnosed stage IV CRC patients before therapy (n = 17). A subset of CRC patients (n = 10) provided follow-up samples 3-6 months after therapy. 16S rRNA microbial profiling was conducted using the Illumina MiSeq platform. Computational tools were benchmarked using a mock community, with a defined microbial composition. Microbiome and functional analyses included diversity metrics, differential abundance testing, and pathway prediction, with adjustments for age and sex, followed by sensitivity analyses accounting for antibiotic use and immunotherapy.
RESULTS: Among the evaluated computational tools, USEARCH was selected for downstream CRC microbiome analyses based on its performance. CRC patients exhibited progressive dysbiosis, characterised by distinct beta diversity profiles, reduced alpha diversity and a declining Firmicutes/Bacteroidota ratio from cancer-free controls to baseline CRC and post-therapy samples. Differential abundance analysis identified taxa associated with CRC development and therapy response, including Fusobacterium, Muribaculaceae, Intestinimonas, Intestinimonas butyriciproducens and Lactobacillus fermentum. Notably, some potentially beneficial taxa increased progressively across the disease and treatment continuum, suggesting that therapy may promote specific favorable microorganisms while coinciding with broader microbiome dysregulation. Functional pathway analysis revealed widespread alterations in microbial functional capacity, including potential therapy-associated shifts.
CONCLUSION: This study represents a pioneering effort in gut microbiome profiling of Lebanese population with advanced CRC, establishing a molecular reference map during a period of rising CRC incidence and dietary transition. Computational benchmarking using a mock community supported the robustness of the analytical workflow. The results may facilitate the discovery of microbial signatures associated with CRC development and therapy response, providing insights into cancer prevention and clinical intervention.},
}
RevDate: 2026-06-29
Targeting the crosstalk between Alzheimer's disease and gastrointestinal cancers.
Molecular medicine (Cambridge, Mass.) pii:10.1186/s10020-026-01545-x [Epub ahead of print].
Epidemiological studies have revealed an inverse association between Alzheimer's disease and cancer. Here, we discuss the mechanisms involved in the relationship between Alzheimer's disease and gastrointestinal cancers, particularly pancreatic and gastric-colorectal cancers. The gut‒brain axis and pancreas‒brain axis connect the central nervous system with peripheral organs and form immune‒metabolic networks. We focus on bidirectional tumor-brain communication, involving cell-death pathways, apoptosis, metabolic dysregulation, microbiota, metabolic dysregulation, neuroinflammation, immune system and sensory-sympathetic circuits, and neural remodeling. Furthermore, we discuss potential integrated, multitarget therapeutic strategies, including metabolic regulation, microbiome interventions, and immune modulation. Prospective longitudinal cohorts incorporating prediagnostic exposures and molecular pathology are needed to establish temporality.
Additional Links: PMID-42374181
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@article {pmid42374181,
year = {2026},
author = {Gong, R and Wang, H and Cao, L and Niu, H and Rominger, A and Luo, Z and Ni, R},
title = {Targeting the crosstalk between Alzheimer's disease and gastrointestinal cancers.},
journal = {Molecular medicine (Cambridge, Mass.)},
volume = {},
number = {},
pages = {},
doi = {10.1186/s10020-026-01545-x},
pmid = {42374181},
issn = {1528-3658},
abstract = {Epidemiological studies have revealed an inverse association between Alzheimer's disease and cancer. Here, we discuss the mechanisms involved in the relationship between Alzheimer's disease and gastrointestinal cancers, particularly pancreatic and gastric-colorectal cancers. The gut‒brain axis and pancreas‒brain axis connect the central nervous system with peripheral organs and form immune‒metabolic networks. We focus on bidirectional tumor-brain communication, involving cell-death pathways, apoptosis, metabolic dysregulation, microbiota, metabolic dysregulation, neuroinflammation, immune system and sensory-sympathetic circuits, and neural remodeling. Furthermore, we discuss potential integrated, multitarget therapeutic strategies, including metabolic regulation, microbiome interventions, and immune modulation. Prospective longitudinal cohorts incorporating prediagnostic exposures and molecular pathology are needed to establish temporality.},
}
RevDate: 2026-06-29
Metagenomic profiling of gut microbiome in post-cholecystectomy patients with diarrhea: a nested case-control study.
BMC microbiology pii:10.1186/s12866-026-05346-4 [Epub ahead of print].
BACKGROUND: Cholecystectomy can cause diarrhea, with an incidence as high as 57.2%, seriously impacting patient prognosis. To investigate the gut dysbiosis following cholecystectomy and identify microbial biomarkers and functional genomics associated with post-cholecystectomy diarrhea (PCD), we conducted a nested case-control study within a prospective cohort.
METHODS: We enrolled a cohort of 160 patients. At follow-up completion, 30 patients who developed PCD were matched with 30 non-PCD (NPCD) controls. 16 S rRNA sequencing was used to analyze gut microbiota structure and diversity (mainly at genus level). Representative fecal samples underwent metagenomic sequencing for species level and genetic differential analysis.
RESULTS: The potentially pathogenic bacterial species Coprococcus comes and Blautia sp. were significantly enriched in the gut microbiota of PCD patients, with their abundance positively correlated with the degree of intestinal inflammation. In contrast, the potentially beneficial bacterial species Bacteroides intestinalis and Prevotella copri, known to contribute to lipid metabolism and play a role in modulating gut immunity and suppressing inflammatory responses, were found to be significantly depleted in PCD patients. Further metagenomic functional analysis revealed significant enrichment of pathways related to cell motility, membrane transport, and sulfur metabolism in PCD patients.
CONCLUSIONS: This work identified potential beneficial and pathogenic bacterial species associated with the onset of PCD, as well as significantly enriched functional pathways within the intestinal microbiota. These findings provide a scientific basis for elucidating the relationship between PCD and gut microbiota, and provide candidate microbial signatures and functional pathways that may inform future microbiota-targeted strategies, pending external and mechanistic validation.
Additional Links: PMID-42374196
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@article {pmid42374196,
year = {2026},
author = {Ye, J and Mao, P and Li, B and Hao, Y and Chen, Y and Li, K},
title = {Metagenomic profiling of gut microbiome in post-cholecystectomy patients with diarrhea: a nested case-control study.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05346-4},
pmid = {42374196},
issn = {1471-2180},
abstract = {BACKGROUND: Cholecystectomy can cause diarrhea, with an incidence as high as 57.2%, seriously impacting patient prognosis. To investigate the gut dysbiosis following cholecystectomy and identify microbial biomarkers and functional genomics associated with post-cholecystectomy diarrhea (PCD), we conducted a nested case-control study within a prospective cohort.
METHODS: We enrolled a cohort of 160 patients. At follow-up completion, 30 patients who developed PCD were matched with 30 non-PCD (NPCD) controls. 16 S rRNA sequencing was used to analyze gut microbiota structure and diversity (mainly at genus level). Representative fecal samples underwent metagenomic sequencing for species level and genetic differential analysis.
RESULTS: The potentially pathogenic bacterial species Coprococcus comes and Blautia sp. were significantly enriched in the gut microbiota of PCD patients, with their abundance positively correlated with the degree of intestinal inflammation. In contrast, the potentially beneficial bacterial species Bacteroides intestinalis and Prevotella copri, known to contribute to lipid metabolism and play a role in modulating gut immunity and suppressing inflammatory responses, were found to be significantly depleted in PCD patients. Further metagenomic functional analysis revealed significant enrichment of pathways related to cell motility, membrane transport, and sulfur metabolism in PCD patients.
CONCLUSIONS: This work identified potential beneficial and pathogenic bacterial species associated with the onset of PCD, as well as significantly enriched functional pathways within the intestinal microbiota. These findings provide a scientific basis for elucidating the relationship between PCD and gut microbiota, and provide candidate microbial signatures and functional pathways that may inform future microbiota-targeted strategies, pending external and mechanistic validation.},
}
RevDate: 2026-06-30
Dysbiosis of oral bacteriome and mycobiome associated with the severity of heart failure.
BMC oral health pii:10.1186/s12903-026-08977-1 [Epub ahead of print].
BACKGROUND: Heart failure (HF) is accompanied by chronic inflammation and metabolic stress, but the relationship between HF severity and the oral microbial ecosystem remains incompletely understood. This study aimed to investigate bacterial, fungal, and predicted functional alterations in supragingival plaque from patients with HF.
METHODS: This case-control study enrolled 63 patients with HF and 31 healthy controls (HC). Supragingival plaque samples were profiled by 16S rRNA and ITS sequencing. Community structure, differential amplicon sequence variants (ASVs), bacterial-fungal co-abundance networks, HF severity-associated ASVs and predicted MetaCyc pathways were analyzed using QIIME2, SparCC, weighted LASSO regression, and PICRUSt2. Pathway-ASV correlations were further assessed to explore links between taxonomic and predicted functional shifts.
RESULTS: HF status and NYHA class were among the strongest explanatory factors for oral bacterial and fungal community variation. Differential abundance analysis identified 102 bacterial and 68 fungal ASVs between HF and control groups. Weighted LASSO analysis retained six ASVs associated with the NYHA III-IV phenotype: ASV586 (Geotrichum candidum), ASV238 (Nectriaceae), and ASV182 (Neisseria bacilliformis) showed positive coefficients, whereas Haemophilus (ASV1), Streptococcus (ASV0), and Pseudopropionibacterium (ASV148) showed negative coefficients. A combined 6-ASV score discriminated HF from controls with an AUC of 0.804 and NYHA III-IV from the remaining cohort with an AUC of 0.842. PICRUSt2 identified 165 pathways differing between HF and controls. TCA cycle I was enriched in HF and positively correlated with NYHA class, whereas pyruvate fermentation to butanoate, a butyrate-related fermentative pathway, was enriched in controls and negatively correlated with NYHA class. Robust pathway-ASV correlations linked HC-enriched oral biofilm taxa with HC-enriched functional modules, suggesting functional uncoupling of the supragingival plaque ecosystem in more severe HF.
CONCLUSIONS: HF severity is associated with oral bacterial-fungal dysbiosis, characterized by enrichment of opportunistic pathogens, depletion of commensal biofilm organisms and predicted functional shifts involving microbial TCA cycle and fermentative capacity. These findings support an "oral-heart axis" in HF and warrant validation by longitudinal multi-omics studies.
Additional Links: PMID-42374463
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@article {pmid42374463,
year = {2026},
author = {Li, H and Wu, Q and Wang, Z and Hu, X and Zhang, S},
title = {Dysbiosis of oral bacteriome and mycobiome associated with the severity of heart failure.},
journal = {BMC oral health},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12903-026-08977-1},
pmid = {42374463},
issn = {1472-6831},
support = {82270405//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Heart failure (HF) is accompanied by chronic inflammation and metabolic stress, but the relationship between HF severity and the oral microbial ecosystem remains incompletely understood. This study aimed to investigate bacterial, fungal, and predicted functional alterations in supragingival plaque from patients with HF.
METHODS: This case-control study enrolled 63 patients with HF and 31 healthy controls (HC). Supragingival plaque samples were profiled by 16S rRNA and ITS sequencing. Community structure, differential amplicon sequence variants (ASVs), bacterial-fungal co-abundance networks, HF severity-associated ASVs and predicted MetaCyc pathways were analyzed using QIIME2, SparCC, weighted LASSO regression, and PICRUSt2. Pathway-ASV correlations were further assessed to explore links between taxonomic and predicted functional shifts.
RESULTS: HF status and NYHA class were among the strongest explanatory factors for oral bacterial and fungal community variation. Differential abundance analysis identified 102 bacterial and 68 fungal ASVs between HF and control groups. Weighted LASSO analysis retained six ASVs associated with the NYHA III-IV phenotype: ASV586 (Geotrichum candidum), ASV238 (Nectriaceae), and ASV182 (Neisseria bacilliformis) showed positive coefficients, whereas Haemophilus (ASV1), Streptococcus (ASV0), and Pseudopropionibacterium (ASV148) showed negative coefficients. A combined 6-ASV score discriminated HF from controls with an AUC of 0.804 and NYHA III-IV from the remaining cohort with an AUC of 0.842. PICRUSt2 identified 165 pathways differing between HF and controls. TCA cycle I was enriched in HF and positively correlated with NYHA class, whereas pyruvate fermentation to butanoate, a butyrate-related fermentative pathway, was enriched in controls and negatively correlated with NYHA class. Robust pathway-ASV correlations linked HC-enriched oral biofilm taxa with HC-enriched functional modules, suggesting functional uncoupling of the supragingival plaque ecosystem in more severe HF.
CONCLUSIONS: HF severity is associated with oral bacterial-fungal dysbiosis, characterized by enrichment of opportunistic pathogens, depletion of commensal biofilm organisms and predicted functional shifts involving microbial TCA cycle and fermentative capacity. These findings support an "oral-heart axis" in HF and warrant validation by longitudinal multi-omics studies.},
}
RevDate: 2026-06-30
Uncovering transcriptional processes in microbial communities adapted to differing saline conditions in salt-weathered historic buildings.
Microbiome pii:10.1186/s40168-026-02383-z [Epub ahead of print].
BACKGROUND: Microbial colonization of architectural surfaces in historic buildings can cause not only aesthetic damage but also biodeterioration. One example is the colonizing microbiome on salt-weathered architectural surfaces. Halotolerant and halophilic communities on such surfaces produce colored pigments that visually alter cultural heritage sites and could potentially degrade organic binders used for mural paintings. Although the microorganisms involved in these deterioration processes have already been described, detailed information about the molecular processes that allow these communities to succeed, survive, and thrive under such extreme conditions is still lacking.
RESULTS: A combined metagenome and metatranscriptome approach were employed to investigate three sampling sites located in two Austrian historic buildings displaying different environmental and saline compositions. The chapel of St. Virgil (Vienna) is a subsurface, climate-controlled environment. In contrast, the Charterhouse Mauerbach (Lower Austria) is exposed to natural fluctuations in temperature and humidity. DNA and total RNA were extracted from each sampling site simultaneously and sequenced. Two methods for gene assembly were compared and functionally evaluated. Results showed a minor bias in both methods, with improved results when they were combined. Comparison between DNA and RNA showed interesting variations in the taxonomic composition between the DNA- and RNA-based dataset, distinguishing the dormant from the active microbiome. The annotated halotolerance mechanisms in the metatranscriptomes indicated genome and proteome adaptations, showing high GC content, proteome acidification, with elevated aspartate and glutamate levels, and low isoelectric point profiles. Furthermore, the communities used both "salt-in" and "salt-out" osmoregulatory mechanisms. Pigment production was confirmed in all sampling points, revealing diverse pathways for carotenoid biosynthesis. Various protective mechanisms against oxidative stress were detected, such as those against reactive oxygen species (ROS), but also detoxification, protein folding, protein and DNA repair, and RNA chaperones. Key metabolic pathways revealed diverse pathways related to carbon, nitrogen, and sulfur cycling, linked to varying oxygen concentrations within biofilms. The results also highlighted the need for an in-depth analysis of the capabilities of the involved microorganisms.
CONCLUSIONS: The study shows highly specialized and cooperative adaptations, using both "salt-in" and "salt-out" strategies, diverse phototrophic and redox metabolisms that tightly couple C-N-S cycling.
Additional Links: PMID-42374590
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PubMed:
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@article {pmid42374590,
year = {2026},
author = {Fürnwein, L and Tichy, J and Waldherr, M and Lehner, E and Ortbauer, M and Vassallo, Y and Sipek, B and Sterflinger, K and Piñar, G and Graf, AB},
title = {Uncovering transcriptional processes in microbial communities adapted to differing saline conditions in salt-weathered historic buildings.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02383-z},
pmid = {42374590},
issn = {2049-2618},
support = {Heritage_2020-005_RESTOROMIC//Österreichischen Akademie der Wissenschaften/ ; },
abstract = {BACKGROUND: Microbial colonization of architectural surfaces in historic buildings can cause not only aesthetic damage but also biodeterioration. One example is the colonizing microbiome on salt-weathered architectural surfaces. Halotolerant and halophilic communities on such surfaces produce colored pigments that visually alter cultural heritage sites and could potentially degrade organic binders used for mural paintings. Although the microorganisms involved in these deterioration processes have already been described, detailed information about the molecular processes that allow these communities to succeed, survive, and thrive under such extreme conditions is still lacking.
RESULTS: A combined metagenome and metatranscriptome approach were employed to investigate three sampling sites located in two Austrian historic buildings displaying different environmental and saline compositions. The chapel of St. Virgil (Vienna) is a subsurface, climate-controlled environment. In contrast, the Charterhouse Mauerbach (Lower Austria) is exposed to natural fluctuations in temperature and humidity. DNA and total RNA were extracted from each sampling site simultaneously and sequenced. Two methods for gene assembly were compared and functionally evaluated. Results showed a minor bias in both methods, with improved results when they were combined. Comparison between DNA and RNA showed interesting variations in the taxonomic composition between the DNA- and RNA-based dataset, distinguishing the dormant from the active microbiome. The annotated halotolerance mechanisms in the metatranscriptomes indicated genome and proteome adaptations, showing high GC content, proteome acidification, with elevated aspartate and glutamate levels, and low isoelectric point profiles. Furthermore, the communities used both "salt-in" and "salt-out" osmoregulatory mechanisms. Pigment production was confirmed in all sampling points, revealing diverse pathways for carotenoid biosynthesis. Various protective mechanisms against oxidative stress were detected, such as those against reactive oxygen species (ROS), but also detoxification, protein folding, protein and DNA repair, and RNA chaperones. Key metabolic pathways revealed diverse pathways related to carbon, nitrogen, and sulfur cycling, linked to varying oxygen concentrations within biofilms. The results also highlighted the need for an in-depth analysis of the capabilities of the involved microorganisms.
CONCLUSIONS: The study shows highly specialized and cooperative adaptations, using both "salt-in" and "salt-out" strategies, diverse phototrophic and redox metabolisms that tightly couple C-N-S cycling.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Perinatal ampicillin exposure alters murine maternal fecal bile acid and acylcarnitine profiles.
Gut microbes, 18(1):2690698.
Maternal intrapartum antibiotic prophylaxis (IAP) and postpartum maternal antibiotic usage are increasingly common and have been linked to altered growth and immune development in offspring. However, the mechanisms underlying these effects, particularly those arising from indirect early-life exposure to antibiotics, remain poorly understood. Here, using a preclinical murine model, we examined the impact of in vivo antepartum and postpartum maternal ampicillin administration on the maternal fecal microbiome and metabolome. Ampicillin treatment resulted in a significant depletion of bacterial species belonging to the Muribaculaceae family, including Muribaculum intestinale and Duncaniella dubosii, accompanied by a cohort-dependent enrichment of Enterococcus and Prevotella species. These microbial shifts coincided with substantial and reproducible metabolic remodeling, including elevated fecal acylcarnitines and altered bile acid profiles. Notably, we identified two previously uncharacterized trihydroxylated bile acids conjugated to a hexose moiety, which we annotated as cholic acid-galactose and taurocholic acid-galactose and synthesized. These metabolites were consistently associated with antibiotic exposure across public metabolomics data repositories. Finally, alterations in the maternal fecal microbiome and metabolome were associated with increased weight gain in offspring, suggesting potential pathways by which maternal antibiotic exposure may influence early developmental outcomes. These findings highlight microbial and metabolic signatures linked to perinatal antibiotic use and underscore the need to balance infection control with long-term infant health considerations.
Additional Links: PMID-42374604
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@article {pmid42374604,
year = {2026},
author = {Zuffa, S and Thomas, SP and Patan, A and Mohanty, I and El Abiead, Y and Deleray, V and Kvitne, KE and Kousha, A and Suzuki, E and Tsai, CM and Nguyen, G and Ho, B and Y Liu, G and Nizet, V and Dorrestein, PC and Askarian, F and Tsunoda, SM},
title = {Perinatal ampicillin exposure alters murine maternal fecal bile acid and acylcarnitine profiles.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2690698},
doi = {10.1080/19490976.2026.2690698},
pmid = {42374604},
issn = {1949-0984},
mesh = {Animals ; Female ; *Ampicillin/adverse effects/administration & dosage ; *Bile Acids and Salts/metabolism/chemistry/analysis ; *Anti-Bacterial Agents/adverse effects/administration & dosage ; *Feces/chemistry/microbiology ; Pregnancy ; Mice ; *Carnitine/analogs & derivatives/metabolism/analysis ; Bacteria/classification/drug effects/isolation & purification/genetics ; Metabolome/drug effects ; *Gastrointestinal Microbiome/drug effects ; Mice, Inbred C57BL ; },
abstract = {Maternal intrapartum antibiotic prophylaxis (IAP) and postpartum maternal antibiotic usage are increasingly common and have been linked to altered growth and immune development in offspring. However, the mechanisms underlying these effects, particularly those arising from indirect early-life exposure to antibiotics, remain poorly understood. Here, using a preclinical murine model, we examined the impact of in vivo antepartum and postpartum maternal ampicillin administration on the maternal fecal microbiome and metabolome. Ampicillin treatment resulted in a significant depletion of bacterial species belonging to the Muribaculaceae family, including Muribaculum intestinale and Duncaniella dubosii, accompanied by a cohort-dependent enrichment of Enterococcus and Prevotella species. These microbial shifts coincided with substantial and reproducible metabolic remodeling, including elevated fecal acylcarnitines and altered bile acid profiles. Notably, we identified two previously uncharacterized trihydroxylated bile acids conjugated to a hexose moiety, which we annotated as cholic acid-galactose and taurocholic acid-galactose and synthesized. These metabolites were consistently associated with antibiotic exposure across public metabolomics data repositories. Finally, alterations in the maternal fecal microbiome and metabolome were associated with increased weight gain in offspring, suggesting potential pathways by which maternal antibiotic exposure may influence early developmental outcomes. These findings highlight microbial and metabolic signatures linked to perinatal antibiotic use and underscore the need to balance infection control with long-term infant health considerations.},
}
MeSH Terms:
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hide MeSH Terms
Animals
Female
*Ampicillin/adverse effects/administration & dosage
*Bile Acids and Salts/metabolism/chemistry/analysis
*Anti-Bacterial Agents/adverse effects/administration & dosage
*Feces/chemistry/microbiology
Pregnancy
Mice
*Carnitine/analogs & derivatives/metabolism/analysis
Bacteria/classification/drug effects/isolation & purification/genetics
Metabolome/drug effects
*Gastrointestinal Microbiome/drug effects
Mice, Inbred C57BL
RevDate: 2026-06-30
CmpDate: 2026-06-30
Microbiome and metabolites impact enteric and central nervous systems in ALS.
Gut microbes, 18(1):2692737.
Amyotrophic lateral sclerosis (ALS) has been linked to gastrointestinal symptoms and alterations in the gut microbiota. The enteric nervous system (ENS) coordinates intestinal function and sits at the host-microbe interface. The mechanisms by which luminal changes relay to the central nervous system (CNS), where motor neurons reside, have yet to be completely defined. In this narrative review, we first present evidence from ALS patient cohorts and preclinical models alongside mechanistic studies of infection, dysbiosis, and related neurodegenerative diseases to discuss how the microbiota and its metabolites may affect the ENS and CNS in ALS. Next, we propose a plausible mechanism of ALS pathogenesis through the gut-microbiome-brain axis. We further offer a summary of clinical trials that have studied the impacts of the microbiota on human ALS. Finally, we discuss future directions for studies of microbiota-ENS-CNS interactions in ALS. Better understanding of the dynamic interactions among the microbiota, microbial metabolites, neuroactive metabolites, and inflammation through the ENS/CNS in ALS will provide innovative insights into ALS prevention and treatment.
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@article {pmid42374626,
year = {2026},
author = {Walton, EI and Sun, J},
title = {Microbiome and metabolites impact enteric and central nervous systems in ALS.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2692737},
doi = {10.1080/19490976.2026.2692737},
pmid = {42374626},
issn = {1949-0984},
mesh = {*Amyotrophic Lateral Sclerosis/microbiology/metabolism/physiopathology ; Humans ; *Central Nervous System/metabolism/microbiology/physiopathology ; *Enteric Nervous System/metabolism/physiopathology/microbiology ; *Gastrointestinal Microbiome/physiology ; Animals ; Dysbiosis/microbiology ; },
abstract = {Amyotrophic lateral sclerosis (ALS) has been linked to gastrointestinal symptoms and alterations in the gut microbiota. The enteric nervous system (ENS) coordinates intestinal function and sits at the host-microbe interface. The mechanisms by which luminal changes relay to the central nervous system (CNS), where motor neurons reside, have yet to be completely defined. In this narrative review, we first present evidence from ALS patient cohorts and preclinical models alongside mechanistic studies of infection, dysbiosis, and related neurodegenerative diseases to discuss how the microbiota and its metabolites may affect the ENS and CNS in ALS. Next, we propose a plausible mechanism of ALS pathogenesis through the gut-microbiome-brain axis. We further offer a summary of clinical trials that have studied the impacts of the microbiota on human ALS. Finally, we discuss future directions for studies of microbiota-ENS-CNS interactions in ALS. Better understanding of the dynamic interactions among the microbiota, microbial metabolites, neuroactive metabolites, and inflammation through the ENS/CNS in ALS will provide innovative insights into ALS prevention and treatment.},
}
MeSH Terms:
show MeSH Terms
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*Amyotrophic Lateral Sclerosis/microbiology/metabolism/physiopathology
Humans
*Central Nervous System/metabolism/microbiology/physiopathology
*Enteric Nervous System/metabolism/physiopathology/microbiology
*Gastrointestinal Microbiome/physiology
Animals
Dysbiosis/microbiology
RevDate: 2026-06-30
CmpDate: 2026-06-30
Intraoral microbiome components identified in Polish patients assessed in terms of threats to human health with infectious factors.
Annals of agricultural and environmental medicine : AAEM, 33(2):161-166.
INTRODUCTION AND OBJECTIVE: The human oral cavity, the main part of masticatory system, is a dynamic environment still requiring quality research. The aim of the study is assessment of the status of the oral cavity and composition of intraoral microbiome of Polish patients in terms of threats to human health with infectious factors.
MATERIAL AND METHODS: The study utilised the data of generally healthy persons: 30 young aged 16-26 years and 30 middle-aged patients, aged 42-52 years. Intraoral swabs were assessed microscopically and by in vitro culture methods to detect/ identify microbiota.
RESULTS: Different microorganisms occurr in the oral cavity, including non-resident species. Parasitic protozoans Trichomonas tenax and Entamoeba gingivalis, facultative parasitic Acanthamoeba strains, yeast-like fungi of Candida albicans group, opportunistic and pathogenic bacteria, including endosymbionts, were identified with various frequency in particular regions of the oral cavity. Higher prevalences of bacteria and fungi strains occurred in middle-aged patients.
CONCLUSIONS: The relationship between microbiota of the human oral cavity remains a rare subject of research. This study has shown the ability of different microorganisms to coexist intraorally. These components may pose clinically important threat that should be taken into account as infectious factors. Recognition of microbiome components as potentially contagious, early identification/monitoring/assessment of concomitant species, preventive elimination of the infectious strains during the treatment should be taken into consideration. Further quality research on the intraoral microbiome species that may pose severe local/general clinical diseases are needed to reduce the risk to human health.
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@article {pmid42374673,
year = {2026},
author = {Perkowski, K and Dybicz, M and Szubińska-Lelonkiewicz, DM and Szaflik, J and Kuligowska, A and Łazicka-Gałecka, ME and Conn, DB and Zawadzki, P and Szostakowska, B and Baltaza, W and Zadurska, M and Chomicz, L},
title = {Intraoral microbiome components identified in Polish patients assessed in terms of threats to human health with infectious factors.},
journal = {Annals of agricultural and environmental medicine : AAEM},
volume = {33},
number = {2},
pages = {161-166},
doi = {10.26444/aaem/218097},
pmid = {42374673},
issn = {1898-2263},
mesh = {Humans ; Poland ; *Microbiota ; Adult ; *Mouth/microbiology/parasitology ; Female ; Young Adult ; *Bacteria/isolation & purification/classification/genetics ; Adolescent ; Middle Aged ; *Fungi/isolation & purification/classification/genetics ; Male ; },
abstract = {INTRODUCTION AND OBJECTIVE: The human oral cavity, the main part of masticatory system, is a dynamic environment still requiring quality research. The aim of the study is assessment of the status of the oral cavity and composition of intraoral microbiome of Polish patients in terms of threats to human health with infectious factors.
MATERIAL AND METHODS: The study utilised the data of generally healthy persons: 30 young aged 16-26 years and 30 middle-aged patients, aged 42-52 years. Intraoral swabs were assessed microscopically and by in vitro culture methods to detect/ identify microbiota.
RESULTS: Different microorganisms occurr in the oral cavity, including non-resident species. Parasitic protozoans Trichomonas tenax and Entamoeba gingivalis, facultative parasitic Acanthamoeba strains, yeast-like fungi of Candida albicans group, opportunistic and pathogenic bacteria, including endosymbionts, were identified with various frequency in particular regions of the oral cavity. Higher prevalences of bacteria and fungi strains occurred in middle-aged patients.
CONCLUSIONS: The relationship between microbiota of the human oral cavity remains a rare subject of research. This study has shown the ability of different microorganisms to coexist intraorally. These components may pose clinically important threat that should be taken into account as infectious factors. Recognition of microbiome components as potentially contagious, early identification/monitoring/assessment of concomitant species, preventive elimination of the infectious strains during the treatment should be taken into consideration. Further quality research on the intraoral microbiome species that may pose severe local/general clinical diseases are needed to reduce the risk to human health.},
}
MeSH Terms:
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Humans
Poland
*Microbiota
Adult
*Mouth/microbiology/parasitology
Female
Young Adult
*Bacteria/isolation & purification/classification/genetics
Adolescent
Middle Aged
*Fungi/isolation & purification/classification/genetics
Male
RevDate: 2026-06-30
Rapeseed root phospholipid metabolism orchestrates low phosphorus-induced microbiome changes and the interaction with beneficial Massilia.
Plant communications pii:S2590-3462(26)00289-0 [Epub ahead of print].
Phosphorus (P) is an essential macronutrient for plant development, and the role of microorganisms in enhancing plant P acquisition has attracted increasing attention. However, the genetic factors that enable plants to shape a microbiome responsive to low-P conditions remain largely elusive. In this study, we demonstrate that phospholipid metabolism influences low-P-induced changes in the root microbiome of rapeseed. Notably, the genus Massilia is identified as a key biomarker, whose abundance is significantly regulated by phospholipase-associated genetic factors. Experimental inoculation with Massilia significantly promoted plant growth and increased membrane phospholipid levels. Furthermore, phospholipids produced by Massilia serve as bioavailable P sources for the host plant, while the plant-derived phospholipid metabolite glyceric acid functions as a carbon source for the bacterium. These findings provide genetic insights into how plant phospholipid metabolism, mediated by phospholipases, orchestrates root microbial communities under low-P stress. This study also highlights the potential of Massilia as a bioinoculant to improve crop resilience in P-deficient soils.
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@article {pmid42374738,
year = {2026},
author = {Dong, X and Luo, Y and Chen, Y and Yang, B and Guo, L and Li, N},
title = {Rapeseed root phospholipid metabolism orchestrates low phosphorus-induced microbiome changes and the interaction with beneficial Massilia.},
journal = {Plant communications},
volume = {},
number = {},
pages = {101981},
doi = {10.1016/j.xplc.2026.101981},
pmid = {42374738},
issn = {2590-3462},
abstract = {Phosphorus (P) is an essential macronutrient for plant development, and the role of microorganisms in enhancing plant P acquisition has attracted increasing attention. However, the genetic factors that enable plants to shape a microbiome responsive to low-P conditions remain largely elusive. In this study, we demonstrate that phospholipid metabolism influences low-P-induced changes in the root microbiome of rapeseed. Notably, the genus Massilia is identified as a key biomarker, whose abundance is significantly regulated by phospholipase-associated genetic factors. Experimental inoculation with Massilia significantly promoted plant growth and increased membrane phospholipid levels. Furthermore, phospholipids produced by Massilia serve as bioavailable P sources for the host plant, while the plant-derived phospholipid metabolite glyceric acid functions as a carbon source for the bacterium. These findings provide genetic insights into how plant phospholipid metabolism, mediated by phospholipases, orchestrates root microbial communities under low-P stress. This study also highlights the potential of Massilia as a bioinoculant to improve crop resilience in P-deficient soils.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Shenfu Decoction Extends Survival Time of Seawater-Induced Hypothermia in Rats: The Role of Metabolomics and Gut Microbiota.
Current drug metabolism, 27(1):58-74.
INTRODUCTION: Shenfu decoction (SFD), a Traditional Chinese Medicine formula, is used in clinical emergencies. Its effects on seawater-induced hypothermia remain unclear. This study investigates the therapeutic mechanisms of SFD in improving the survival of hypothermic rats through metabolomics and gut microbiota analysis.
METHODS: Hypothermia was induced in rats via seawater immersion. The chemical constituents of SFD were analyzed using ultra-performance liquid chromatography quadrupole timeof- flight mass spectrometry (UPLC-Q-TOF-MS). Survival time and rates of low-temperature water-immersed rats were assessed. Rat blood samples were obtained for analysis of hematologic parameters, electrolytes, hepatic and renal function, cardiac injury, and inflammatory cytokines. To investigate the potential mechanism underlying the survival-prolonging effect of SFD on seawater-immersed hypothermic rats, untargeted blood metabolomics and gut microbiota profiling were employed for preliminary screening.
RESULTS: UPLC-Q-TOF-MS identified almost 50 compounds in SFD, and 1.35 g/kg SFD significantly extended the survival time of seawater-induced hypothermia rats by 6 hours. After hypothermic seawater immersion, the levels of red blood cells, hemoglobin, hematocrit, as well as serum calcium, phosphorus, blood urea nitrogen, alkaline phosphatase, total protein, cardiac troponin T, and interleukin-6 were significantly increased. However, pretreatment with 1.35 g/kg SFD in rats markedly decreased these parameters. The induction of hypothermic seawater immersion elevated blood glucose, and the administration of SFD exacerbated this increase in rats. Metabolomic analysis revealed elevated levels of valerenic acid and benzoylmesaconine in the SFD group, suggesting the restoration of metabolic homeostasis. This recovery was associated with modulation of the gut microbiota, notably an enhancement of beneficial genera, such as Enterococcus.
DISCUSSION: The findings demonstrated that SFD significantly prolonged survival in a rat model of seawater-immersion hypothermia. The protective mechanism involved a dual action: mitigating hypothermia-induced organ damage and hematological disturbances, coupled with restoring metabolic homeostasis and modulating gut microbiota. SFD has been found to possess specifically enriched beneficial bacterial genera, linked to the activation of brown adipose tissue and non-shivering thermogenesis. This study has provided initial evidence for a gut microbiota-metabolism axis mediating SFD's protective effect.
CONCLUSION: SFD prolonged survival in rats with seawater-induced hypothermia, likely by enhancing thermogenesis and regulating lipid metabolism through gut microbiota changes. The findings highlighted the potential of SFD for hypothermia prevention; however, its exact underlying mechanisms require further validation.
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@article {pmid42374767,
year = {2026},
author = {Wang, YJ and Chen, HZ and Wang, ZB and Sun, CY and Guo, CY and Ruan, Y and Li, CT and Zou, B and Yin, ZF and Gu, W},
title = {Shenfu Decoction Extends Survival Time of Seawater-Induced Hypothermia in Rats: The Role of Metabolomics and Gut Microbiota.},
journal = {Current drug metabolism},
volume = {27},
number = {1},
pages = {58-74},
pmid = {42374767},
issn = {1875-5453},
mesh = {Animals ; Male ; Metabolomics ; *Drugs, Chinese Herbal/pharmacology/therapeutic use ; Seawater/adverse effects ; Rats ; *Gastrointestinal Microbiome/drug effects ; Rats, Sprague-Dawley ; *Hypothermia/drug therapy/metabolism ; },
abstract = {INTRODUCTION: Shenfu decoction (SFD), a Traditional Chinese Medicine formula, is used in clinical emergencies. Its effects on seawater-induced hypothermia remain unclear. This study investigates the therapeutic mechanisms of SFD in improving the survival of hypothermic rats through metabolomics and gut microbiota analysis.
METHODS: Hypothermia was induced in rats via seawater immersion. The chemical constituents of SFD were analyzed using ultra-performance liquid chromatography quadrupole timeof- flight mass spectrometry (UPLC-Q-TOF-MS). Survival time and rates of low-temperature water-immersed rats were assessed. Rat blood samples were obtained for analysis of hematologic parameters, electrolytes, hepatic and renal function, cardiac injury, and inflammatory cytokines. To investigate the potential mechanism underlying the survival-prolonging effect of SFD on seawater-immersed hypothermic rats, untargeted blood metabolomics and gut microbiota profiling were employed for preliminary screening.
RESULTS: UPLC-Q-TOF-MS identified almost 50 compounds in SFD, and 1.35 g/kg SFD significantly extended the survival time of seawater-induced hypothermia rats by 6 hours. After hypothermic seawater immersion, the levels of red blood cells, hemoglobin, hematocrit, as well as serum calcium, phosphorus, blood urea nitrogen, alkaline phosphatase, total protein, cardiac troponin T, and interleukin-6 were significantly increased. However, pretreatment with 1.35 g/kg SFD in rats markedly decreased these parameters. The induction of hypothermic seawater immersion elevated blood glucose, and the administration of SFD exacerbated this increase in rats. Metabolomic analysis revealed elevated levels of valerenic acid and benzoylmesaconine in the SFD group, suggesting the restoration of metabolic homeostasis. This recovery was associated with modulation of the gut microbiota, notably an enhancement of beneficial genera, such as Enterococcus.
