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ESP: PubMed Auto Bibliography 14 Jun 2025 at 01:52 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2025-06-13
Editorial: Statistical approaches, applications, and software for longitudinal microbiome data analysis and microbiome multi-omics data integration.
Frontiers in genetics, 16:1624791.
Additional Links: PMID-40510813
PubMed:
Citation:
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@article {pmid40510813,
year = {2025},
author = {Li, H and Chen, J and Fenger, M and Jiang, Y},
title = {Editorial: Statistical approaches, applications, and software for longitudinal microbiome data analysis and microbiome multi-omics data integration.},
journal = {Frontiers in genetics},
volume = {16},
number = {},
pages = {1624791},
pmid = {40510813},
issn = {1664-8021},
}
RevDate: 2025-06-13
CmpDate: 2025-06-13
Characterization of the salivary microbiome in healthy individuals under fatigue status.
Frontiers in cellular and infection microbiology, 15:1506723.
BACKGROUND & AIMS: Limited understanding exists regarding the characteristics and biological significance of the salivary microbiome in healthy individuals experiencing physiological fatigue. This study aimed to delineate the structural and functional alterations in the salivary microbiome of healthy individuals undergoing physiological fatigue compared to energetic controls, and to explore its potential as a biomarker for fatigue status.
METHODS: A cohort of 7 healthy individuals experiencing acute physiological fatigue (induced by prolonged study and confirmed via electroencephalography; Fatigue group, FTG) and 63 energetic healthy controls (Energetic group, ENG) were enrolled. Saliva samples were collected, from which microbial DNA was extracted. The V3-V4 hypervariable region of the 16S rRNA gene was subsequently sequenced using high-throughput technology. Bioinformatics analyses encompassed assessment of alpha and beta diversity, identification of differential taxa using Linear discriminant analysis Effect Size (LEfSe) with multi-method cross-validation, construction of microbial co-occurrence networks, and screening of fatigue-associated biomarker genera via the Boruta-SHAP algorithm. Microbial community phenotypes and potential functional pathways were predicted using BugBase and PICRUSt2, respectively.
RESULTS: The FTG group exhibited significantly diminished alpha diversity (Simpson index, p=0.01071) relative to the ENG group. Beta diversity analysis demonstrated significant dissimilarities in microbial community structure between the groups (p<0.05). Taxonomic profiling revealed a significant enrichment in the relative abundance of potential periodontopathogenic genera, including Streptococcus and Filifactor, within the FTG group, concomitantly with a significant depletion of health-associated genera such as Rothia and Neisseria. A predictive model constructed using the Boruta-SHAP algorithm, based on 15 key genera, effectively discriminated between fatigue and non-fatigue states, achieving an area under the receiver operating characteristic curve (AUC) of 0.948. Phenotypic predictions indicated a significant increase in the proportion of bacteria harboring Mobile Genetic Elements (MGEs) (p=0.048), alongside significant reductions in the proportion of aerobic bacteria (p=0.006) and biofilm-forming capacity (p=0.002) in the FTG group. Functional pathway analysis (PICRUSt2) revealed an enrichment of pathways such as "Neuroactive ligand-receptor interaction" in the FTG group, whereas pathways pertinent to energy metabolism (e.g., Citrate cycle (TCA cycle), Oxidative phosphorylation) and amino acid metabolism (e.g., Phenylalanine metabolism, Histidine metabolism) were significantly enriched in the ENG group.
CONCLUSION: This study provides novel evidence that physiological fatigue induces significant structural and functional alterations in the salivary microbiome of healthy individuals. These perturbations include diminished microbial diversity, disrupted community architecture, enrichment of potential opportunistic pathogens, and marked shifts in key metabolic pathways, particularly those governing neuroactivity and energy metabolism. These findings suggest that the salivary microbiome may be implicated in the physiological regulation of fatigue, potentially via an "oral-microbiome-brain axis," and underscore its potential as a source of non-invasive biomarkers for assessing fatigue status. Further mechanistic investigations are warranted to elucidate these interactions.
Additional Links: PMID-40510800
PubMed:
Citation:
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@article {pmid40510800,
year = {2025},
author = {Peng, X and Han, N and Gong, Y and He, L and Xu, Y and Xiao, D and Zhang, T and Qiang, Y and Li, X and Zhang, W and Zhang, J},
title = {Characterization of the salivary microbiome in healthy individuals under fatigue status.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1506723},
pmid = {40510800},
issn = {2235-2988},
mesh = {Humans ; *Saliva/microbiology ; *Microbiota ; RNA, Ribosomal, 16S/genetics ; Male ; Adult ; Female ; *Fatigue/microbiology ; Healthy Volunteers ; Biomarkers/analysis ; *Bacteria/classification/genetics/isolation & purification ; DNA, Bacterial/genetics ; Young Adult ; High-Throughput Nucleotide Sequencing ; Computational Biology ; Sequence Analysis, DNA ; Middle Aged ; },
abstract = {BACKGROUND & AIMS: Limited understanding exists regarding the characteristics and biological significance of the salivary microbiome in healthy individuals experiencing physiological fatigue. This study aimed to delineate the structural and functional alterations in the salivary microbiome of healthy individuals undergoing physiological fatigue compared to energetic controls, and to explore its potential as a biomarker for fatigue status.
METHODS: A cohort of 7 healthy individuals experiencing acute physiological fatigue (induced by prolonged study and confirmed via electroencephalography; Fatigue group, FTG) and 63 energetic healthy controls (Energetic group, ENG) were enrolled. Saliva samples were collected, from which microbial DNA was extracted. The V3-V4 hypervariable region of the 16S rRNA gene was subsequently sequenced using high-throughput technology. Bioinformatics analyses encompassed assessment of alpha and beta diversity, identification of differential taxa using Linear discriminant analysis Effect Size (LEfSe) with multi-method cross-validation, construction of microbial co-occurrence networks, and screening of fatigue-associated biomarker genera via the Boruta-SHAP algorithm. Microbial community phenotypes and potential functional pathways were predicted using BugBase and PICRUSt2, respectively.
RESULTS: The FTG group exhibited significantly diminished alpha diversity (Simpson index, p=0.01071) relative to the ENG group. Beta diversity analysis demonstrated significant dissimilarities in microbial community structure between the groups (p<0.05). Taxonomic profiling revealed a significant enrichment in the relative abundance of potential periodontopathogenic genera, including Streptococcus and Filifactor, within the FTG group, concomitantly with a significant depletion of health-associated genera such as Rothia and Neisseria. A predictive model constructed using the Boruta-SHAP algorithm, based on 15 key genera, effectively discriminated between fatigue and non-fatigue states, achieving an area under the receiver operating characteristic curve (AUC) of 0.948. Phenotypic predictions indicated a significant increase in the proportion of bacteria harboring Mobile Genetic Elements (MGEs) (p=0.048), alongside significant reductions in the proportion of aerobic bacteria (p=0.006) and biofilm-forming capacity (p=0.002) in the FTG group. Functional pathway analysis (PICRUSt2) revealed an enrichment of pathways such as "Neuroactive ligand-receptor interaction" in the FTG group, whereas pathways pertinent to energy metabolism (e.g., Citrate cycle (TCA cycle), Oxidative phosphorylation) and amino acid metabolism (e.g., Phenylalanine metabolism, Histidine metabolism) were significantly enriched in the ENG group.
CONCLUSION: This study provides novel evidence that physiological fatigue induces significant structural and functional alterations in the salivary microbiome of healthy individuals. These perturbations include diminished microbial diversity, disrupted community architecture, enrichment of potential opportunistic pathogens, and marked shifts in key metabolic pathways, particularly those governing neuroactivity and energy metabolism. These findings suggest that the salivary microbiome may be implicated in the physiological regulation of fatigue, potentially via an "oral-microbiome-brain axis," and underscore its potential as a source of non-invasive biomarkers for assessing fatigue status. Further mechanistic investigations are warranted to elucidate these interactions.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Saliva/microbiology
*Microbiota
RNA, Ribosomal, 16S/genetics
Male
Adult
Female
*Fatigue/microbiology
Healthy Volunteers
Biomarkers/analysis
*Bacteria/classification/genetics/isolation & purification
DNA, Bacterial/genetics
Young Adult
High-Throughput Nucleotide Sequencing
Computational Biology
Sequence Analysis, DNA
Middle Aged
RevDate: 2025-06-13
Association between oral microbiome diversity and kidney stones: a cross-sectional study.
Frontiers in microbiology, 16:1600961.
BACKGROUND: Kidney stones are a common urologic disorder that imposes a significant burden on global public health. This study aimed to determine the association between oral microbiome diversity and kidney stones.
METHODS: The data for this study came from the National Health and Nutrition Examination Survey 2009-2012 survey cycle. Use of alpha diversity to assess oral microbiome diversity. Multivariate logistic regression modeling was used to assess the association between different alpha-diversity indicators and kidney stones. Subgroup analyses and interaction tests were used to assess the stability of the association between alpha-diversity and kidney stones. Restricted cubic spline plots were used to assess non-linear associations and dose-response relationships.
RESULTS: The study included 5,870 eligible participants with a mean age of 43.74 years at baseline. After adjusting for all covariates, the observed oral microbiome diversity was significantly negatively associated with the risk of kidney stones (P < 0.05). Subgroup analyses showed that oral microbiome diversity was negatively associated with the risk of kidney stones in certain populations, particularly among those aged 40-60 years, men, obese, with moderate to high cardiovascular health scores, smokers, and those without hypertension. Restricted cubic spline analysis suggested a significant non-linear negative correlation between the Shannon and Simpson diversity indices and the risk of kidney stones (p for non-linear < 0.05). Since our study was a cross-sectional design, the main limitation was the inability to prove causality.