DISCUSSION: The findings demonstrated that SFD significantly prolonged survival in a rat model of seawater-immersion hypothermia. The protective mechanism involved a dual action: mitigating hypothermia-induced organ damage and hematological disturbances, coupled with restoring metabolic homeostasis and modulating gut microbiota. SFD has been found to possess specifically enriched beneficial bacterial genera, linked to the activation of brown adipose tissue and non-shivering thermogenesis. This study has provided initial evidence for a gut microbiota-metabolism axis mediating SFD's protective effect.
CONCLUSION: SFD prolonged survival in rats with seawater-induced hypothermia, likely by enhancing thermogenesis and regulating lipid metabolism through gut microbiota changes. The findings highlighted the potential of SFD for hypothermia prevention; however, its exact underlying mechanisms require further validation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Male
Metabolomics
*Drugs, Chinese Herbal/pharmacology/therapeutic use
Seawater/adverse effects
Rats
*Gastrointestinal Microbiome/drug effects
Rats, Sprague-Dawley
*Hypothermia/drug therapy/metabolism
RevDate: 2026-06-30
The gut-heart axis in cardio-oncology.
Cardiovascular research pii:8721926 [Epub ahead of print].
As cancer survival rates improve, the long-term burden of treatment has become increasingly evident. Cancer survivors face a markedly higher risk of cardiovascular-related complications and premature, non-cancer-related mortality. In particular, cardiovascular disease (CVD) is disproportionately prevalent, with survivors approximately 40% more likely to develop and die from CVD compared to the general population. Although this increased morbidity reflects both acute cardiotoxic events and the later development and progression of more chronic CVDs, traditionally viewed as direct consequences of cancer therapies, the underlying mechanisms, especially those that are feasible to modify, are poorly understood. Emerging evidence positions the gut-heart axis as a central regulator of cardiovascular risk in cardio-oncology. This avenue is especially compelling to explore as the gut microbiome is well documented to be altered by cancer therapies, including chemotherapy, immune checkpoint inhibitors, targeted therapies, and radiation, with profound and persistent changes in diversity, composition and function widely reported across clinical cohorts. Comparable microbial changes have been observed in non-cancer cohorts with cardiovascular disease. For example, specific microbial metabolites have been reported to exert cardiovascular protective benefits in hypertension. Thus, there is a compelling opportunity to explore the gut microbiome to advance our understanding and ability to prevent cardiovascular disease in cancer survivors. This review synthesises current evidence linking the gut microbiome to cancer therapy-related cardiac dysfunction (CTRCD), evaluates microbial metabolites as predictive biomarkers of cardiotoxicity, and discusses microbiome-targeted modulation as an emerging strategy for improving cardiovascular outcomes in cancer survivors.
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@article {pmid42374831,
year = {2026},
author = {Chan, NSL and Cross, C and Bowen, J and Prestidge, C and Ryan, FJ and Dorraki, M and Liyanage, S and Sharma, S and Pathy, R and Bursill, CA and Psaltis, PJ and Marques, FZ and Wardill, HR and Joyce, P},
title = {The gut-heart axis in cardio-oncology.},
journal = {Cardiovascular research},
volume = {},
number = {},
pages = {},
doi = {10.1093/cvr/cvag146},
pmid = {42374831},
issn = {1755-3245},
abstract = {As cancer survival rates improve, the long-term burden of treatment has become increasingly evident. Cancer survivors face a markedly higher risk of cardiovascular-related complications and premature, non-cancer-related mortality. In particular, cardiovascular disease (CVD) is disproportionately prevalent, with survivors approximately 40% more likely to develop and die from CVD compared to the general population. Although this increased morbidity reflects both acute cardiotoxic events and the later development and progression of more chronic CVDs, traditionally viewed as direct consequences of cancer therapies, the underlying mechanisms, especially those that are feasible to modify, are poorly understood. Emerging evidence positions the gut-heart axis as a central regulator of cardiovascular risk in cardio-oncology. This avenue is especially compelling to explore as the gut microbiome is well documented to be altered by cancer therapies, including chemotherapy, immune checkpoint inhibitors, targeted therapies, and radiation, with profound and persistent changes in diversity, composition and function widely reported across clinical cohorts. Comparable microbial changes have been observed in non-cancer cohorts with cardiovascular disease. For example, specific microbial metabolites have been reported to exert cardiovascular protective benefits in hypertension. Thus, there is a compelling opportunity to explore the gut microbiome to advance our understanding and ability to prevent cardiovascular disease in cancer survivors. This review synthesises current evidence linking the gut microbiome to cancer therapy-related cardiac dysfunction (CTRCD), evaluates microbial metabolites as predictive biomarkers of cardiotoxicity, and discusses microbiome-targeted modulation as an emerging strategy for improving cardiovascular outcomes in cancer survivors.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Regulatory effects of leflunomide on gut microecology during IgA nephropathy treatment.
Renal failure, 48(1):2650023.
Growing evidence suggests that the gut-kidney axis may contribute to the pathogenesis of IgA nephropathy (IgAN). However, the effects of immunosuppressants on the intestinal microbiome remain unclear. We investigated how different therapeutic strategies influence gut microbial composition in IgAN patients. We enrolled 46 patients with IgAN and 37 healthy controls (HC). Patients were stratified by treatment regimen into a supportive care group or an immunosuppressive therapy group, with subgroups defined by the use of leflunomide and systemic glucocorticoids. Fecal samples from patients in clinical remission were analyzed and 16S rRNA gene sequencing was performed. We examined microbial α- and β-diversity, taxonomic differences, and predicted functional pathways using Linear Discriminant Analysis Effect Size and Kyoto Encyclopedia of Genes and Genomes (KEGG)-based annotation. Compared with HCs, IgAN patients showed significantly reduced microbial α-diversity, depletion of beneficial taxa such as Faecalibacterium, and enrichment of potential pathogens, including Enterobacteriaceae. Neither supportive care and systemic glucocorticoid therapy were not associated with an apparent restoration of overall microbial diversity or community structure. Conversely, leflunomide treatment was associated with higher microbial diversity and a taxonomic profile that showed a trend toward similarity with healthy controls. Notably, anti-inflammatory bacteria, including Dysosmobacter welbionis, Ruthenibacterium lactatiformans, and Intestinimonas butyriciproducens were significantly enriched (all p < 0.01). KEGG-based predictions revealed downregulation of pro-inflammatory pathways, accompanied by reduced levels of inflammatory markers (p < 0.05). Overall, the therapeutic efficacy of leflunomide in IgA nephropathy is associated with specific characteristics of the patients' gut microbiota, which may be linked to its potential to reverse dysbiosis and enhance anti-inflammatory effects.
Additional Links: PMID-42374850
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PubMed:
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@article {pmid42374850,
year = {2026},
author = {Ren, P and Wen, X and Lin, X and Zhao, W and Xu, G and Jiang, H and Chen, J},
title = {Regulatory effects of leflunomide on gut microecology during IgA nephropathy treatment.},
journal = {Renal failure},
volume = {48},
number = {1},
pages = {2650023},
doi = {10.1080/0886022X.2026.2650023},
pmid = {42374850},
issn = {1525-6049},
mesh = {Humans ; *Leflunomide/therapeutic use/pharmacology ; *Glomerulonephritis, IGA/drug therapy/microbiology ; Female ; Male ; Adult ; *Gastrointestinal Microbiome/drug effects ; *Immunosuppressive Agents/therapeutic use/pharmacology ; Feces/microbiology ; Case-Control Studies ; Glucocorticoids/therapeutic use ; Middle Aged ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Growing evidence suggests that the gut-kidney axis may contribute to the pathogenesis of IgA nephropathy (IgAN). However, the effects of immunosuppressants on the intestinal microbiome remain unclear. We investigated how different therapeutic strategies influence gut microbial composition in IgAN patients. We enrolled 46 patients with IgAN and 37 healthy controls (HC). Patients were stratified by treatment regimen into a supportive care group or an immunosuppressive therapy group, with subgroups defined by the use of leflunomide and systemic glucocorticoids. Fecal samples from patients in clinical remission were analyzed and 16S rRNA gene sequencing was performed. We examined microbial α- and β-diversity, taxonomic differences, and predicted functional pathways using Linear Discriminant Analysis Effect Size and Kyoto Encyclopedia of Genes and Genomes (KEGG)-based annotation. Compared with HCs, IgAN patients showed significantly reduced microbial α-diversity, depletion of beneficial taxa such as Faecalibacterium, and enrichment of potential pathogens, including Enterobacteriaceae. Neither supportive care and systemic glucocorticoid therapy were not associated with an apparent restoration of overall microbial diversity or community structure. Conversely, leflunomide treatment was associated with higher microbial diversity and a taxonomic profile that showed a trend toward similarity with healthy controls. Notably, anti-inflammatory bacteria, including Dysosmobacter welbionis, Ruthenibacterium lactatiformans, and Intestinimonas butyriciproducens were significantly enriched (all p < 0.01). KEGG-based predictions revealed downregulation of pro-inflammatory pathways, accompanied by reduced levels of inflammatory markers (p < 0.05). Overall, the therapeutic efficacy of leflunomide in IgA nephropathy is associated with specific characteristics of the patients' gut microbiota, which may be linked to its potential to reverse dysbiosis and enhance anti-inflammatory effects.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Leflunomide/therapeutic use/pharmacology
*Glomerulonephritis, IGA/drug therapy/microbiology
Female
Male
Adult
*Gastrointestinal Microbiome/drug effects
*Immunosuppressive Agents/therapeutic use/pharmacology
Feces/microbiology
Case-Control Studies
Glucocorticoids/therapeutic use
Middle Aged
RNA, Ribosomal, 16S/genetics
RevDate: 2026-06-30
Males are worse mothers: Comparing care patterns in a facultatively caring beetle.
Insect science [Epub ahead of print].
During biparental pre- and post-hatching care, parents take on energy-consuming tasks for the offspring's benefit and further reduce their own individual costs by specializing in different care aspects. But how is biparental care evolutionarily stable when biparental care is facultative, that is, when offspring survival does not obligately rely on post-hatching care? We examine this phenomenon in the carrion-breeding beetle Nicrophorus vespilloides, whose facultative biparental care involves microbiome control of the carcass nursery through continued application of antimicrobial exudates, shielding offspring from adverse environmental conditions. While evidence suggests synergistic effects of biparental care in Nicrophorus, any adaptive benefits in terms of social immunity are unknown in this genus. We presented Nicrophorus adults with a microbial challenge while manipulating parental care patterns during the period of post-hatching care, investigating consequences in parent and offspring performance. We found that microbial environment and parental care pattern influence larval development and survival. Additionally, we show for the first time that both factors affect personal immunity response in Nicrophorus offspring, responding to challenging conditions. Simultaneously, we show that biparentally caring beetles lose more weight during post-hatching care than uniparentally caring beetles, indicating higher investment and/or higher competition with mates or offspring. We present new evidence that burying beetle offspring adjust their personal immunity based on their microbial and social environment, and that biparental care may allow parents to sustain parental care under challenging conditions, raising further questions about the interplay of care patterns and the microbial environment on immune-regulatory and developmental processes in offspring.
Additional Links: PMID-42375078
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@article {pmid42375078,
year = {2026},
author = {Müller, L and Limburg, P and Körner, M},
title = {Males are worse mothers: Comparing care patterns in a facultatively caring beetle.},
journal = {Insect science},
volume = {},
number = {},
pages = {},
doi = {10.1111/1744-7917.70313},
pmid = {42375078},
issn = {1744-7917},
support = {531480526//Deutsche Forschungsgemeinschaft/ ; },
abstract = {During biparental pre- and post-hatching care, parents take on energy-consuming tasks for the offspring's benefit and further reduce their own individual costs by specializing in different care aspects. But how is biparental care evolutionarily stable when biparental care is facultative, that is, when offspring survival does not obligately rely on post-hatching care? We examine this phenomenon in the carrion-breeding beetle Nicrophorus vespilloides, whose facultative biparental care involves microbiome control of the carcass nursery through continued application of antimicrobial exudates, shielding offspring from adverse environmental conditions. While evidence suggests synergistic effects of biparental care in Nicrophorus, any adaptive benefits in terms of social immunity are unknown in this genus. We presented Nicrophorus adults with a microbial challenge while manipulating parental care patterns during the period of post-hatching care, investigating consequences in parent and offspring performance. We found that microbial environment and parental care pattern influence larval development and survival. Additionally, we show for the first time that both factors affect personal immunity response in Nicrophorus offspring, responding to challenging conditions. Simultaneously, we show that biparentally caring beetles lose more weight during post-hatching care than uniparentally caring beetles, indicating higher investment and/or higher competition with mates or offspring. We present new evidence that burying beetle offspring adjust their personal immunity based on their microbial and social environment, and that biparental care may allow parents to sustain parental care under challenging conditions, raising further questions about the interplay of care patterns and the microbial environment on immune-regulatory and developmental processes in offspring.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Development of Quorum Sensing Modulators of Streptococcus constellatus.
Chembiochem : a European journal of chemical biology, 27(13):e70444.
Streptococcus constellatus inhabits the healthy human gastrointestinal tract and oral microbiome; however, the incidence of this species becoming opportunistically pathogenic has increased in recent decades. S. constellatus has the potential to cause severe pyogenic infections requiring combination antibiotic therapy or surgical intervention. Some virulence processes in S. constellatus, such as genetic competence, are regulated through quorum sensing (QS), facilitated by its 16-mer competence stimulating peptide (CSP). Several target residues on the CSP molecule were identified that can be mutated to enhance the peptide activity and/or lead to competitive inhibition of the competence regulon QS circuitry, thereby modulating related pathogenic phenotypes. Using a rational design approach, second-generation peptide analog libraries were designed and screened, resulting in optimization of a competitive QS inhibitor, CSP-D1AI4AM6A, with an IC50 of 38.3 nM. Overall, this work provides a rational framework upon which novel QS modulators can be designed to attenuate virulence processes in this opportunistic pathogen.
Additional Links: PMID-42375126
PubMed:
Citation:
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@article {pmid42375126,
year = {2026},
author = {Rodriguez, KM and Elliott, DN and Lemieux, ER and Liu, OS and Tal-Gan, Y},
title = {Development of Quorum Sensing Modulators of Streptococcus constellatus.},
journal = {Chembiochem : a European journal of chemical biology},
volume = {27},
number = {13},
pages = {e70444},
pmid = {42375126},
issn = {1439-7633},
support = {CHE-2316599//National Science Foundation/ ; GM145539/NH/NIH HHS/United States ; },
mesh = {*Quorum Sensing/drug effects ; *Bacterial Proteins/metabolism/chemistry/genetics ; *Peptides/chemistry/pharmacology/chemical synthesis ; *Anti-Bacterial Agents/pharmacology/chemistry/chemical synthesis ; Humans ; },
abstract = {Streptococcus constellatus inhabits the healthy human gastrointestinal tract and oral microbiome; however, the incidence of this species becoming opportunistically pathogenic has increased in recent decades. S. constellatus has the potential to cause severe pyogenic infections requiring combination antibiotic therapy or surgical intervention. Some virulence processes in S. constellatus, such as genetic competence, are regulated through quorum sensing (QS), facilitated by its 16-mer competence stimulating peptide (CSP). Several target residues on the CSP molecule were identified that can be mutated to enhance the peptide activity and/or lead to competitive inhibition of the competence regulon QS circuitry, thereby modulating related pathogenic phenotypes. Using a rational design approach, second-generation peptide analog libraries were designed and screened, resulting in optimization of a competitive QS inhibitor, CSP-D1AI4AM6A, with an IC50 of 38.3 nM. Overall, this work provides a rational framework upon which novel QS modulators can be designed to attenuate virulence processes in this opportunistic pathogen.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Quorum Sensing/drug effects
*Bacterial Proteins/metabolism/chemistry/genetics
*Peptides/chemistry/pharmacology/chemical synthesis
*Anti-Bacterial Agents/pharmacology/chemistry/chemical synthesis
Humans
RevDate: 2026-06-30
CmpDate: 2026-06-30
Vaginal microbiota and genitourinary syndrome of menopause in premenopausal breast cancer patients receiving endocrine therapy: a longitudinal cohort study protocol.
Frontiers in medicine, 13:1826064.
BACKGROUND: Endocrine therapy with ovarian function suppression combined with aromatase inhibitors or tamoxifen is essential for hormone receptor-positive breast cancer in premenopausal women, but often induces genitourinary syndrome of menopause (GSM) via hypoestrogenism. Existing research focuses on natural menopause, with limited longitudinal data on vaginal microbiome changes in breast cancer survivors, especially amid rising cases among young Chinese women.
OBJECTIVES: To (1) assess temporal effects of endocrine therapy on vaginal microbiome α- and β-diversity and dominant taxa (e.g., Lactobacillus); (2) explore dose-response links between microbiome shifts and GSM severity; and (3) compare OFS + AI versus OFS + TAM impacts on vaginal microecology.
METHODS: This single-center prospective cohort at Women's Hospital, Zhejiang University School of Medicine, will enroll 110 premenopausal women (18-45 years) with hormone receptor-positive breast cancer, allocated to OFS + AI or OFS + TAM based on clinical regimens. Vaginal swabs collected at baseline and 1, 3, 6, 12 months undergo 16S rRNA sequencing (V3-V4 region) with DADA2-based ASV analysis via QIIME 2 for species-level resolution. Assessments include Vaginal Health Index (VHI), GSM symptoms (VAS for dryness, dyspareunia, burning), s, and urinary symptoms (ICIQ-SF). Primary outcomes: microbiome diversity (Simpson index) and Lactobacillus abundance. Secondary: VHI, VAS, urinary scores. Analyses use repeated measures ANOVA and generalized estimating equations; sample size accounts for medium effect (d = 0.8) and 10% attrition. Ethically approved and registered in Chinese Clinical Trial Registry.
CONCLUSION: As a longitudinal study on vaginal microecology in this population, this protocol integrates molecular and clinical data to reveal GSM mechanisms, informing personalized interventions for better quality of life and adherence.
CLINICAL TRIAL REGISTRATION: http://www.chictr.org.cn/showproj.html?proj=296570, Identifier (No. ChiCTR2500115283).
Additional Links: PMID-42375202
PubMed:
Citation:
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@article {pmid42375202,
year = {2026},
author = {Chen, F and Bo, Z and Fan, Y and Huang, Y and Chen, Y and Wan, F},
title = {Vaginal microbiota and genitourinary syndrome of menopause in premenopausal breast cancer patients receiving endocrine therapy: a longitudinal cohort study protocol.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1826064},
pmid = {42375202},
issn = {2296-858X},
abstract = {BACKGROUND: Endocrine therapy with ovarian function suppression combined with aromatase inhibitors or tamoxifen is essential for hormone receptor-positive breast cancer in premenopausal women, but often induces genitourinary syndrome of menopause (GSM) via hypoestrogenism. Existing research focuses on natural menopause, with limited longitudinal data on vaginal microbiome changes in breast cancer survivors, especially amid rising cases among young Chinese women.
OBJECTIVES: To (1) assess temporal effects of endocrine therapy on vaginal microbiome α- and β-diversity and dominant taxa (e.g., Lactobacillus); (2) explore dose-response links between microbiome shifts and GSM severity; and (3) compare OFS + AI versus OFS + TAM impacts on vaginal microecology.
METHODS: This single-center prospective cohort at Women's Hospital, Zhejiang University School of Medicine, will enroll 110 premenopausal women (18-45 years) with hormone receptor-positive breast cancer, allocated to OFS + AI or OFS + TAM based on clinical regimens. Vaginal swabs collected at baseline and 1, 3, 6, 12 months undergo 16S rRNA sequencing (V3-V4 region) with DADA2-based ASV analysis via QIIME 2 for species-level resolution. Assessments include Vaginal Health Index (VHI), GSM symptoms (VAS for dryness, dyspareunia, burning), s, and urinary symptoms (ICIQ-SF). Primary outcomes: microbiome diversity (Simpson index) and Lactobacillus abundance. Secondary: VHI, VAS, urinary scores. Analyses use repeated measures ANOVA and generalized estimating equations; sample size accounts for medium effect (d = 0.8) and 10% attrition. Ethically approved and registered in Chinese Clinical Trial Registry.
CONCLUSION: As a longitudinal study on vaginal microecology in this population, this protocol integrates molecular and clinical data to reveal GSM mechanisms, informing personalized interventions for better quality of life and adherence.
CLINICAL TRIAL REGISTRATION: http://www.chictr.org.cn/showproj.html?proj=296570, Identifier (No. ChiCTR2500115283).},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Comparative analysis of gut microbiota in Bombyx mori fed on M. alba and M. nigra using 16S rRNA amplicon sequencing.
Open veterinary journal, 16(1):275-286.
BACKGROUND: Bombyx mori is a key species in the sericulture industry and depends on mulberry leaves for growth and silk production.
AIM: This study characterized the gut microbiota of B. mori fed on two mulberry species using 16S rRNA amplicon sequencing.
METHODS: Ten healthy fifth instar larvae were randomly selected from each treatment group. The larvae were dissected under sterile conditions to extract the gut tissues to obtain a pooled sample. DNA was extracted using a QIAamp DNA Microbiome kit, and the primer set 27F (5-AGAGTTTGATCCTGGCTCAG-3) and 1492-R (5-GGTTACCTTGTTACGACTT-3) was used to amplify variable regions V3-V4 of the 16S rRNA gene using Illumina sequencing. Using the EzBioCloud platform, Operational Taxonomic Unit data were used to estimate the bacterial species richness and evenness. The microbial communities' phylum to genus level were grouped. Raw paired-end reads (FASTQ format) were imported into Qiime2 v2021.4 software, and a Krona plot was constructed.
RESULTS: The gut microbiota of B. mori larvae fed on Morus alba was predominantly composed of Proteobacteria (36.46%), Bacteroidota (22.98%), Firmicutes (20.31%), and Actinobacteriota (20.15%). All of these play critical roles in nitrogen fixation, carbohydrate breakdown, and immune modulation, thereby supporting optimal gut health and nutrient absorption. In contrast, silkworms fed on Morus nigra exhibited a microbiota dominated by Proteobacteria (31.74%), Verrucomicrobiota (23.35%), Bacteroidota (12.58%), and Bdellovibrionota (12.30%). Bdellovibrionota is a predatory bacterium that may disrupt the balance and potentially affect silkworm health and growth. Proximate analysis further supported the differences in microbiota composition of M. alba and M. nigra. M. alba had significantly higher levels of crude protein (26.16%) and crude fat (4.53%) than M. nigra (19.50% and 3.20%, respectively). Silkworms fed with M. alba exhibited superior growth across all molting stages compared with those fed with M. nigra.
CONCLUSION: Future studies should focus on the effects of probiotic supplementation on microbial diversity, growth performance, and cocoon production. Increasing the sample size would provide more comprehensive results and individual-level variations in gut microbiota. These insights will contribute to the optimization of sericulture strategies for silkworm growth and silk yield.
Additional Links: PMID-42375244
PubMed:
Citation:
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@article {pmid42375244,
year = {2026},
author = {Shafique, M and Ali, W and Bukhari, SM and Mehmood, S},
title = {Comparative analysis of gut microbiota in Bombyx mori fed on M. alba and M. nigra using 16S rRNA amplicon sequencing.},
journal = {Open veterinary journal},
volume = {16},
number = {1},
pages = {275-286},
pmid = {42375244},
issn = {2218-6050},
mesh = {Animals ; *Bombyx/microbiology/growth & development ; *Morus ; RNA, Ribosomal, 16S/analysis ; *Gastrointestinal Microbiome ; Larva/microbiology/growth & development ; Bacteria/classification/genetics/isolation & purification ; Animal Feed/analysis ; },
abstract = {BACKGROUND: Bombyx mori is a key species in the sericulture industry and depends on mulberry leaves for growth and silk production.
AIM: This study characterized the gut microbiota of B. mori fed on two mulberry species using 16S rRNA amplicon sequencing.
METHODS: Ten healthy fifth instar larvae were randomly selected from each treatment group. The larvae were dissected under sterile conditions to extract the gut tissues to obtain a pooled sample. DNA was extracted using a QIAamp DNA Microbiome kit, and the primer set 27F (5-AGAGTTTGATCCTGGCTCAG-3) and 1492-R (5-GGTTACCTTGTTACGACTT-3) was used to amplify variable regions V3-V4 of the 16S rRNA gene using Illumina sequencing. Using the EzBioCloud platform, Operational Taxonomic Unit data were used to estimate the bacterial species richness and evenness. The microbial communities' phylum to genus level were grouped. Raw paired-end reads (FASTQ format) were imported into Qiime2 v2021.4 software, and a Krona plot was constructed.
RESULTS: The gut microbiota of B. mori larvae fed on Morus alba was predominantly composed of Proteobacteria (36.46%), Bacteroidota (22.98%), Firmicutes (20.31%), and Actinobacteriota (20.15%). All of these play critical roles in nitrogen fixation, carbohydrate breakdown, and immune modulation, thereby supporting optimal gut health and nutrient absorption. In contrast, silkworms fed on Morus nigra exhibited a microbiota dominated by Proteobacteria (31.74%), Verrucomicrobiota (23.35%), Bacteroidota (12.58%), and Bdellovibrionota (12.30%). Bdellovibrionota is a predatory bacterium that may disrupt the balance and potentially affect silkworm health and growth. Proximate analysis further supported the differences in microbiota composition of M. alba and M. nigra. M. alba had significantly higher levels of crude protein (26.16%) and crude fat (4.53%) than M. nigra (19.50% and 3.20%, respectively). Silkworms fed with M. alba exhibited superior growth across all molting stages compared with those fed with M. nigra.
CONCLUSION: Future studies should focus on the effects of probiotic supplementation on microbial diversity, growth performance, and cocoon production. Increasing the sample size would provide more comprehensive results and individual-level variations in gut microbiota. These insights will contribute to the optimization of sericulture strategies for silkworm growth and silk yield.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Bombyx/microbiology/growth & development
*Morus
RNA, Ribosomal, 16S/analysis
*Gastrointestinal Microbiome
Larva/microbiology/growth & development
Bacteria/classification/genetics/isolation & purification
Animal Feed/analysis
RevDate: 2026-07-01
CmpDate: 2026-06-30
Decoding the reproductive microbiome: enabling clinical and biological insights through machine and deep learning.
Frontiers in endocrinology, 17:1812407.
BACKGROUND: Technological advances have revolutionised the microbiome research in the field of human reproduction, identifying the microbiome as important regulator of reproductive health and functions, where microbes are now linked to sperm quality, ovarian function, endometrial receptivity, embryo implantation, and pregnancy outcomes, including miscarriage and preterm birth. However, the field faces a 'descriptive phase' due to the fragmentation of datasets and a lack of functional integration. To progress towards broader understanding and clinical utility, robust computational frameworks are required to translate complex microbial signatures into predictive insights.
METHODS: This review classifies the application of machine learning (ML) and deep learning (DL) into essential methodological pillars. We evaluate the entire computational workflow from sequencing data generation to predictive modelling, including data pre-processing for sparsity and compositionality, exploratory, diversity, functional and differential abundance analyses, and advanced data integration to harmonise data across samples, independent datasets, and multiple 16S regions. Particular emphasis is placed on feature selection for biomarker signatures, synthetic data generation, and phenotype classification. Where reproductive-specific evidence is currently limited, normally due to scarce study cohorts, we present proof-of-concept studies from other human niches to demonstrate potential applications. Furthermore, we address the need for Explainable Artificial Intelligence (XAI) to ensure biological interpretability and guide clinical decisions effectively.
CONCLUSION: Transitioning from descriptive to predictive reproductive medicine relies on integrating ML/DL approaches with biological knowledge. Challenges like small cohort sizes can be overcome through the integration and harmonisation of independent datasets. On a methodological level, researchers should adopt ensemble-based differential abundance and feature selection to reduce data and tool-specific biases. Crucially, any steps altering data nature-such as synthetic data generation-must be strictly confined to training sets to prevent data leakage and preserve model validity. Alongside these technical precautions, standardising analytical workflows and prioritising interpretability are key practical steps. While clinical translation requires extensive validation, moving toward predictive studies is a fundamental first step for future personalised reproductive care. With the current review, we highlight the methodological considerations of ML/DL and provide recommendations for future microbiome studies in the field.
Additional Links: PMID-42375331
PubMed:
Citation:
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@article {pmid42375331,
year = {2026},
author = {Garach Vélez, I and Leonés-Baños, I and Folch, BA and Antequera, L and Rojas, I and Ortuño, F and Lara, MJS and Altmäe, S and Herrera, LJ},
title = {Decoding the reproductive microbiome: enabling clinical and biological insights through machine and deep learning.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1812407},
pmid = {42375331},
issn = {1664-2392},
mesh = {Humans ; *Deep Learning ; *Microbiota/physiology ; *Machine Learning ; *Reproduction/physiology ; Female ; Predictive Learning Models ; Data Analytics ; },
abstract = {BACKGROUND: Technological advances have revolutionised the microbiome research in the field of human reproduction, identifying the microbiome as important regulator of reproductive health and functions, where microbes are now linked to sperm quality, ovarian function, endometrial receptivity, embryo implantation, and pregnancy outcomes, including miscarriage and preterm birth. However, the field faces a 'descriptive phase' due to the fragmentation of datasets and a lack of functional integration. To progress towards broader understanding and clinical utility, robust computational frameworks are required to translate complex microbial signatures into predictive insights.
METHODS: This review classifies the application of machine learning (ML) and deep learning (DL) into essential methodological pillars. We evaluate the entire computational workflow from sequencing data generation to predictive modelling, including data pre-processing for sparsity and compositionality, exploratory, diversity, functional and differential abundance analyses, and advanced data integration to harmonise data across samples, independent datasets, and multiple 16S regions. Particular emphasis is placed on feature selection for biomarker signatures, synthetic data generation, and phenotype classification. Where reproductive-specific evidence is currently limited, normally due to scarce study cohorts, we present proof-of-concept studies from other human niches to demonstrate potential applications. Furthermore, we address the need for Explainable Artificial Intelligence (XAI) to ensure biological interpretability and guide clinical decisions effectively.
CONCLUSION: Transitioning from descriptive to predictive reproductive medicine relies on integrating ML/DL approaches with biological knowledge. Challenges like small cohort sizes can be overcome through the integration and harmonisation of independent datasets. On a methodological level, researchers should adopt ensemble-based differential abundance and feature selection to reduce data and tool-specific biases. Crucially, any steps altering data nature-such as synthetic data generation-must be strictly confined to training sets to prevent data leakage and preserve model validity. Alongside these technical precautions, standardising analytical workflows and prioritising interpretability are key practical steps. While clinical translation requires extensive validation, moving toward predictive studies is a fundamental first step for future personalised reproductive care. With the current review, we highlight the methodological considerations of ML/DL and provide recommendations for future microbiome studies in the field.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Deep Learning
*Microbiota/physiology
*Machine Learning
*Reproduction/physiology
Female
Predictive Learning Models
Data Analytics
RevDate: 2026-06-30
CmpDate: 2026-06-30
Molecular studies on the impact of microbiome on anticancer drug resistance.
Frontiers in immunology, 17:1848345.
Cancer remains a leading global health challenge, with drug resistance posing a critical barrier to the durable efficacy of anticancer therapies, including chemotherapy, immunotherapy, and targeted treatments. Growing evidence highlights the gut microbiome as a key modulator in this resistance process. The gut microbiome-a dynamic and diverse microbial ecosystem-can influence drug efficacy through multiple mechanisms, including the biotransformation of chemotherapeutics, modulation of immune responses, alteration of host drug-metabolizing enzymes, and reshaping of the tumor microenvironment. Notably, specific bacterial taxa can enzymatically inactivate chemotherapeutic drugs, while microbial metabolites and signaling pathways further promote resistance by rewiring cellular survival and immune-regulatory programs. In this review, we synthesize recent molecular insights into microbiome-driven anticancer drug resistance and discuss emerging microbiome-targeted strategies, such as dietary intervention, probiotics and prebiotics, fecal microbiota transplantation, and advanced drug delivery systems. A deeper understanding of host-microbiome-drug interactions may provide new opportunities to overcome therapeutic resistance and advance precision oncology.
Additional Links: PMID-42375360
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Citation:
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@article {pmid42375360,
year = {2026},
author = {Zhou, K and Lu, P and Xu, H and Wang, L and Liang, X},
title = {Molecular studies on the impact of microbiome on anticancer drug resistance.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1848345},
pmid = {42375360},
issn = {1664-3224},
mesh = {Humans ; *Drug Resistance, Neoplasm/immunology ; Animals ; *Antineoplastic Agents/therapeutic use/pharmacology ; *Gastrointestinal Microbiome/immunology/drug effects ; *Neoplasms/drug therapy/microbiology/immunology ; Tumor Microenvironment/immunology ; Probiotics ; Prebiotics ; Fecal Microbiota Transplantation ; },
abstract = {Cancer remains a leading global health challenge, with drug resistance posing a critical barrier to the durable efficacy of anticancer therapies, including chemotherapy, immunotherapy, and targeted treatments. Growing evidence highlights the gut microbiome as a key modulator in this resistance process. The gut microbiome-a dynamic and diverse microbial ecosystem-can influence drug efficacy through multiple mechanisms, including the biotransformation of chemotherapeutics, modulation of immune responses, alteration of host drug-metabolizing enzymes, and reshaping of the tumor microenvironment. Notably, specific bacterial taxa can enzymatically inactivate chemotherapeutic drugs, while microbial metabolites and signaling pathways further promote resistance by rewiring cellular survival and immune-regulatory programs. In this review, we synthesize recent molecular insights into microbiome-driven anticancer drug resistance and discuss emerging microbiome-targeted strategies, such as dietary intervention, probiotics and prebiotics, fecal microbiota transplantation, and advanced drug delivery systems. A deeper understanding of host-microbiome-drug interactions may provide new opportunities to overcome therapeutic resistance and advance precision oncology.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Drug Resistance, Neoplasm/immunology
Animals
*Antineoplastic Agents/therapeutic use/pharmacology
*Gastrointestinal Microbiome/immunology/drug effects
*Neoplasms/drug therapy/microbiology/immunology
Tumor Microenvironment/immunology
Probiotics
Prebiotics
Fecal Microbiota Transplantation
RevDate: 2026-06-30
CmpDate: 2026-06-30
Invasive Ureaplasma urealyticum infection mimicking diffuse large B-cell lymphoma relapse: A case report.
IDCases, 45:e02637.
Ureaplasma spp. are typically benign colonizers of the urogenital tract but may cause invasive disease in immunocompromised patients. In rare cases, such infections may mimic malignancy and lead to significant diagnostic delay. Diagnosis is challenging due to non-specific clinical manifestations, poor visibility on Gram stain, and limitations of standard culture methods. We report a rare case of invasive Ureaplasma urealyticum infection in a patient in complete remission after rituximab-based chemoimmunotherapy for diffuse large B-cell lymphoma transformed from follicular lymphoma. The infection manifested as a progressively destructive soft tissue lesion involving the scrotum and abdominal wall and was suspected to represent lymphoma progression. Conventional microbiologic investigations remained negative, and the diagnosis was ultimately established through microbiome analysis based on 16S rRNA gene amplicon sequencing. Antimicrobial susceptibility testing guided prolonged dual-agent therapy with doxycycline and moxifloxacin, resulting in complete resolution. Clinicians should consider invasive Ureaplasma infection in immunocompromised patients with persistent culture-negative infections or PET-positive lesions suggestive of malignancy, as early molecular diagnostics may prevent diagnostic delay and unnecessary invasive procedures.
Additional Links: PMID-42375500
PubMed:
Citation:
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@article {pmid42375500,
year = {2026},
author = {Østergaard, S and Nielsen, XC and Jensen, JS and Grüner, JM and Gjerdrum, LMR and Pedersen, LM},
title = {Invasive Ureaplasma urealyticum infection mimicking diffuse large B-cell lymphoma relapse: A case report.},
journal = {IDCases},
volume = {45},
number = {},
pages = {e02637},
pmid = {42375500},
issn = {2214-2509},
abstract = {Ureaplasma spp. are typically benign colonizers of the urogenital tract but may cause invasive disease in immunocompromised patients. In rare cases, such infections may mimic malignancy and lead to significant diagnostic delay. Diagnosis is challenging due to non-specific clinical manifestations, poor visibility on Gram stain, and limitations of standard culture methods. We report a rare case of invasive Ureaplasma urealyticum infection in a patient in complete remission after rituximab-based chemoimmunotherapy for diffuse large B-cell lymphoma transformed from follicular lymphoma. The infection manifested as a progressively destructive soft tissue lesion involving the scrotum and abdominal wall and was suspected to represent lymphoma progression. Conventional microbiologic investigations remained negative, and the diagnosis was ultimately established through microbiome analysis based on 16S rRNA gene amplicon sequencing. Antimicrobial susceptibility testing guided prolonged dual-agent therapy with doxycycline and moxifloxacin, resulting in complete resolution. Clinicians should consider invasive Ureaplasma infection in immunocompromised patients with persistent culture-negative infections or PET-positive lesions suggestive of malignancy, as early molecular diagnostics may prevent diagnostic delay and unnecessary invasive procedures.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
The Nasopharyngeal Microbiome: A Narrative Review of the Hidden Regulator of Ear, Nose, and Throat (ENT) Inflammations.
Cureus, 18(5):e109921.