CONCLUSIONS: In this study, we found an inverse relationship between oral microbiome diversity and kidney stone risk observed in alpha diversity. This reveals the complexity of host-microbiome interactions, and further mechanistic studies are necessary to elucidate these complex roles in the future.
Additional Links: PMID-40510677
PubMed:
Citation:
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@article {pmid40510677,
year = {2025},
author = {Zhang, Z and Guan, S and Chen, L and Jiang, F and Dong, H and Chen, Z and Lv, L and Song, H and Sun, W and He, D and Jiang, S and Tian, F},
title = {Association between oral microbiome diversity and kidney stones: a cross-sectional study.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1600961},
pmid = {40510677},
issn = {1664-302X},
abstract = {BACKGROUND: Kidney stones are a common urologic disorder that imposes a significant burden on global public health. This study aimed to determine the association between oral microbiome diversity and kidney stones.
METHODS: The data for this study came from the National Health and Nutrition Examination Survey 2009-2012 survey cycle. Use of alpha diversity to assess oral microbiome diversity. Multivariate logistic regression modeling was used to assess the association between different alpha-diversity indicators and kidney stones. Subgroup analyses and interaction tests were used to assess the stability of the association between alpha-diversity and kidney stones. Restricted cubic spline plots were used to assess non-linear associations and dose-response relationships.
RESULTS: The study included 5,870 eligible participants with a mean age of 43.74 years at baseline. After adjusting for all covariates, the observed oral microbiome diversity was significantly negatively associated with the risk of kidney stones (P < 0.05). Subgroup analyses showed that oral microbiome diversity was negatively associated with the risk of kidney stones in certain populations, particularly among those aged 40-60 years, men, obese, with moderate to high cardiovascular health scores, smokers, and those without hypertension. Restricted cubic spline analysis suggested a significant non-linear negative correlation between the Shannon and Simpson diversity indices and the risk of kidney stones (p for non-linear < 0.05). Since our study was a cross-sectional design, the main limitation was the inability to prove causality.
CONCLUSIONS: In this study, we found an inverse relationship between oral microbiome diversity and kidney stone risk observed in alpha diversity. This reveals the complexity of host-microbiome interactions, and further mechanistic studies are necessary to elucidate these complex roles in the future.},
}
RevDate: 2025-06-13
Rhinoceromics: a multi-amplicon study with clinical markers to transferrin saturation levels in ex-situ black rhinoceros (Diceros bicornis michaeli).
Frontiers in microbiology, 16:1515939.
Iron overload disorder (IOD) is a common condition in ex-situ black rhinoceroses (Diceros bicornis), although it has not been reported in the wild. This study aimed to gain a deeper understanding of the relationship between 25-hydroxy vitamin D [25(OH)D], inflammatory markers, insulin levels, the gut microbiome, dietary components, and transferrin saturation (TS) in ex-situ black rhinoceroses. Blood and fecal samples from 11 black rhinoceroses at five different European zoological institutions were monitored over a 1-year period. Inflammatory markers such as interleukin 6 (IL-6), serum amyloid A (SAA), interferon γ (IFN-γ), and tumor necrosis factor α (TNF-α) were analyzed. Our study corroborates the findings of previous research, which demonstrated that insulin, inflammatory markers, and TS% are higher in ex-situ black rhinoceroses compared to published wild ranges. Our data show no correlations between insulin, 25(OH)D, TS%, inflammatory markers, or short-chain fatty acids (SFCAs). Serum 25(OH)D exhibited significantly higher levels in summer than in winter. Transferrin saturation was influenced by age, which is consistent with previous studies. The microbiome did not differ significantly among individuals, institutions, sex, or season, unlike the mycobiome, which exhibited significant differences across institutions. The impact of the mycobiome differences on the physiology of the animals could not be determined from this study.