The nasopharyngeal microbiome is a central regulator of respiratory health. The upper airway microbial community acts as the primary gatekeeper against respiratory pathogens and maintains homeostasis in the upper respiratory tract (URT). This community is established at birth and influenced by the delivery method and antibiotic exposure. Disruptions to this balance are recognised as a major driver of chronic inflammatory ear, nose, and throat (ENT) diseases. This review analyses the literature on the relationship between the nasopharyngeal microbiome and inflammatory ENT diseases. We searched recent literature (2015-2025) via PubMed and Scopus, focusing on 16S rRNA and metagenomic studies of the upper respiratory tract. We examined papers that linked microbial shifts to clinical outcomes in otitis media, rhinosinusitis, and allergic rhinitis, as well as studies applying machine learning to diagnostic modelling. Clinical health is associated with stable colonisation by Dolosigranulum and Corynebacterium. These commensals protect the host by maintaining the mucosal barrier and competing against pathogens. Chronic disease, in contrast, is marked by a bloom of Streptococcus, Haemophilus, or Moraxella. In chronic rhinosinusitis, loss of bacterial diversity and S. aureus biofilm formation often lead to treatment failure. Machine learning tools like Random Forest and XGBoost classifiers have been applied to nasopharyngeal microbiome data. In published cohorts, these models have achieved sensitivity and specificity values of 80-90% for identifying dysbiotic profiles associated with disease, outperforming standard culture in speed and taxonomic resolution. These findings support a shift from broad antibiotic use toward microbiome-informed treatment. Standardising sampling and sequencing methods remains the next necessary step.
Additional Links: PMID-42375904
PubMed:
Citation:
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@article {pmid42375904,
year = {2026},
author = {Panagiotidi, K and Markidis, A and Karamatzanis, I and Almomani, M and Omirou, R and Kosmidou, P},
title = {The Nasopharyngeal Microbiome: A Narrative Review of the Hidden Regulator of Ear, Nose, and Throat (ENT) Inflammations.},
journal = {Cureus},
volume = {18},
number = {5},
pages = {e109921},
pmid = {42375904},
issn = {2168-8184},
abstract = {The nasopharyngeal microbiome is a central regulator of respiratory health. The upper airway microbial community acts as the primary gatekeeper against respiratory pathogens and maintains homeostasis in the upper respiratory tract (URT). This community is established at birth and influenced by the delivery method and antibiotic exposure. Disruptions to this balance are recognised as a major driver of chronic inflammatory ear, nose, and throat (ENT) diseases. This review analyses the literature on the relationship between the nasopharyngeal microbiome and inflammatory ENT diseases. We searched recent literature (2015-2025) via PubMed and Scopus, focusing on 16S rRNA and metagenomic studies of the upper respiratory tract. We examined papers that linked microbial shifts to clinical outcomes in otitis media, rhinosinusitis, and allergic rhinitis, as well as studies applying machine learning to diagnostic modelling. Clinical health is associated with stable colonisation by Dolosigranulum and Corynebacterium. These commensals protect the host by maintaining the mucosal barrier and competing against pathogens. Chronic disease, in contrast, is marked by a bloom of Streptococcus, Haemophilus, or Moraxella. In chronic rhinosinusitis, loss of bacterial diversity and S. aureus biofilm formation often lead to treatment failure. Machine learning tools like Random Forest and XGBoost classifiers have been applied to nasopharyngeal microbiome data. In published cohorts, these models have achieved sensitivity and specificity values of 80-90% for identifying dysbiotic profiles associated with disease, outperforming standard culture in speed and taxonomic resolution. These findings support a shift from broad antibiotic use toward microbiome-informed treatment. Standardising sampling and sequencing methods remains the next necessary step.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Comparative gut microbial enzyme functions in human amoebiasis: Implications for host-microbe interactions and veterinary parasitic models.
Open veterinary journal, 16(4):2212-2231.
BACKGROUND: The intestinal microbiome is a critical component of host defense and metabolic regulation in both humans and animals. Parasitic infections such as amebiasis disrupt microbial enzyme activities, potentially influencing host physiology.
AIM: To investigate functional differences in gut microbial enzymes between humans infected with Entameba histolytica and healthy controls and to provide insights relevant to comparative parasitic pathobiology.
METHODS: Stool samples collected from patients diagnosed with amebiasis, as well as from healthy control individuals, were analyzed using 16S rRNA gene sequencing. KEGG-based annotation tools were used to generate functional enzyme predictions, and differential pathway enrichment was assessed across hierarchical metabolic levels.
RESULTS: The results showed that healthy controls displayed greater representation of metabolic, genetic, and environmental information pathways. In contrast, amebiasis patients showed enrichment in membrane transport and energy metabolism. Glycolytic and oxidative stress-related enzymes, including 6-phosphofructokinase, phosphoglycerate mutase, and peroxiredoxin, were significantly more abundant in the infected group. Conversely, enzymes linked to amino acid biosynthesis and DNA repair-such as phosphoglycolate phosphatase and NADH: ubiquinone reductase-were markedly reduced, indicating a functional shift toward energy mobilization and stress adaptation.
CONCLUSION: In conclusion, amebiasis induces the reorganization of gut microbial enzyme functions, enhancing glycolytic and transport activities while suppressing biosynthetic and repair processes. These findings may also provide valuable comparative insights for veterinary medicine, as similar host-parasite-microbiome interactions occur in several protozoal infections affecting domestic and wild animals. Understanding microbial enzyme responses during protozoal infection could therefore contribute to improved interpretation of microbiome-associated pathophysiology in veterinary parasitology.
Additional Links: PMID-42375950
PubMed:
Citation:
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@article {pmid42375950,
year = {2026},
author = {Abuljadayel, DA},
title = {Comparative gut microbial enzyme functions in human amoebiasis: Implications for host-microbe interactions and veterinary parasitic models.},
journal = {Open veterinary journal},
volume = {16},
number = {4},
pages = {2212-2231},
pmid = {42375950},
issn = {2218-6050},
mesh = {Humans ; *Entamoeba histolytica/physiology ; *Gastrointestinal Microbiome ; *Host Microbial Interactions ; Animals ; RNA, Ribosomal, 16S/analysis ; *Entamoebiasis/microbiology/parasitology ; *Bacteria/enzymology ; },
abstract = {BACKGROUND: The intestinal microbiome is a critical component of host defense and metabolic regulation in both humans and animals. Parasitic infections such as amebiasis disrupt microbial enzyme activities, potentially influencing host physiology.
AIM: To investigate functional differences in gut microbial enzymes between humans infected with Entameba histolytica and healthy controls and to provide insights relevant to comparative parasitic pathobiology.
METHODS: Stool samples collected from patients diagnosed with amebiasis, as well as from healthy control individuals, were analyzed using 16S rRNA gene sequencing. KEGG-based annotation tools were used to generate functional enzyme predictions, and differential pathway enrichment was assessed across hierarchical metabolic levels.
RESULTS: The results showed that healthy controls displayed greater representation of metabolic, genetic, and environmental information pathways. In contrast, amebiasis patients showed enrichment in membrane transport and energy metabolism. Glycolytic and oxidative stress-related enzymes, including 6-phosphofructokinase, phosphoglycerate mutase, and peroxiredoxin, were significantly more abundant in the infected group. Conversely, enzymes linked to amino acid biosynthesis and DNA repair-such as phosphoglycolate phosphatase and NADH: ubiquinone reductase-were markedly reduced, indicating a functional shift toward energy mobilization and stress adaptation.
CONCLUSION: In conclusion, amebiasis induces the reorganization of gut microbial enzyme functions, enhancing glycolytic and transport activities while suppressing biosynthetic and repair processes. These findings may also provide valuable comparative insights for veterinary medicine, as similar host-parasite-microbiome interactions occur in several protozoal infections affecting domestic and wild animals. Understanding microbial enzyme responses during protozoal infection could therefore contribute to improved interpretation of microbiome-associated pathophysiology in veterinary parasitology.},
}
MeSH Terms:
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Humans
*Entamoeba histolytica/physiology
*Gastrointestinal Microbiome
*Host Microbial Interactions
Animals
RNA, Ribosomal, 16S/analysis
*Entamoebiasis/microbiology/parasitology
*Bacteria/enzymology
RevDate: 2026-06-30
CmpDate: 2026-06-30
Microbial community characterization of multi-crop growouts in the XROOTS aeroponic-hydroponic system on the International Space Station.
Frontiers in microbiomes, 5:1779816.
Plant growth systems tested on the International Space Station (ISS) are small-area growth units that mostly use solid media. With NASA's plan to send astronauts on long-duration exploration missions, there is a need to produce larger amounts of fresh food with limited upmass and resources. The eXposed Root On-Orbit Test System (XROOTS) is an aeroponic-hydroponic nutrient delivery system designed for exploration missions and was tested on the ISS. Post-harvest samples were returned for microbiological analyses of the plant leaves, roots, and fruit from lettuce, mizuna mustard, wheat, radish, tomato, and pea plants grown in the XROOTS. The microbiological food safety of crops was evaluated through culture-based microbial enumeration and identification. The microbial communities were compared between different plants and plant tissues by sequencing the prokaryotic V4 variable region of the 16S ribosomal RNA (rRNA) gene amplicons and fungal internal transcribed spacer (ITS) region. The microbial counts from the root module surface samples demonstrated a reduction after cleansing. The bacterial counts in the nutrient solution ranged from 65 to 3,800 CFU/ml. The bacterial counts in the distal leaf sections were lower than those in the leaf proximal, wick, and roots in all plant samples. The tomato fruit and the pea pod samples had the lowest average counts. The microbial counts from the leaves and wicks harvested from XROOTS were similar to the ranges found on previous Veggie (Vegetable Production System)-grown leafy greens. All screening tests for potential foodborne pathogenic bacteria were negative. Sequencing analyses showed that diversity was low in the leaves and higher in the roots, and the microbial community was more diversified in the XROOTS samples compared with previous Veggie experiments. Pseudomonas had the highest relative abundance in the majority of samples. Although some microbes were shared in the majority of plant tissues, unique microbes were identified for each plant type grown in XROOTS and when compared with previous Veggie demonstrations. Microbial surveys of ISS-grown plants and the associated hardware provide valuable data that can reveal potential challenges in deep-space crop production operations and ensure the quality of crops intended for crew consumption.
Additional Links: PMID-42376193
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Citation:
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@article {pmid42376193,
year = {2026},
author = {Khodadad, CLM and Spern, CJ and Hummerick, ME and Gooden, JL and Morales, CJ and Wheeler, RM and Melendez, O and Morrow, R and Wetzel, J and Zhang, Y},
title = {Microbial community characterization of multi-crop growouts in the XROOTS aeroponic-hydroponic system on the International Space Station.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1779816},
pmid = {42376193},
issn = {2813-4338},
abstract = {Plant growth systems tested on the International Space Station (ISS) are small-area growth units that mostly use solid media. With NASA's plan to send astronauts on long-duration exploration missions, there is a need to produce larger amounts of fresh food with limited upmass and resources. The eXposed Root On-Orbit Test System (XROOTS) is an aeroponic-hydroponic nutrient delivery system designed for exploration missions and was tested on the ISS. Post-harvest samples were returned for microbiological analyses of the plant leaves, roots, and fruit from lettuce, mizuna mustard, wheat, radish, tomato, and pea plants grown in the XROOTS. The microbiological food safety of crops was evaluated through culture-based microbial enumeration and identification. The microbial communities were compared between different plants and plant tissues by sequencing the prokaryotic V4 variable region of the 16S ribosomal RNA (rRNA) gene amplicons and fungal internal transcribed spacer (ITS) region. The microbial counts from the root module surface samples demonstrated a reduction after cleansing. The bacterial counts in the nutrient solution ranged from 65 to 3,800 CFU/ml. The bacterial counts in the distal leaf sections were lower than those in the leaf proximal, wick, and roots in all plant samples. The tomato fruit and the pea pod samples had the lowest average counts. The microbial counts from the leaves and wicks harvested from XROOTS were similar to the ranges found on previous Veggie (Vegetable Production System)-grown leafy greens. All screening tests for potential foodborne pathogenic bacteria were negative. Sequencing analyses showed that diversity was low in the leaves and higher in the roots, and the microbial community was more diversified in the XROOTS samples compared with previous Veggie experiments. Pseudomonas had the highest relative abundance in the majority of samples. Although some microbes were shared in the majority of plant tissues, unique microbes were identified for each plant type grown in XROOTS and when compared with previous Veggie demonstrations. Microbial surveys of ISS-grown plants and the associated hardware provide valuable data that can reveal potential challenges in deep-space crop production operations and ensure the quality of crops intended for crew consumption.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Metagenomic analysis of human feces reveals gut microbiome role in colorectal cancer.
Frontiers in cellular and infection microbiology, 16:1828012.
BACKGROUND: This study aimed to identify the microbiota and specific genes that are closely associated with colorectal cancer (CRC) through metagenomic sequencing and integrative multi-omics analysis.
METHODS: Fecal samples were collected from 11 healthy volunteers and 20 patients with CRC. Genomic DNA was extracted for metagenomic analysis and high-throughput sequencing. Compositional differences and correlations of the gut microbiome were compared based on species and functional diversity.
RESULTS: The overall species composition included 1,980 species, with 1,707 species identified in the CRC group and 1,525 in the healthy control group. Alpha diversity was significantly lower in the CRC group than in the healthy control group (p = 0.014). Beta diversity analysis revealed significant differences between the two groups (stress = 0.1308, p = 0.021). Based on LEfSe analysis, Shigella, Porphyromonas, Proteus, Bacteroides, Alistipes, Fusobacterium, and Escherichia were more abundant in patients with CRC, whereas Eubacterium, Clostridium, Dialister, Faecalibacterium, Blautia, Coprococcus, Dorea, Subdoligranulum, Megamonas, Roseburia, and Prevotella were significantly more abundant in the healthy control group (p < 0.05).
CONCLUSION: A multidimensional microbial diagnostic model, incorporating Shigella, Porphyromonas, Proteus, Bacteroides, Fusobacterium, Escherichia, Eubacterium, Clostridium, Dialister, Faecalibacterium, Blautia, Coprococcus, Dorea, Subdoligranulum, Megamonas, Roseburia, and Prevotella, suggests the potential to enhance early CRC screening performance. Furthermore, LptA, tnaA, envC, and argB may represent promising candidates for novel therapeutic targets, warranting further investigation.
Additional Links: PMID-42376319
PubMed:
Citation:
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@article {pmid42376319,
year = {2026},
author = {Gu, Z and Tan, Q and Mao, D and Zhang, Y and Wang, Y and He, D and Chen, S},
title = {Metagenomic analysis of human feces reveals gut microbiome role in colorectal cancer.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1828012},
pmid = {42376319},
issn = {2235-2988},
mesh = {Humans ; *Colorectal Neoplasms/microbiology ; *Feces/microbiology ; *Metagenomics/methods ; *Gastrointestinal Microbiome/genetics ; Female ; Male ; Middle Aged ; *Bacteria/classification/genetics/isolation & purification ; Aged ; Multiomics ; High-Throughput Nucleotide Sequencing ; Adult ; Metagenome ; },
abstract = {BACKGROUND: This study aimed to identify the microbiota and specific genes that are closely associated with colorectal cancer (CRC) through metagenomic sequencing and integrative multi-omics analysis.
METHODS: Fecal samples were collected from 11 healthy volunteers and 20 patients with CRC. Genomic DNA was extracted for metagenomic analysis and high-throughput sequencing. Compositional differences and correlations of the gut microbiome were compared based on species and functional diversity.
RESULTS: The overall species composition included 1,980 species, with 1,707 species identified in the CRC group and 1,525 in the healthy control group. Alpha diversity was significantly lower in the CRC group than in the healthy control group (p = 0.014). Beta diversity analysis revealed significant differences between the two groups (stress = 0.1308, p = 0.021). Based on LEfSe analysis, Shigella, Porphyromonas, Proteus, Bacteroides, Alistipes, Fusobacterium, and Escherichia were more abundant in patients with CRC, whereas Eubacterium, Clostridium, Dialister, Faecalibacterium, Blautia, Coprococcus, Dorea, Subdoligranulum, Megamonas, Roseburia, and Prevotella were significantly more abundant in the healthy control group (p < 0.05).
CONCLUSION: A multidimensional microbial diagnostic model, incorporating Shigella, Porphyromonas, Proteus, Bacteroides, Fusobacterium, Escherichia, Eubacterium, Clostridium, Dialister, Faecalibacterium, Blautia, Coprococcus, Dorea, Subdoligranulum, Megamonas, Roseburia, and Prevotella, suggests the potential to enhance early CRC screening performance. Furthermore, LptA, tnaA, envC, and argB may represent promising candidates for novel therapeutic targets, warranting further investigation.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Colorectal Neoplasms/microbiology
*Feces/microbiology
*Metagenomics/methods
*Gastrointestinal Microbiome/genetics
Female
Male
Middle Aged
*Bacteria/classification/genetics/isolation & purification
Aged
Multiomics
High-Throughput Nucleotide Sequencing
Adult
Metagenome
RevDate: 2026-06-30
CmpDate: 2026-06-30
Carceral settings as institutional exposures in caries microbiome research.
Journal of oral microbiology, 18(1):2694733.
Additional Links: PMID-42376429
PubMed:
Citation:
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@article {pmid42376429,
year = {2026},
author = {Yusroni, A and Anwar, MK and Sari, YEK},
title = {Carceral settings as institutional exposures in caries microbiome research.},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2694733},
pmid = {42376429},
issn = {2000-2297},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Oral fungal microbiome in gout: composition, cross-kingdom interactions, and effects of intervention.
Journal of oral microbiology, 18(1):2680789.
BACKGROUND: Oral fungi, despite their low abundance, may influence microbial interactions, host responses, and disease progression; however, their role in gout remains poorly understood.
MATERIALS AND METHODS: Between March and December 2024, patients with chronic gouty arthritis (CGA), acute gouty arthritis (AGA), and age- and sex-matched healthy controls (HC) were enrolled. Unstimulated saliva underwent ITS2 sequencing. Analyses included α/β-diversity, differential abundance, and genus-level co-occurrence networks. Cross-kingdom associations were assessed using partial Spearman correlation integrating 16S rRNA data. A subset received lifestyle intervention and urate-lowering therapy with follow-up.
RESULTS: A total of 76 participants (35 CGA, 17 AGA, 24 HC) were included. Alpha-diversity showed no significant difference, while β-diversity distinguished patients from HC (P = 0.0018). Ascomycota and Basidiomycota predominated. Alternaria, Eutypella, and Saccharomyces was enriched in CGA. Whereas Eutypella was enriched in AGA. Network analysis revealed progressive loss of fungal-fungal and fungal-bacterial interactions, with strengthened pathogenic fungi-bacteria associations. Follow-up indicated partial restoration of fungal-fungal networks preceding compositional recovery.
CONCLUSION: This study provides the first characterization of the oral mycobiome in gout, highlighting weakened microbial connectivity and reinforced pathogen associations. Interventions may restore network integrity before compositional normalization, suggesting the oral mycobiome as a potential target in gout.
Additional Links: PMID-42376430
PubMed:
Citation:
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@article {pmid42376430,
year = {2026},
author = {Yao, M and Han, Y and Huang, C and Dai, M and Zhang, X and Zhang, Y and Zeng, X},
title = {Oral fungal microbiome in gout: composition, cross-kingdom interactions, and effects of intervention.},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2680789},
pmid = {42376430},
issn = {2000-2297},
abstract = {BACKGROUND: Oral fungi, despite their low abundance, may influence microbial interactions, host responses, and disease progression; however, their role in gout remains poorly understood.
MATERIALS AND METHODS: Between March and December 2024, patients with chronic gouty arthritis (CGA), acute gouty arthritis (AGA), and age- and sex-matched healthy controls (HC) were enrolled. Unstimulated saliva underwent ITS2 sequencing. Analyses included α/β-diversity, differential abundance, and genus-level co-occurrence networks. Cross-kingdom associations were assessed using partial Spearman correlation integrating 16S rRNA data. A subset received lifestyle intervention and urate-lowering therapy with follow-up.
RESULTS: A total of 76 participants (35 CGA, 17 AGA, 24 HC) were included. Alpha-diversity showed no significant difference, while β-diversity distinguished patients from HC (P = 0.0018). Ascomycota and Basidiomycota predominated. Alternaria, Eutypella, and Saccharomyces was enriched in CGA. Whereas Eutypella was enriched in AGA. Network analysis revealed progressive loss of fungal-fungal and fungal-bacterial interactions, with strengthened pathogenic fungi-bacteria associations. Follow-up indicated partial restoration of fungal-fungal networks preceding compositional recovery.
CONCLUSION: This study provides the first characterization of the oral mycobiome in gout, highlighting weakened microbial connectivity and reinforced pathogen associations. Interventions may restore network integrity before compositional normalization, suggesting the oral mycobiome as a potential target in gout.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Buffalo rumen microbial cellulase as a candidate enzyme for hydrolysis of rice straw into glucose: A preliminary study.
Open veterinary journal, 15(12):6342-6350.
BACKGROUND: The buffalo rumen microbiome is enriched in functional genes, notably those encoding beta-glucosidase, which participate in polysaccharide breakdown. However, the characterization of enzymes and the application of buffalo rumen in biomass fermentation remain underdeveloped.
AIM: This study aimed to elucidate the enzymatic profile of buffalo rumen microbiota and assess the effect of heat of ammonia-based pretreatment combined with enzymatic hydrolysis isolated from buffalo ruminal fluid in rice straw to produce bioethanol.
METHODS: A factorial experiment was performed with heat (H) and enzyme (E) combinations. The treatment was as follows: (1) no heat and commercial enzyme (H0E1), (2) heat and commercial enzyme (H1E1), (3) no heat and buffalo rumen enzyme (H0E2), and (4) heat and buffalo rumen enzyme (H1E2) with three replications. The enzyme activity, glucose, and ethanol levels were measured.
RESULTS: Beta-glucosidase enzyme was the highest activity (64.23 ± 12.37 U/g) in buffalo rumen fluid. The activities of carboxymethyl cellulase, xylanase, and exoglucanase were 50.36 ± 8.05, 17.44 ± 5.95, and 0.20 ± 0.03 U/g, respectively. The interaction treatments impacted (p < 0.01) the glucose production. H1E1 treatment had the highest glucose content (193.94 ± 14.51 g/L) among all treatments. Moreover, the glucose level in the H0E1 group was higher than that in the H0E2 and H1E2 groups (102.96 ± 27.59 vs. 0.91 ± 0.15 and 1.32 ± 0.37 g/L, respectively). The combination treatments had no effect (p > 0.05) on ethanol production. Heat treatment did not (p > 0.05) influence the ethanol content. However, enzyme treatment affected (p < 0.01) the ethanol level. The ethanol production in the H0E1 and H1E1 groups (0.55% ± 0.13% and 0.99% ± 0.02% v/v) was higher than the ethanol content in the H0E2 and H1E2 treatments (0.19% ± 0.11% and 0.28% ± 0.10% v/v).
CONCLUSION: Buffalo rumen-derived cellulase can convert cellulose in rice straw into glucose. However, the glucose content in the buffalo rumen enzyme treatment was lower than that of the commercial enzyme.
Additional Links: PMID-42376535
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@article {pmid42376535,
year = {2025},
author = {Prabowo, A and Hartanto, S and Ludfiani, DD and Haryanto, B and Pertiwi, MD and Wasil, AA and Wardani, MLD and Suretno, ND and Hayati, RN and Arianti, FD and Santoso, AD and Megawati, M and Astuti, W and Pandupuspitasari, NS and Kurniawati, A and Bachruddin, Z},
title = {Buffalo rumen microbial cellulase as a candidate enzyme for hydrolysis of rice straw into glucose: A preliminary study.},
journal = {Open veterinary journal},
volume = {15},
number = {12},
pages = {6342-6350},
pmid = {42376535},
issn = {2218-6050},
mesh = {Animals ; *Buffaloes/microbiology ; *Rumen/microbiology/enzymology ; *Cellulase/metabolism ; *Glucose/metabolism ; *Oryza/chemistry/metabolism ; Hydrolysis ; Fermentation ; Ethanol/metabolism ; *Gastrointestinal Microbiome ; },
abstract = {BACKGROUND: The buffalo rumen microbiome is enriched in functional genes, notably those encoding beta-glucosidase, which participate in polysaccharide breakdown. However, the characterization of enzymes and the application of buffalo rumen in biomass fermentation remain underdeveloped.
AIM: This study aimed to elucidate the enzymatic profile of buffalo rumen microbiota and assess the effect of heat of ammonia-based pretreatment combined with enzymatic hydrolysis isolated from buffalo ruminal fluid in rice straw to produce bioethanol.
METHODS: A factorial experiment was performed with heat (H) and enzyme (E) combinations. The treatment was as follows: (1) no heat and commercial enzyme (H0E1), (2) heat and commercial enzyme (H1E1), (3) no heat and buffalo rumen enzyme (H0E2), and (4) heat and buffalo rumen enzyme (H1E2) with three replications. The enzyme activity, glucose, and ethanol levels were measured.
RESULTS: Beta-glucosidase enzyme was the highest activity (64.23 ± 12.37 U/g) in buffalo rumen fluid. The activities of carboxymethyl cellulase, xylanase, and exoglucanase were 50.36 ± 8.05, 17.44 ± 5.95, and 0.20 ± 0.03 U/g, respectively. The interaction treatments impacted (p < 0.01) the glucose production. H1E1 treatment had the highest glucose content (193.94 ± 14.51 g/L) among all treatments. Moreover, the glucose level in the H0E1 group was higher than that in the H0E2 and H1E2 groups (102.96 ± 27.59 vs. 0.91 ± 0.15 and 1.32 ± 0.37 g/L, respectively). The combination treatments had no effect (p > 0.05) on ethanol production. Heat treatment did not (p > 0.05) influence the ethanol content. However, enzyme treatment affected (p < 0.01) the ethanol level. The ethanol production in the H0E1 and H1E1 groups (0.55% ± 0.13% and 0.99% ± 0.02% v/v) was higher than the ethanol content in the H0E2 and H1E2 treatments (0.19% ± 0.11% and 0.28% ± 0.10% v/v).
CONCLUSION: Buffalo rumen-derived cellulase can convert cellulose in rice straw into glucose. However, the glucose content in the buffalo rumen enzyme treatment was lower than that of the commercial enzyme.},
}
MeSH Terms:
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Animals
*Buffaloes/microbiology
*Rumen/microbiology/enzymology
*Cellulase/metabolism
*Glucose/metabolism
*Oryza/chemistry/metabolism
Hydrolysis
Fermentation
Ethanol/metabolism
*Gastrointestinal Microbiome
RevDate: 2026-06-30
CmpDate: 2026-06-30
Exploring the Tenebrio molitor gut microbiota response to LDPE and PET: putative genetic indicators and methodological insights.
Frontiers in microbiology, 17:1746922.
Insect gut microbiomes are recognized as potential reservoirs of enzymatic activities relevant to plastic metabolism. Here, we investigated the taxonomic and functional dynamics of the Tenebrio molitor gut microbiota under dietary exposure to low-density polyethylene (LDPE) and polyethylene terephthalate (PET) using 16S rRNA sequencing and shotgun metagenomics. Significant compositional shifts were detected at the ASV level, with plastic-fed cohorts showing enrichment of taxa implicated in xenobiotic metabolism. Predicted functional changes suggested altered abundance of pathways related to aromatic compound processing and redox homeostasis. Metagenomic assembly and functional annotation, performed through a reproducible open-source workflow, revealed several putative proteins with distant homology to enzymes such as phthalate dioxygenases, urethanases, and polyhydroxyalkanoate depolymerases. A metagenome-assembled genome (MAG) assigned to Enterococcus accounted for most recovered protein-coding sequences. Although gene-level comparisons did not show statistically significant differences, Gene Set Enrichment Analysis (GSEA) highlighted ABC transporter signatures and stress-response ATPases under plastic-exposed conditions. Overall, this exploratory study reveals microbial shifts and putative genetic indicators of metabolic potential within the T. molitor gut, providing a reproducible analytical framework for future investigations into the microbial role in plastic bioconversion.
Additional Links: PMID-42376574
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Citation:
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@article {pmid42376574,
year = {2026},
author = {Biełło, K and Rodríguez-Caballero, G and Becerra-Mora, D and Dorado-Blanco, N and Sáez-Melero, LP and Moreno-Vivián, C and Luque-Almagro, VM and Olaya-Abril, A and Roldán, MD},
title = {Exploring the Tenebrio molitor gut microbiota response to LDPE and PET: putative genetic indicators and methodological insights.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1746922},
pmid = {42376574},
issn = {1664-302X},
abstract = {Insect gut microbiomes are recognized as potential reservoirs of enzymatic activities relevant to plastic metabolism. Here, we investigated the taxonomic and functional dynamics of the Tenebrio molitor gut microbiota under dietary exposure to low-density polyethylene (LDPE) and polyethylene terephthalate (PET) using 16S rRNA sequencing and shotgun metagenomics. Significant compositional shifts were detected at the ASV level, with plastic-fed cohorts showing enrichment of taxa implicated in xenobiotic metabolism. Predicted functional changes suggested altered abundance of pathways related to aromatic compound processing and redox homeostasis. Metagenomic assembly and functional annotation, performed through a reproducible open-source workflow, revealed several putative proteins with distant homology to enzymes such as phthalate dioxygenases, urethanases, and polyhydroxyalkanoate depolymerases. A metagenome-assembled genome (MAG) assigned to Enterococcus accounted for most recovered protein-coding sequences. Although gene-level comparisons did not show statistically significant differences, Gene Set Enrichment Analysis (GSEA) highlighted ABC transporter signatures and stress-response ATPases under plastic-exposed conditions. Overall, this exploratory study reveals microbial shifts and putative genetic indicators of metabolic potential within the T. molitor gut, providing a reproducible analytical framework for future investigations into the microbial role in plastic bioconversion.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Tissue-specific changes in endophytic bacterial and fungal communities of two pine species associated with pine wilt disease.
Frontiers in microbiology, 17:1864084.
Pine wilt disease severely threatens pine forests worldwide, yet coordinated shifts in endophytic bacterial and fungal communities across host tissues remain incompletely resolved. We analyzed 16S rRNA gene and ITS amplicons from needles, stems, and roots of healthy trees and naturally infected trees at the mid-to-late stages of disease in Pinus densiflora Siebold & Zucc. (Japanese red pine) and Pinus thunbergii Parl. (Japanese black pine). Tissue-stratified analyses revealed significant disease-associated differentiation of both bacterial and fungal communities in all three tissues. Bacterial communities showed stronger disease-associated restructuring, with significant shifts in both composition and dispersion, indicating centroid changes accompanied by increased within-group heterogeneity. Fungal communities also differed significantly with disease status, but dispersion changes were not detected. Needles harbored the greatest numbers of differential taxa in both bacterial and fungal communities, whereas fungal community-level differentiation was strongest in stems. Host species background significantly modulated needle bacterial communities as well as needle- and stem-associated fungal communities. Overall, pine wilt disease was associated with tissue-specific reorganization of the endophytic microbiome, with bacterial communities exhibiting greater heterogeneity and fungal communities showing compositional differentiation without detectable dispersion shifts.
Additional Links: PMID-42376581
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@article {pmid42376581,
year = {2026},
author = {Xu, Y and Huang, R and Yang, H and Li, X and Zhang, S and Shi, J},
title = {Tissue-specific changes in endophytic bacterial and fungal communities of two pine species associated with pine wilt disease.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1864084},
pmid = {42376581},
issn = {1664-302X},
abstract = {Pine wilt disease severely threatens pine forests worldwide, yet coordinated shifts in endophytic bacterial and fungal communities across host tissues remain incompletely resolved. We analyzed 16S rRNA gene and ITS amplicons from needles, stems, and roots of healthy trees and naturally infected trees at the mid-to-late stages of disease in Pinus densiflora Siebold & Zucc. (Japanese red pine) and Pinus thunbergii Parl. (Japanese black pine). Tissue-stratified analyses revealed significant disease-associated differentiation of both bacterial and fungal communities in all three tissues. Bacterial communities showed stronger disease-associated restructuring, with significant shifts in both composition and dispersion, indicating centroid changes accompanied by increased within-group heterogeneity. Fungal communities also differed significantly with disease status, but dispersion changes were not detected. Needles harbored the greatest numbers of differential taxa in both bacterial and fungal communities, whereas fungal community-level differentiation was strongest in stems. Host species background significantly modulated needle bacterial communities as well as needle- and stem-associated fungal communities. Overall, pine wilt disease was associated with tissue-specific reorganization of the endophytic microbiome, with bacterial communities exhibiting greater heterogeneity and fungal communities showing compositional differentiation without detectable dispersion shifts.},
}
RevDate: 2026-06-30
Impact of the invasive diatom species Cymbella janischii on riverine microbial biofilm communities and a potential role of bacterially produced zeatin.
Journal of phycology [Epub ahead of print].
The diatom Cymbella janischii is an invasive species in Japan, causing nuisance blooms by forming thick mats in rivers. To date, there are no documented studies on the microbiome associations in C. janischii mats or the processes that drive bloom formation. This study used metabarcoding of diatoms, bacteria, and fungi to identify key species and assess the effects of C. janischii blooms on the benthic microbial communities. C. janischii blooms reduced diatom and bacterial species diversity, while fungal diversity remained stable. In addition, the diatom Nitzschia paleacea and the bacterium Flavobacterium sp. were observed to co-occur and vary in abundance, indicating a possible ecological link that may affect mat structure or function. Metagenomic predictions of bacterial functions showed that compared to benthic stones without visible C. janischii mats, mat-associated bacteria had enriched pathways related to the metabolism of carbohydrates, nucleotides, and amino acids, along with zeatin biosynthesis. Zeatin is a cytokinin phytohormone that stimulates plant growth and development. In vitro exposure of C. janischii to varying zeatin concentrations confirmed its growth-promoting effects, inducing cell proliferation and stalk formation. This study shows that zeatin stimulates the growth of C. janischii. The findings of this study provide new insights into microbiome diversity, identifying key taxa associated with C. janischii mats to help better understand bloom formation.
Additional Links: PMID-42376710
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@article {pmid42376710,
year = {2026},
author = {Arguelles, EDLR and Mugikura, K and Sato, S},
title = {Impact of the invasive diatom species Cymbella janischii on riverine microbial biofilm communities and a potential role of bacterially produced zeatin.},
journal = {Journal of phycology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jpy.70195},
pmid = {42376710},
issn = {1529-8817},
support = {21A402//Japan Society for the Promotion of Science/ ; 23K05398//Japan Society for the Promotion of Science/ ; 26K01814//Japan Society for the Promotion of Science/ ; //Ministry of Education, Culture, Sports, Science and Technology/ ; },
abstract = {The diatom Cymbella janischii is an invasive species in Japan, causing nuisance blooms by forming thick mats in rivers. To date, there are no documented studies on the microbiome associations in C. janischii mats or the processes that drive bloom formation. This study used metabarcoding of diatoms, bacteria, and fungi to identify key species and assess the effects of C. janischii blooms on the benthic microbial communities. C. janischii blooms reduced diatom and bacterial species diversity, while fungal diversity remained stable. In addition, the diatom Nitzschia paleacea and the bacterium Flavobacterium sp. were observed to co-occur and vary in abundance, indicating a possible ecological link that may affect mat structure or function. Metagenomic predictions of bacterial functions showed that compared to benthic stones without visible C. janischii mats, mat-associated bacteria had enriched pathways related to the metabolism of carbohydrates, nucleotides, and amino acids, along with zeatin biosynthesis. Zeatin is a cytokinin phytohormone that stimulates plant growth and development. In vitro exposure of C. janischii to varying zeatin concentrations confirmed its growth-promoting effects, inducing cell proliferation and stalk formation. This study shows that zeatin stimulates the growth of C. janischii. The findings of this study provide new insights into microbiome diversity, identifying key taxa associated with C. janischii mats to help better understand bloom formation.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Immune-Inflammatory Imbalance in Mice Under High Humidity and Three Different Ambient Temperatures: Insights From Gut Microbiome and Serum Metabolomics.
Environmental microbiology, 28(7):e70365.
Gut microbiota and metabolites have been increasingly implicated in the pathogenesis of immune inflammation, which may be affected by environmental factors. This study aimed to explore the influence of co-exposure to high humidity and temperatures (low, normal or high) on biomarkers of immune inflammation and potential mechanisms. We established C57BL/6J mice models (with equal numbers of males and females) of high humidity and low temperature (HH-LT), normal temperature (HH-NT) or high temperature (HH-HT) co-exposure environments to observe the impact of high humidity and different temperature co-exposure environments for 28 and 56 consecutive days. Following exposure, results showed that all six combined exposure conditions significantly increased pro-inflammatory cytokines (TNF-α, IL-1β, IL-12p70), decreased anti-inflammatory cytokines (IL-4, IL-10) and elevated the Teff/Treg ratio in the spleen. Gut microbiota analysis revealed reduced Akkermansia and increased Desulfovibrio and Enterorhabdus. Serum metabolomics identified widespread disturbances enriched in pathways including protein digestion and absorption, lysine degradation, phenylalanine metabolism and unsaturated fatty acid biosynthesis. Pearson correlation analysis confirmed significant associations among microbial shifts, immune-inflammatory dysregulation and metabolic perturbations-suggesting that high humidity combined with different temperatures correlated with immune imbalance, likely mediated by gut dysbiosis and serum metabolic disruption.
Additional Links: PMID-42376743
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@article {pmid42376743,
year = {2026},
author = {Yang, H and Wei, S and Ou, X and Jiang, W and Lu, W and Lan, T},
title = {Immune-Inflammatory Imbalance in Mice Under High Humidity and Three Different Ambient Temperatures: Insights From Gut Microbiome and Serum Metabolomics.},
journal = {Environmental microbiology},
volume = {28},
number = {7},
pages = {e70365},
doi = {10.1111/1462-2920.70365},
pmid = {42376743},
issn = {1462-2920},
support = {SZ2021ZZ1002//the Specific Fund of State Key Laboratory of Dampness Syndrome of Chinese Medicine/ ; SZ2021ZZ12//the Specific Fund of State Key Laboratory of Dampness Syndrome of Chinese Medicine/ ; SZ2021ZZ26//the Specific Fund of State Key Laboratory of Dampness Syndrome of Chinese Medicine/ ; SZ2021ZZ46//the Specific Fund of State Key Laboratory of Dampness Syndrome of Chinese Medicine/ ; HQL2024PZ036//Research and Cultivation Project of Chinese Medicine Guangdong Laboratory/ ; 2024A03J0739//Guangzhou Basic and Applied Basic Research Foundation/ ; },
mesh = {Animals ; *Humidity ; Mice ; Male ; Female ; Mice, Inbred C57BL ; *Gastrointestinal Microbiome ; Metabolomics ; *Inflammation/immunology/microbiology ; Cytokines/blood ; *Temperature ; Metabolome ; Biomarkers/blood ; },
abstract = {Gut microbiota and metabolites have been increasingly implicated in the pathogenesis of immune inflammation, which may be affected by environmental factors. This study aimed to explore the influence of co-exposure to high humidity and temperatures (low, normal or high) on biomarkers of immune inflammation and potential mechanisms. We established C57BL/6J mice models (with equal numbers of males and females) of high humidity and low temperature (HH-LT), normal temperature (HH-NT) or high temperature (HH-HT) co-exposure environments to observe the impact of high humidity and different temperature co-exposure environments for 28 and 56 consecutive days. Following exposure, results showed that all six combined exposure conditions significantly increased pro-inflammatory cytokines (TNF-α, IL-1β, IL-12p70), decreased anti-inflammatory cytokines (IL-4, IL-10) and elevated the Teff/Treg ratio in the spleen. Gut microbiota analysis revealed reduced Akkermansia and increased Desulfovibrio and Enterorhabdus. Serum metabolomics identified widespread disturbances enriched in pathways including protein digestion and absorption, lysine degradation, phenylalanine metabolism and unsaturated fatty acid biosynthesis. Pearson correlation analysis confirmed significant associations among microbial shifts, immune-inflammatory dysregulation and metabolic perturbations-suggesting that high humidity combined with different temperatures correlated with immune imbalance, likely mediated by gut dysbiosis and serum metabolic disruption.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Humidity
Mice
Male
Female
Mice, Inbred C57BL
*Gastrointestinal Microbiome
Metabolomics
*Inflammation/immunology/microbiology
Cytokines/blood
*Temperature
Metabolome
Biomarkers/blood
RevDate: 2026-06-30
CmpDate: 2026-06-30
Emergence of invasive Escherichia coli pathobionts in gut microbiome promotes cancer stemness via targeting Hippo pathways.
Gut microbes, 18(1):2694795.
Growing evidence suggests a pivotal role of the microbiome in tumorigenesis, extending beyond genetics. Apc(Min/+) mice exhibit reduced tumor load when housed in germ-free conditions. Nevertheless, how genetic factors shape microbiota and how dysbiosis fits into the genetic paradigm of intestinal carcinogenesis remain elusive. Epithelial stemness is regulated by Wnt/Apc/β-catenin pathway, whereas Apc mutations and Hippo signaling are associated with tumor growth. Invasive pathobionts emerge from microbiota as a result of epithelial barrier dysfunction. We hypothesize that the emergence of invasive pathobionts and dysbiosis of epithelial microbiota contribute to increased cancer stemness. The epithelial and fecal microbiota are longitudinally monitored in Apc(Min/+) and wild-type littermates born to wild-type surrogate dams. Segregation of epithelial microbiota between Apc(Min/+) and wild-type mice was observed as early as eight weeks after birth, whereas fecal microbiota diverged at 20 weeks of age. Epithelial dysbiosis and barrier defects were observed in Apc(Min/+) mice, characterized by intraepithelial Escherichia coli with invasive features. While antibiotic treatment reduced cancer burden, invasive E. coli infection promoted tumorsphere formation. Higher expression of Vgll3 and Tead4 (Hippo effectors) and Cd44 (a cancer stemness marker) was observed in bacteria-infected tumorspheres. Mechanistically, bacteria augmented epithelial clonogenicity by enhancing VGLL3/TEAD4-mediated CD44 promoter activity. Invasive E. coli genetic signatures were verified in 86% of human colorectal carcinoma specimens, and a positive correlation with TEAD4 expression was observed. In conclusion, Apc mutation drives the expansion of invasive pathobionts to promote cancer stemness via a VGLL3/TEAD4/CD44 axis. Bacteria-targeting interventions could be an alternative strategy for patients with hereditary tumors.
Additional Links: PMID-42376755
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PubMed:
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@article {pmid42376755,
year = {2026},
author = {Yu, LC and Wei, SC and Lin, BR and Li, YH and Liao, YC and Peng, YW and Lin, CH and Hu, PT and Pai, YC and Lai, LC and Chen, YT and Huang, CY and Jeng, YM and Ni, YH},
title = {Emergence of invasive Escherichia coli pathobionts in gut microbiome promotes cancer stemness via targeting Hippo pathways.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2694795},
doi = {10.1080/19490976.2026.2694795},
pmid = {42376755},
issn = {1949-0984},
mesh = {Animals ; *Protein Serine-Threonine Kinases/metabolism/genetics ; Mice ; *Signal Transduction ; *Escherichia coli/pathogenicity/physiology/growth & development ; Hippo Signaling Pathway ; Humans ; *Gastrointestinal Microbiome ; Feces/microbiology ; *Neoplastic Stem Cells ; Dysbiosis/microbiology ; Transcription Factors/metabolism/genetics ; *Escherichia coli Infections/microbiology ; },
abstract = {Growing evidence suggests a pivotal role of the microbiome in tumorigenesis, extending beyond genetics. Apc(Min/+) mice exhibit reduced tumor load when housed in germ-free conditions. Nevertheless, how genetic factors shape microbiota and how dysbiosis fits into the genetic paradigm of intestinal carcinogenesis remain elusive. Epithelial stemness is regulated by Wnt/Apc/β-catenin pathway, whereas Apc mutations and Hippo signaling are associated with tumor growth. Invasive pathobionts emerge from microbiota as a result of epithelial barrier dysfunction. We hypothesize that the emergence of invasive pathobionts and dysbiosis of epithelial microbiota contribute to increased cancer stemness. The epithelial and fecal microbiota are longitudinally monitored in Apc(Min/+) and wild-type littermates born to wild-type surrogate dams. Segregation of epithelial microbiota between Apc(Min/+) and wild-type mice was observed as early as eight weeks after birth, whereas fecal microbiota diverged at 20 weeks of age. Epithelial dysbiosis and barrier defects were observed in Apc(Min/+) mice, characterized by intraepithelial Escherichia coli with invasive features. While antibiotic treatment reduced cancer burden, invasive E. coli infection promoted tumorsphere formation. Higher expression of Vgll3 and Tead4 (Hippo effectors) and Cd44 (a cancer stemness marker) was observed in bacteria-infected tumorspheres. Mechanistically, bacteria augmented epithelial clonogenicity by enhancing VGLL3/TEAD4-mediated CD44 promoter activity. Invasive E. coli genetic signatures were verified in 86% of human colorectal carcinoma specimens, and a positive correlation with TEAD4 expression was observed. In conclusion, Apc mutation drives the expansion of invasive pathobionts to promote cancer stemness via a VGLL3/TEAD4/CD44 axis. Bacteria-targeting interventions could be an alternative strategy for patients with hereditary tumors.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Protein Serine-Threonine Kinases/metabolism/genetics
Mice
*Signal Transduction
*Escherichia coli/pathogenicity/physiology/growth & development
Hippo Signaling Pathway
Humans
*Gastrointestinal Microbiome
Feces/microbiology
*Neoplastic Stem Cells
Dysbiosis/microbiology
Transcription Factors/metabolism/genetics
*Escherichia coli Infections/microbiology
RevDate: 2026-06-30
Pharmacological Modulation of Immunosenescence and Inflammaging: Senolytics, Senomorphics, and Emerging Therapies.
Immunological investigations [Epub ahead of print].
BACKGROUND: Ageing is a major risk factor for chronic inflammatory and immune-mediated diseases and is characterised by progressive immune dysfunction. This process, termed immunosenescence, affects both innate and adaptive immunity, resulting in reduced naïve T and B cell production, accumulation of senescent immune cells, impaired pathogen recognition, and weakened immune surveillance. These changes are accompanied by a persistent, low-grade inflammatory state known as inflammaging, which occurs even in the absence of infection and contributes to increased susceptibility to infections, poor vaccine responses, and age-related disorders.
METHODS: This review integrates evidence from basic, translational, and clinical studies to elucidate the molecular and cellular mechanisms linking immunosenescence and inflammaging, with a focus on immune cell alterations and the role of senescent cells and their secretory phenotype.
RESULTS: Accumulation of senescent cells and the senescence-associated secretory phenotype (SASP) play a central role in sustaining chronic inflammation and disrupting tissue homeostasis. These processes impair immune function and tissue repair, increasing vulnerability to disease. Emerging therapeutic strategies, including senolytics, senomorphics, metabolic modulators, repurposed drugs, and microbiome-targeted interventions such as postbiotics, show potential in modulating these pathways.
CONCLUSION: Immunosenescence and inflammaging are closely interconnected drivers of age-related disease. Targeting senescent cells and inflammatory signalling pathways may offer promising strategies to restore immune resilience, reduce chronic inflammation, and promote healthy ageing. Further research is required to translate these approaches into clinical practice.
Additional Links: PMID-42376766
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@article {pmid42376766,
year = {2026},
author = {R, B and Sandur V, R},
title = {Pharmacological Modulation of Immunosenescence and Inflammaging: Senolytics, Senomorphics, and Emerging Therapies.},
journal = {Immunological investigations},
volume = {},
number = {},
pages = {1-26},
doi = {10.1080/08820139.2026.2695165},
pmid = {42376766},
issn = {1532-4311},
abstract = {BACKGROUND: Ageing is a major risk factor for chronic inflammatory and immune-mediated diseases and is characterised by progressive immune dysfunction. This process, termed immunosenescence, affects both innate and adaptive immunity, resulting in reduced naïve T and B cell production, accumulation of senescent immune cells, impaired pathogen recognition, and weakened immune surveillance. These changes are accompanied by a persistent, low-grade inflammatory state known as inflammaging, which occurs even in the absence of infection and contributes to increased susceptibility to infections, poor vaccine responses, and age-related disorders.
METHODS: This review integrates evidence from basic, translational, and clinical studies to elucidate the molecular and cellular mechanisms linking immunosenescence and inflammaging, with a focus on immune cell alterations and the role of senescent cells and their secretory phenotype.
RESULTS: Accumulation of senescent cells and the senescence-associated secretory phenotype (SASP) play a central role in sustaining chronic inflammation and disrupting tissue homeostasis. These processes impair immune function and tissue repair, increasing vulnerability to disease. Emerging therapeutic strategies, including senolytics, senomorphics, metabolic modulators, repurposed drugs, and microbiome-targeted interventions such as postbiotics, show potential in modulating these pathways.
CONCLUSION: Immunosenescence and inflammaging are closely interconnected drivers of age-related disease. Targeting senescent cells and inflammatory signalling pathways may offer promising strategies to restore immune resilience, reduce chronic inflammation, and promote healthy ageing. Further research is required to translate these approaches into clinical practice.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Optimization of Preclinical Rodent Research Models of Human Shock: Part 2 Trauma, Burn, and the Gut Microbiome.
Shock (Augusta, Ga.), 66(1):4-12.
Rodent models are critical tools in the study of trauma and burn injury, giving mechanistic insights into the unique pathophysiological response and the systemic complications that follow. These models allow researchers to control injury patterns, longitudinally assess immune and metabolic responses, and evaluate therapeutic strategies in ways that are not feasible in human subjects. In this second part of our review, we examine how experimental trauma and burn models have evolved to better replicate the clinical trajectory of critically ill patients, with emphasis on polytrauma, burn injury, and translational relevance. We also highlight the role of the gut microbiome in the pathogenesis of shock within sepsis, trauma, and burn and review how rodent models have been used to investigate dysbiosis and test microbiome-targeted interventions. Although interspecies differences pose translational challenges, ongoing refinements in model selection, injury models, microbiome characterization, and reverse-translational approaches continue to expand the utility of rodent models, allowing researchers to discover vital insights into the complex pathophysiology of these critically ill patients and potential therapeutic targets that guide further investigation.
Additional Links: PMID-42376926
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PubMed:
Citation:
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@article {pmid42376926,
year = {2026},
author = {Rodhouse, C and Bertram Wiggins, W and Michael, Z and Byskosh, A and Boeno, FP and Hernandez-Rios, M and Park, G and Dumitrescu, S and Fisler, GM and Taylor, MD and Abraham, MN and Vo, Q and Charles, A and Lederer, J and Laitano, O and Rincon, J and Nagpal, R and Chakrabarty, P and Casadesus, G and Osuchowski, MF and Deutschman, CS and Mohr, A and Maile, R and Scott, M and Efron, P and Bible, L},
title = {Optimization of Preclinical Rodent Research Models of Human Shock: Part 2 Trauma, Burn, and the Gut Microbiome.},
journal = {Shock (Augusta, Ga.)},
volume = {66},
number = {1},
pages = {4-12},
doi = {10.1097/SHK.0000000000002872},
pmid = {42376926},
issn = {1540-0514},
mesh = {Animals ; *Burns/microbiology ; Humans ; Disease Models, Animal ; *Gastrointestinal Microbiome/physiology ; *Shock/microbiology ; Rodentia ; *Wounds and Injuries ; },
abstract = {Rodent models are critical tools in the study of trauma and burn injury, giving mechanistic insights into the unique pathophysiological response and the systemic complications that follow. These models allow researchers to control injury patterns, longitudinally assess immune and metabolic responses, and evaluate therapeutic strategies in ways that are not feasible in human subjects. In this second part of our review, we examine how experimental trauma and burn models have evolved to better replicate the clinical trajectory of critically ill patients, with emphasis on polytrauma, burn injury, and translational relevance. We also highlight the role of the gut microbiome in the pathogenesis of shock within sepsis, trauma, and burn and review how rodent models have been used to investigate dysbiosis and test microbiome-targeted interventions. Although interspecies differences pose translational challenges, ongoing refinements in model selection, injury models, microbiome characterization, and reverse-translational approaches continue to expand the utility of rodent models, allowing researchers to discover vital insights into the complex pathophysiology of these critically ill patients and potential therapeutic targets that guide further investigation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Burns/microbiology
Humans
Disease Models, Animal
*Gastrointestinal Microbiome/physiology
*Shock/microbiology
Rodentia
*Wounds and Injuries
RevDate: 2026-06-30
Cadmium toxicity to the human gut microbiome varies depending on composition.
Applied and environmental microbiology [Epub ahead of print].
Cadmium (Cd(II), hereafter Cd) is a toxic heavy metal that has detrimental effects on the gut microbiota. We investigated the effects of acute Cd exposure on human fecal microbiotas using 24-h in vitro cultures from 20 healthy adult donors. Regression analysis of butyrate production in the absence (-Cd) versus presence (+Cd) of Cd identified three categories of microbial responses: sensitive, intermediate, and resilient. Under Cd stress, sensitive microbiomes exhibited significant decreases in butyrate, coupled with elevated acetate and lactate production, while resilient microbiomes did not show significant changes in butyrate and exhibited attenuated increases in lactate compared with sensitive microbiomes. Several genera differed significantly between sensitive and resilient communities after exposure to Cd, but the most striking difference was in Anaerostipes. Network analysis revealed a significantly greater disruption of microbial interactions in sensitive communities compared with resilient communities. In resilient communities, butyrate production was primarily associated with Faecalibacterium in the absence of Cd and Anaerostipes in the presence of Cd. Furthermore, supplementation of sensitive microbiotas with Anaerostipes species restored butyrate production in the presence of Cd. These findings highlight distinct gut microbial responses to acute Cd exposure and provide a foundation to investigate microbiota features underlying Cd sensitivity or resilience.IMPORTANCECadmium (Cd) is a widespread environmental contaminant that enters the human intestine, where it can disrupt the gut microbial community and negatively impact digestive and systemic health. However, this study demonstrates that human gut microbiomes vary in their responses to cadmium exposure: sensitive communities exhibit losses of beneficial organisms, particularly butyrate-producing taxa that contribute to intestinal integrity and metabolic balance, whereas resilient communities retain microorganisms with this key functional capacity. Anaerostipes appeared to be involved, at least in part, with Cd resilience. This work advances our understanding of how gut microbial functions may mitigate the adverse effects of cadmium exposure by identifying the compositional features that distinguish sensitive from resilient microbiomes. These findings highlight the importance of elucidating microbiome-mediated mechanisms that sustain host health and lay the groundwork for deeper mechanistic studies to mitigate cadmium toxicity.
Additional Links: PMID-42377019
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PubMed:
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@article {pmid42377019,
year = {2026},
author = {Perez-Donado, CE and Liu, S and Seravalli, J and Auchtung, JM and Rose, DJ},
title = {Cadmium toxicity to the human gut microbiome varies depending on composition.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0064526},
doi = {10.1128/aem.00645-26},
pmid = {42377019},
issn = {1098-5336},
abstract = {Cadmium (Cd(II), hereafter Cd) is a toxic heavy metal that has detrimental effects on the gut microbiota. We investigated the effects of acute Cd exposure on human fecal microbiotas using 24-h in vitro cultures from 20 healthy adult donors. Regression analysis of butyrate production in the absence (-Cd) versus presence (+Cd) of Cd identified three categories of microbial responses: sensitive, intermediate, and resilient. Under Cd stress, sensitive microbiomes exhibited significant decreases in butyrate, coupled with elevated acetate and lactate production, while resilient microbiomes did not show significant changes in butyrate and exhibited attenuated increases in lactate compared with sensitive microbiomes. Several genera differed significantly between sensitive and resilient communities after exposure to Cd, but the most striking difference was in Anaerostipes. Network analysis revealed a significantly greater disruption of microbial interactions in sensitive communities compared with resilient communities. In resilient communities, butyrate production was primarily associated with Faecalibacterium in the absence of Cd and Anaerostipes in the presence of Cd. Furthermore, supplementation of sensitive microbiotas with Anaerostipes species restored butyrate production in the presence of Cd. These findings highlight distinct gut microbial responses to acute Cd exposure and provide a foundation to investigate microbiota features underlying Cd sensitivity or resilience.IMPORTANCECadmium (Cd) is a widespread environmental contaminant that enters the human intestine, where it can disrupt the gut microbial community and negatively impact digestive and systemic health. However, this study demonstrates that human gut microbiomes vary in their responses to cadmium exposure: sensitive communities exhibit losses of beneficial organisms, particularly butyrate-producing taxa that contribute to intestinal integrity and metabolic balance, whereas resilient communities retain microorganisms with this key functional capacity. Anaerostipes appeared to be involved, at least in part, with Cd resilience. This work advances our understanding of how gut microbial functions may mitigate the adverse effects of cadmium exposure by identifying the compositional features that distinguish sensitive from resilient microbiomes. These findings highlight the importance of elucidating microbiome-mediated mechanisms that sustain host health and lay the groundwork for deeper mechanistic studies to mitigate cadmium toxicity.},
}
RevDate: 2026-06-30
Signatures in the gut microbiome of German elite athletes: insights from a matched-subgroup analysis.
mSystems [Epub ahead of print].
Elite athletes undergo intense physical training and experience substantial physiological stress, which could affect the composition and function of their gut microbiome. This study compared the gut microbiomes of 148 German junior and senior elite athletes with those of 108 healthy adults to identify taxonomic and functional features associated with elite athletic status. Group comparisons were conducted between healthy adults, senior athletes, and junior athletes, and a matched-subgroup analysis was performed in adults only, controlling for age, sex, body mass index, and dietary pattern. Significant differences in taxonomic composition were observed between athletes and healthy adults. Healthy adults exhibited greater microbial evenness and diversity than junior athletes, whereas senior athletes displayed higher microbial richness. Principal coordinate analysis revealed distinct clustering by athletic status. Linear discriminant analysis effect size identified taxa such as Escherichia-Shigella as being enriched in athletes. Predictive metagenomic profiling (PICRUSt2) indicated differences in microbial functional potential between adult athletes and matched controls, including pathways related to amino acid metabolism, glycolysis, fatty acid β-oxidation, and quinone biosynthesis. Together, these findings demonstrate distinct taxonomic and predicted functional microbiome signatures associated with elite athletic status.IMPORTANCEElite athletic training and lifestyle are associated with the gut microbiome. Our research has revealed distinct microbial structures in elite athletes, characterized by reduced evenness in junior athletes and increased richness in senior athletes, compared to healthy adults. Matched-subgroup analyses confirmed these group-specific differences. The gut microbiomes of athletes were enriched in pathways related to amino acid biosynthesis, glycolysis, fatty acid β-oxidation, and quinone synthesis. These microbiome features may be relevant for metabolic efficiency and resilience to oxidative stress. Combining taxonomic and functional prediction data from a uniquely characterized cohort of junior and senior elite athletes provides novel insight into microbiome signatures associated with sustained physical and psychological stress, with potential implications for performance, recovery, and health.CLINICAL TRIALSThis study is registered with ClinicalTrials.gov as NCT03582020.
Additional Links: PMID-42377028
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PubMed:
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@article {pmid42377028,
year = {2026},
author = {Lenz, C and Seel, W and Dombrowski, T and Hacker, S and Simon, M-C and Zentgraf, K and Dawczynski, C and Krüger, K},
title = {Signatures in the gut microbiome of German elite athletes: insights from a matched-subgroup analysis.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0048926},
doi = {10.1128/msystems.00489-26},
pmid = {42377028},
issn = {2379-5077},
abstract = {Elite athletes undergo intense physical training and experience substantial physiological stress, which could affect the composition and function of their gut microbiome. This study compared the gut microbiomes of 148 German junior and senior elite athletes with those of 108 healthy adults to identify taxonomic and functional features associated with elite athletic status. Group comparisons were conducted between healthy adults, senior athletes, and junior athletes, and a matched-subgroup analysis was performed in adults only, controlling for age, sex, body mass index, and dietary pattern. Significant differences in taxonomic composition were observed between athletes and healthy adults. Healthy adults exhibited greater microbial evenness and diversity than junior athletes, whereas senior athletes displayed higher microbial richness. Principal coordinate analysis revealed distinct clustering by athletic status. Linear discriminant analysis effect size identified taxa such as Escherichia-Shigella as being enriched in athletes. Predictive metagenomic profiling (PICRUSt2) indicated differences in microbial functional potential between adult athletes and matched controls, including pathways related to amino acid metabolism, glycolysis, fatty acid β-oxidation, and quinone biosynthesis. Together, these findings demonstrate distinct taxonomic and predicted functional microbiome signatures associated with elite athletic status.IMPORTANCEElite athletic training and lifestyle are associated with the gut microbiome. Our research has revealed distinct microbial structures in elite athletes, characterized by reduced evenness in junior athletes and increased richness in senior athletes, compared to healthy adults. Matched-subgroup analyses confirmed these group-specific differences. The gut microbiomes of athletes were enriched in pathways related to amino acid biosynthesis, glycolysis, fatty acid β-oxidation, and quinone synthesis. These microbiome features may be relevant for metabolic efficiency and resilience to oxidative stress. Combining taxonomic and functional prediction data from a uniquely characterized cohort of junior and senior elite athletes provides novel insight into microbiome signatures associated with sustained physical and psychological stress, with potential implications for performance, recovery, and health.CLINICAL TRIALSThis study is registered with ClinicalTrials.gov as NCT03582020.},
}
RevDate: 2026-06-30
Draft genome sequence of Streptococcus infantarius strain UMPGM isolated from individual withdrawing from methamphetamine.
Microbiology resource announcements [Epub ahead of print].
We report draft the genome sequence of Streptococcus infantarius strain UMPGM (1,791,962 bp, guanine-cytosine [GC] content of 37.70%) isolated from an individual recovering from methamphetamine use disorder. The organism was isolated from a stool sample on de Man, Rogosa, and Sharpe agar under anaerobic condition.
Additional Links: PMID-42377267
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PubMed:
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@article {pmid42377267,
year = {2026},
author = {Kiraman, SK and Mohd Arshad, N and Ahmad, HF},
title = {Draft genome sequence of Streptococcus infantarius strain UMPGM isolated from individual withdrawing from methamphetamine.},
journal = {Microbiology resource announcements},
volume = {},
number = {},
pages = {e0036826},
doi = {10.1128/mra.00368-26},
pmid = {42377267},
issn = {2576-098X},
abstract = {We report draft the genome sequence of Streptococcus infantarius strain UMPGM (1,791,962 bp, guanine-cytosine [GC] content of 37.70%) isolated from an individual recovering from methamphetamine use disorder. The organism was isolated from a stool sample on de Man, Rogosa, and Sharpe agar under anaerobic condition.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
The Putative Role of Oral Microbiome in Premature Aging during HIV Infection: What Do We Know?.
Puerto Rico health sciences journal, 45(2):50-56.
Despite improvements in life expectancy, people with HIV (PWH) are at risk of developing HIV-associated comorbidities at a younger age when compared to HIV-uninfected individuals. This premature aging process can be attributed to various factors, such as the prolonged exposure to combination antiretroviral therapy (cART), inflammation, microbial perturbances and oxidative stress. Similarly to the gut, oral dysbiosis occurs in HIV-1 infection, with cART and inflammation playing a crucial role. This gives rise to an enrichment of pathogenic microorganisms that in turn, elicit an immune response tied to chronic inflammation. Consequently, cART exposure, dysbiosis and persistent inflammation in HIV-1 infection have been associated with the production of reactive oxygen species, mitochondrial dysfunction and telomere shortening, which are known hallmarks of aging. Although looking into these factors provides insight into the mechanisms underlying premature aging in PWH, there is still much we do not know about the oral microbiome and its relationship to HIV-1 infection. The objective of this review is to synthetize current evidence to better elucidate the role of the oral microbiome in HIV-1 infection and its contribution to inflammation and oxidative stress. By addressing these gaps, we aim to provide a novel perspective on the premature biological aging process in PWH and ultimately improve overall health in this population.
Additional Links: PMID-42377329
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Citation:
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@article {pmid42377329,
year = {2026},
author = {Solá-Morlá, C and Alcalá-Zúñiga, D and Araujo, J and Bonecini-Almeida, MDG and Roy, U and Pérez-Santiago, J},
title = {The Putative Role of Oral Microbiome in Premature Aging during HIV Infection: What Do We Know?.},
journal = {Puerto Rico health sciences journal},
volume = {45},
number = {2},
pages = {50-56},
pmid = {42377329},
issn = {2373-6011},
mesh = {Humans ; *HIV Infections/drug therapy/complications/microbiology ; *Aging, Premature/microbiology/etiology ; *Microbiota ; Oxidative Stress ; Inflammation/microbiology ; *Mouth/microbiology ; Dysbiosis/microbiology ; },
abstract = {Despite improvements in life expectancy, people with HIV (PWH) are at risk of developing HIV-associated comorbidities at a younger age when compared to HIV-uninfected individuals. This premature aging process can be attributed to various factors, such as the prolonged exposure to combination antiretroviral therapy (cART), inflammation, microbial perturbances and oxidative stress. Similarly to the gut, oral dysbiosis occurs in HIV-1 infection, with cART and inflammation playing a crucial role. This gives rise to an enrichment of pathogenic microorganisms that in turn, elicit an immune response tied to chronic inflammation. Consequently, cART exposure, dysbiosis and persistent inflammation in HIV-1 infection have been associated with the production of reactive oxygen species, mitochondrial dysfunction and telomere shortening, which are known hallmarks of aging. Although looking into these factors provides insight into the mechanisms underlying premature aging in PWH, there is still much we do not know about the oral microbiome and its relationship to HIV-1 infection. The objective of this review is to synthetize current evidence to better elucidate the role of the oral microbiome in HIV-1 infection and its contribution to inflammation and oxidative stress. By addressing these gaps, we aim to provide a novel perspective on the premature biological aging process in PWH and ultimately improve overall health in this population.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*HIV Infections/drug therapy/complications/microbiology
*Aging, Premature/microbiology/etiology
*Microbiota
Oxidative Stress
Inflammation/microbiology
*Mouth/microbiology
Dysbiosis/microbiology
RevDate: 2026-06-30
R-5780, a SagA-engineered Lactococcus lactis, is a safe oral synthetic-biology microbial therapy that potentiates PD-1 blockade.
Cancer immunology, immunotherapy : CII pii:10.1007/s00262-026-04480-2 [Epub ahead of print].
Immune checkpoint inhibitors (ICIs) targeting programmed cell death protein 1 (PD-1) have transformed cancer therapy, yet response rates remain limited across solid tumors. Modulation of the gut microbiome has emerged as a promising strategy to enhance immunotherapy efficacy. R-5780 is an engineered Lactococcus lactis strain expressing the peptidoglycan hydrolase Secreted Antigen A (SagA), which generates muramyl dipeptide (MDP), a natural ligand of the nucleotide-binding oligomerization domain 2 (NOD2) receptor involved in innate immune activation and antigen-presenting cell maturation. Therapeutic potential of R-5780 was assessed in vivo murine models. Using the CT26 murine colorectal carcinoma model, oral administration of R-5780 with anti-PD-1 significantly inhibited tumor growth in both prophylactic and therapeutic settings compared to ICI therapy alone. Mechanistic studies revealed that R-5780 enhanced dendritic-cell activation and promoted a pro-inflammatory tumor microenvironment characterized by elevated interleukin-1 beta (IL-1β). Multiplex cytokine profiling and flow cytometry further showed that R-5780 reduced CD8[+] T-cell exhaustion, with decreased expression of PD-1, LAG-3, and TIM-3 on intratumoral T cells. In murine toxicology studies, R-5780 was well tolerated, with no adverse events or systemic inflammation observed following oral administration. Together, these results identify R-5780 as a safe and potent NOD2 activator that synergizes with PD-1 blockade to enhance antitumor immunity and support its advancement toward clinical evaluation.
Additional Links: PMID-42377551
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PubMed:
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@article {pmid42377551,
year = {2026},
author = {Fukuhara, M and Sahay, B and Fanger, GR and Freguia, CF},
title = {R-5780, a SagA-engineered Lactococcus lactis, is a safe oral synthetic-biology microbial therapy that potentiates PD-1 blockade.},
journal = {Cancer immunology, immunotherapy : CII},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00262-026-04480-2},
pmid = {42377551},
issn = {1432-0851},
abstract = {Immune checkpoint inhibitors (ICIs) targeting programmed cell death protein 1 (PD-1) have transformed cancer therapy, yet response rates remain limited across solid tumors. Modulation of the gut microbiome has emerged as a promising strategy to enhance immunotherapy efficacy. R-5780 is an engineered Lactococcus lactis strain expressing the peptidoglycan hydrolase Secreted Antigen A (SagA), which generates muramyl dipeptide (MDP), a natural ligand of the nucleotide-binding oligomerization domain 2 (NOD2) receptor involved in innate immune activation and antigen-presenting cell maturation. Therapeutic potential of R-5780 was assessed in vivo murine models. Using the CT26 murine colorectal carcinoma model, oral administration of R-5780 with anti-PD-1 significantly inhibited tumor growth in both prophylactic and therapeutic settings compared to ICI therapy alone. Mechanistic studies revealed that R-5780 enhanced dendritic-cell activation and promoted a pro-inflammatory tumor microenvironment characterized by elevated interleukin-1 beta (IL-1β). Multiplex cytokine profiling and flow cytometry further showed that R-5780 reduced CD8[+] T-cell exhaustion, with decreased expression of PD-1, LAG-3, and TIM-3 on intratumoral T cells. In murine toxicology studies, R-5780 was well tolerated, with no adverse events or systemic inflammation observed following oral administration. Together, these results identify R-5780 as a safe and potent NOD2 activator that synergizes with PD-1 blockade to enhance antitumor immunity and support its advancement toward clinical evaluation.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
The interplay between gut microbiota and Alzheimer's disease: mechanistic insights from dysbiosis to disease modulation.
Metabolic brain disease, 41(1):.
Alzheimer's disease (AD) is a chronic, progressive, neurodegenerative condition marked by memory loss and cognitive decline. It is characterized by neuropathological features such as amyloid plaque accumulation, neurofibrillary tangles of tau protein, and inflammatory changes in the brain. Recent research emphasizes how gut microbes influence the onset and progression of AD primarily through the gut-brain connection, a bidirectional communication system. The human gastrointestinal tract (GI) contains trillions of bacteria, primarily Bacteroidetes, Firmicutes, and Actinobacteria, which play vital roles in digestion, metabolic regulation, and immune modulation. However, factors such as diet, lifestyle, and environmental exposure can disrupt microbial balance, weaken intestinal barrier function, and initiate systemic inflammation. Such dysbiosis has been linked to defective regulation of the amyloid precursor protein (APP), leading to increased deposition of amyloidogenic peptides (Aβ). Moreover, the enteric nervous system, which expresses APP, may serve as an initial site of amyloid deposition, affecting gastrointestinal motility and inflammatory susceptibility. The gut microbiota also produces key bioactive compounds, including neurotransmitters such as serotonin, dopamine, acetylcholine, histamine, and gamma-aminobutyric acid (GABA), which influence the central nervous system (CNS) through neural, immune, and endocrine pathways. An imbalance in these neuroactive molecules may disrupt synaptic signaling and contribute to Alzheimer's-related cognitive dysfunction. Therefore, improving our understanding of gut-brain communication may advance knowledge of AD development and support the creation of new therapies. This review highlights the strong association between intestinal microbes and Alzheimer's pathogenesis, emphasizing microbiota modulation through probiotics, prebiotics, postbiotics, synbiotics, and antibiotics as potential therapeutic approaches, supported by emerging clinical trial evidence.
Additional Links: PMID-42377735
PubMed:
Citation:
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@article {pmid42377735,
year = {2026},
author = {Das, K and Khatun, R and Begum, S and Bhattacharyya, K and Datta, M and Saha, D and Sarma, A and Mehta, P and Das, BK},
title = {The interplay between gut microbiota and Alzheimer's disease: mechanistic insights from dysbiosis to disease modulation.},
journal = {Metabolic brain disease},
volume = {41},
number = {1},
pages = {},
pmid = {42377735},
issn = {1573-7365},
mesh = {Humans ; *Alzheimer Disease/metabolism/microbiology ; *Gastrointestinal Microbiome/physiology ; *Dysbiosis/metabolism/microbiology ; Animals ; Brain/metabolism ; Amyloid beta-Peptides/metabolism ; },
abstract = {Alzheimer's disease (AD) is a chronic, progressive, neurodegenerative condition marked by memory loss and cognitive decline. It is characterized by neuropathological features such as amyloid plaque accumulation, neurofibrillary tangles of tau protein, and inflammatory changes in the brain. Recent research emphasizes how gut microbes influence the onset and progression of AD primarily through the gut-brain connection, a bidirectional communication system. The human gastrointestinal tract (GI) contains trillions of bacteria, primarily Bacteroidetes, Firmicutes, and Actinobacteria, which play vital roles in digestion, metabolic regulation, and immune modulation. However, factors such as diet, lifestyle, and environmental exposure can disrupt microbial balance, weaken intestinal barrier function, and initiate systemic inflammation. Such dysbiosis has been linked to defective regulation of the amyloid precursor protein (APP), leading to increased deposition of amyloidogenic peptides (Aβ). Moreover, the enteric nervous system, which expresses APP, may serve as an initial site of amyloid deposition, affecting gastrointestinal motility and inflammatory susceptibility. The gut microbiota also produces key bioactive compounds, including neurotransmitters such as serotonin, dopamine, acetylcholine, histamine, and gamma-aminobutyric acid (GABA), which influence the central nervous system (CNS) through neural, immune, and endocrine pathways. An imbalance in these neuroactive molecules may disrupt synaptic signaling and contribute to Alzheimer's-related cognitive dysfunction. Therefore, improving our understanding of gut-brain communication may advance knowledge of AD development and support the creation of new therapies. This review highlights the strong association between intestinal microbes and Alzheimer's pathogenesis, emphasizing microbiota modulation through probiotics, prebiotics, postbiotics, synbiotics, and antibiotics as potential therapeutic approaches, supported by emerging clinical trial evidence.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Alzheimer Disease/metabolism/microbiology
*Gastrointestinal Microbiome/physiology
*Dysbiosis/metabolism/microbiology
Animals
Brain/metabolism
Amyloid beta-Peptides/metabolism
RevDate: 2026-06-30
Precision Exercise for Breast Cancer-Related Outcomes: Towards Personalised Training Based on Tumour, Treatment and Patient Characteristics.
Sports medicine (Auckland, N.Z.) [Epub ahead of print].
Exercise is a promising strategy associated with improved cancer-related outcomes through multiple biological mechanisms. However, current exercise guidelines largely adopt a one-size-fits-all approach and overlook inter-individual variability in response. Given the heterogeneity of breast cancer, precision exercise prescriptions may better target biological pathways linked to therapeutic efficacy and long-term prognosis. Observational studies consistently show that higher physical activity levels are associated with improved survival outcomes, including reduced all-cause and breast cancer-specific mortality. In contrast, evidence from interventional trials remains limited and inconsistent, with effects on tumour response and survival largely derived from secondary or exploratory analyses. These discrepancies likely reflect differences in study design, exercise dose, adherence and treatment-related factors, and may indicate that null findings are partly attributable to an insufficient or inconsistent exercise stimulus rather than a true biological non-response. Exercise influences key pathways involved in tumour progression and treatment response, including immune function, inflammation, metabolism, tumour perfusion and the gut microbiome. As these responses may vary according to tumour subtype, treatment context and host characteristics, a uniform approach to exercise prescription may fail to optimise its therapeutic potential. This review proposes a precision exercise framework that integrates tumour, treatment and patient-specific factors such as genetic and epigenetic profiles, metabolic status and body composition, systemic inflammation and the gut microbiome to guide precision exercise strategies. It also highlights the potential of digital tools, including wearable technologies and artificial intelligence, to enable data-driven personalisation and real-time adaptation, alongside key considerations for safe clinical implementation. While this framework is supported by biological plausibility, whether variability in these upstream biological responses translates into differences in cancer-related outcomes remains unknown. As such, this approach remains hypothesis generating. Future research should focus on adequately powered trials and mechanistic studies to determine whether precision exercise can meaningfully improve cancer-related outcomes in breast cancer.