Additional Links: PMID-40510676
PubMed:
Citation:
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@article {pmid40510676,
year = {2025},
author = {Bruins-van Sonsbeek, LGR and Verschuren, MCM and Kaal, S and Lindenburg, PW and Rodenburg, KCW and Clauss, M and Speksnijder, AGCL and Rutten, VPMG and Bonnet, BFJ and Wittink, F},
title = {Rhinoceromics: a multi-amplicon study with clinical markers to transferrin saturation levels in ex-situ black rhinoceros (Diceros bicornis michaeli).},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1515939},
pmid = {40510676},
issn = {1664-302X},
abstract = {Iron overload disorder (IOD) is a common condition in ex-situ black rhinoceroses (Diceros bicornis), although it has not been reported in the wild. This study aimed to gain a deeper understanding of the relationship between 25-hydroxy vitamin D [25(OH)D], inflammatory markers, insulin levels, the gut microbiome, dietary components, and transferrin saturation (TS) in ex-situ black rhinoceroses. Blood and fecal samples from 11 black rhinoceroses at five different European zoological institutions were monitored over a 1-year period. Inflammatory markers such as interleukin 6 (IL-6), serum amyloid A (SAA), interferon γ (IFN-γ), and tumor necrosis factor α (TNF-α) were analyzed. Our study corroborates the findings of previous research, which demonstrated that insulin, inflammatory markers, and TS% are higher in ex-situ black rhinoceroses compared to published wild ranges. Our data show no correlations between insulin, 25(OH)D, TS%, inflammatory markers, or short-chain fatty acids (SFCAs). Serum 25(OH)D exhibited significantly higher levels in summer than in winter. Transferrin saturation was influenced by age, which is consistent with previous studies. The microbiome did not differ significantly among individuals, institutions, sex, or season, unlike the mycobiome, which exhibited significant differences across institutions. The impact of the mycobiome differences on the physiology of the animals could not be determined from this study.},
}
RevDate: 2025-06-13
Impact of the soil layer on the soil microbial diversity and composition of Pinus yunnanensis at the Ailao Mountains subtropical forest.
Frontiers in microbiology, 16:1558906.
Microbial communities residing in forest soils play crucial roles in decomposing organic matter and recycling nutrients, making these ecosystems one of the most diverse habitats on Earth. However, the composition and function of these complex and diverse microbiomes across different soil layers remain largely unknown. In this study, we collected soil samples from various layers and analysed the bacterial and fungal community compositions in experimental forest ecosystems using sequencing techniques. Our findings revealed that the soil layer was the primary factor influencing microbial communities, whereas sampling season had only a marginal effect. The most prevalent bacterial phyla and fungal classes were Acidobacteria, Actinobacteria, Armatimonadetes, Bacteroidetes, Firmicutes, Planctomycetes, Proteobacteria, Verrucomicrobia, and Agaricomycetes. Owing to the heterogeneity of the soil layer environment, we observed distinct patterns in the bacterial and fungal microbiomes across different layers. Moreover, the soil layer affected the network complexity, with fungi exhibiting higher complexity in the upper layer, whereas bacteria showed the opposite trend. Additionally, the dominant bacterial and fungal taxa across all soil layers belonged predominantly to Acidobacteria and Agaricomycetes, respectively. These findings underscore the significance of soil layers in shaping soil microbial communities and highlight the composition and co-occurrence patterns of the microbial communities within these layers.
Additional Links: PMID-40510675
PubMed:
Citation:
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@article {pmid40510675,
year = {2025},
author = {Qiao, H and Zeng, Q and Martin, F and Wang, Q},
title = {Impact of the soil layer on the soil microbial diversity and composition of Pinus yunnanensis at the Ailao Mountains subtropical forest.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1558906},
pmid = {40510675},
issn = {1664-302X},
abstract = {Microbial communities residing in forest soils play crucial roles in decomposing organic matter and recycling nutrients, making these ecosystems one of the most diverse habitats on Earth. However, the composition and function of these complex and diverse microbiomes across different soil layers remain largely unknown. In this study, we collected soil samples from various layers and analysed the bacterial and fungal community compositions in experimental forest ecosystems using sequencing techniques. Our findings revealed that the soil layer was the primary factor influencing microbial communities, whereas sampling season had only a marginal effect. The most prevalent bacterial phyla and fungal classes were Acidobacteria, Actinobacteria, Armatimonadetes, Bacteroidetes, Firmicutes, Planctomycetes, Proteobacteria, Verrucomicrobia, and Agaricomycetes. Owing to the heterogeneity of the soil layer environment, we observed distinct patterns in the bacterial and fungal microbiomes across different layers. Moreover, the soil layer affected the network complexity, with fungi exhibiting higher complexity in the upper layer, whereas bacteria showed the opposite trend. Additionally, the dominant bacterial and fungal taxa across all soil layers belonged predominantly to Acidobacteria and Agaricomycetes, respectively. These findings underscore the significance of soil layers in shaping soil microbial communities and highlight the composition and co-occurrence patterns of the microbial communities within these layers.},
}
RevDate: 2025-06-13
Intermittent fasting inhibits the development of colorectal cancer in APC [Min/+] mice through gut microbiota and its related metabolites.
Frontiers in microbiology, 16:1563224.
BACKGROUND AND OBJECTIVES: Intermittent fasting is an emerging dietary approach, but its specific role in colorectal cancer (CRC) is not yet clear. In this study, we investigated the relationship between intermittent fasting and colorectal development in mice.
METHODS: First, APC [Min/+] mouse models (a spontaneous model of colorectal cancer) were subjected to intermittent fasting intervention (2 days/week) with regular monitoring of body weight changes. Subsequently, 16S rRNA sequencing and untargeted metabolomics were employed to analyze alterations in fecal microbial community structure and metabolic profiles following the fasting intervention. Tumor development was quantitatively assessed by enumerating CRC lesions using HE staining, while histopathological evaluation was performed to determine the degree of neoplastic progression. Concurrently, western blotting was conducted to examine the expression levels of intestinal barrier function-related proteins. Finally, in vitro validation experiments, including colony formation assay and transwell invasion assay, were performed to investigate the effects of the key microbial metabolite isovaleric acid on the proliferative and invasive capacities of CRC cells.
RESULTS: Intermittent fasting significantly reduced tumor incidence by approximately 50% compared to the control group (1.25 ± 0.38 vs 2.50 ± 0.38 tumors/mouse, P = 0.017) and markedly attenuated tumor progression. 16S rRNA sequencing analysis revealed significant enrichment of two key bacterial genera, Alistipes (P = 0.030) and Odoribacter (P = 0.030), along with a significant reduction in fecal isovaleric acid levels (P < 0.05) in the intermittent fasting group. Furthermore, intermittent fasting effectively controlled body weight gain (P < 0.05) and significantly improved intestinal barrier function (P < 0.05). In vitro experiments further demonstrated that isovaleric acid directly promoted CRC cell proliferation (P < 0.05) and enhanced their invasive capacity (P < 0.05).
CONCLUSION: Intermittent fasting suppresses CRC development in mice through its effects on gut microbiota and related metabolites.
Additional Links: PMID-40510674
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Citation:
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@article {pmid40510674,
year = {2025},
author = {Chen, J and Su, R and He, Y and Chen, J},
title = {Intermittent fasting inhibits the development of colorectal cancer in APC [Min/+] mice through gut microbiota and its related metabolites.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1563224},
pmid = {40510674},
issn = {1664-302X},
abstract = {BACKGROUND AND OBJECTIVES: Intermittent fasting is an emerging dietary approach, but its specific role in colorectal cancer (CRC) is not yet clear. In this study, we investigated the relationship between intermittent fasting and colorectal development in mice.
METHODS: First, APC [Min/+] mouse models (a spontaneous model of colorectal cancer) were subjected to intermittent fasting intervention (2 days/week) with regular monitoring of body weight changes. Subsequently, 16S rRNA sequencing and untargeted metabolomics were employed to analyze alterations in fecal microbial community structure and metabolic profiles following the fasting intervention. Tumor development was quantitatively assessed by enumerating CRC lesions using HE staining, while histopathological evaluation was performed to determine the degree of neoplastic progression. Concurrently, western blotting was conducted to examine the expression levels of intestinal barrier function-related proteins. Finally, in vitro validation experiments, including colony formation assay and transwell invasion assay, were performed to investigate the effects of the key microbial metabolite isovaleric acid on the proliferative and invasive capacities of CRC cells.
RESULTS: Intermittent fasting significantly reduced tumor incidence by approximately 50% compared to the control group (1.25 ± 0.38 vs 2.50 ± 0.38 tumors/mouse, P = 0.017) and markedly attenuated tumor progression. 16S rRNA sequencing analysis revealed significant enrichment of two key bacterial genera, Alistipes (P = 0.030) and Odoribacter (P = 0.030), along with a significant reduction in fecal isovaleric acid levels (P < 0.05) in the intermittent fasting group. Furthermore, intermittent fasting effectively controlled body weight gain (P < 0.05) and significantly improved intestinal barrier function (P < 0.05). In vitro experiments further demonstrated that isovaleric acid directly promoted CRC cell proliferation (P < 0.05) and enhanced their invasive capacity (P < 0.05).
CONCLUSION: Intermittent fasting suppresses CRC development in mice through its effects on gut microbiota and related metabolites.},
}
RevDate: 2025-06-13
Plant developmental stage drives the assembly and functional adaptability of endophytic microbial communities.
Frontiers in microbiology, 16:1492141.
INTRODUCTION: The seeds of Amorphophallus muelleri represent a unique category of herbaceous seeds that arise from triploid apomixis. They necessitate an exceptionally protracted maturation phase of 8 months, followed by a dormancy period of 4 months, before they can germinate and give rise to fully formed new plants. Currently, the connection between endophytic microbial communities in A. muelleri seeds and the host plant's development is largely unexplored.
METHODS: Herein, we analyzed the temporal dynamics of the endophytic bacterial and fungal communities from seed germination to seedling establishment (seven stages) through amplicon sequencing.