Additional Links: PMID-42377761
PubMed:
Citation:
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@article {pmid42377761,
year = {2026},
author = {Crespo-Garcia, C and Borsati, A and Taaffe, DR and Peddle-McIntyre, CJ and Campbell, JP and Avancini, A and Jeffery, E and Galvao, DA and Newton, RU},
title = {Precision Exercise for Breast Cancer-Related Outcomes: Towards Personalised Training Based on Tumour, Treatment and Patient Characteristics.},
journal = {Sports medicine (Auckland, N.Z.)},
volume = {},
number = {},
pages = {},
pmid = {42377761},
issn = {1179-2035},
abstract = {Exercise is a promising strategy associated with improved cancer-related outcomes through multiple biological mechanisms. However, current exercise guidelines largely adopt a one-size-fits-all approach and overlook inter-individual variability in response. Given the heterogeneity of breast cancer, precision exercise prescriptions may better target biological pathways linked to therapeutic efficacy and long-term prognosis. Observational studies consistently show that higher physical activity levels are associated with improved survival outcomes, including reduced all-cause and breast cancer-specific mortality. In contrast, evidence from interventional trials remains limited and inconsistent, with effects on tumour response and survival largely derived from secondary or exploratory analyses. These discrepancies likely reflect differences in study design, exercise dose, adherence and treatment-related factors, and may indicate that null findings are partly attributable to an insufficient or inconsistent exercise stimulus rather than a true biological non-response. Exercise influences key pathways involved in tumour progression and treatment response, including immune function, inflammation, metabolism, tumour perfusion and the gut microbiome. As these responses may vary according to tumour subtype, treatment context and host characteristics, a uniform approach to exercise prescription may fail to optimise its therapeutic potential. This review proposes a precision exercise framework that integrates tumour, treatment and patient-specific factors such as genetic and epigenetic profiles, metabolic status and body composition, systemic inflammation and the gut microbiome to guide precision exercise strategies. It also highlights the potential of digital tools, including wearable technologies and artificial intelligence, to enable data-driven personalisation and real-time adaptation, alongside key considerations for safe clinical implementation. While this framework is supported by biological plausibility, whether variability in these upstream biological responses translates into differences in cancer-related outcomes remains unknown. As such, this approach remains hypothesis generating. Future research should focus on adequately powered trials and mechanistic studies to determine whether precision exercise can meaningfully improve cancer-related outcomes in breast cancer.},
}
RevDate: 2026-06-30
Time-series dynamics and biocontrol potential of postharvest bacteria in litchi microbiota.
Science China. Life sciences [Epub ahead of print].
Postharvest surface microbiota plays a pivotal role in fruit spoilage and disease development, directly influencing shelf life and food safety. In this study, we systematically investigated the dynamic changes of peel-associated microbial communities in two litchi cultivars with distinct storability (Huaizhi and Nuomici), under both natural and fungicide (prochloraz) treatments over a 9 d storage period. Amplicon sequencing, time-series analysis, and a random forest model identified five key genera-Acetobacter, Methylobacterium, Sphingomonas, Gluconobacter, and Pantoea-strongly associated with storage time. Notably, culturable isolates from these genera exhibited significant antagonistic activity against the common postharvest fungal pathogens Peronophythora litchii and Colletotrichum gloeosporioides, with Gluconobacter sp. Lc45 demonstrating high-efficiency antagonism. Furthermore, a random forest model based on microbial biomarkers accurately predicted fruit freshness (R[2]>0.9). This study highlights the ecological and biocontrol significance of surface microbiota on litchi, and proposes microbial-based strategies as promising eco-friendly alternatives for postharvest disease control and freshness prediction in subtropical fruits.
Additional Links: PMID-42377893
PubMed:
Citation:
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@article {pmid42377893,
year = {2026},
author = {Hou, H and Lyu, H and Yang, H and Wang, Y and Zhang, T and Yang, J and Yousuf, S and Luo, H and Yao, X and Liu, YX},
title = {Time-series dynamics and biocontrol potential of postharvest bacteria in litchi microbiota.},
journal = {Science China. Life sciences},
volume = {},
number = {},
pages = {},
pmid = {42377893},
issn = {1869-1889},
abstract = {Postharvest surface microbiota plays a pivotal role in fruit spoilage and disease development, directly influencing shelf life and food safety. In this study, we systematically investigated the dynamic changes of peel-associated microbial communities in two litchi cultivars with distinct storability (Huaizhi and Nuomici), under both natural and fungicide (prochloraz) treatments over a 9 d storage period. Amplicon sequencing, time-series analysis, and a random forest model identified five key genera-Acetobacter, Methylobacterium, Sphingomonas, Gluconobacter, and Pantoea-strongly associated with storage time. Notably, culturable isolates from these genera exhibited significant antagonistic activity against the common postharvest fungal pathogens Peronophythora litchii and Colletotrichum gloeosporioides, with Gluconobacter sp. Lc45 demonstrating high-efficiency antagonism. Furthermore, a random forest model based on microbial biomarkers accurately predicted fruit freshness (R[2]>0.9). This study highlights the ecological and biocontrol significance of surface microbiota on litchi, and proposes microbial-based strategies as promising eco-friendly alternatives for postharvest disease control and freshness prediction in subtropical fruits.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Small Intestinal Bacterial Overgrowth: Microbiome Dysregulation, Gut-Brain Axis Disruption, and Systemic Consequences.
Molecular nutrition & food research, 70(13):e70541.
Small intestinal bacterial overgrowth (SIBO) is a gastrointestinal disorder characterized by excessive bacterial colonization in the small intestine, leading to impaired digestion and nutrient malabsorption. Increasing evidence indicates that SIBO exerts systemic effects beyond the gut, contributing to metabolic, neurological, cardiovascular, dermatological, and autoimmune conditions. Current management strategies include nonsystemic antibiotics such as rifaximin, dietary interventions (low-FODMAP and biphasic diets), and nutraceuticals including berberine, oregano oil, peppermint oil, garlic derivatives, vitamins, and magnesium. Despite demonstrated clinical efficacy, challenges persist, including high recurrence rates, antimicrobial resistance, and long-term disruption of gut microbiota. Nutraceutical and dietary approaches offer promising patient-centered alternatives but require stronger clinical validation. This review critically examines the multifactorial pathophysiology of SIBO, emphasizing gut-brain axis dysregulation, microbial dysbiosis, oxidative stress, impaired intestinal motility, anatomical abnormalities, hypochlorhydria, bile acid malabsorption, and immune dysfunction. It synthesizes current diagnostic and therapeutic strategies, highlighting antibiotics, dietary approaches, and nutraceuticals, while distinguishing robust evidence from observational or preclinical findings. Finally, it identifies key research priorities, including improved diagnostics, global clinical trials, and microbiome- and genetics-based personalized treatments for sustained remission.
Additional Links: PMID-42378001
Publisher:
PubMed:
Citation:
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@article {pmid42378001,
year = {2026},
author = {Furqan, A and Sultan, MT and Khalid, MU and Waqar, M and Maaz, M and Tanvir, L and Naeem, R and Zarrish, M and Ibrahim, SRM and Mohamed, GA and Hossain, MS and Mohamed, HM},
title = {Small Intestinal Bacterial Overgrowth: Microbiome Dysregulation, Gut-Brain Axis Disruption, and Systemic Consequences.},
journal = {Molecular nutrition & food research},
volume = {70},
number = {13},
pages = {e70541},
doi = {10.1002/mnfr.70541},
pmid = {42378001},
issn = {1613-4133},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Dysbiosis ; *Intestine, Small/microbiology/physiopathology ; Animals ; *Brain-Gut Axis/physiology ; *Blind Loop Syndrome/microbiology/physiopathology ; Dietary Supplements ; Anti-Bacterial Agents/pharmacology/therapeutic use ; },
abstract = {Small intestinal bacterial overgrowth (SIBO) is a gastrointestinal disorder characterized by excessive bacterial colonization in the small intestine, leading to impaired digestion and nutrient malabsorption. Increasing evidence indicates that SIBO exerts systemic effects beyond the gut, contributing to metabolic, neurological, cardiovascular, dermatological, and autoimmune conditions. Current management strategies include nonsystemic antibiotics such as rifaximin, dietary interventions (low-FODMAP and biphasic diets), and nutraceuticals including berberine, oregano oil, peppermint oil, garlic derivatives, vitamins, and magnesium. Despite demonstrated clinical efficacy, challenges persist, including high recurrence rates, antimicrobial resistance, and long-term disruption of gut microbiota. Nutraceutical and dietary approaches offer promising patient-centered alternatives but require stronger clinical validation. This review critically examines the multifactorial pathophysiology of SIBO, emphasizing gut-brain axis dysregulation, microbial dysbiosis, oxidative stress, impaired intestinal motility, anatomical abnormalities, hypochlorhydria, bile acid malabsorption, and immune dysfunction. It synthesizes current diagnostic and therapeutic strategies, highlighting antibiotics, dietary approaches, and nutraceuticals, while distinguishing robust evidence from observational or preclinical findings. Finally, it identifies key research priorities, including improved diagnostics, global clinical trials, and microbiome- and genetics-based personalized treatments for sustained remission.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology
Dysbiosis
*Intestine, Small/microbiology/physiopathology
Animals
*Brain-Gut Axis/physiology
*Blind Loop Syndrome/microbiology/physiopathology
Dietary Supplements
Anti-Bacterial Agents/pharmacology/therapeutic use
RevDate: 2026-06-30
CmpDate: 2026-06-30
Is Fusobacterium nucleatum the key mediator between oral infections and systemic diseases? Mechanistic insights and therapeutic implications.
Gut microbes, 18(1):2694819.
Fusobacterium nucleatum has emerged as a pathobiont that associates oral dysbiosis with systemic diseases through coaggregation, hematogenous dissemination, and immune modulation. This review provides molecular insights through which they are involved in systemic diseases such as colorectal cancer, adverse pregnancy outcomes, cardiovascular diseases, neurodegenerative disorders, and diabetes mellitus. Key virulence factors include the adhesins of FadA, Fap2, and RadD, lipopolysaccharides, and outer membrane vesicles, which mediate epithelial invasion and endothelial permeafbility and facilitate immune suppression through TLR4-NF-κB, β-catenin/Wnt, and MAPK signaling pathways. These interactions result in impaired tissue homeostasis, propagate chronic inflammation, and promote oncogenic and metabolic modulation. Systemic pleiotropy of F. nucleatum is further substantiated by its involvement in chemoresistance, placental dysfunction, vascular inflammation, and neuronal injury, substantiating its systemic pleiotropy. Emerging therapeutic strategies, such as blocking adhesins, neutralizing outer membrane vesicles, microbiome manipulation, and using CRISPR-based clearance, provide precision techniques for mitigating diseases. Therefore, this review identifies F. nucleatum as the primary microbial mediator of oral-systemic pathology and its translational significance in the development of targeted antimicrobial and host-directed therapies.
Additional Links: PMID-42378068
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PubMed:
Citation:
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@article {pmid42378068,
year = {2026},
author = {Siddarth Ragunagam, G and Anbarasu, A and Kodiveri Muthukaliannan, G},
title = {Is Fusobacterium nucleatum the key mediator between oral infections and systemic diseases? Mechanistic insights and therapeutic implications.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2694819},
doi = {10.1080/19490976.2026.2694819},
pmid = {42378068},
issn = {1949-0984},
mesh = {Humans ; *Fusobacterium nucleatum/pathogenicity/physiology/genetics ; Animals ; Virulence Factors/metabolism ; *Fusobacterium Infections/microbiology ; Dysbiosis/microbiology ; Female ; Cardiovascular Diseases/microbiology ; Neurodegenerative Diseases/microbiology ; Diabetes Mellitus/microbiology ; Pregnancy ; },
abstract = {Fusobacterium nucleatum has emerged as a pathobiont that associates oral dysbiosis with systemic diseases through coaggregation, hematogenous dissemination, and immune modulation. This review provides molecular insights through which they are involved in systemic diseases such as colorectal cancer, adverse pregnancy outcomes, cardiovascular diseases, neurodegenerative disorders, and diabetes mellitus. Key virulence factors include the adhesins of FadA, Fap2, and RadD, lipopolysaccharides, and outer membrane vesicles, which mediate epithelial invasion and endothelial permeafbility and facilitate immune suppression through TLR4-NF-κB, β-catenin/Wnt, and MAPK signaling pathways. These interactions result in impaired tissue homeostasis, propagate chronic inflammation, and promote oncogenic and metabolic modulation. Systemic pleiotropy of F. nucleatum is further substantiated by its involvement in chemoresistance, placental dysfunction, vascular inflammation, and neuronal injury, substantiating its systemic pleiotropy. Emerging therapeutic strategies, such as blocking adhesins, neutralizing outer membrane vesicles, microbiome manipulation, and using CRISPR-based clearance, provide precision techniques for mitigating diseases. Therefore, this review identifies F. nucleatum as the primary microbial mediator of oral-systemic pathology and its translational significance in the development of targeted antimicrobial and host-directed therapies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Fusobacterium nucleatum/pathogenicity/physiology/genetics
Animals
Virulence Factors/metabolism
*Fusobacterium Infections/microbiology
Dysbiosis/microbiology
Female
Cardiovascular Diseases/microbiology
Neurodegenerative Diseases/microbiology
Diabetes Mellitus/microbiology
Pregnancy
RevDate: 2026-06-30
Exploring Emerging Concepts in the Pathophysiology of PCOS: Microbiome Dysbiosis and Immunological Dysregulation.
Reproduction & fertility pii:RAF-25-0187 [Epub ahead of print].
ABSTRACT: Polycystic ovarian syndrome (PCOS) is a complex yet common endocrine disorder, affecting 5-20% of reproductive-age women, characterised by a combination of hyperandrogenism, anovulation, and metabolic dysfunction. This combination of factors has traditionally been assumed to be the causative factors for the subfertility associated with PCOS, but significant microbial dysbiosis and alterations in immune function are identified in women with PCOS, suggesting a more complicated multifactorial impact on reproduction. Microbiome alterations vary between different PCOS subtypes, suggesting that hyperandrogenism and insulin resistance can impact microbial communities. The immunological implications of these microbiome changes are still poorly understood, along with their impact on reproductive outcomes such as implantation, miscarriage, and assisted reproduction success rates. Although therapeutic interventions are chosen based on their endocrine and metabolic effects, many of these also target the microbiome and have immunomodulatory effects. Understanding these microbiome-host interactions and immunological factors provides new insights into the complex spectrum of PCOS pathophysiology and provides the potential for novel therapeutic approaches.
LAY SUMMARY: Polycystic Ovary Syndrome (PCOS) is a common hormonal condition affecting up to one in five women of reproductive age. It can cause irregular periods, excess hair growth, acne, and difficulties with fertility. Recent research suggests that PCOS is not only a hormonal disorder but also involves changes in the body's bacteria, known as the microbiome, and disturbances in the immune system. These changes may contribute to inflammation, insulin resistance, and hormone imbalance. Understanding how the microbiome and immune system interact in PCOS could lead to new ways to diagnose and treat the condition. Future therapies may focus on restoring a healthy microbiome to improve metabolic and reproductive health.
Additional Links: PMID-42378109
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PubMed:
Citation:
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@article {pmid42378109,
year = {2026},
author = {Kumar, P and O'Reilly, M and McGowan, K and Harrity, C},
title = {Exploring Emerging Concepts in the Pathophysiology of PCOS: Microbiome Dysbiosis and Immunological Dysregulation.},
journal = {Reproduction & fertility},
volume = {},
number = {},
pages = {},
doi = {10.1530/RAF-25-0187},
pmid = {42378109},
issn = {2633-8386},
abstract = {ABSTRACT: Polycystic ovarian syndrome (PCOS) is a complex yet common endocrine disorder, affecting 5-20% of reproductive-age women, characterised by a combination of hyperandrogenism, anovulation, and metabolic dysfunction. This combination of factors has traditionally been assumed to be the causative factors for the subfertility associated with PCOS, but significant microbial dysbiosis and alterations in immune function are identified in women with PCOS, suggesting a more complicated multifactorial impact on reproduction. Microbiome alterations vary between different PCOS subtypes, suggesting that hyperandrogenism and insulin resistance can impact microbial communities. The immunological implications of these microbiome changes are still poorly understood, along with their impact on reproductive outcomes such as implantation, miscarriage, and assisted reproduction success rates. Although therapeutic interventions are chosen based on their endocrine and metabolic effects, many of these also target the microbiome and have immunomodulatory effects. Understanding these microbiome-host interactions and immunological factors provides new insights into the complex spectrum of PCOS pathophysiology and provides the potential for novel therapeutic approaches.
LAY SUMMARY: Polycystic Ovary Syndrome (PCOS) is a common hormonal condition affecting up to one in five women of reproductive age. It can cause irregular periods, excess hair growth, acne, and difficulties with fertility. Recent research suggests that PCOS is not only a hormonal disorder but also involves changes in the body's bacteria, known as the microbiome, and disturbances in the immune system. These changes may contribute to inflammation, insulin resistance, and hormone imbalance. Understanding how the microbiome and immune system interact in PCOS could lead to new ways to diagnose and treat the condition. Future therapies may focus on restoring a healthy microbiome to improve metabolic and reproductive health.},
}
RevDate: 2026-06-30
Vaginal Estrogen for Urinary Tract Infection Prevention: A Narrative Review of Evidence, Guidelines, and Regulatory Gaps.
Gynecologic and obstetric investigation pii:000553344 [Epub ahead of print].
BACKGROUND: Recurrent urinary tract infections (rUTIs) are common in peri- and postmenopausal women and impose substantial symptom, quality of life, and antimicrobial stewardship burdens, with particularly high incidence and hospitalization costs documented in England and UK primary care populations. Vaginal estrogen, by restoring urogenital epithelium and the lactobacillus-dominant microbiome, is recommended in several guidelines for preventing rUTI; including UK antimicrobial prescribing guidance for rUTIs and European Association of Urology recommendations. However, most formulations are licensed only for genitourinary syndrome of menopause, not for UTI prophylaxis. This creates a mismatch between the growing clinical evidence base and the absence of a specific regulatory indication for rUTI prevention across major regulatory agencies, including the U.S. Food and Drug Administration (FDA), the European Medicines Agency (EMA), and the UK Medicines and Healthcare products Regulatory Agency (MHRA), which may contribute to underuse and clinician uncertainty.
OBJECTIVES: To review and summarize the evidence on vaginal estrogen for prevention of recurrent urinary tract infections in peri- and postmenopausal women, with a particular focus on its use alone and in combination with antibiotic therapy, and on the gap between clinical guideline recommendations and regulatory product labelling.
METHODS: We conducted a structured narrative review focusing on randomized controlled trials and clinical practice guidelines that evaluate intravaginal estrogen for the prevention of rUTI in peri- and postmenopausal women. PubMed and Embase searches were performed using key terms for estrogen, urinary tract infection, and menopause, and were supplemented with targeted searches of major guidelines. Data were described in terms of study design, participant characteristics, estrogen formulations and dosing regimens, timing of initiation, comparators, outcome measures, and reported safety outcomes.
OUTCOME: Evidence from five RCTs reported that low-dose vaginal estrogen, administered as creams, tablets, rings, or gels, reduced culture-confirmed rUTI episodes and improved vaginal health indices, with no clear superiority of any single formulation and a favorable local safety profile. One trial found estriol pessaries less effective than nitrofurantoin prophylaxis, indicating that estrogen may complement rather than fully replace antibiotics in some women. Initiation was predominantly prophylactic or post-antibiotic, and no identified trial evaluated co-initiation of vaginal estrogen with antibiotics at the onset of acute UTI, highlighting a persisting evidence gap regarding optimal timing of therapy.
CONCLUSIONS AND OUTLOOK: Vaginal estrogen is an evidence-based yet underutilized strategy for rUTI prevention in peri- and postmenopausal women, supported by RCT data and guideline recommendations, but not recognized in current FDA-approved indications for vaginal estrogen products. Closing this evidence licensing gap will require regulatory reconsideration informed by existing trial data, alongside new pragmatic studies to refine timing, dosing, and formulation choices, to evaluate co-administration with antibiotics, and to explore women's knowledge, preferences, and adherence to support patient-centered implementation in routine care.
Additional Links: PMID-42378201
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PubMed:
Citation:
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@article {pmid42378201,
year = {2026},
author = {Ghasoub, R and Mackay, W and Shepherd, A},
title = {Vaginal Estrogen for Urinary Tract Infection Prevention: A Narrative Review of Evidence, Guidelines, and Regulatory Gaps.},
journal = {Gynecologic and obstetric investigation},
volume = {},
number = {},
pages = {1-12},
doi = {10.1159/000553344},
pmid = {42378201},
issn = {1423-002X},
abstract = {BACKGROUND: Recurrent urinary tract infections (rUTIs) are common in peri- and postmenopausal women and impose substantial symptom, quality of life, and antimicrobial stewardship burdens, with particularly high incidence and hospitalization costs documented in England and UK primary care populations. Vaginal estrogen, by restoring urogenital epithelium and the lactobacillus-dominant microbiome, is recommended in several guidelines for preventing rUTI; including UK antimicrobial prescribing guidance for rUTIs and European Association of Urology recommendations. However, most formulations are licensed only for genitourinary syndrome of menopause, not for UTI prophylaxis. This creates a mismatch between the growing clinical evidence base and the absence of a specific regulatory indication for rUTI prevention across major regulatory agencies, including the U.S. Food and Drug Administration (FDA), the European Medicines Agency (EMA), and the UK Medicines and Healthcare products Regulatory Agency (MHRA), which may contribute to underuse and clinician uncertainty.
OBJECTIVES: To review and summarize the evidence on vaginal estrogen for prevention of recurrent urinary tract infections in peri- and postmenopausal women, with a particular focus on its use alone and in combination with antibiotic therapy, and on the gap between clinical guideline recommendations and regulatory product labelling.
METHODS: We conducted a structured narrative review focusing on randomized controlled trials and clinical practice guidelines that evaluate intravaginal estrogen for the prevention of rUTI in peri- and postmenopausal women. PubMed and Embase searches were performed using key terms for estrogen, urinary tract infection, and menopause, and were supplemented with targeted searches of major guidelines. Data were described in terms of study design, participant characteristics, estrogen formulations and dosing regimens, timing of initiation, comparators, outcome measures, and reported safety outcomes.
OUTCOME: Evidence from five RCTs reported that low-dose vaginal estrogen, administered as creams, tablets, rings, or gels, reduced culture-confirmed rUTI episodes and improved vaginal health indices, with no clear superiority of any single formulation and a favorable local safety profile. One trial found estriol pessaries less effective than nitrofurantoin prophylaxis, indicating that estrogen may complement rather than fully replace antibiotics in some women. Initiation was predominantly prophylactic or post-antibiotic, and no identified trial evaluated co-initiation of vaginal estrogen with antibiotics at the onset of acute UTI, highlighting a persisting evidence gap regarding optimal timing of therapy.
CONCLUSIONS AND OUTLOOK: Vaginal estrogen is an evidence-based yet underutilized strategy for rUTI prevention in peri- and postmenopausal women, supported by RCT data and guideline recommendations, but not recognized in current FDA-approved indications for vaginal estrogen products. Closing this evidence licensing gap will require regulatory reconsideration informed by existing trial data, alongside new pragmatic studies to refine timing, dosing, and formulation choices, to evaluate co-administration with antibiotics, and to explore women's knowledge, preferences, and adherence to support patient-centered implementation in routine care.},
}
RevDate: 2026-06-30
CmpDate: 2026-06-30
Plastic Diets Drive Microbiome and Metabolic Reprogramming in Wax Moth Larvae (Achroia grisella).
Archives of insect biochemistry and physiology, 122(3):e70180.
The burgeoning global plastic crisis necessitates transformative solutions beyond current recycling and disposal methods. This study investigates the ability of wax moth larvae (Achroia grisella) to biodegrade low-density polyethylene (LDPE) and polylactic acid (PLA), emphasizing the complex interactions between the physiology of larvae, their gut microbiome, and the plastic degradation process. Using 16S ribosomal RNA sequencing, Seahorse bioassays, and advanced metabolomic and lipidomic profiling, we demonstrate that plastic consumption is associated with microbial and metabolic restructuring in larvae. LDPE-fed larvae displayed elevated microbial diversity, dominated by Bacillus spp., which correlated with shifts in carbohydrate metabolism and amino acid biosynthesis pathways critical for energy production and detoxification. Conversely, PLA-fed larvae were enriched with Enterococcus spp., linked to oxidative stress mitigation and nucleotide turnover. These diet-induced adaptations, such as the proliferation of Bacillus spp. in LDPE‑fed larvae, known to express alkane‑hydroxylase enzymes that initiate polyethylene depolymerization, and enrichment of Enterococcus spp. in PLA‑fed larvae, linked to ester bond hydrolysis, underscore a symbiotic co-metabolism that may play a contributory role in plastic processing, albeit at the cost of reduced larval growth and suppressed mitochondrial function. By unraveling these complex biological interactions, this study establishes a foundation for harnessing insect-microbiome ecosystems to develop scalable and eco-friendly strategies for plastic waste management. Future research should explore the genetic and enzymatic mechanisms underpinning plastic metabolism in insect-microbiome ecosystems.
Additional Links: PMID-42378406
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PubMed:
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@article {pmid42378406,
year = {2026},
author = {Shah, R and Marcora, A and Ruffell, A and Sinclair, GM and Vanwonterghem, I and Bissett, A and Hulthen, A and Wijffels, G and Paull, C and Beale, DJ},
title = {Plastic Diets Drive Microbiome and Metabolic Reprogramming in Wax Moth Larvae (Achroia grisella).},
journal = {Archives of insect biochemistry and physiology},
volume = {122},
number = {3},
pages = {e70180},
doi = {10.1002/arch.70180},
pmid = {42378406},
issn = {1520-6327},
mesh = {Animals ; *Moths/microbiology/metabolism/growth & development ; Larva/microbiology/metabolism/growth & development ; *Gastrointestinal Microbiome/drug effects ; Diet ; *Polyethylene/metabolism ; Polyesters/metabolism ; Biodegradation, Environmental ; RNA, Ribosomal, 16S ; *Plastics/metabolism ; },
abstract = {The burgeoning global plastic crisis necessitates transformative solutions beyond current recycling and disposal methods. This study investigates the ability of wax moth larvae (Achroia grisella) to biodegrade low-density polyethylene (LDPE) and polylactic acid (PLA), emphasizing the complex interactions between the physiology of larvae, their gut microbiome, and the plastic degradation process. Using 16S ribosomal RNA sequencing, Seahorse bioassays, and advanced metabolomic and lipidomic profiling, we demonstrate that plastic consumption is associated with microbial and metabolic restructuring in larvae. LDPE-fed larvae displayed elevated microbial diversity, dominated by Bacillus spp., which correlated with shifts in carbohydrate metabolism and amino acid biosynthesis pathways critical for energy production and detoxification. Conversely, PLA-fed larvae were enriched with Enterococcus spp., linked to oxidative stress mitigation and nucleotide turnover. These diet-induced adaptations, such as the proliferation of Bacillus spp. in LDPE‑fed larvae, known to express alkane‑hydroxylase enzymes that initiate polyethylene depolymerization, and enrichment of Enterococcus spp. in PLA‑fed larvae, linked to ester bond hydrolysis, underscore a symbiotic co-metabolism that may play a contributory role in plastic processing, albeit at the cost of reduced larval growth and suppressed mitochondrial function. By unraveling these complex biological interactions, this study establishes a foundation for harnessing insect-microbiome ecosystems to develop scalable and eco-friendly strategies for plastic waste management. Future research should explore the genetic and enzymatic mechanisms underpinning plastic metabolism in insect-microbiome ecosystems.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Moths/microbiology/metabolism/growth & development
Larva/microbiology/metabolism/growth & development
*Gastrointestinal Microbiome/drug effects
Diet
*Polyethylene/metabolism
Polyesters/metabolism
Biodegradation, Environmental
RNA, Ribosomal, 16S
*Plastics/metabolism
RevDate: 2026-06-30
CmpDate: 2026-07-01
Multiomics analysis dissects the molecular foundation of perianal fistulas associated with Crohn's disease and of cryptoglandular origin.
Journal of Crohn's & colitis, 20(6):.
BACKGROUND AND OBJECTIVE: Perianal fistulas, either of cryptoglandular origin (CgF) or associated with Crohn's disease (CDF), have limited treatment options and pose a tremendous burden for affected patients. We recently showed that the epithelial-mesenchymal transition (EMT) contributes to CDF pathogenesis, but detailed mechanisms need further evaluation. Here, we performed multiomics analysis to gain further molecular insights into fistula pathogenesis.
DESIGN: Rectal biopsies, swabs, fistula curettage, and serum samples were derived from patients with either CDF (n = 23) or CgF (n = 17) and analyzed by bulk RNA sequencing, metagenomics, untargeted metabolomics, or multiplex-ELISA, where appropriate.
RESULTS: Transcriptomics revealed striking differences in gene expression between rectal mucosa and fistula tract samples. However, the transcriptomes of CDF and CgF were comparable, and genes involved in EMT, inflammation and tumor necrosis factor signaling were prominent in both fistula types. A set of 18 genes was found to be differentially expressed in CDF and CgF and might allow discrimination. The overall microbiome composition within fistula tracts did not differ between CDF and CgF patients, but there was a significant difference in rectal microbiome compositions. On a species level, we detected an enrichment of disease-specific, pathogenic species in the fistula tracts. Of note, Bacteroides ssp., Fusobacterium animalis, and Staphylococcus aureus prevailed within CDF.
CONCLUSION: Our data demonstrate only minor differences in the transcriptome and the microbiome between CDF and CgF, but clear differences when compared to rectal mucosa biopsies. Thus, our data suggest that the molecular makeup underlying the pathophysiology of fistulas might be comparable between CDF and CgF.
Additional Links: PMID-42378712
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@article {pmid42378712,
year = {2026},
author = {Mamie, C and Cabalzar-Wondberg, D and Turina, M and Wawrzyniak, M and Misselwitz, B and Zamboni, N and Gottier, C and Lang, S and Rogler, G and Avivar-Valderas, A and de la Rosa, O and Candela, N and Tang, J and Morsy, Y and Scharl, M},
title = {Multiomics analysis dissects the molecular foundation of perianal fistulas associated with Crohn's disease and of cryptoglandular origin.},
journal = {Journal of Crohn's & colitis},
volume = {20},
number = {6},
pages = {},
doi = {10.1093/ecco-jcc/jjag080},
pmid = {42378712},
issn = {1876-4479},
support = {//Takeda Pharmaceutical Company Ltd/ ; },
mesh = {Humans ; *Crohn Disease/complications/genetics/microbiology ; *Rectal Fistula/genetics/microbiology/etiology/pathology/metabolism ; Multiomics ; Female ; Male ; Adult ; Epithelial-Mesenchymal Transition/genetics ; Transcriptome ; Middle Aged ; Intestinal Mucosa/pathology/metabolism ; Gastrointestinal Microbiome/genetics ; Gene Expression Profiling ; Metabolomics ; },
abstract = {BACKGROUND AND OBJECTIVE: Perianal fistulas, either of cryptoglandular origin (CgF) or associated with Crohn's disease (CDF), have limited treatment options and pose a tremendous burden for affected patients. We recently showed that the epithelial-mesenchymal transition (EMT) contributes to CDF pathogenesis, but detailed mechanisms need further evaluation. Here, we performed multiomics analysis to gain further molecular insights into fistula pathogenesis.
DESIGN: Rectal biopsies, swabs, fistula curettage, and serum samples were derived from patients with either CDF (n = 23) or CgF (n = 17) and analyzed by bulk RNA sequencing, metagenomics, untargeted metabolomics, or multiplex-ELISA, where appropriate.
RESULTS: Transcriptomics revealed striking differences in gene expression between rectal mucosa and fistula tract samples. However, the transcriptomes of CDF and CgF were comparable, and genes involved in EMT, inflammation and tumor necrosis factor signaling were prominent in both fistula types. A set of 18 genes was found to be differentially expressed in CDF and CgF and might allow discrimination. The overall microbiome composition within fistula tracts did not differ between CDF and CgF patients, but there was a significant difference in rectal microbiome compositions. On a species level, we detected an enrichment of disease-specific, pathogenic species in the fistula tracts. Of note, Bacteroides ssp., Fusobacterium animalis, and Staphylococcus aureus prevailed within CDF.
CONCLUSION: Our data demonstrate only minor differences in the transcriptome and the microbiome between CDF and CgF, but clear differences when compared to rectal mucosa biopsies. Thus, our data suggest that the molecular makeup underlying the pathophysiology of fistulas might be comparable between CDF and CgF.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Crohn Disease/complications/genetics/microbiology
*Rectal Fistula/genetics/microbiology/etiology/pathology/metabolism
Multiomics
Female
Male
Adult
Epithelial-Mesenchymal Transition/genetics
Transcriptome
Middle Aged
Intestinal Mucosa/pathology/metabolism
Gastrointestinal Microbiome/genetics
Gene Expression Profiling
Metabolomics
RevDate: 2026-06-30
The chemistry of the cobalt corrinoids - Recent advances and emerging themes. Part 3. Cobalamins and health.
Journal of inorganic biochemistry, 283:113395 pii:S0162-0134(26)00184-4 [Epub ahead of print].
Vitamin B12 (cobalamin) is an essential micronutrient whose biological importance extends beyond its traditional classification as a haematinic vitamin. This third and final part of a review covering work published between 2020 and 2025 synthesises selected illustrative studies that have advanced understanding of B12 physiology, nutrition, deficiency, delivery, and systems-level biology. At the molecular level, B12 functions as a cofactor in one‑carbon metabolism and mitochondrial pathways, influencing DNA synthesis, methylation capacity, and energy metabolism. These biochemical roles translate into organism-level consequences, particularly in the nervous system, where deficiency may cause irreversible neurological injury even in the absence of overt haematological abnormalities.Population-level analyses show that B12 status reflects the interaction of didetary intake, absorption efficiency, life stage, and food-system dynamics. Although animal-source foods remain the most reliable sources, shifts towards plant-based diets and inconsistent fortification practices are altering risk profiles. Clinical evidence further indicates that B12 deficiency is heterogeneous, frequently under-recognised, and complicated by the limitations of conventional biomarkers. Advances in delivery science point towards more controlled and targeted interventions, including encapsulation technologies, alternative administration routes, and receptor-mediated transport strategies. Emerging evidence also suggests biological activities for cobalamin derivatives beyond classical cofactor function, while microbiome research increasingly implicates corrinoid metabolism in host-microbe interactions relevant to immune and metabolic regulation. These developments support an integrated systems-level view of B12 biology spanning dietary supply, physiology, microbial ecology, and therapeutic innovation. SYNOPSIS: The final part of this review examines recent advances in vitamin B12 biology, spanning physiology, nutrition, deficiency, biomarker limitations, therapeutic delivery, and microbiome-linked corrinoid metabolism. These developments support an integrated systems-level view linking molecular function, dietary ecology, population health, and emerging therapeutic opportunities.
Additional Links: PMID-42378725
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PubMed:
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@article {pmid42378725,
year = {2026},
author = {Marques, HM},
title = {The chemistry of the cobalt corrinoids - Recent advances and emerging themes. Part 3. Cobalamins and health.},
journal = {Journal of inorganic biochemistry},
volume = {283},
number = {},
pages = {113395},
doi = {10.1016/j.jinorgbio.2026.113395},
pmid = {42378725},
issn = {1873-3344},
abstract = {Vitamin B12 (cobalamin) is an essential micronutrient whose biological importance extends beyond its traditional classification as a haematinic vitamin. This third and final part of a review covering work published between 2020 and 2025 synthesises selected illustrative studies that have advanced understanding of B12 physiology, nutrition, deficiency, delivery, and systems-level biology. At the molecular level, B12 functions as a cofactor in one‑carbon metabolism and mitochondrial pathways, influencing DNA synthesis, methylation capacity, and energy metabolism. These biochemical roles translate into organism-level consequences, particularly in the nervous system, where deficiency may cause irreversible neurological injury even in the absence of overt haematological abnormalities.Population-level analyses show that B12 status reflects the interaction of didetary intake, absorption efficiency, life stage, and food-system dynamics. Although animal-source foods remain the most reliable sources, shifts towards plant-based diets and inconsistent fortification practices are altering risk profiles. Clinical evidence further indicates that B12 deficiency is heterogeneous, frequently under-recognised, and complicated by the limitations of conventional biomarkers. Advances in delivery science point towards more controlled and targeted interventions, including encapsulation technologies, alternative administration routes, and receptor-mediated transport strategies. Emerging evidence also suggests biological activities for cobalamin derivatives beyond classical cofactor function, while microbiome research increasingly implicates corrinoid metabolism in host-microbe interactions relevant to immune and metabolic regulation. These developments support an integrated systems-level view of B12 biology spanning dietary supply, physiology, microbial ecology, and therapeutic innovation. SYNOPSIS: The final part of this review examines recent advances in vitamin B12 biology, spanning physiology, nutrition, deficiency, biomarker limitations, therapeutic delivery, and microbiome-linked corrinoid metabolism. These developments support an integrated systems-level view linking molecular function, dietary ecology, population health, and emerging therapeutic opportunities.},
}
RevDate: 2026-06-30
Chemical ecology in phytoremediation: Mechanistic insights, knowledge gaps, and future research directions.
The Science of the total environment, 1046:182009 pii:S0048-9697(26)00673-X [Epub ahead of print].
Phytoremediation harnesses plants efficiently to mitigate environmental pollutants, providing an eco-friendly alternative to conventional remediation technologies. Despite of decades physiological and molecular research, phytoremediation performance often remains context-dependent and challenging to predict, partly due to an incomplete understanding of chemically mediated interactions among plants, microbes, and contaminants in complex soil and water environments. This review synthesizes insights from chemical ecology to evaluate how root exudates, volatile organic compounds (VOCs), and allelochemicals orchestrate rhizosphere dynamics, microbial community assembly, and contaminant speciation and transformation. We focus on key knowledge gaps, including limited mechanistic validation of metabolite-microbe-pollutant interactions, insufficient integration of multi-omics datasets with ecological and physicochemical variables, and methodological challenges in field translation. While recent multi-omics approaches have expanded molecular resolution, their integration with ecological context and spatiotemporal dynamics remains limited. By highlighting emerging approaches and interdisciplinary strategies, this review outlines key research directions toward mechanistic, predictive, and ecologically grounded phytoremediation frameworks. It is a roadmap for advancing predictive, ecologically informed phytoremediation systems.
Additional Links: PMID-42378882
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PubMed:
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@article {pmid42378882,
year = {2026},
author = {Akpinar, A and Bakhshpour-Yücel, M},
title = {Chemical ecology in phytoremediation: Mechanistic insights, knowledge gaps, and future research directions.},
journal = {The Science of the total environment},
volume = {1046},
number = {},
pages = {182009},
doi = {10.1016/j.scitotenv.2026.182009},
pmid = {42378882},
issn = {1879-1026},
abstract = {Phytoremediation harnesses plants efficiently to mitigate environmental pollutants, providing an eco-friendly alternative to conventional remediation technologies. Despite of decades physiological and molecular research, phytoremediation performance often remains context-dependent and challenging to predict, partly due to an incomplete understanding of chemically mediated interactions among plants, microbes, and contaminants in complex soil and water environments. This review synthesizes insights from chemical ecology to evaluate how root exudates, volatile organic compounds (VOCs), and allelochemicals orchestrate rhizosphere dynamics, microbial community assembly, and contaminant speciation and transformation. We focus on key knowledge gaps, including limited mechanistic validation of metabolite-microbe-pollutant interactions, insufficient integration of multi-omics datasets with ecological and physicochemical variables, and methodological challenges in field translation. While recent multi-omics approaches have expanded molecular resolution, their integration with ecological context and spatiotemporal dynamics remains limited. By highlighting emerging approaches and interdisciplinary strategies, this review outlines key research directions toward mechanistic, predictive, and ecologically grounded phytoremediation frameworks. It is a roadmap for advancing predictive, ecologically informed phytoremediation systems.},
}
RevDate: 2026-06-30
Interkingdom signaling dynamics in the cereal holobiont: microbiome-mediated pathways to drought resilience.
Plant physiology and biochemistry : PPB, 237:111523 pii:S0981-9428(26)00509-7 [Epub ahead of print].
Root-associated microbiomes are increasingly recognized as important contributors to drought adaptation in cereal crops. Rather than functioning solely through improved nutrient acquisition, beneficial microorganisms can reshape host stress responses by modulating interconnected signaling, metabolic, transcriptional, and epigenetic pathways. Emerging evidence suggests that the plant-microbiome interactions operate through complex interkingdom signaling networks that coordinate root physiology, hormonal regulation, reactive oxygen species homeostasis, and stress-responsive gene expression, ultimately reinforcing drought resilience. However, current understanding of microbiome-mediated drought adaptation remains fragmented across ecological, omics, and molecular signaling perspectives. In this review, we synthesize current knowledge on microbiome-mediated signaling mechanisms underlying drought resilience in cereals from a holobiont-oriented perspective, in which plants and their root-associated microbiomes are viewed as integrated adaptive systems. We discuss how drought-responsive microbiomes influence plant adaptation through genomic and functional complementarity, multi-omics reprogramming, and modulation of core regulatory hubs, including protein kinases, transcription factors, phytohormones, reactive oxygen species, small signaling peptides, miRNAs, lncRNA-associated networks, and epigenetic regulation. Finally, we highlight major mechanistic gaps, technological challenges, and emerging opportunities for microbiome-informed engineering strategies aimed at improving cereal drought resilience.
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PubMed:
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@article {pmid42378887,
year = {2026},
author = {Gholizadeh, S and Nemati, I and Malekian, B and Barnes, CJ and Gholizadeh, H and Vestergård, M and Elango, D and Nicolaisen, M},
title = {Interkingdom signaling dynamics in the cereal holobiont: microbiome-mediated pathways to drought resilience.},
journal = {Plant physiology and biochemistry : PPB},
volume = {237},
number = {},
pages = {111523},
doi = {10.1016/j.plaphy.2026.111523},
pmid = {42378887},
issn = {1873-2690},
abstract = {Root-associated microbiomes are increasingly recognized as important contributors to drought adaptation in cereal crops. Rather than functioning solely through improved nutrient acquisition, beneficial microorganisms can reshape host stress responses by modulating interconnected signaling, metabolic, transcriptional, and epigenetic pathways. Emerging evidence suggests that the plant-microbiome interactions operate through complex interkingdom signaling networks that coordinate root physiology, hormonal regulation, reactive oxygen species homeostasis, and stress-responsive gene expression, ultimately reinforcing drought resilience. However, current understanding of microbiome-mediated drought adaptation remains fragmented across ecological, omics, and molecular signaling perspectives. In this review, we synthesize current knowledge on microbiome-mediated signaling mechanisms underlying drought resilience in cereals from a holobiont-oriented perspective, in which plants and their root-associated microbiomes are viewed as integrated adaptive systems. We discuss how drought-responsive microbiomes influence plant adaptation through genomic and functional complementarity, multi-omics reprogramming, and modulation of core regulatory hubs, including protein kinases, transcription factors, phytohormones, reactive oxygen species, small signaling peptides, miRNAs, lncRNA-associated networks, and epigenetic regulation. Finally, we highlight major mechanistic gaps, technological challenges, and emerging opportunities for microbiome-informed engineering strategies aimed at improving cereal drought resilience.},
}
RevDate: 2026-06-30
From coarse-grained metabolic rules to fine-grained control of microbial communities.
Current opinion in microbiology, 92:102788 pii:S1369-5274(26)00082-2 [Epub ahead of print].
Over the past decade, microbial ecology has revealed remarkable coarse-grained regularities in community assembly and metabolic function. Across diverse systems, distinct taxonomic compositions can converge on similar functional outputs, and simple physiological principles can predict steady-state outcomes. These findings suggest that complex microbiomes may, in some regimes, be governed by emergent simplicity and therefore be predictable. Yet many of the traits we want to understand or engineer seem to depend on fine-grained dynamics that may be transient, strain-specific, and history dependent. Here, we argue that bridging the gap between coarse-grained metabolic rules and fine-grained metabolic complexity is essential for a predictive and engineering-oriented microbiome ecology. While progress is limited by the lack of (or insufficient) temporal, spatial, and chemical resolution, we highlight both conceptual advances and emerging technologies that may help fill that gap by providing temporal, spatial, single-cell resolved, dynamic, quantitative measurements.
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PubMed:
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@article {pmid42378946,
year = {2026},
author = {Vila, JC and Estrela, S},
title = {From coarse-grained metabolic rules to fine-grained control of microbial communities.},
journal = {Current opinion in microbiology},
volume = {92},
number = {},
pages = {102788},
doi = {10.1016/j.mib.2026.102788},
pmid = {42378946},
issn = {1879-0364},
abstract = {Over the past decade, microbial ecology has revealed remarkable coarse-grained regularities in community assembly and metabolic function. Across diverse systems, distinct taxonomic compositions can converge on similar functional outputs, and simple physiological principles can predict steady-state outcomes. These findings suggest that complex microbiomes may, in some regimes, be governed by emergent simplicity and therefore be predictable. Yet many of the traits we want to understand or engineer seem to depend on fine-grained dynamics that may be transient, strain-specific, and history dependent. Here, we argue that bridging the gap between coarse-grained metabolic rules and fine-grained metabolic complexity is essential for a predictive and engineering-oriented microbiome ecology. While progress is limited by the lack of (or insufficient) temporal, spatial, and chemical resolution, we highlight both conceptual advances and emerging technologies that may help fill that gap by providing temporal, spatial, single-cell resolved, dynamic, quantitative measurements.},
}
RevDate: 2026-06-30
The role of the antimicrobial peptide nisin as a clean label food preservative.
Current opinion in microbiology, 92:102786 pii:S1369-5274(26)00080-9 [Epub ahead of print].
The bacteriocin nisin can play a role in addressing the global need for safe, effective, and 'clean label' preservation strategies. Nisin A and its variants are among the most extensively studied antimicrobial peptides. Despite many advantages, nisin exhibits limitations in complex food matrices, including reduced solubility at neutral pH, susceptibility to proteolytic degradation, and poor activity against Gram-negative bacteria. We highlight recent advances aimed at overcoming these challenges, including novel delivery systems and the development of novel nisin variants with improved physicochemical properties, resistance to enzymatic degradation, and expanded antimicrobial spectra. Additionally, emerging research suggests a potential role for nisin as a functional food component capable of modulating the gut microbiome, although its effects appear context-dependent and require further investigation. We suggest that a diversified portfolio of nisin variants combined with advances in delivery strategies can position nisin and its variants as a key tool in the development of sustainable, safe, and minimally processed food.
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@article {pmid42378947,
year = {2026},
author = {Murphy, IL and Hill, C and Field, D},
title = {The role of the antimicrobial peptide nisin as a clean label food preservative.},
journal = {Current opinion in microbiology},
volume = {92},
number = {},
pages = {102786},
doi = {10.1016/j.mib.2026.102786},
pmid = {42378947},
issn = {1879-0364},
abstract = {The bacteriocin nisin can play a role in addressing the global need for safe, effective, and 'clean label' preservation strategies. Nisin A and its variants are among the most extensively studied antimicrobial peptides. Despite many advantages, nisin exhibits limitations in complex food matrices, including reduced solubility at neutral pH, susceptibility to proteolytic degradation, and poor activity against Gram-negative bacteria. We highlight recent advances aimed at overcoming these challenges, including novel delivery systems and the development of novel nisin variants with improved physicochemical properties, resistance to enzymatic degradation, and expanded antimicrobial spectra. Additionally, emerging research suggests a potential role for nisin as a functional food component capable of modulating the gut microbiome, although its effects appear context-dependent and require further investigation. We suggest that a diversified portfolio of nisin variants combined with advances in delivery strategies can position nisin and its variants as a key tool in the development of sustainable, safe, and minimally processed food.},
}
RevDate: 2026-06-30
Early-life gut microbiome composition and rotavirus vaccine-induced IgA responses in U.S. infants: a longitudinal cohort study.
EBioMedicine, 129:106360 pii:S2352-3964(26)00243-4 [Epub ahead of print].
BACKGROUND: Rotavirus remains a leading cause of childhood mortality worldwide, despite the widespread introduction of oral rotavirus vaccines. Evidence linking the gut microbiome to vaccine response is inconsistent and limited in U.S.
POPULATIONS: This study investigates the development of the infant gut microbiome and its association with immunogenicity following RotaTeq administration in U.S. infants.
METHODS: We conducted a longitudinal analysis of infants in Rochester, New York, using 16S rRNA sequencing to assess microbiome composition at one (M1), sixth (M6), and twelfth (M12) months of age. Rotavirus-IgA serologies were measured at M6 and M12 to assess RotaTeq vaccine seroresponse. Clinical metadata were used to assess factors associated with microbial diversity and rotavirus-IgA titres over the first year of life. We examined associations between (1) M1 microbiome and M6 rotavirus-IgA; (2) M6 microbiome and M6 rotavirus-IgA; and (3) M6 microbiome and M12 rotavirus-IgA.
FINDINGS: Higher gut microbial alpha diversity at M1 was associated with higher rotavirus-IgA titres at M6 (N = 47, β: 2·06, 95% CI: [0·31-3·99], p = 0·024). Alpha diversity at M6 was not associated with concurrent rotavirus-IgA responses (N = 56, β: 0·73, 95% CI: [-0·856, 2·313], p = 0·36) but was associated with higher rotavirus-IgA at M12 (N = 52, β: 1·47, 95% CI: [0·127, 2·805], p = 0·033). Rotavirus-IgA responses were associated with specific microbial taxa across timepoints, with both positive and negative associations observed.
INTERPRETATION: In a healthy U.S. infant cohort, early-life gut microbiome diversity and composition were associated with rotavirus-IgA responses following RotaTeq vaccination. This study advances understanding of microbiome-vaccine interactions in high-income settings.
FUNDING: Office of the Director of the National Institutes of Health, National Institute of Mental Health of the National Institutes of Health, and the National Center for Advancing Translational Sciences of the National Institutes of Health.
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Citation:
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@article {pmid42378964,
year = {2026},
author = {Narváez-Miranda, J and Sohn, MB and Velasquez-Portocarrero, D and Gill, AL and Beblavy, R and Castro-Melendez, D and Ejiofor, K and Qiu, X and Laniewski, N and Groff, B and Brunner, J and Ras, M and Leger, A and Macomber, A and Caddy, SL and Jiang, B and O'Connor, T and Gill, SR and Scheible, K},
title = {Early-life gut microbiome composition and rotavirus vaccine-induced IgA responses in U.S. infants: a longitudinal cohort study.},
journal = {EBioMedicine},
volume = {129},
number = {},
pages = {106360},
doi = {10.1016/j.ebiom.2026.106360},
pmid = {42378964},
issn = {2352-3964},
abstract = {BACKGROUND: Rotavirus remains a leading cause of childhood mortality worldwide, despite the widespread introduction of oral rotavirus vaccines. Evidence linking the gut microbiome to vaccine response is inconsistent and limited in U.S.
POPULATIONS: This study investigates the development of the infant gut microbiome and its association with immunogenicity following RotaTeq administration in U.S. infants.
METHODS: We conducted a longitudinal analysis of infants in Rochester, New York, using 16S rRNA sequencing to assess microbiome composition at one (M1), sixth (M6), and twelfth (M12) months of age. Rotavirus-IgA serologies were measured at M6 and M12 to assess RotaTeq vaccine seroresponse. Clinical metadata were used to assess factors associated with microbial diversity and rotavirus-IgA titres over the first year of life. We examined associations between (1) M1 microbiome and M6 rotavirus-IgA; (2) M6 microbiome and M6 rotavirus-IgA; and (3) M6 microbiome and M12 rotavirus-IgA.
FINDINGS: Higher gut microbial alpha diversity at M1 was associated with higher rotavirus-IgA titres at M6 (N = 47, β: 2·06, 95% CI: [0·31-3·99], p = 0·024). Alpha diversity at M6 was not associated with concurrent rotavirus-IgA responses (N = 56, β: 0·73, 95% CI: [-0·856, 2·313], p = 0·36) but was associated with higher rotavirus-IgA at M12 (N = 52, β: 1·47, 95% CI: [0·127, 2·805], p = 0·033). Rotavirus-IgA responses were associated with specific microbial taxa across timepoints, with both positive and negative associations observed.
INTERPRETATION: In a healthy U.S. infant cohort, early-life gut microbiome diversity and composition were associated with rotavirus-IgA responses following RotaTeq vaccination. This study advances understanding of microbiome-vaccine interactions in high-income settings.
FUNDING: Office of the Director of the National Institutes of Health, National Institute of Mental Health of the National Institutes of Health, and the National Center for Advancing Translational Sciences of the National Institutes of Health.},
}
RevDate: 2026-06-28
L-Glutamine Plus L-Glutamic Acid Enhances Antioxidant Status and Ammonia Toxicity Resilience, Upregulates Interleukin IL-10 Gene, and Improves Gut Microbiota and Survival in Juvenile Nile Tilapia.
Journal of animal physiology and animal nutrition [Epub ahead of print].
Glutamine (Gln) and glutamic acid (Glu) are the most abundant free amino acids (AAs) in the fish body. Although classified as non-essential AAs, their supplementation can be a strategy to optimize the growth performance and health of fish. This study aimed to investigate the effects of dietary Gln and Glu blend on growth performance, biochemical parameters, gut microbiota composition, short-chain fatty acids (SCFAs) production, digestive enzyme activity, histomorphometry, and liver mRNA levels of glutamine synthetase (GS), peroxisome proliferator-activated receptor alpha (PPAR-α), anti-inflammatory interleukin 10 (IL-10), pro-inflammatory interleukin 1β (IL-1β), and antioxidant status of juvenile Nile tilapia. Fish (n = 216; 0.99 ± 0.01 g) were randomly allocated into eight aquariums containing 27 fish each, in a four-replicate design. Fish were hand-fed a Glu + Gln unsupplemented basal diet (CON) or a basal diet supplemented with 20 g kg[-1] Glu + Gln (AMG) six times daily until apparent satiety for 60 days. Relative to fish fed CON diet, fish fed AMG diet exhibited enhanced feed conversion ratio (FCR; -5.6%), energy retention efficiency (+8.20%), and protein retention efficiency (+7.69%), and a trend towards a higher survival rate (+5.9%), suggesting improved nutrient utilization. Although the general structure of the microbiota of fish fed AMG diet remained similar to that of fish fed CON diet, it was observed that Gln + Glu supplementation promoted increased relative abundance of Enterococcus sp., a potential probiotic. Notably, fish fed AMG diet showed higher SCFA production than those fed CON diet, enhancing intestinal fold development. Fish fed AMG diet also exhibited higher liver activity of superoxide dismutase (SOD) and glutathione-S-transferase (GST), resulting in lower malondialdehyde (MDA) concentration and indicating a healthier intestinal mucosal state. Furthermore, fish fed AMG diet showed higher mRNA expression of IL-10 and GS, indicating enhanced anti-inflammatory responses and ammonia metabolism, respectively. In conclusion, 20 g kg[-1] dietary Gln plus Glu enhanced FCR, nutrient retention, and survival by favorably modulating the microbiota and improving intestinal function, thereby optimizing antioxidant responses and innate immunity in juvenile Nile tilapia. These findings highlight the potential of Gln and Glu blend to improve profitability and sustainability in Nile tilapia aquaculture.
Additional Links: PMID-42365622
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@article {pmid42365622,
year = {2026},
author = {Carneiro, CLDS and Cruz, TPD and Monteiro, LCP and Glugoski, L and Feldhaus, MV and Lipinski, LC and Vicari, MR and Nogaroto, V and Barriviera, VR and Furuya, WM},
title = {L-Glutamine Plus L-Glutamic Acid Enhances Antioxidant Status and Ammonia Toxicity Resilience, Upregulates Interleukin IL-10 Gene, and Improves Gut Microbiota and Survival in Juvenile Nile Tilapia.},
journal = {Journal of animal physiology and animal nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1111/jpn.70086},
pmid = {42365622},
issn = {1439-0396},
support = {176820/2023-0//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; //Coordenação de Aperfeiçoamento de Pessoal de Nível Superior/ ; },
abstract = {Glutamine (Gln) and glutamic acid (Glu) are the most abundant free amino acids (AAs) in the fish body. Although classified as non-essential AAs, their supplementation can be a strategy to optimize the growth performance and health of fish. This study aimed to investigate the effects of dietary Gln and Glu blend on growth performance, biochemical parameters, gut microbiota composition, short-chain fatty acids (SCFAs) production, digestive enzyme activity, histomorphometry, and liver mRNA levels of glutamine synthetase (GS), peroxisome proliferator-activated receptor alpha (PPAR-α), anti-inflammatory interleukin 10 (IL-10), pro-inflammatory interleukin 1β (IL-1β), and antioxidant status of juvenile Nile tilapia. Fish (n = 216; 0.99 ± 0.01 g) were randomly allocated into eight aquariums containing 27 fish each, in a four-replicate design. Fish were hand-fed a Glu + Gln unsupplemented basal diet (CON) or a basal diet supplemented with 20 g kg[-1] Glu + Gln (AMG) six times daily until apparent satiety for 60 days. Relative to fish fed CON diet, fish fed AMG diet exhibited enhanced feed conversion ratio (FCR; -5.6%), energy retention efficiency (+8.20%), and protein retention efficiency (+7.69%), and a trend towards a higher survival rate (+5.9%), suggesting improved nutrient utilization. Although the general structure of the microbiota of fish fed AMG diet remained similar to that of fish fed CON diet, it was observed that Gln + Glu supplementation promoted increased relative abundance of Enterococcus sp., a potential probiotic. Notably, fish fed AMG diet showed higher SCFA production than those fed CON diet, enhancing intestinal fold development. Fish fed AMG diet also exhibited higher liver activity of superoxide dismutase (SOD) and glutathione-S-transferase (GST), resulting in lower malondialdehyde (MDA) concentration and indicating a healthier intestinal mucosal state. Furthermore, fish fed AMG diet showed higher mRNA expression of IL-10 and GS, indicating enhanced anti-inflammatory responses and ammonia metabolism, respectively. In conclusion, 20 g kg[-1] dietary Gln plus Glu enhanced FCR, nutrient retention, and survival by favorably modulating the microbiota and improving intestinal function, thereby optimizing antioxidant responses and innate immunity in juvenile Nile tilapia. These findings highlight the potential of Gln and Glu blend to improve profitability and sustainability in Nile tilapia aquaculture.},
}
RevDate: 2026-06-28
CmpDate: 2026-06-28
Current perspectives on the pathogenesis of multiple sclerosis: A minireview.
Endocrine regulations, 60(1):72-85 pii:enr-2026-0009.
Multiple sclerosis (MS) is a chronic immune-mediated demyelinating disease of the central nervous system characterized by inflammation, reactive gliosis, and progressive neuroaxonal damage resulting in heterogeneous clinical and histopathological manifestations. As MS often leads to disability at a young age, it represents a substantial socio-economic burden in developed countries. The etiopathogenesis of MS is multifactorial and incompletely understood, involving genetic, immunologic, and environmental factors. Recent research highlights immune responses to Epstein-Barr virus, blood-brain barrier disruption, microbiome-gut-brain axis alterations, oxidative damage, and mitochondrial dysfunction. Studying patients with newly diagnosed MS without significant comorbidities provides insight into early disease mechanisms before disability development or long-term treatment effects. This mini-review focuses on early vascular and metabolic alterations that may contribute to MS, including lipoprotein subfractions as markers of incipient atherosclerosis, endothelial dysfunction as an initiating vascular event, and autonomic nervous system imbalance during disease progression. It also addresses insulin sensitivity as a key metabolic factor alongside chronic inflammation and oxidative damage as interconnected mechanisms driving tissue injury. Metabolic changes reflecting neuronal impairment, mitochondrial dysfunction, and astroglial activation are detectable in both lesional and normal-appearing white matter in early stages. Reduced antioxidant capacity supports a role of oxidative damage in MS pathogenesis. Accelerated vascular aging, independent of traditional cardiovascular risk factors, may progress from endothelial dysfunction to structural atherosclerotic changes. Subtle alterations in lipoprotein profiles further suggest an increased risk of atherosclerosis, potentially influenced by inflammatory activity and oxidative damage, with possible sex-specific differences. Autonomic dysfunction appears to develop secondary to disease progression rather than as a primary driver of pathogenesis.
Additional Links: PMID-42365629
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@article {pmid42365629,
year = {2026},
author = {Radikova, Z and Tibensky, M and Mosna, L and Penesova, A and Havranova, A and Vlcek, M and Imrich, R},
title = {Current perspectives on the pathogenesis of multiple sclerosis: A minireview.},
journal = {Endocrine regulations},
volume = {60},
number = {1},
pages = {72-85},
doi = {10.2478/enr-2026-0009},
pmid = {42365629},
issn = {1336-0329},
mesh = {Humans ; *Multiple Sclerosis/etiology/metabolism/physiopathology/immunology/pathology ; Oxidative Stress/physiology ; Animals ; Inflammation ; Disease Progression ; },
abstract = {Multiple sclerosis (MS) is a chronic immune-mediated demyelinating disease of the central nervous system characterized by inflammation, reactive gliosis, and progressive neuroaxonal damage resulting in heterogeneous clinical and histopathological manifestations. As MS often leads to disability at a young age, it represents a substantial socio-economic burden in developed countries. The etiopathogenesis of MS is multifactorial and incompletely understood, involving genetic, immunologic, and environmental factors. Recent research highlights immune responses to Epstein-Barr virus, blood-brain barrier disruption, microbiome-gut-brain axis alterations, oxidative damage, and mitochondrial dysfunction. Studying patients with newly diagnosed MS without significant comorbidities provides insight into early disease mechanisms before disability development or long-term treatment effects. This mini-review focuses on early vascular and metabolic alterations that may contribute to MS, including lipoprotein subfractions as markers of incipient atherosclerosis, endothelial dysfunction as an initiating vascular event, and autonomic nervous system imbalance during disease progression. It also addresses insulin sensitivity as a key metabolic factor alongside chronic inflammation and oxidative damage as interconnected mechanisms driving tissue injury. Metabolic changes reflecting neuronal impairment, mitochondrial dysfunction, and astroglial activation are detectable in both lesional and normal-appearing white matter in early stages. Reduced antioxidant capacity supports a role of oxidative damage in MS pathogenesis. Accelerated vascular aging, independent of traditional cardiovascular risk factors, may progress from endothelial dysfunction to structural atherosclerotic changes. Subtle alterations in lipoprotein profiles further suggest an increased risk of atherosclerosis, potentially influenced by inflammatory activity and oxidative damage, with possible sex-specific differences. Autonomic dysfunction appears to develop secondary to disease progression rather than as a primary driver of pathogenesis.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Multiple Sclerosis/etiology/metabolism/physiopathology/immunology/pathology
Oxidative Stress/physiology
Animals
Inflammation
Disease Progression
RevDate: 2026-06-28
CmpDate: 2026-06-28
Early life adversity influences brain development through neuroendocrine, immune, and microbiota-related mechanisms: A review.
Endocrine regulations, 60(1):86-97 pii:enr-2026-0010.
The early life experiences have an important impact on the development of the brain and behavior and early life adversities (ELA) may affect several biological systems including the hypothalamic-pituitary-adrenal (HPA) axis, neurotransmitter and immune signaling systems, and microbiota composition. Dysregulation of these systems may result in an altered stress reactivity in both early life and the adulthood periods leading to maladaptive responses to the environmental stimuli. The activation of certain neuropeptides, including oxytocin, stimulation of the HPA axis, and increased glucocorticoid levels, may also play an important role in the early adaptive processes. In terms of brain maturation, ELA can directly or indirectly elicit structural changes in neurite growth, neurogenesis, neuronal connectivities, and signaling processes, which may contribute to the production of the long-term behavioral changes associated with an increased risk of the neuropsychiatric disorders' development in later periods of the life. In this review, we summarize the effect of ELA on the HPA axis function, stress-related hormonal balance, immune responses, and the gut microbiome indicating how these changes may affect the brain function and behavior in the early stages of the life and adulthood. We also provide insight into animal studies revealing the responses of corticotropin-releasing hormone, urocortins, and corticosterone in various neural circuits in response to ELA evoked by maternal separation and limited bedding paradigms.
Additional Links: PMID-42365631
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@article {pmid42365631,
year = {2026},
author = {Vargovic, P and Osacka, J and Horvathova, L and Tillinger, A and Mihalj, D and Bodorova, BB and Dziewiczova, L and Havranek, T and Bacova, Z and Bakos, J},
title = {Early life adversity influences brain development through neuroendocrine, immune, and microbiota-related mechanisms: A review.},
journal = {Endocrine regulations},
volume = {60},
number = {1},
pages = {86-97},
doi = {10.2478/enr-2026-0010},
pmid = {42365631},
issn = {1336-0329},
mesh = {Humans ; Animals ; *Brain/growth & development/immunology/metabolism ; *Hypothalamo-Hypophyseal System/metabolism/physiopathology ; *Pituitary-Adrenal System/metabolism/physiopathology ; *Adverse Childhood Experiences ; *Stress, Psychological/immunology/physiopathology/metabolism ; *Gastrointestinal Microbiome/physiology ; *Neurosecretory Systems ; Neurodevelopment ; *Immune System ; *Microbiota/physiology ; },
abstract = {The early life experiences have an important impact on the development of the brain and behavior and early life adversities (ELA) may affect several biological systems including the hypothalamic-pituitary-adrenal (HPA) axis, neurotransmitter and immune signaling systems, and microbiota composition. Dysregulation of these systems may result in an altered stress reactivity in both early life and the adulthood periods leading to maladaptive responses to the environmental stimuli. The activation of certain neuropeptides, including oxytocin, stimulation of the HPA axis, and increased glucocorticoid levels, may also play an important role in the early adaptive processes. In terms of brain maturation, ELA can directly or indirectly elicit structural changes in neurite growth, neurogenesis, neuronal connectivities, and signaling processes, which may contribute to the production of the long-term behavioral changes associated with an increased risk of the neuropsychiatric disorders' development in later periods of the life. In this review, we summarize the effect of ELA on the HPA axis function, stress-related hormonal balance, immune responses, and the gut microbiome indicating how these changes may affect the brain function and behavior in the early stages of the life and adulthood. We also provide insight into animal studies revealing the responses of corticotropin-releasing hormone, urocortins, and corticosterone in various neural circuits in response to ELA evoked by maternal separation and limited bedding paradigms.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Animals
*Brain/growth & development/immunology/metabolism
*Hypothalamo-Hypophyseal System/metabolism/physiopathology
*Pituitary-Adrenal System/metabolism/physiopathology
*Adverse Childhood Experiences
*Stress, Psychological/immunology/physiopathology/metabolism
*Gastrointestinal Microbiome/physiology
*Neurosecretory Systems
Neurodevelopment
*Immune System
*Microbiota/physiology
RevDate: 2026-06-28
CmpDate: 2026-06-28
Hepatocrinology: New Conceptual Frameworks Linking Endocrine Disorders to Chronic Liver Pathology.
Journal of gastrointestinal and liver diseases : JGLD, 35(2):286-295.
Hepatocrinology is an emerging interdisciplinary field that examines the bidirectional interactions between the liver and the endocrine system, emphasizing how hepatic dysfunction influences hormonal regulation and how endocrine disorders, in turn, shape liver metabolism, inflammation, and disease progression. This review summarizes current theoretical frameworks, including hepato-endocrine axes, hepatokine signaling, and multi-organ communication models, highlighting the liver's role as a central endocrine hub. Key hepatic hormones, transport proteins, and hepatokines such as fetuin-A, fibroblast growth factor 21, and selenoprotein P are discussed in relation to metabolic disorders including metabolic dysfunction-associated steatotic liver disease, metabolic dysfunction-associated steatohepatitis, polycystic ovary syndrome, diabetes, and advanced chronic liver disease. The review further explores hormonal axes involving the thyroid, pancreas, adrenal glands, parathyroids, and gonads, illustrating their complex interplay with hepatic physiology. Current challenges, such as limited long-term studies and therapeutic controversies, are examined alongside emerging directions involving hepatokine-targeted therapies, precision medicine, and microbiome-driven modulation. Understanding these interconnected pathways is essential for improving diagnostic accuracy, risk stratification, and therapeutic strategies in hepato-endocrine disorders.
Additional Links: PMID-42365641
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@article {pmid42365641,
year = {2026},
author = {Gherman-Lencu, CC and Bud, MG and Perne, MG and Gavris, MD and David, LE and Alexescu, TG},
title = {Hepatocrinology: New Conceptual Frameworks Linking Endocrine Disorders to Chronic Liver Pathology.},
journal = {Journal of gastrointestinal and liver diseases : JGLD},
volume = {35},
number = {2},
pages = {286-295},
doi = {10.15403/jgld-6940},
pmid = {42365641},
issn = {1842-1121},
mesh = {Humans ; *Liver/metabolism/pathology/physiopathology ; *Endocrine System Diseases/metabolism/physiopathology/complications ; *Liver Diseases/metabolism/physiopathology ; *Endocrine System/metabolism/physiopathology ; Chronic Disease ; Animals ; Signal Transduction ; },
abstract = {Hepatocrinology is an emerging interdisciplinary field that examines the bidirectional interactions between the liver and the endocrine system, emphasizing how hepatic dysfunction influences hormonal regulation and how endocrine disorders, in turn, shape liver metabolism, inflammation, and disease progression. This review summarizes current theoretical frameworks, including hepato-endocrine axes, hepatokine signaling, and multi-organ communication models, highlighting the liver's role as a central endocrine hub. Key hepatic hormones, transport proteins, and hepatokines such as fetuin-A, fibroblast growth factor 21, and selenoprotein P are discussed in relation to metabolic disorders including metabolic dysfunction-associated steatotic liver disease, metabolic dysfunction-associated steatohepatitis, polycystic ovary syndrome, diabetes, and advanced chronic liver disease. The review further explores hormonal axes involving the thyroid, pancreas, adrenal glands, parathyroids, and gonads, illustrating their complex interplay with hepatic physiology. Current challenges, such as limited long-term studies and therapeutic controversies, are examined alongside emerging directions involving hepatokine-targeted therapies, precision medicine, and microbiome-driven modulation. Understanding these interconnected pathways is essential for improving diagnostic accuracy, risk stratification, and therapeutic strategies in hepato-endocrine disorders.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Liver/metabolism/pathology/physiopathology
*Endocrine System Diseases/metabolism/physiopathology/complications
*Liver Diseases/metabolism/physiopathology
*Endocrine System/metabolism/physiopathology
Chronic Disease
Animals
Signal Transduction
RevDate: 2026-06-28
Lifestyle-associated blood metabolic pathways and functional performance in cognitive aging.
Scientific reports pii:10.1038/s41598-026-58782-7 [Epub ahead of print].
Functional decline is a major clinical feature of Alzheimer's disease (AD), yet the blood metabolic pathways associated with lifestyle factors and multidimensional functional performance across cognitive stages remain incompletely characterized. We applied a pathway-level blood metabolomics framework to harmonized, de-identified data from aging and dementia-related cohort resources spanning cognitively normal aging (CN), mild cognitive impairment (MCI), and AD. Metabolites were mapped to curated pathways and summarized into pathway activity scores across five domains: energy metabolism, amino acid metabolism, lipid metabolism, inflammation/oxidative stress, and microbiome-linked metabolism. We evaluated associations among physical activity, diet quality, pathway activity scores, and functional outcomes, including activities of daily living, gait speed, grip strength, global cognition, composite function, and frailty. To summarize pathway patterns jointly associated with physical activity and diet quality, we derived a lifestyle-modulated metabolic pathway score (LMPS) using elastic net regression with cross-validation, out-of-fold score estimation, and bootstrap stability assessment. Lifestyle-associated pathway activity showed coordinated patterns across metabolic domains and was associated with functional performance across cognitive groups. Higher LMPS values were associated with better physical and cognitive function and lower frailty, with graded differences observed across CN, MCI, and AD. Internal robustness analyses indicated greater stability at the pathway-domain level than at the individual-pathway coefficient level. Sensitivity analyses adjusting for cognitive group attenuated but did not eliminate the directionally consistent associations between LMPS and major functional outcomes. Convergent pathway patterns involved mitochondrial energy metabolism, lipid remodeling, inflammatory regulation, and microbiome-related metabolism. Pathway-level blood metabolomics identified lifestyle-associated metabolic patterns related to multidimensional functional outcomes across the cognitive aging spectrum. LMPS provides a data-driven summary of lifestyle-associated pathway variation in this cohort and may help generate hypotheses about metabolic correlates of functional performance. Independent and longitudinal validation will be required to determine its reproducibility, temporal relevance, and translational utility.
Additional Links: PMID-42366201
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PubMed:
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@article {pmid42366201,
year = {2026},
author = {Chen, Y and Gui, H and Ma, K and Zhang, Z and Zhao, T and Wang, M},
title = {Lifestyle-associated blood metabolic pathways and functional performance in cognitive aging.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-58782-7},
pmid = {42366201},
issn = {2045-2322},
abstract = {Functional decline is a major clinical feature of Alzheimer's disease (AD), yet the blood metabolic pathways associated with lifestyle factors and multidimensional functional performance across cognitive stages remain incompletely characterized. We applied a pathway-level blood metabolomics framework to harmonized, de-identified data from aging and dementia-related cohort resources spanning cognitively normal aging (CN), mild cognitive impairment (MCI), and AD. Metabolites were mapped to curated pathways and summarized into pathway activity scores across five domains: energy metabolism, amino acid metabolism, lipid metabolism, inflammation/oxidative stress, and microbiome-linked metabolism. We evaluated associations among physical activity, diet quality, pathway activity scores, and functional outcomes, including activities of daily living, gait speed, grip strength, global cognition, composite function, and frailty. To summarize pathway patterns jointly associated with physical activity and diet quality, we derived a lifestyle-modulated metabolic pathway score (LMPS) using elastic net regression with cross-validation, out-of-fold score estimation, and bootstrap stability assessment. Lifestyle-associated pathway activity showed coordinated patterns across metabolic domains and was associated with functional performance across cognitive groups. Higher LMPS values were associated with better physical and cognitive function and lower frailty, with graded differences observed across CN, MCI, and AD. Internal robustness analyses indicated greater stability at the pathway-domain level than at the individual-pathway coefficient level. Sensitivity analyses adjusting for cognitive group attenuated but did not eliminate the directionally consistent associations between LMPS and major functional outcomes. Convergent pathway patterns involved mitochondrial energy metabolism, lipid remodeling, inflammatory regulation, and microbiome-related metabolism. Pathway-level blood metabolomics identified lifestyle-associated metabolic patterns related to multidimensional functional outcomes across the cognitive aging spectrum. LMPS provides a data-driven summary of lifestyle-associated pathway variation in this cohort and may help generate hypotheses about metabolic correlates of functional performance. Independent and longitudinal validation will be required to determine its reproducibility, temporal relevance, and translational utility.},
}
RevDate: 2026-06-28
CmpDate: 2026-06-28
Biologics for cardiovascular diseases: from bench to bedside.
Signal transduction and targeted therapy, 11(1):.