RESULTS AND DISCUSSION: The results showed that plant developmental stage explained the large variation in endophytic bacterial and fungal communities in A. muelleri and that multiple microbial attributes (e.g., α, β-diversity, community composition, and bacterial and fungal ecological networks) are driven by the developmental state of A. muelleri. Metagenomic analyses further indicated that the four stages after rooting have higher microbial functional diversity. Microbial functional genes involved in cell wall/membrane/envelope biogenesis, inorganic ion transport and metabolism, and carbon degradation were abundant in A. muelleri seeds from Stage 1 to Stage 3 (before rooting). From Stage 4 to Stage 7 (after rooting), microbial functional genes involved in the carbon, nitrogen and phosphorus cycles, starch and sucrose metabolism, and energy production and conversion were more abundant. Coincidentally, more abundant Proteobacteria, and Basidiomycota taxa related to carbon degradation were found in stages 1-3, while more Allorhizobium-Neorhizobium-Pararhizobium-Rhizobium and Stenotrophomonas taxa associated with nitrogen cycling and plant growth promotion were observed in stages 4-7. These findings have greatly improved our basic understanding of the assembly and functional adaptability of the endophytic microbiome during A. muelleri plant development and are helpful for the mining, development and utilization of functional microbial resources.
Additional Links: PMID-40510672
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Citation:
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@article {pmid40510672,
year = {2025},
author = {Yang, M and Wang, J and Qi, Y and Gao, P and Li, L and Guo, J and Zhao, Y and Liu, J and Chen, Z and Zhao, J and Yu, L},
title = {Plant developmental stage drives the assembly and functional adaptability of endophytic microbial communities.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1492141},
pmid = {40510672},
issn = {1664-302X},
abstract = {INTRODUCTION: The seeds of Amorphophallus muelleri represent a unique category of herbaceous seeds that arise from triploid apomixis. They necessitate an exceptionally protracted maturation phase of 8 months, followed by a dormancy period of 4 months, before they can germinate and give rise to fully formed new plants. Currently, the connection between endophytic microbial communities in A. muelleri seeds and the host plant's development is largely unexplored.
METHODS: Herein, we analyzed the temporal dynamics of the endophytic bacterial and fungal communities from seed germination to seedling establishment (seven stages) through amplicon sequencing.
RESULTS AND DISCUSSION: The results showed that plant developmental stage explained the large variation in endophytic bacterial and fungal communities in A. muelleri and that multiple microbial attributes (e.g., α, β-diversity, community composition, and bacterial and fungal ecological networks) are driven by the developmental state of A. muelleri. Metagenomic analyses further indicated that the four stages after rooting have higher microbial functional diversity. Microbial functional genes involved in cell wall/membrane/envelope biogenesis, inorganic ion transport and metabolism, and carbon degradation were abundant in A. muelleri seeds from Stage 1 to Stage 3 (before rooting). From Stage 4 to Stage 7 (after rooting), microbial functional genes involved in the carbon, nitrogen and phosphorus cycles, starch and sucrose metabolism, and energy production and conversion were more abundant. Coincidentally, more abundant Proteobacteria, and Basidiomycota taxa related to carbon degradation were found in stages 1-3, while more Allorhizobium-Neorhizobium-Pararhizobium-Rhizobium and Stenotrophomonas taxa associated with nitrogen cycling and plant growth promotion were observed in stages 4-7. These findings have greatly improved our basic understanding of the assembly and functional adaptability of the endophytic microbiome during A. muelleri plant development and are helpful for the mining, development and utilization of functional microbial resources.},
}
RevDate: 2025-06-13
CmpDate: 2025-06-13
Gut Microbiota in Lactose Intolerance: A Mendelian Randomization Study on Microbial Mechanisms and Potential Links to Tumor Inflammatory Microenvironments.
Mediators of inflammation, 2025:8181816.
Background: Previous observational studies have suggested an association between the composition of the intestinal microbiome and lactose intolerance (LI). However, the causal direction remains unclear. This study utilized Mendelian randomization (MR) to rigorously evaluate the potential causal link between the gut microbiome and LI. Methods: Genome-wide association studies (GWASs) summary statistics for gut microbiota and LI were sourced from previously published GWAS studies. Multiple methods, such as Simple mode, MR-Egger regression, weighted median, inverse variance-weighted (IVW), and weighted model, were used to determine the causal relationship between gut microbiota and LI. To validate the primary findings from the MR analyses, several sensitivity analyses were conducted. Furthermore, a reverse MR analysis was executed on bacterial taxa previously identified to have a potential causal link with LI risk, aiming to evaluate the possibility of reverse causation. Results: The IVW results revealed that the genus Lachnospiraceae UCG008 (OR = 0.584, 95%CI 0.356-0.958, p=0.0330), genus Eubacterium hallii group (OR = 0.467, 95% CI 0.242-0.899, p=0.023), and genus Ruminococcus gauvreauii group (OR = 0.506, 95% CI 0.2653-0.968, p=0.039) have a protective effect against LI. In contrast, the genus Holdemania (OR = 1.86, 95% CI 1.105-3.131, p=0.0194) displayed a predisposing effect. Sensitivity analyses did not detect any outlier single-nucleotide polymorphisms (SNPs). Further analyses reinforced the association between specific gut microbiota compositions and LI. No evidence suggested reverse causality between LI and the bacterial taxa identified in the reverse MR analysis. Conclusions: From a genetic standpoint, this MR study indicates a causal relationship between variations in gut microbiota composition and LI. This not only underscores the potential of gut microbiota-centric treatments for LI but also provides a foundation for exploring the role of gut microbiota in LI development. Further study of the mechanism of Lachnospiraceae in the treatment of IL is conducive to the discovery of new therapeutic targets for IL.
Additional Links: PMID-40510587
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@article {pmid40510587,
year = {2025},
author = {Xie, Y and Cao, Q and Huang, Z and Zou, X},
title = {Gut Microbiota in Lactose Intolerance: A Mendelian Randomization Study on Microbial Mechanisms and Potential Links to Tumor Inflammatory Microenvironments.},
journal = {Mediators of inflammation},
volume = {2025},
number = {},
pages = {8181816},
pmid = {40510587},
issn = {1466-1861},
mesh = {*Gastrointestinal Microbiome/genetics/physiology ; Humans ; *Mendelian Randomization Analysis/methods ; *Lactose Intolerance/microbiology/genetics ; Genome-Wide Association Study ; Polymorphism, Single Nucleotide/genetics ; *Inflammation/microbiology ; },
abstract = {Background: Previous observational studies have suggested an association between the composition of the intestinal microbiome and lactose intolerance (LI). However, the causal direction remains unclear. This study utilized Mendelian randomization (MR) to rigorously evaluate the potential causal link between the gut microbiome and LI. Methods: Genome-wide association studies (GWASs) summary statistics for gut microbiota and LI were sourced from previously published GWAS studies. Multiple methods, such as Simple mode, MR-Egger regression, weighted median, inverse variance-weighted (IVW), and weighted model, were used to determine the causal relationship between gut microbiota and LI. To validate the primary findings from the MR analyses, several sensitivity analyses were conducted. Furthermore, a reverse MR analysis was executed on bacterial taxa previously identified to have a potential causal link with LI risk, aiming to evaluate the possibility of reverse causation. Results: The IVW results revealed that the genus Lachnospiraceae UCG008 (OR = 0.584, 95%CI 0.356-0.958, p=0.0330), genus Eubacterium hallii group (OR = 0.467, 95% CI 0.242-0.899, p=0.023), and genus Ruminococcus gauvreauii group (OR = 0.506, 95% CI 0.2653-0.968, p=0.039) have a protective effect against LI. In contrast, the genus Holdemania (OR = 1.86, 95% CI 1.105-3.131, p=0.0194) displayed a predisposing effect. Sensitivity analyses did not detect any outlier single-nucleotide polymorphisms (SNPs). Further analyses reinforced the association between specific gut microbiota compositions and LI. No evidence suggested reverse causality between LI and the bacterial taxa identified in the reverse MR analysis. Conclusions: From a genetic standpoint, this MR study indicates a causal relationship between variations in gut microbiota composition and LI. This not only underscores the potential of gut microbiota-centric treatments for LI but also provides a foundation for exploring the role of gut microbiota in LI development. Further study of the mechanism of Lachnospiraceae in the treatment of IL is conducive to the discovery of new therapeutic targets for IL.},
}
MeSH Terms:
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*Gastrointestinal Microbiome/genetics/physiology
Humans
*Mendelian Randomization Analysis/methods
*Lactose Intolerance/microbiology/genetics
Genome-Wide Association Study
Polymorphism, Single Nucleotide/genetics
*Inflammation/microbiology
RevDate: 2025-06-13
The early-life gut microbiome in common pediatric diseases: roles and therapeutic implications.
Frontiers in nutrition, 12:1597206.
The early-life gut microbiome has been increasingly recognized as a contributing factor for pediatric health and diseases. Studies have reported that the human gut microbiota colonization commences at birth and progresses over the course of the first three years of life, until it reaches a mature and stable diversity and composition. During this critical window, the gut microbiome is vulnerably subjected to environmental factors, leading to transient microbial reprogramming and functional changes. The dynamic early-life intestinal microbiota is frequently manipulated by environmental factors, which impact the composition and function of the gut microflora, hence confer to short-and/or long-term health outcomes extending to adulthood. Evidence has shown that the imbalanced gut microbial community early in life is associated with several childhood diseases and disorders, such as inflammatory bowel diseases, allergies, attention-deficit/hyperactivity disorder and pediatric obesity. Manipulating the early-life intestinal microbes can either ameliorate or impair host's immunological and metabolic responses, impacting overall health conditions later in life. This narrative review article discusses the recent understanding and implications of the early-life gut microbiome in common pediatric diseases and potential intervention approaches.