The rise of biologics, including recombinant proteins, gene therapies, and cell therapies, is reshaping the landscape of modern therapeutics, offering new strategies to address previously "undruggable" targets. Cardiovascular diseases (CVDs), the leading cause of mortality worldwide, remain inadequately managed by traditional therapies, but biologics offer a paradigm shift from symptom control to disease modification. This review provides a comprehensive analysis of biologics in cardiovascular medicine, focusing on five key biological processes: cardiac regeneration, cardiac reverse remodeling, genetic cardiomyopathy correction, vascular function modulation, and lipid metabolism modulation. Advances in cardiac regeneration are highlighted by the transplantation of pluripotent stem cells, direct reprogramming, stimulation of endogenous adult cardiomyocyte proliferation, and noncell strategies, all of which aim to restore cardiac tissue integrity. In reverse cardiac remodeling, therapies targeting key signaling pathways, metabolic processes, and contractility-enhancing agents offer promising new approaches for CVD management. The development of gene therapies targeting genetic cardiomyopathies, including gene replacement, genome editing, and gene silencing, is discussed. For vascular function modulation, therapies targeting angiotensinogen, natriuretic peptide receptor 1, and the gut microbiome have been explored as innovative approaches to regulate vascular tone and hemodynamics. Finally, lipid modulation therapies, including agents targeting proprotein convertase subtilisin/kexin type 9 (PCSK9) and atherogenic lipoproteins, have redefined the management of dyslipidemia and cardiovascular risk. Collectively, these advancements underscore the transformative potential of biologics to provide targeted, personalized, and disease-modifying treatments for CVD. By addressing both the pathophysiological roots and clinical manifestations of CVDs, biologics represent a promising frontier in cardiovascular medicine.
Additional Links: PMID-42366210
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Citation:
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@article {pmid42366210,
year = {2026},
author = {Sun, X and Wang, X and Jia, R and Tang, J and Zeng, X and Zhao, F and Zeng, F and Huang, N and Li, J and Cui, K},
title = {Biologics for cardiovascular diseases: from bench to bedside.},
journal = {Signal transduction and targeted therapy},
volume = {11},
number = {1},
pages = {},
pmid = {42366210},
issn = {2059-3635},
mesh = {Humans ; *Cardiovascular Diseases/genetics/therapy/pathology/metabolism ; Proprotein Convertase 9/genetics ; *Biological Products/therapeutic use ; Animals ; *Genetic Therapy ; Lipid Metabolism/genetics/drug effects ; },
abstract = {The rise of biologics, including recombinant proteins, gene therapies, and cell therapies, is reshaping the landscape of modern therapeutics, offering new strategies to address previously "undruggable" targets. Cardiovascular diseases (CVDs), the leading cause of mortality worldwide, remain inadequately managed by traditional therapies, but biologics offer a paradigm shift from symptom control to disease modification. This review provides a comprehensive analysis of biologics in cardiovascular medicine, focusing on five key biological processes: cardiac regeneration, cardiac reverse remodeling, genetic cardiomyopathy correction, vascular function modulation, and lipid metabolism modulation. Advances in cardiac regeneration are highlighted by the transplantation of pluripotent stem cells, direct reprogramming, stimulation of endogenous adult cardiomyocyte proliferation, and noncell strategies, all of which aim to restore cardiac tissue integrity. In reverse cardiac remodeling, therapies targeting key signaling pathways, metabolic processes, and contractility-enhancing agents offer promising new approaches for CVD management. The development of gene therapies targeting genetic cardiomyopathies, including gene replacement, genome editing, and gene silencing, is discussed. For vascular function modulation, therapies targeting angiotensinogen, natriuretic peptide receptor 1, and the gut microbiome have been explored as innovative approaches to regulate vascular tone and hemodynamics. Finally, lipid modulation therapies, including agents targeting proprotein convertase subtilisin/kexin type 9 (PCSK9) and atherogenic lipoproteins, have redefined the management of dyslipidemia and cardiovascular risk. Collectively, these advancements underscore the transformative potential of biologics to provide targeted, personalized, and disease-modifying treatments for CVD. By addressing both the pathophysiological roots and clinical manifestations of CVDs, biologics represent a promising frontier in cardiovascular medicine.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Cardiovascular Diseases/genetics/therapy/pathology/metabolism
Proprotein Convertase 9/genetics
*Biological Products/therapeutic use
Animals
*Genetic Therapy
Lipid Metabolism/genetics/drug effects
RevDate: 2026-06-28
Deep metagenomics uncovers functional adaptations and pathogenic risks in the gut microbiome of Antarctic fur seals (Arctocephalus gazella).
Environmental microbiome pii:10.1186/s40793-026-00919-2 [Epub ahead of print].
The Antarctic fur seal (Arctocephalus gazella) plays a key role in the Antarctic marine ecosystem by regulating krill, fish, and cephalopod populations through selective foraging, promoting Southern Ocean productivity via excretion, and influencing coastal island ecosystems during breeding season. Despite the importance of the gut microbiota in reflecting diet, health, and environmental adaptation, the gut microbiome of the Antarctic fur seal remains poorly characterized. To address this gap and evaluate its potential as a bioindicator of Antarctic marine environmental health, we employed shotgun metagenomics and 16S rRNA amplicon sequencing on fresh fecal samples collected from four Antarctic fur seals (designated S59, S62, S63, and S64) at King George Island, Western Antarctica. Despite inter-individual variation, both approaches identified Bacillota as the dominant phylum but showed genus-level discrepancies, with Fusobacterium prevailing in metagenomes and Clostridium in 16S amplicons. Viral communities constituted up to 5.3% of the microbiome, including an immunodeficiency-associated Lentivirus. Chitin-degrading capacity was ubiquitous, consistent with the host's krill-based diet. Metagenome-assembled genomes (MAGs) resolved distinct taxonomic contributions to discrete steps of chitin hydrolysis, suggesting that complete depolymerization requires metabolic cross-feeding among functionally complementary taxa. Notably, Helicobacter MAGs were abundant in individual S62, suggesting potential pathogenicity. Additionally, 16 antibiotic resistance gene types were detected, with bacitracin, polymyxin, and multidrug resistance dominating the resistome. These findings not only elucidate the community composition, functional potential, and ecological adaptation of the Antarctic fur seal gut microbiota but also establish a comprehensive baseline for assessing environmental change and human impacts on the Antarctic marine ecosystem, thereby offering valuable scientific data and methodological insights for the conservation of polar marine mammals.
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PubMed:
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@article {pmid42366391,
year = {2026},
author = {Lai, T and Liu, Y and Duan, Z and Su, S and Ding, H and Dai, Y and Gao, M and Ji, M and Liao, L},
title = {Deep metagenomics uncovers functional adaptations and pathogenic risks in the gut microbiome of Antarctic fur seals (Arctocephalus gazella).},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-026-00919-2},
pmid = {42366391},
issn = {2524-6372},
support = {2022YFC2807501//National Key Research and Development Program of China/ ; 42476264//National Natural Science Foundation of China/ ; },
abstract = {The Antarctic fur seal (Arctocephalus gazella) plays a key role in the Antarctic marine ecosystem by regulating krill, fish, and cephalopod populations through selective foraging, promoting Southern Ocean productivity via excretion, and influencing coastal island ecosystems during breeding season. Despite the importance of the gut microbiota in reflecting diet, health, and environmental adaptation, the gut microbiome of the Antarctic fur seal remains poorly characterized. To address this gap and evaluate its potential as a bioindicator of Antarctic marine environmental health, we employed shotgun metagenomics and 16S rRNA amplicon sequencing on fresh fecal samples collected from four Antarctic fur seals (designated S59, S62, S63, and S64) at King George Island, Western Antarctica. Despite inter-individual variation, both approaches identified Bacillota as the dominant phylum but showed genus-level discrepancies, with Fusobacterium prevailing in metagenomes and Clostridium in 16S amplicons. Viral communities constituted up to 5.3% of the microbiome, including an immunodeficiency-associated Lentivirus. Chitin-degrading capacity was ubiquitous, consistent with the host's krill-based diet. Metagenome-assembled genomes (MAGs) resolved distinct taxonomic contributions to discrete steps of chitin hydrolysis, suggesting that complete depolymerization requires metabolic cross-feeding among functionally complementary taxa. Notably, Helicobacter MAGs were abundant in individual S62, suggesting potential pathogenicity. Additionally, 16 antibiotic resistance gene types were detected, with bacitracin, polymyxin, and multidrug resistance dominating the resistome. These findings not only elucidate the community composition, functional potential, and ecological adaptation of the Antarctic fur seal gut microbiota but also establish a comprehensive baseline for assessing environmental change and human impacts on the Antarctic marine ecosystem, thereby offering valuable scientific data and methodological insights for the conservation of polar marine mammals.},
}
RevDate: 2026-06-28
The gastrointestinal microbiome and constituent short-chain fatty acids: a narrative review of an underexplored axis in acute lymphoblastic leukemia.
Gut pathogens pii:10.1186/s13099-026-00855-z [Epub ahead of print].
Acute Lymphoblastic Leukemia (ALL) is an aggressive malignancy of lymphoid progenitors, and remains the most commonly diagnosed hematological cancer in the pediatric population. Although 5-year overall survival rates now exceed 90%, standard-of-care therapies are associated with substantial acute and long-term toxicities, underscoring the need for novel and supportive strategies that preserve treatment efficacy whilst reducing dose-limiting side effects. Increasing evidence linking the microbiome to therapeutic response and toxicity in oncology highlights the potential relevance of microbial-derived metabolites, particularly short-chain fatty acids (SCFAs), in hematological malignancies. This review critically examines the emerging, yet limited, evidence supporting a role for SCFAs in ALL, integrating mechanistic insights from metabolic, immunological, and oncological studies to propose biologically plausible pathways of involvement. Specifically, we suggest how SCFAs may influence treatment response, mitigate therapy-related toxicity, reduce treatment-related morbidity and modulate early-life factors associated with ALL risk. Whilst direct ALL-specific evidence remains sparse, we propose that SCFAs represent a compelling and underexplored axis for microbiome-ALL research, and we aim to stimulate targeted experimental and clinical investigations to define their therapeutic potential.
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@article {pmid42366393,
year = {2026},
author = {Cheney, CV and Page, EC and Yeung, DT and White, DL},
title = {The gastrointestinal microbiome and constituent short-chain fatty acids: a narrative review of an underexplored axis in acute lymphoblastic leukemia.},
journal = {Gut pathogens},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13099-026-00855-z},
pmid = {42366393},
issn = {1757-4749},
abstract = {Acute Lymphoblastic Leukemia (ALL) is an aggressive malignancy of lymphoid progenitors, and remains the most commonly diagnosed hematological cancer in the pediatric population. Although 5-year overall survival rates now exceed 90%, standard-of-care therapies are associated with substantial acute and long-term toxicities, underscoring the need for novel and supportive strategies that preserve treatment efficacy whilst reducing dose-limiting side effects. Increasing evidence linking the microbiome to therapeutic response and toxicity in oncology highlights the potential relevance of microbial-derived metabolites, particularly short-chain fatty acids (SCFAs), in hematological malignancies. This review critically examines the emerging, yet limited, evidence supporting a role for SCFAs in ALL, integrating mechanistic insights from metabolic, immunological, and oncological studies to propose biologically plausible pathways of involvement. Specifically, we suggest how SCFAs may influence treatment response, mitigate therapy-related toxicity, reduce treatment-related morbidity and modulate early-life factors associated with ALL risk. Whilst direct ALL-specific evidence remains sparse, we propose that SCFAs represent a compelling and underexplored axis for microbiome-ALL research, and we aim to stimulate targeted experimental and clinical investigations to define their therapeutic potential.},
}
RevDate: 2026-06-29
Comments on: The Biliary Multi-Omics Landscape: Integrating Microbiome and Metabolomics in Gallbladder Cancer: Biliary Stasis, Microbial Viability, and Host Antimicrobial Defenses.
Additional Links: PMID-42366510
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@article {pmid42366510,
year = {2026},
author = {Bather, K},
title = {Comments on: The Biliary Multi-Omics Landscape: Integrating Microbiome and Metabolomics in Gallbladder Cancer: Biliary Stasis, Microbial Viability, and Host Antimicrobial Defenses.},
journal = {Journal of gastroenterology and hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jgh.70538},
pmid = {42366510},
issn = {1440-1746},
}
RevDate: 2026-06-29
CmpDate: 2026-06-29
[Microbiota and microbiome of the lacrimal drainage system].
Vestnik oftalmologii, 142(3):91-100.
This review analyzes current concepts of the role of the microbiota and microbiome in the physiology and pathology of the human lacrimal drainage system (LDS). The terms are clearly differentiated: microbiota is the collection of living microorganisms, whereas microbiome also includes their genetic material and habitat. The article describes anatomical features of the LDS and involutional changes in adults (atrophy of the lacrimal puncta, canalicular fibrosis, and nasolacrimal duct stenosis), which predispose to tear stagnation and inflammation. The review includes a comparative analysis of the microbiological spectrum in healthy individuals and patients with dacryocystitis and canaliculitis. The composition of the flora was found to differ substantially depending on age (predominance of S. pneumoniae in children versus Staphylococcus spp. in adults) and geographical region. Metagenomic sequencing data (16S rRNA) demonstrate significantly greater microbial diversity compared with conventional culture methods, revealing a broad spectrum of aerobes, anaerobes, and fungi. The work pays particular attention to regional resistance patterns, including the high prevalence of methicillin-resistant Staphylococcus aureus (MRSA) in several Asian countries. Based on the literature data this study proposes and algorithm for empirical antibacterial therapy, taking into account the likely pathogens, as well as the indications for surgical correction, and emphasizes the prospects for creating a national map of the LDS microbiome in the Russian Federation to optimize treatment strategies for dacryocystitis and dacryostenosis.
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@article {pmid42366665,
year = {2026},
author = {Kuzbekov, SR},
title = {[Microbiota and microbiome of the lacrimal drainage system].},
journal = {Vestnik oftalmologii},
volume = {142},
number = {3},
pages = {91-100},
doi = {10.17116/oftalma202614203191},
pmid = {42366665},
issn = {0042-465X},
mesh = {Humans ; *Microbiota ; *Lacrimal Apparatus/microbiology/physiopathology/pathology ; *Dacryocystitis/microbiology/diagnosis/physiopathology ; *Lacrimal Duct Obstruction/diagnosis ; Anti-Bacterial Agents/pharmacology ; },
abstract = {This review analyzes current concepts of the role of the microbiota and microbiome in the physiology and pathology of the human lacrimal drainage system (LDS). The terms are clearly differentiated: microbiota is the collection of living microorganisms, whereas microbiome also includes their genetic material and habitat. The article describes anatomical features of the LDS and involutional changes in adults (atrophy of the lacrimal puncta, canalicular fibrosis, and nasolacrimal duct stenosis), which predispose to tear stagnation and inflammation. The review includes a comparative analysis of the microbiological spectrum in healthy individuals and patients with dacryocystitis and canaliculitis. The composition of the flora was found to differ substantially depending on age (predominance of S. pneumoniae in children versus Staphylococcus spp. in adults) and geographical region. Metagenomic sequencing data (16S rRNA) demonstrate significantly greater microbial diversity compared with conventional culture methods, revealing a broad spectrum of aerobes, anaerobes, and fungi. The work pays particular attention to regional resistance patterns, including the high prevalence of methicillin-resistant Staphylococcus aureus (MRSA) in several Asian countries. Based on the literature data this study proposes and algorithm for empirical antibacterial therapy, taking into account the likely pathogens, as well as the indications for surgical correction, and emphasizes the prospects for creating a national map of the LDS microbiome in the Russian Federation to optimize treatment strategies for dacryocystitis and dacryostenosis.},
}
MeSH Terms:
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Humans
*Microbiota
*Lacrimal Apparatus/microbiology/physiopathology/pathology
*Dacryocystitis/microbiology/diagnosis/physiopathology
*Lacrimal Duct Obstruction/diagnosis
Anti-Bacterial Agents/pharmacology
RevDate: 2026-06-29
CmpDate: 2026-06-29
Microbiota and serum tumor markers in patients with pancreatic cystic neoplasm.
Polski przeglad chirurgiczny, 97(3):46-52.
Introduction: One of the main precursory lesions for pancreatic carcinoma is pancreatic cystic neoplasms (PCN). Differentiation between the various types of cysts is a clinical challenge.
Aim: The aim of the study was to assess the microbiological status and the serum tumor markers compared with biochemical parameters and histopathological results in patients with PCN.
Materials and methods: A total of 59 patients diagnosed with PCN and treated between 2022 and 2023 were included in the study. Preoperative levels of serum inflammatory and tumor markers were assessed. Bacterial culture samples were collected from the nasal vestibule, the skin of the groin, and from cyst fluid and bile (in the case of cholecystectomy), and histopathology reports were examined.
Results: Seven (41.18%) patients with positive culture had cancer compared with 12 (28.57%) negative patients (p = 0.35). In the cystic pancreatic cancer group CA19-9 level was higher (190.43 427.80 ng/ml) than among benign lesions (100.16 506.22 ng/ml) (p = 0.02). Among patients with positive culture, C-reactive protein (CRP) level was higher (31.84 70.91 mg/l) comparing with patients with negative culture (10.94 28.75 mg/l; p = 0.03). Serum alpha fetoprotein (AFP) levels were lower in patients with positive culture (2.34 1.13 vs. 4.08 2.44 ng/ml, respectively; p = 0.04). Furthermore, CRP level was positively correlated with CA19-9, and CA125 levels and negatively correlated with AFP level and hospitalization period.
Conclusions: Patients with positive cultures tended to have a higher incidence of cancers, CRP levels, and longer hospitalization periods. Further analyses of pancreatic cyst microbiome are definitely required.
Additional Links: PMID-42366719
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PubMed:
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@article {pmid42366719,
year = {2025},
author = {Malik, P and Tyczkowska-Sieroń, E and Durczyński, A and Hogendorf, P and Strzelczyk, J and Wlaźlak, M and Grzegory, A},
title = {Microbiota and serum tumor markers in patients with pancreatic cystic neoplasm.},
journal = {Polski przeglad chirurgiczny},
volume = {97},
number = {3},
pages = {46-52},
doi = {10.5604/01.3001.0054.9921},
pmid = {42366719},
issn = {2299-2847},
mesh = {Humans ; Female ; *Pancreatic Neoplasms/blood/microbiology/pathology ; Male ; *Biomarkers, Tumor/blood ; Middle Aged ; Aged ; Adult ; *Microbiota ; *Pancreatic Cyst/blood/microbiology ; CA-19-9 Antigen/blood ; },
abstract = {Introduction: One of the main precursory lesions for pancreatic carcinoma is pancreatic cystic neoplasms (PCN). Differentiation between the various types of cysts is a clinical challenge.
Aim: The aim of the study was to assess the microbiological status and the serum tumor markers compared with biochemical parameters and histopathological results in patients with PCN.
Materials and methods: A total of 59 patients diagnosed with PCN and treated between 2022 and 2023 were included in the study. Preoperative levels of serum inflammatory and tumor markers were assessed. Bacterial culture samples were collected from the nasal vestibule, the skin of the groin, and from cyst fluid and bile (in the case of cholecystectomy), and histopathology reports were examined.
Results: Seven (41.18%) patients with positive culture had cancer compared with 12 (28.57%) negative patients (p = 0.35). In the cystic pancreatic cancer group CA19-9 level was higher (190.43 427.80 ng/ml) than among benign lesions (100.16 506.22 ng/ml) (p = 0.02). Among patients with positive culture, C-reactive protein (CRP) level was higher (31.84 70.91 mg/l) comparing with patients with negative culture (10.94 28.75 mg/l; p = 0.03). Serum alpha fetoprotein (AFP) levels were lower in patients with positive culture (2.34 1.13 vs. 4.08 2.44 ng/ml, respectively; p = 0.04). Furthermore, CRP level was positively correlated with CA19-9, and CA125 levels and negatively correlated with AFP level and hospitalization period.
Conclusions: Patients with positive cultures tended to have a higher incidence of cancers, CRP levels, and longer hospitalization periods. Further analyses of pancreatic cyst microbiome are definitely required.},
}
MeSH Terms:
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Humans
Female
*Pancreatic Neoplasms/blood/microbiology/pathology
Male
*Biomarkers, Tumor/blood
Middle Aged
Aged
Adult
*Microbiota
*Pancreatic Cyst/blood/microbiology
CA-19-9 Antigen/blood
RevDate: 2026-06-29
Full-length 16S rRNA metabarcoding characterization of facial skin microbiota in acne patients: a case study in the Mekong Delta of Viet Nam.
Dermatology reports [Epub ahead of print].
Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous unit in which skin microbiome dysbiosis plays a key pathogenic role. This study, based on full-length 16S rRNA gene amplicon sequencing (V1-V9), characterized facial microbial diversity in 45 participants classified as healthy (n=15), mild acne (n=15), and moderate-severe acne (n=15), using pooled samples for downstream microbiome analyses. Samples from the skin surface and sebaceous follicles were analyzed by 16S rRNA (V1-V9) sequencing using Illumina MiniSeq and processed via QIIME2. Alpha diversity (observed taxa, Shannon index), beta diversity (Bray-Curtis dissimilarity, permutational multivariate analysis of variance [PERMANOVA]), and biomarker taxa (linear discriminant analysis effect size [LEfSe]) were assessed. Bacillota, mainly Staphylococcus spp., predominated on the skin surface, with relative abundance increasing with acne severity, whereas follicles were dominated by Cutibacterium acnes (Actinomycetota). Follicular samples showed lower richness and Shannon diversity than surface samples, though intergroup differences were not significant. Principal coordinates analysis (PCoA) explained >65% of variation, revealing greater dispersion among surface communities but no clear clustering by severity (PERMANOVA p>0.3). LEfSe identified distinct bacterial biomarkers across clinical groups. Overall, site-specific microbial shifts - particularly C. acnes and Staphylococcus dysbiosis - appear central to acne development, suggesting microbiome-targeted interventions as potential therapeutic strategies.
Additional Links: PMID-42366944
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PubMed:
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@article {pmid42366944,
year = {2026},
author = {Tu, XM and Nguyen, PT and Nguyen, TN and Nguyen, LTT and Tran, DN and Huynh, PX},
title = {Full-length 16S rRNA metabarcoding characterization of facial skin microbiota in acne patients: a case study in the Mekong Delta of Viet Nam.},
journal = {Dermatology reports},
volume = {},
number = {},
pages = {},
doi = {10.4081/dr.2026.10643},
pmid = {42366944},
issn = {2036-7392},
abstract = {Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous unit in which skin microbiome dysbiosis plays a key pathogenic role. This study, based on full-length 16S rRNA gene amplicon sequencing (V1-V9), characterized facial microbial diversity in 45 participants classified as healthy (n=15), mild acne (n=15), and moderate-severe acne (n=15), using pooled samples for downstream microbiome analyses. Samples from the skin surface and sebaceous follicles were analyzed by 16S rRNA (V1-V9) sequencing using Illumina MiniSeq and processed via QIIME2. Alpha diversity (observed taxa, Shannon index), beta diversity (Bray-Curtis dissimilarity, permutational multivariate analysis of variance [PERMANOVA]), and biomarker taxa (linear discriminant analysis effect size [LEfSe]) were assessed. Bacillota, mainly Staphylococcus spp., predominated on the skin surface, with relative abundance increasing with acne severity, whereas follicles were dominated by Cutibacterium acnes (Actinomycetota). Follicular samples showed lower richness and Shannon diversity than surface samples, though intergroup differences were not significant. Principal coordinates analysis (PCoA) explained >65% of variation, revealing greater dispersion among surface communities but no clear clustering by severity (PERMANOVA p>0.3). LEfSe identified distinct bacterial biomarkers across clinical groups. Overall, site-specific microbial shifts - particularly C. acnes and Staphylococcus dysbiosis - appear central to acne development, suggesting microbiome-targeted interventions as potential therapeutic strategies.},
}
RevDate: 2026-06-29
Engineered nanoparticles at the redox interface: Rewiring ROS signaling and stress responses in plants.
Journal of integrative plant biology [Epub ahead of print].
Engineered nanoparticles (ENPs) are increasingly recognized as promising tools for modulating plant stress responses; however, their underlying mechanisms and associated risks remain under debate. This review integrates recent advances showing that ENPs can reprogram plant redox homeostasis through multiple pathways, including direct surface redox activity, nanozyme-like catalysis, ion release, and disruption of organellar electron transport. In addition, ENPs influence membrane physicochemical properties, transcriptional regulation, metabolic fluxes, hormonal crosstalk, epigenetic modifications, and the structure of the plant-associated microbiome. These processes produce distinct reactive oxygen and nitrogen species (ROS/RNS) signatures that activate Ca[2+] fluxes, mitogen-activated protein kinase (MAPK) cascades, and downstream transcriptional networks. We emphasize the importance of dose-dependent-often hormetic-responses, the critical role of the rhizosphere microbiome, and the application of spatially resolved techniques (e.g., μ-XRF, NanoSIMS, and spatial omics) to link NP fate with localized redox dynamics. Finally, we propose a safe-by-design framework that incorporates standardized NP characterization, appropriate ionic and inert controls, and predictive modeling approaches. This framework aims to facilitate the risk-informed and sustainable deployment of ENPs in agriculture.
Additional Links: PMID-42367109
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PubMed:
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@article {pmid42367109,
year = {2026},
author = {Jamei, M and Jamei, R},
title = {Engineered nanoparticles at the redox interface: Rewiring ROS signaling and stress responses in plants.},
journal = {Journal of integrative plant biology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jipb.70316},
pmid = {42367109},
issn = {1744-7909},
abstract = {Engineered nanoparticles (ENPs) are increasingly recognized as promising tools for modulating plant stress responses; however, their underlying mechanisms and associated risks remain under debate. This review integrates recent advances showing that ENPs can reprogram plant redox homeostasis through multiple pathways, including direct surface redox activity, nanozyme-like catalysis, ion release, and disruption of organellar electron transport. In addition, ENPs influence membrane physicochemical properties, transcriptional regulation, metabolic fluxes, hormonal crosstalk, epigenetic modifications, and the structure of the plant-associated microbiome. These processes produce distinct reactive oxygen and nitrogen species (ROS/RNS) signatures that activate Ca[2+] fluxes, mitogen-activated protein kinase (MAPK) cascades, and downstream transcriptional networks. We emphasize the importance of dose-dependent-often hormetic-responses, the critical role of the rhizosphere microbiome, and the application of spatially resolved techniques (e.g., μ-XRF, NanoSIMS, and spatial omics) to link NP fate with localized redox dynamics. Finally, we propose a safe-by-design framework that incorporates standardized NP characterization, appropriate ionic and inert controls, and predictive modeling approaches. This framework aims to facilitate the risk-informed and sustainable deployment of ENPs in agriculture.},
}
RevDate: 2026-06-29
Engineered diazotrophs with host-inducible nitrogen supply systems: Transforming rice farming through innovative nitrogen biofertilizers.
Journal of integrative plant biology [Epub ahead of print].
Nitrogen pollution represents a critical challenge in the 21st century, highlighting the urgent need for sustainable alternatives to industrial nitrogen fixation. Diazotrophic bacteria, which uniquely convert dinitrogen (N2) into bioavailable forms, offer a promising solution through biological nitrogen fixation (BNF). These bacteria typically perform nitrogen fixation under nitrogen-limited conditions. Over the past 50 years, extensive research has elucidated the molecular mechanisms and regulatory pathways governing BNF. Recent microbiome studies have revealed that wild rice accessions harbor a greater abundance of diazotrophic bacteria, whereas a substantial proportion of these beneficial microbes have been lost in modern cultivated varieties. Advancements in synthetic biology have enabled the engineering of nitrogen‑exporting diazotrophs, potentially reducing dependence on industrial nitrogen fertilizers. This review emphasizes the importance of targeted research to develop customized diazotrophic microbes in conjunction with synthetic microbial community that can serve as nitrogen exporters for rice. Furthermore, it highlights the necessity of identifying rice cultivars that are particularly responsive to these microbial interventions. Finally, it provides a comprehensive roadmap addressing key challenges and opportunities in deploying BNF to supplement plant nitrogen nutrition and advance sustainable agriculture.
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@article {pmid42367143,
year = {2026},
author = {Sengupta, A and Sahoo, RN and Sinharoy, S},
title = {Engineered diazotrophs with host-inducible nitrogen supply systems: Transforming rice farming through innovative nitrogen biofertilizers.},
journal = {Journal of integrative plant biology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jipb.70320},
pmid = {42367143},
issn = {1744-7909},
abstract = {Nitrogen pollution represents a critical challenge in the 21st century, highlighting the urgent need for sustainable alternatives to industrial nitrogen fixation. Diazotrophic bacteria, which uniquely convert dinitrogen (N2) into bioavailable forms, offer a promising solution through biological nitrogen fixation (BNF). These bacteria typically perform nitrogen fixation under nitrogen-limited conditions. Over the past 50 years, extensive research has elucidated the molecular mechanisms and regulatory pathways governing BNF. Recent microbiome studies have revealed that wild rice accessions harbor a greater abundance of diazotrophic bacteria, whereas a substantial proportion of these beneficial microbes have been lost in modern cultivated varieties. Advancements in synthetic biology have enabled the engineering of nitrogen‑exporting diazotrophs, potentially reducing dependence on industrial nitrogen fertilizers. This review emphasizes the importance of targeted research to develop customized diazotrophic microbes in conjunction with synthetic microbial community that can serve as nitrogen exporters for rice. Furthermore, it highlights the necessity of identifying rice cultivars that are particularly responsive to these microbial interventions. Finally, it provides a comprehensive roadmap addressing key challenges and opportunities in deploying BNF to supplement plant nitrogen nutrition and advance sustainable agriculture.},
}
RevDate: 2026-06-29
CmpDate: 2026-06-29
Cnidarian-algal partnerships structure bacterial communities during strobilation in Cassiopea xamachana.
ISME communications, 6(1):ycag147.
Cnidarian-algal (Symbiodiniaceae) symbioses rely on complex interactions among the cnidarian host, algal symbionts, and associated bacterial communities. In the upside-down jellyfish Cassiopea xamachana, the polyp-to-medusa transition (strobilation) requires the establishment of symbiosis with Symbiodiniaceae algal partners, yet bacterial community dynamics during this developmental process remain unknown. Here, we experimentally induced symbiosis in aposymbiotic polyps using four algal treatments: xenic Symbiodinium microadriaticum (native symbiont), xenic Breviolum minutum, antibiotic-treated B. minutum, and a photosynthetically impaired B. minutum mutant. We combined 16S rRNA gene sequencing with measurements of photosynthetic efficiency, asexual budding, and algal surface N-glycan profiles to characterize holobiont assembly during symbiosis onset and strobilation. Algal treatment structured bacterial communities in both algal cultures and polyp tissues. Our analyses identified a set of amplicon sequence variants that consistently distinguished strobilating polyps from non-strobilating aposymbiotic and mutant polyps, in addition to potential bacterial biomarkers associated with successful metamorphosis. Strobilation was associated with the enrichment of bacterial communities putatively involved in sulfur and nitrogen cycling, whereas non-strobilating aposymbiotic and mutant polyps were characterized by opportunistic bacteria and increased community variability. Together, these results reveal coordinated changes in algal physiology, surface glycan profiles, and bacterial community structure associated with successful strobilation in C. xamachana and support a model in which tripartite host-alga-bacteria interactions influence cnidarian life stage transitions.
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@article {pmid42367188,
year = {2026},
author = {Montesanto, F and McCauley, M and Bedgood, SA and Miner, C and Steinworth, B and Sharp, V and Ohdera, AH and Oluokun, A and Fowowe, M and Oluokun, O and Mechref, Y and Xiang, T and Medina, M and Weis, VM and Martindale, MQ and Loesgen, S},
title = {Cnidarian-algal partnerships structure bacterial communities during strobilation in Cassiopea xamachana.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag147},
pmid = {42367188},
issn = {2730-6151},
abstract = {Cnidarian-algal (Symbiodiniaceae) symbioses rely on complex interactions among the cnidarian host, algal symbionts, and associated bacterial communities. In the upside-down jellyfish Cassiopea xamachana, the polyp-to-medusa transition (strobilation) requires the establishment of symbiosis with Symbiodiniaceae algal partners, yet bacterial community dynamics during this developmental process remain unknown. Here, we experimentally induced symbiosis in aposymbiotic polyps using four algal treatments: xenic Symbiodinium microadriaticum (native symbiont), xenic Breviolum minutum, antibiotic-treated B. minutum, and a photosynthetically impaired B. minutum mutant. We combined 16S rRNA gene sequencing with measurements of photosynthetic efficiency, asexual budding, and algal surface N-glycan profiles to characterize holobiont assembly during symbiosis onset and strobilation. Algal treatment structured bacterial communities in both algal cultures and polyp tissues. Our analyses identified a set of amplicon sequence variants that consistently distinguished strobilating polyps from non-strobilating aposymbiotic and mutant polyps, in addition to potential bacterial biomarkers associated with successful metamorphosis. Strobilation was associated with the enrichment of bacterial communities putatively involved in sulfur and nitrogen cycling, whereas non-strobilating aposymbiotic and mutant polyps were characterized by opportunistic bacteria and increased community variability. Together, these results reveal coordinated changes in algal physiology, surface glycan profiles, and bacterial community structure associated with successful strobilation in C. xamachana and support a model in which tripartite host-alga-bacteria interactions influence cnidarian life stage transitions.},
}
RevDate: 2026-06-29
CmpDate: 2026-06-29
Antibiotic course frequency and recovery strategies alter gut microbial composition and metabolism.
ISME communications, 6(1):ycag145.
Antibiotics profoundly alter the gut microbiome, but how exposure frequencies shape microbial recovery remains unclear. The effectiveness of post-antibiotic interventions, e.g. probiotics or autologous fecal microbiota transplantation, (aFMT) requires further exploration. This study investigated how antibiotic course timing and recovery strategies influence gut microbiome and metabolism in male Wistar rats. A single oral dose of vancomycin-ciprofloxacin (VC) caused rapid urinary and fecal metabolic shifts within 8-12 h and reduced bacterial α-diversity in cecal and colonic contents. When three VC courses were administered at regular (every 3 weeks; VCr) or irregular (1-3 weeks; VCi) intervals, VCr showed greater suppression of fecal α-diversity and stronger disruption of amino acid and host-microbial co-metabolism than VCi. Over the 3-week recovery period, VCr exhibited slower fecal α-diversity restoration; at week 3, β-diversity remained significantly different between groups, and cecal butyrate levels were persistently reduced in VCr. Both groups showed elevated levels of 5-aminovalerate in feces and colon compared with controls, whereas only VCi showed reductions in jejunal and ileal amino acids. Probiotics or aFMT had limited influence on small intestinal alterations, though aFMT accelerated fecal α-diversity recovery, and both interventions promoted partial normalization of fecal amino acids and 5-aminovalerate, without achieving complete restoration. Overall, shorter antibiotic intervals exerted stronger effects on the small intestinal luminal chemical environment, whereas longer intervals led to greater suppression of colonic and fecal microbial metabolism. Probiotics and aFMT supported selective metabolic recovery without fully reversing antibiotics-induced disturbances, highlighting the need for more targeted restoration strategies across gastrointestinal regions.
Additional Links: PMID-42367194
PubMed:
Citation:
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@article {pmid42367194,
year = {2026},
author = {Abaakil, K and Liu, Z and Wang, M and Kuznecova, E and Sung, MSC and Marchesi, JR and Mausz, MA and Li, JV},
title = {Antibiotic course frequency and recovery strategies alter gut microbial composition and metabolism.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag145},
pmid = {42367194},
issn = {2730-6151},
abstract = {Antibiotics profoundly alter the gut microbiome, but how exposure frequencies shape microbial recovery remains unclear. The effectiveness of post-antibiotic interventions, e.g. probiotics or autologous fecal microbiota transplantation, (aFMT) requires further exploration. This study investigated how antibiotic course timing and recovery strategies influence gut microbiome and metabolism in male Wistar rats. A single oral dose of vancomycin-ciprofloxacin (VC) caused rapid urinary and fecal metabolic shifts within 8-12 h and reduced bacterial α-diversity in cecal and colonic contents. When three VC courses were administered at regular (every 3 weeks; VCr) or irregular (1-3 weeks; VCi) intervals, VCr showed greater suppression of fecal α-diversity and stronger disruption of amino acid and host-microbial co-metabolism than VCi. Over the 3-week recovery period, VCr exhibited slower fecal α-diversity restoration; at week 3, β-diversity remained significantly different between groups, and cecal butyrate levels were persistently reduced in VCr. Both groups showed elevated levels of 5-aminovalerate in feces and colon compared with controls, whereas only VCi showed reductions in jejunal and ileal amino acids. Probiotics or aFMT had limited influence on small intestinal alterations, though aFMT accelerated fecal α-diversity recovery, and both interventions promoted partial normalization of fecal amino acids and 5-aminovalerate, without achieving complete restoration. Overall, shorter antibiotic intervals exerted stronger effects on the small intestinal luminal chemical environment, whereas longer intervals led to greater suppression of colonic and fecal microbial metabolism. Probiotics and aFMT supported selective metabolic recovery without fully reversing antibiotics-induced disturbances, highlighting the need for more targeted restoration strategies across gastrointestinal regions.},
}
RevDate: 2026-06-29
CmpDate: 2026-06-29
Microbiota-miR-101 interactions in obesity-associated colorectal cancer: from barrier dysfunction to precision therapeutic strategies.
Frontiers in pharmacology, 17:1850919.
Colorectal cancer (CRC) remains a leading cause of cancer-related morbidity and mortality worldwide, with obesity recognized as a major modifiable risk factor. Obesity-associated CRC is characterized by systemic low-grade inflammation, altered lipid metabolism, and gut microbial dysbiosis, all of which converge to create a pro-inflammatory niche. Emerging evidence implicates murine miR-101a/b, an ortholog of the human miR-101 family, as a key molecular mediator linking metabolic dysfunction, promoting inflammation, endotoxemia, and affecting epithelial homeostasis. Traditionally, the miR-101 family is considered a tumor suppressor by repressing oncogenes such as EZH2, MCL-1, and COX-2; miR-101a appears to exhibit a paradoxical microenvironment-modulating role in obese colon. Recent studies demonstrate that elevated dietary and microbiota-derived ethanolamine induces miR-101a overexpression in colonic epithelial cells. Mechanistically, miR-101a directly destabilizes the mRNA encoding the tight junction protein (ZO-1; TJP1), thereby impairing epithelial barrier integrity, increasing intestinal permeability, and promoting chronic inflammation. The chronic inflammation promotes epithelial proliferation, generates mutagenic reactive oxygen species, and activates pro-survival pathways such as STAT3 and AKT, collectively contributing to a tumor-permissive microenvironment that may support adenoma initiation and progression. The resulting chronic inflammatory milieu promotes epithelial stress, proliferative signaling, and accumulation of DNA damage, contributing to conditions that favor colorectal carcinogenesis. Importantly, this ethanolamine-miR-101a axis represents a novel mechanistic link between diet, microbiota, and cancer biology. Translationally, miR-101a holds promise as a biomarker of early barrier dysfunction and CRC risk, as detectable in tissue, serum, or fecal samples. Furthermore, microbiome-targeted interventions, dietary modifications, or direct inhibition of miR-101a may offer innovative therapeutic strategies. Collectively, these findings support the development of precision microbiome-miRNA-based approaches and highlight the importance of context-dependent miRNA regulation in obesity-associated CRC.
Additional Links: PMID-42367298
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Citation:
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@article {pmid42367298,
year = {2026},
author = {Mishra, SP and Jacobson, R and Wang, B and Prajapati, S and Sanberg, P and Brechot, C and Jain, S and Yadav, H},
title = {Microbiota-miR-101 interactions in obesity-associated colorectal cancer: from barrier dysfunction to precision therapeutic strategies.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1850919},
pmid = {42367298},
issn = {1663-9812},
abstract = {Colorectal cancer (CRC) remains a leading cause of cancer-related morbidity and mortality worldwide, with obesity recognized as a major modifiable risk factor. Obesity-associated CRC is characterized by systemic low-grade inflammation, altered lipid metabolism, and gut microbial dysbiosis, all of which converge to create a pro-inflammatory niche. Emerging evidence implicates murine miR-101a/b, an ortholog of the human miR-101 family, as a key molecular mediator linking metabolic dysfunction, promoting inflammation, endotoxemia, and affecting epithelial homeostasis. Traditionally, the miR-101 family is considered a tumor suppressor by repressing oncogenes such as EZH2, MCL-1, and COX-2; miR-101a appears to exhibit a paradoxical microenvironment-modulating role in obese colon. Recent studies demonstrate that elevated dietary and microbiota-derived ethanolamine induces miR-101a overexpression in colonic epithelial cells. Mechanistically, miR-101a directly destabilizes the mRNA encoding the tight junction protein (ZO-1; TJP1), thereby impairing epithelial barrier integrity, increasing intestinal permeability, and promoting chronic inflammation. The chronic inflammation promotes epithelial proliferation, generates mutagenic reactive oxygen species, and activates pro-survival pathways such as STAT3 and AKT, collectively contributing to a tumor-permissive microenvironment that may support adenoma initiation and progression. The resulting chronic inflammatory milieu promotes epithelial stress, proliferative signaling, and accumulation of DNA damage, contributing to conditions that favor colorectal carcinogenesis. Importantly, this ethanolamine-miR-101a axis represents a novel mechanistic link between diet, microbiota, and cancer biology. Translationally, miR-101a holds promise as a biomarker of early barrier dysfunction and CRC risk, as detectable in tissue, serum, or fecal samples. Furthermore, microbiome-targeted interventions, dietary modifications, or direct inhibition of miR-101a may offer innovative therapeutic strategies. Collectively, these findings support the development of precision microbiome-miRNA-based approaches and highlight the importance of context-dependent miRNA regulation in obesity-associated CRC.},
}
RevDate: 2026-06-29
Caecal microbiome transplant inhibits transmission and intestinal colonisation of Campylobacter jejuni in broiler chickens.
Poultry science and management, 3(1):13.
Campylobacter jejuni is the most frequent cause of foodborne bacterial gastroenteritis with poultry products the most frequent source of infection. C. jejuni can colonise the intestinal tract of the chicken and in particular the large blind caeca to a high level accompanied by faecal shedding and rapid transmission in flocks. As such, reducing transmission and intestinal colonisation in poultry meat production is considered a key target to reduce human infection. Whilst vaccines and feed-based approaches including modulation of the microbiome are considered most likely to reduce numbers in the chicken caeca, neither have yet shown the capacity to lead to significant reductions. We have previously shown that administration of a caecal microbiome transplant (CMT) at hatch acts to modify the microbiome, increasing diversity and reducing Enterobacteriacae levels associated with poor gut health and increased Campylobacter susceptibility. When challenged at 21 days old with C. jejuni M1 in a seeder bird infection model, birds in groups receiving CMT showed reduced transmission and significantly lower levels of C. jejuni at post-mortem examination at 35 days of age than control birds or birds treated with a commercial microflora competitive exclusion product (Aviguard). These data show that a microbiome-based intervention has the potential to inhibit C. jejuni transmission and decrease levels in the caeca at slaughter age. This is modelled to lead to a significant reduction in human cases. CMT offers a valuable tool to determine protective taxa in the chicken gut, aiding rational development of microbial interventions as well as a low-cost platform to help understand immunological development in the chicken gut.
Additional Links: PMID-42367597
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Citation:
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@article {pmid42367597,
year = {2026},
author = {Gilroy, R and Chaloner, G and Wedley, A and Richards-Rios, P and Pottenger, S and Wigley, P},
title = {Caecal microbiome transplant inhibits transmission and intestinal colonisation of Campylobacter jejuni in broiler chickens.},
journal = {Poultry science and management},
volume = {3},
number = {1},
pages = {13},
pmid = {42367597},
issn = {3005-0715},
abstract = {Campylobacter jejuni is the most frequent cause of foodborne bacterial gastroenteritis with poultry products the most frequent source of infection. C. jejuni can colonise the intestinal tract of the chicken and in particular the large blind caeca to a high level accompanied by faecal shedding and rapid transmission in flocks. As such, reducing transmission and intestinal colonisation in poultry meat production is considered a key target to reduce human infection. Whilst vaccines and feed-based approaches including modulation of the microbiome are considered most likely to reduce numbers in the chicken caeca, neither have yet shown the capacity to lead to significant reductions. We have previously shown that administration of a caecal microbiome transplant (CMT) at hatch acts to modify the microbiome, increasing diversity and reducing Enterobacteriacae levels associated with poor gut health and increased Campylobacter susceptibility. When challenged at 21 days old with C. jejuni M1 in a seeder bird infection model, birds in groups receiving CMT showed reduced transmission and significantly lower levels of C. jejuni at post-mortem examination at 35 days of age than control birds or birds treated with a commercial microflora competitive exclusion product (Aviguard). These data show that a microbiome-based intervention has the potential to inhibit C. jejuni transmission and decrease levels in the caeca at slaughter age. This is modelled to lead to a significant reduction in human cases. CMT offers a valuable tool to determine protective taxa in the chicken gut, aiding rational development of microbial interventions as well as a low-cost platform to help understand immunological development in the chicken gut.},
}
RevDate: 2026-06-29
CmpDate: 2026-06-29
The fourth trimester and challenges for the lupus patient.
EULAR rheumatology open, 1(4):403-412.
Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease that primarily affects persons of reproductive age. While SLE management during pregnancy has been previously studied, the unique challenges of the postpartum period, particularly the first 3 months after delivery, remain underexplored. The postpartum period is a time of significant physiological, social, and psychological change for both the birthing parent and infant. This review aims to summarise the available evidence regarding postpartum SLE flares, thrombosis, breastfeeding, perinatal microbiome, perinatal mood and anxiety disorders, maternal-infant bonding, and social support. Additionally, the review identifies significant knowledge gaps in postpartum SLE care and highlights priorities for future research to improve short-term and long-term outcomes for birthing parents with SLE and their infants.
Additional Links: PMID-42367655
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@article {pmid42367655,
year = {2025},
author = {Fleming, EG and Chen, J and Mohideen, S and Broder, A and Oladipo, AF},
title = {The fourth trimester and challenges for the lupus patient.},
journal = {EULAR rheumatology open},
volume = {1},
number = {4},
pages = {403-412},
pmid = {42367655},
issn = {3050-7081},
abstract = {Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease that primarily affects persons of reproductive age. While SLE management during pregnancy has been previously studied, the unique challenges of the postpartum period, particularly the first 3 months after delivery, remain underexplored. The postpartum period is a time of significant physiological, social, and psychological change for both the birthing parent and infant. This review aims to summarise the available evidence regarding postpartum SLE flares, thrombosis, breastfeeding, perinatal microbiome, perinatal mood and anxiety disorders, maternal-infant bonding, and social support. Additionally, the review identifies significant knowledge gaps in postpartum SLE care and highlights priorities for future research to improve short-term and long-term outcomes for birthing parents with SLE and their infants.},
}
RevDate: 2026-06-29
CmpDate: 2026-06-29
Autoimmune gastritis: a comprehensive review of pathophysiology, risk stratification, and management.
Frontiers in immunology, 17:1878128.
Autoimmune gastritis (AIG) is a chronic, organ-specific autoimmune disease characterized by the immune-mediated destruction of gastric parietal cells, leading to impaired acid secretion, vitamin B12 deficiency, and an increased risk of gastric malignancies. The diagnosis of AIG relies on endoscopic findings combined with serological markers and histopathological confirmation. This review synthesizes current knowledge on the pathophysiology, diagnosis, and management of AIG, with a special focus on familial aggregation, polyglandular autoimmunity, and emerging therapeutic strategies. We discuss the diagnostic challenges posed by serological variability, the complex interplay with Helicobacter pylori infection, and the diagnostic pitfalls of macrocytic anemia. Furthermore, we explore precision risk stratification models for gastric neuroendocrine tumors (gNETs) and gastric adenocarcinoma, emphasizing the roles of endoscopic surveillance and molecular biomarkers. Finally, we review emerging therapeutic options, including novel immunomodulators and microbiome-targeted interventions. This review provides a comprehensive framework for clinicians to navigate the complexities of AIG, from early diagnosis to long-term management, with the goal of improving patient outcomes and mitigating the risk of malignant transformation.
Additional Links: PMID-42367768
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Citation:
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@article {pmid42367768,
year = {2026},
author = {Feng, M and Xu, W and Zhu, H},
title = {Autoimmune gastritis: a comprehensive review of pathophysiology, risk stratification, and management.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1878128},
pmid = {42367768},
issn = {1664-3224},
mesh = {Humans ; *Gastritis/therapy/diagnosis/immunology/etiology/physiopathology ; *Autoimmune Diseases/therapy/diagnosis/immunology/etiology ; Animals ; Risk Assessment ; Helicobacter Infections ; Disease Management ; Genetic Predisposition to Disease ; },
abstract = {Autoimmune gastritis (AIG) is a chronic, organ-specific autoimmune disease characterized by the immune-mediated destruction of gastric parietal cells, leading to impaired acid secretion, vitamin B12 deficiency, and an increased risk of gastric malignancies. The diagnosis of AIG relies on endoscopic findings combined with serological markers and histopathological confirmation. This review synthesizes current knowledge on the pathophysiology, diagnosis, and management of AIG, with a special focus on familial aggregation, polyglandular autoimmunity, and emerging therapeutic strategies. We discuss the diagnostic challenges posed by serological variability, the complex interplay with Helicobacter pylori infection, and the diagnostic pitfalls of macrocytic anemia. Furthermore, we explore precision risk stratification models for gastric neuroendocrine tumors (gNETs) and gastric adenocarcinoma, emphasizing the roles of endoscopic surveillance and molecular biomarkers. Finally, we review emerging therapeutic options, including novel immunomodulators and microbiome-targeted interventions. This review provides a comprehensive framework for clinicians to navigate the complexities of AIG, from early diagnosis to long-term management, with the goal of improving patient outcomes and mitigating the risk of malignant transformation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastritis/therapy/diagnosis/immunology/etiology/physiopathology
*Autoimmune Diseases/therapy/diagnosis/immunology/etiology
Animals
Risk Assessment
Helicobacter Infections
Disease Management
Genetic Predisposition to Disease
RevDate: 2026-06-29
CmpDate: 2026-06-29
Metagenomic characterization of gut microbiota in rheumatoid arthritis-associated interstitial lung disease: taxonomic shifts and clinical correlations.
Frontiers in immunology, 17:1868704.
BACKGROUND: Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is a severe extra-articular manifestation with limited diagnostic biomarkers. While gut microbiota dysbiosis contributes to rheumatoid arthritis (RA) pathogenesis, its specific role in RA-ILD remains poorly characterized.
METHODS: We performed shotgun metagenomic sequencing on fecal samples from 41 participants: 10 RA-ILD patients, 20 RA patients without ILD (RA-non-ILD), and 11 healthy controls (HCs). We assessed alpha and beta diversity, differential abundance (Wilcoxon rank-sum tests with FDR correction), Spearman correlations with clinical parameters, microbial co-occurrence networks, and random forest classification.
RESULTS: Alpha and beta diversity did not differ significantly among groups. After FDR correction, no genus differed significantly between RA-ILD and RA-non-ILD. Exploratory analysis (uncorrected P < 0.05) revealed enrichment of Escherichia/Shigella in RA-ILD (11.72% vs. 2.66%, P = 0.003) and depletion of Roseburia (1.05% vs. 3.77%, P = 0.005) and Ruminococcus (5.98% vs. 7.85%, P = 0.032), while Faecalibacterium showed a trend toward depletion without reaching nominal significance (4.45% vs. 4.66%, P = 0.409). Correlation analysis revealed a dichotomous pattern: pro-inflammatory genera correlated positively with disease activity, while butyrate-producing genera correlated negatively. Co-occurrence network analysis showed RA patients had a more complex network than HC and RA-ILD. Random forest classification identified Bifidobacterium, unclassified_ Oscillospiraceae, and unclassified_Lachnospiraceae as top discriminators between HC and RA, and unclassified_ Bacteroidaceae, Parabacteroides, and Blautia for RA-ILD vs RA.
CONCLUSIONS: RA-ILD is associated with specific gut microbial alterations-notably Escherichia/Shigella enrichment and depletion of Roseburia and Ruminococcus-despite preserved overall diversity. These changes correlate with systemic inflammation and suggest a role for the gut microbiota in RA-ILD pathogenesis via the gut-lung axis. The identified taxa warrant validation as candidate biomarkers in larger cohorts.
Additional Links: PMID-42367778
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Citation:
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@article {pmid42367778,
year = {2026},
author = {Fan, R and Zang, Q and Xu, Y and Gao, L and Zhou, J and Zang, Y},
title = {Metagenomic characterization of gut microbiota in rheumatoid arthritis-associated interstitial lung disease: taxonomic shifts and clinical correlations.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1868704},
pmid = {42367778},
issn = {1664-3224},
mesh = {Humans ; *Arthritis, Rheumatoid/complications/microbiology ; *Lung Diseases, Interstitial/microbiology/etiology ; Female ; *Metagenomics/methods ; Male ; *Gastrointestinal Microbiome/genetics ; Middle Aged ; Feces/microbiology ; Aged ; *Bacteria/classification/genetics ; Dysbiosis/microbiology ; *Metagenome ; },
abstract = {BACKGROUND: Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is a severe extra-articular manifestation with limited diagnostic biomarkers. While gut microbiota dysbiosis contributes to rheumatoid arthritis (RA) pathogenesis, its specific role in RA-ILD remains poorly characterized.
METHODS: We performed shotgun metagenomic sequencing on fecal samples from 41 participants: 10 RA-ILD patients, 20 RA patients without ILD (RA-non-ILD), and 11 healthy controls (HCs). We assessed alpha and beta diversity, differential abundance (Wilcoxon rank-sum tests with FDR correction), Spearman correlations with clinical parameters, microbial co-occurrence networks, and random forest classification.
RESULTS: Alpha and beta diversity did not differ significantly among groups. After FDR correction, no genus differed significantly between RA-ILD and RA-non-ILD. Exploratory analysis (uncorrected P < 0.05) revealed enrichment of Escherichia/Shigella in RA-ILD (11.72% vs. 2.66%, P = 0.003) and depletion of Roseburia (1.05% vs. 3.77%, P = 0.005) and Ruminococcus (5.98% vs. 7.85%, P = 0.032), while Faecalibacterium showed a trend toward depletion without reaching nominal significance (4.45% vs. 4.66%, P = 0.409). Correlation analysis revealed a dichotomous pattern: pro-inflammatory genera correlated positively with disease activity, while butyrate-producing genera correlated negatively. Co-occurrence network analysis showed RA patients had a more complex network than HC and RA-ILD. Random forest classification identified Bifidobacterium, unclassified_ Oscillospiraceae, and unclassified_Lachnospiraceae as top discriminators between HC and RA, and unclassified_ Bacteroidaceae, Parabacteroides, and Blautia for RA-ILD vs RA.
CONCLUSIONS: RA-ILD is associated with specific gut microbial alterations-notably Escherichia/Shigella enrichment and depletion of Roseburia and Ruminococcus-despite preserved overall diversity. These changes correlate with systemic inflammation and suggest a role for the gut microbiota in RA-ILD pathogenesis via the gut-lung axis. The identified taxa warrant validation as candidate biomarkers in larger cohorts.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Arthritis, Rheumatoid/complications/microbiology
*Lung Diseases, Interstitial/microbiology/etiology
Female
*Metagenomics/methods
Male
*Gastrointestinal Microbiome/genetics
Middle Aged
Feces/microbiology
Aged
*Bacteria/classification/genetics
Dysbiosis/microbiology
*Metagenome
RevDate: 2026-06-29
CmpDate: 2026-06-29
Rethinking biomarker strategy in gastric cancer immunotherapy: from tumor to host.
Frontiers in immunology, 17:1847526.
Immune checkpoint inhibitors (ICIs) have transformed advanced gastric cancer (GC) treatment, but durable responses remain rare, highlighting the need for better patient selection. Recent studies suggest that host-derived autoantibodies (e.g., ANA, ENA) may serve as prognostic markers in GC patients receiving immunotherapy. These hypothesis-generating observations indicate that pre-existing humoral immunity could reflect a clinically relevant axis of immune fitness. This review critically appraises these findings alongside established and emerging predictive biomarkers. We examine the strengths and limitations of PD-L1, MSI, TMB, and EBV status, and explore the clinical potential of dynamic tools like ctDNA and computational models. We also discuss emerging evidence on intrinsic resistance to PD-1 blockade in MSI-H GC, including PTEN mutations, low TMB within MSI-H tumors, and antigen presentation defects. Murine models have provided key insights into these resistance mechanisms and the immunomodulatory role of the gut microbiome. Collectively, the data support a shift from single-analyte biomarkers toward integrative, dynamic, systems-level models for patient selection, heralding a new era of precision immune-oncology in GC. However, most emerging biomarkers remain investigational and require prospective validation.
Additional Links: PMID-42367810
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Citation:
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@article {pmid42367810,
year = {2026},
author = {Ismaili, N},
title = {Rethinking biomarker strategy in gastric cancer immunotherapy: from tumor to host.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1847526},
pmid = {42367810},
issn = {1664-3224},
mesh = {Humans ; *Stomach Neoplasms/immunology/therapy/genetics ; *Biomarkers, Tumor/immunology/genetics ; *Immunotherapy/methods ; Animals ; Immune Checkpoint Inhibitors/therapeutic use ; Autoantibodies/immunology ; },
abstract = {Immune checkpoint inhibitors (ICIs) have transformed advanced gastric cancer (GC) treatment, but durable responses remain rare, highlighting the need for better patient selection. Recent studies suggest that host-derived autoantibodies (e.g., ANA, ENA) may serve as prognostic markers in GC patients receiving immunotherapy. These hypothesis-generating observations indicate that pre-existing humoral immunity could reflect a clinically relevant axis of immune fitness. This review critically appraises these findings alongside established and emerging predictive biomarkers. We examine the strengths and limitations of PD-L1, MSI, TMB, and EBV status, and explore the clinical potential of dynamic tools like ctDNA and computational models. We also discuss emerging evidence on intrinsic resistance to PD-1 blockade in MSI-H GC, including PTEN mutations, low TMB within MSI-H tumors, and antigen presentation defects. Murine models have provided key insights into these resistance mechanisms and the immunomodulatory role of the gut microbiome. Collectively, the data support a shift from single-analyte biomarkers toward integrative, dynamic, systems-level models for patient selection, heralding a new era of precision immune-oncology in GC. However, most emerging biomarkers remain investigational and require prospective validation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Stomach Neoplasms/immunology/therapy/genetics
*Biomarkers, Tumor/immunology/genetics
*Immunotherapy/methods
Animals
Immune Checkpoint Inhibitors/therapeutic use
Autoantibodies/immunology
RevDate: 2026-06-29
CmpDate: 2026-06-29
Cocaine-Enriched Oral Streptococcus parasanguinis Promotes Neuroimmune Dysfunction and Memory Impairment.
bioRxiv : the preprint server for biology pii:2026.06.12.731966.
Chronic cocaine use is associated with neuroinflammation and cognitive dysfunction, but the underlying mechanisms remain unclear. We previously identified oral enrichment of Streptococcus parasanguinis (SP) and other species in individuals with cocaine use disorder (CUD), and here demonstrate that cocaine selectively enhanced SP growth in vitro . To investigate causality, antibiotic-pretreated wild-type C57BL/6 mice received chronic oral inoculation of SP, S. salivarius , Neisseria flavescens , or vehicle. SP-treated mice exhibited spatial memory impairment, increased brain IL-1β, and non-region-specific microglial activation, without detectable bacterial translocation into the brain. While amyloid-associated signaling changes were observed across all bacterial treatment groups, only SP induced cognitive deficits and neuroinflammation. Untargeted metabolomics identified distinct SP-associated oral-to-brain metabolite signatures, including cysteine S-sulfate (CSS) and altered histamine-associated metabolites. CSS and histamine induced neuroinflammatory and amyloid-associated responses in vitro . Together, these findings identify a cocaine-associated oral pathobiont that promotes neuroinflammation and neurodegeneration, suggesting a novel oral microbiome-brain axis in CUD.
Additional Links: PMID-42367844
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@article {pmid42367844,
year = {2026},
author = {Johnson, D and Salman, T and Noorani, A and Benowitz, B and He, Y and Sundararaj, K and Shelley, H and Luo, Z and Wan, Z and Fitting, S and Penrod, RD and Jiang, W},
title = {Cocaine-Enriched Oral Streptococcus parasanguinis Promotes Neuroimmune Dysfunction and Memory Impairment.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.06.12.731966},
pmid = {42367844},
issn = {2692-8205},
abstract = {Chronic cocaine use is associated with neuroinflammation and cognitive dysfunction, but the underlying mechanisms remain unclear. We previously identified oral enrichment of Streptococcus parasanguinis (SP) and other species in individuals with cocaine use disorder (CUD), and here demonstrate that cocaine selectively enhanced SP growth in vitro . To investigate causality, antibiotic-pretreated wild-type C57BL/6 mice received chronic oral inoculation of SP, S. salivarius , Neisseria flavescens , or vehicle. SP-treated mice exhibited spatial memory impairment, increased brain IL-1β, and non-region-specific microglial activation, without detectable bacterial translocation into the brain. While amyloid-associated signaling changes were observed across all bacterial treatment groups, only SP induced cognitive deficits and neuroinflammation. Untargeted metabolomics identified distinct SP-associated oral-to-brain metabolite signatures, including cysteine S-sulfate (CSS) and altered histamine-associated metabolites. CSS and histamine induced neuroinflammatory and amyloid-associated responses in vitro . Together, these findings identify a cocaine-associated oral pathobiont that promotes neuroinflammation and neurodegeneration, suggesting a novel oral microbiome-brain axis in CUD.},
}
RevDate: 2026-06-29
CmpDate: 2026-06-29
Siphoviridae phage tails co-enrich with ex vivo amyloids.
bioRxiv : the preprint server for biology pii:2026.06.17.733002.
Bacteriophages are ubiquitous in the environment and are part of the natural human microbiome. Despite their abundance, the role of the human phagome in health and disease remains poorly understood. Here, we identify phage tails in ex vivo amyloid extracts from patients with lysozyme amyloidosis (ALys) and light-chain amyloidosis (AL). Using cryo-EM analysis of the ALys dataset, automated model building, and database searches, we assigned the observed tubular assemblies to a phage tail tube protein (TTP). Although we cannot fully rule out the possibility of contamination, the presence of phage tails raises the question of whether they bind to and are co-purified with amyloid fibrils. These structures may provide further insight into the potential relationship between phage-derived assemblies and amyloid remodeling, with possible implications for future therapeutic strategies in human amyloidosis.
Additional Links: PMID-42367858
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@article {pmid42367858,
year = {2026},
author = {Schäfer, JH and O'Neill, RT and Grotjahn, D and Powers, ET and Kelly, JW and Lander, GC},
title = {Siphoviridae phage tails co-enrich with ex vivo amyloids.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.06.17.733002},
pmid = {42367858},
issn = {2692-8205},
abstract = {Bacteriophages are ubiquitous in the environment and are part of the natural human microbiome. Despite their abundance, the role of the human phagome in health and disease remains poorly understood. Here, we identify phage tails in ex vivo amyloid extracts from patients with lysozyme amyloidosis (ALys) and light-chain amyloidosis (AL). Using cryo-EM analysis of the ALys dataset, automated model building, and database searches, we assigned the observed tubular assemblies to a phage tail tube protein (TTP). Although we cannot fully rule out the possibility of contamination, the presence of phage tails raises the question of whether they bind to and are co-purified with amyloid fibrils. These structures may provide further insight into the potential relationship between phage-derived assemblies and amyloid remodeling, with possible implications for future therapeutic strategies in human amyloidosis.},
}
RevDate: 2026-06-29
CmpDate: 2026-06-29
Environmental microbial extracts for longitudinal studies of gut microbiome assembly and maintenance.
bioRxiv : the preprint server for biology pii:2026.06.12.732002.
Animals harbor diverse gut microorganisms that influence host health and fitness. Synthetic microbial communities have been instrumental in enabling reductionist studies of host-microbiome interactions, but some questions require microbial communities with more natural-like complexity while preserving experimental tractability, in vivo monitoring, and quantitative analysis. Here, we describe a method optimized for longitudinal studies of host-microbiome-environment interactions in the nematode Caenorhabditis elegans . In this approach, complex microbial extracts (CMEs) are generated from environmental samples and applied to worm culture plates, providing a diverse yet experimentally convenient microbial environment. We show that CME composition remains stable during cold storage, enabling reproducible longitudinal experiments while minimizing confounding environmental drift over time. As a proof of principle, we apply this method to examine age-dependent changes in the worm gut microbiome, providing support for previous reports of age-dependent increase in the abundance of gut Enterobacteriaceae . CMEs provide a practical and reproducible framework that complements experiments using monocultures or synthetic communities, enabling longitudinal studies of host-microbiome interactions under conditions that better approximate natural microbial complexity.
Additional Links: PMID-42367889
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@article {pmid42367889,
year = {2026},
author = {Bodkhe, R and Choi, R and Shapira, M},
title = {Environmental microbial extracts for longitudinal studies of gut microbiome assembly and maintenance.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.06.12.732002},
pmid = {42367889},
issn = {2692-8205},
abstract = {Animals harbor diverse gut microorganisms that influence host health and fitness. Synthetic microbial communities have been instrumental in enabling reductionist studies of host-microbiome interactions, but some questions require microbial communities with more natural-like complexity while preserving experimental tractability, in vivo monitoring, and quantitative analysis. Here, we describe a method optimized for longitudinal studies of host-microbiome-environment interactions in the nematode Caenorhabditis elegans . In this approach, complex microbial extracts (CMEs) are generated from environmental samples and applied to worm culture plates, providing a diverse yet experimentally convenient microbial environment. We show that CME composition remains stable during cold storage, enabling reproducible longitudinal experiments while minimizing confounding environmental drift over time. As a proof of principle, we apply this method to examine age-dependent changes in the worm gut microbiome, providing support for previous reports of age-dependent increase in the abundance of gut Enterobacteriaceae . CMEs provide a practical and reproducible framework that complements experiments using monocultures or synthetic communities, enabling longitudinal studies of host-microbiome interactions under conditions that better approximate natural microbial complexity.},
}
RevDate: 2026-06-29
CmpDate: 2026-06-29
"What's SUPP" developing an in vitro model for healthy oral biofilms.
bioRxiv : the preprint server for biology pii:2026.06.19.733444.
Human supragingival plaque (SUPP) is a polymicrobial biofilm whose contents undergo dysbiotic transitions during multiple oral diseases. The study of healthy SUPP may lead to future pro or prebiotic therapies, to help prevent or revert dysbiosis during disease. However, many oral plaque models focus on the cultivation of oral pathogens and do not well cultivate commensal SUPP populations. Here, we use a 16S microbiome guided iterative approach to develop a low-cost high sample number SUPP model. Our model demonstrates several findings including a surprisingly minimal impact on salivary preparation methods on model microbiota and the ability to test microbial interactions with added oral strains to assess their fitness. This model provides a reductionist system for the study of healthy oral commensals in a complex polymicrobial framework in the absence of host immune responses.
Additional Links: PMID-42367897
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@article {pmid42367897,
year = {2026},
author = {Labossiere, A and Ramsey, M},
title = {"What's SUPP" developing an in vitro model for healthy oral biofilms.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.06.19.733444},
pmid = {42367897},
issn = {2692-8205},
abstract = {Human supragingival plaque (SUPP) is a polymicrobial biofilm whose contents undergo dysbiotic transitions during multiple oral diseases. The study of healthy SUPP may lead to future pro or prebiotic therapies, to help prevent or revert dysbiosis during disease. However, many oral plaque models focus on the cultivation of oral pathogens and do not well cultivate commensal SUPP populations. Here, we use a 16S microbiome guided iterative approach to develop a low-cost high sample number SUPP model. Our model demonstrates several findings including a surprisingly minimal impact on salivary preparation methods on model microbiota and the ability to test microbial interactions with added oral strains to assess their fitness. This model provides a reductionist system for the study of healthy oral commensals in a complex polymicrobial framework in the absence of host immune responses.},
}
RevDate: 2026-06-29
CmpDate: 2026-06-29
Neuroprotective effects of ursodeoxycholic acid in Parkinson's disease and Alzheimer's disease.
Neuroprotection (Chichester, England), 4(2):111-130.
Neurodegenerative diseases (NDDs) including Parkinson's disease (PD) and Alzheimer's disease (AD), are progressive disorders characterised by shared pathological features, including mitochondrial dysfunction, oxidative stress, apoptosis, neuroinflammation, neurotoxic protein buildup, and impaired protein clearance. Current treatments can only relieve disease symptoms but cannot delay the disease progression. Ursodeoxycholic acid (UDCA), a hydrophilic bile acid traditionally used in hepatology, has recently gained attention for its neuroprotective properties. This review critically evaluates UDCA's mechanisms of action, including the restoration of mitochondrial function, inhibition of apoptosis, reduction of oxidative stress and neuroinflammation, and enhancement of autophagy in both PD and AD models. In vitro and in vivo studies demonstrate UDCA's ability to preserve neuronal integrity, improve motor and cognitive outcomes, and reduce toxic protein aggregates. Although early-phase clinical trials, such as the UDCA for Parkinson's (UP) study in PD, show promising mitochondrial benefits and safety, clinical evidence in AD remains limited. Future directions emphasise the need for large-scale trials, personalised medicine, improved central nervous system (CNS) delivery strategies, or dietary interventions to modulate UDCA production from the gut microbiome. While not a first-line treatment, UDCA represents a compelling mitochondrial stabiliser with disease-modifying potential in NDDs.
Additional Links: PMID-42368200
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@article {pmid42368200,
year = {2026},
author = {Chong, AEY and Sasmita, AO and Koh, RY and Ling, APK},
title = {Neuroprotective effects of ursodeoxycholic acid in Parkinson's disease and Alzheimer's disease.},
journal = {Neuroprotection (Chichester, England)},
volume = {4},
number = {2},
pages = {111-130},
pmid = {42368200},
issn = {2770-730X},
abstract = {Neurodegenerative diseases (NDDs) including Parkinson's disease (PD) and Alzheimer's disease (AD), are progressive disorders characterised by shared pathological features, including mitochondrial dysfunction, oxidative stress, apoptosis, neuroinflammation, neurotoxic protein buildup, and impaired protein clearance. Current treatments can only relieve disease symptoms but cannot delay the disease progression. Ursodeoxycholic acid (UDCA), a hydrophilic bile acid traditionally used in hepatology, has recently gained attention for its neuroprotective properties. This review critically evaluates UDCA's mechanisms of action, including the restoration of mitochondrial function, inhibition of apoptosis, reduction of oxidative stress and neuroinflammation, and enhancement of autophagy in both PD and AD models. In vitro and in vivo studies demonstrate UDCA's ability to preserve neuronal integrity, improve motor and cognitive outcomes, and reduce toxic protein aggregates. Although early-phase clinical trials, such as the UDCA for Parkinson's (UP) study in PD, show promising mitochondrial benefits and safety, clinical evidence in AD remains limited. Future directions emphasise the need for large-scale trials, personalised medicine, improved central nervous system (CNS) delivery strategies, or dietary interventions to modulate UDCA production from the gut microbiome. While not a first-line treatment, UDCA represents a compelling mitochondrial stabiliser with disease-modifying potential in NDDs.},
}
RevDate: 2026-06-29
The Gut Microbiome and Colorectal Cancer: From Association to Causation.
Cancer biome and targeted therapy, 1(2):1-8.
This mini-review discusses the emerging role of the gut microbiome as an active driver of colorectal cancer initiation, progression, and therapeutic response. Key mechanisms include microbiome-induced genomic instability, modulation of host immune responses, and epigenetic reprogramming mediated by tumor-associated bacteria such as Fusobacterium nucleatum. Emerging evidence suggests that specific microbial signatures are not only associated with disease but can functionally shape tumor behavior, influence treatment sensitivity, and serve as clinically actionable biomarkers. These insights highlight the potential of integrating microbiome profiling into precision oncology and underscore the need for mechanistic and translational studies to harness host-microbe interactions for improved cancer prevention and therapy.
Additional Links: PMID-42368406
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42368406,
year = {2026},
author = {Takahashi, T and Goel, A},
title = {The Gut Microbiome and Colorectal Cancer: From Association to Causation.},
journal = {Cancer biome and targeted therapy},
volume = {1},
number = {2},
pages = {1-8},
pmid = {42368406},
issn = {3070-9989},
abstract = {This mini-review discusses the emerging role of the gut microbiome as an active driver of colorectal cancer initiation, progression, and therapeutic response. Key mechanisms include microbiome-induced genomic instability, modulation of host immune responses, and epigenetic reprogramming mediated by tumor-associated bacteria such as Fusobacterium nucleatum. Emerging evidence suggests that specific microbial signatures are not only associated with disease but can functionally shape tumor behavior, influence treatment sensitivity, and serve as clinically actionable biomarkers. These insights highlight the potential of integrating microbiome profiling into precision oncology and underscore the need for mechanistic and translational studies to harness host-microbe interactions for improved cancer prevention and therapy.},
}
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ESP Quick Facts
ESP Origins
In the early 1990's, Robert Robbins was a faculty member at Johns Hopkins, where he directed the informatics core of GDB — the human gene-mapping database of the international human genome project. To share papers with colleagues around the world, he set up a small paper-sharing section on his personal web page. This small project evolved into The Electronic Scholarly Publishing Project.
ESP Support
In 1995, Robbins became the VP/IT of the Fred Hutchinson Cancer Research Center in Seattle, WA. Soon after arriving in Seattle, Robbins secured funding, through the ELSI component of the US Human Genome Project, to create the original ESP.ORG web site, with the formal goal of providing free, world-wide access to the literature of classical genetics.
ESP Rationale
Although the methods of molecular biology can seem almost magical to the uninitiated, the original techniques of classical genetics are readily appreciated by one and all: cross individuals that differ in some inherited trait, collect all of the progeny, score their attributes, and propose mechanisms to explain the patterns of inheritance observed.
ESP Goal
In reading the early works of classical genetics, one is drawn, almost inexorably, into ever more complex models, until molecular explanations begin to seem both necessary and natural. At that point, the tools for understanding genome research are at hand. Assisting readers reach this point was the original goal of The Electronic Scholarly Publishing Project.
ESP Usage
Usage of the site grew rapidly and has remained high. Faculty began to use the site for their assigned readings. Other on-line publishers, ranging from The New York Times to Nature referenced ESP materials in their own publications. Nobel laureates (e.g., Joshua Lederberg) regularly used the site and even wrote to suggest changes and improvements.
ESP Content
When the site began, no journals were making their early content available in digital format. As a result, ESP was obliged to digitize classic literature before it could be made available. For many important papers — such as Mendel's original paper or the first genetic map — ESP had to produce entirely new typeset versions of the works, if they were to be available in a high-quality format.
ESP Help
Early support from the DOE component of the Human Genome Project was critically important for getting the ESP project on a firm foundation. Since that funding ended (nearly 20 years ago), the project has been operated as a purely volunteer effort. Anyone wishing to assist in these efforts should send an email to Robbins.
ESP Plans
With the development of methods for adding typeset side notes to PDF files, the ESP project now plans to add annotated versions of some classical papers to its holdings. We also plan to add new reference and pedagogical material. We have already started providing regularly updated, comprehensive bibliographies to the ESP.ORG site.
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