Additional Links: PMID-40510495
PubMed:
Citation:
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@article {pmid40510495,
year = {2025},
author = {Bankole, T and Li, Y},
title = {The early-life gut microbiome in common pediatric diseases: roles and therapeutic implications.},
journal = {Frontiers in nutrition},
volume = {12},
number = {},
pages = {1597206},
pmid = {40510495},
issn = {2296-861X},
abstract = {The early-life gut microbiome has been increasingly recognized as a contributing factor for pediatric health and diseases. Studies have reported that the human gut microbiota colonization commences at birth and progresses over the course of the first three years of life, until it reaches a mature and stable diversity and composition. During this critical window, the gut microbiome is vulnerably subjected to environmental factors, leading to transient microbial reprogramming and functional changes. The dynamic early-life intestinal microbiota is frequently manipulated by environmental factors, which impact the composition and function of the gut microflora, hence confer to short-and/or long-term health outcomes extending to adulthood. Evidence has shown that the imbalanced gut microbial community early in life is associated with several childhood diseases and disorders, such as inflammatory bowel diseases, allergies, attention-deficit/hyperactivity disorder and pediatric obesity. Manipulating the early-life intestinal microbes can either ameliorate or impair host's immunological and metabolic responses, impacting overall health conditions later in life. This narrative review article discusses the recent understanding and implications of the early-life gut microbiome in common pediatric diseases and potential intervention approaches.},
}
RevDate: 2025-06-13
Partially hydrolyzed guar gum ingestion suppresses atopic dermatitis-like symptoms through prebiotic effect in mice.
Journal of clinical biochemistry and nutrition, 76(3):280-288.
Growing knowledge reveals the association between the gut microbiome and skin, rendering the gut microbiome an appealing potential therapeutic target for atopic dermatitis (AD). In this study, we assessed the effect of partially hydrolyzed guar gum (PHGG) on AD-like symptoms induced by topical 1-Chloro-2,4-dinitrobenzene (DNCB) in BALB/c mice. Four weeks of PHGG feeding prevented the loss of epidermal barrier integrity and epithelial hyperplasia in the AD lesion (p<0.05, effect size >0.80), indicating a reduction in AD-like symptoms. According to the postulated mechanism, PHGG ingestion modulates the gut microbiome resulting in enhanced butyrate production (p<0.05). Butyrate suppresses Th2 function in gut immunity, which is believed to have significance in systemic immune regulation. The lowering of blood Th2 cytokines (IL-4 and IL-10, p<0.05) in the PHGG-fed group confirmed the existence of such a pathway, and butyrate can possibly be considered to have an indirect involvement in the suppression of Th2 immune response in the AD lesions. These findings encourage support for an association between gut microbiome and skin through the immune system, implying that daily PHGG ingestion may be beneficial for suppressing AD symptoms across the gut-immune-skin axis.
Additional Links: PMID-40510389
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Citation:
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@article {pmid40510389,
year = {2025},
author = {Morishima, S and Abe, A and Okamoto, S and Kapoor, MP and Matsuura, S and Kuriya, K and Ozeki, M and Nishio, M and Miura, H and Inoue, R},
title = {Partially hydrolyzed guar gum ingestion suppresses atopic dermatitis-like symptoms through prebiotic effect in mice.},
journal = {Journal of clinical biochemistry and nutrition},
volume = {76},
number = {3},
pages = {280-288},
pmid = {40510389},
issn = {0912-0009},
abstract = {Growing knowledge reveals the association between the gut microbiome and skin, rendering the gut microbiome an appealing potential therapeutic target for atopic dermatitis (AD). In this study, we assessed the effect of partially hydrolyzed guar gum (PHGG) on AD-like symptoms induced by topical 1-Chloro-2,4-dinitrobenzene (DNCB) in BALB/c mice. Four weeks of PHGG feeding prevented the loss of epidermal barrier integrity and epithelial hyperplasia in the AD lesion (p<0.05, effect size >0.80), indicating a reduction in AD-like symptoms. According to the postulated mechanism, PHGG ingestion modulates the gut microbiome resulting in enhanced butyrate production (p<0.05). Butyrate suppresses Th2 function in gut immunity, which is believed to have significance in systemic immune regulation. The lowering of blood Th2 cytokines (IL-4 and IL-10, p<0.05) in the PHGG-fed group confirmed the existence of such a pathway, and butyrate can possibly be considered to have an indirect involvement in the suppression of Th2 immune response in the AD lesions. These findings encourage support for an association between gut microbiome and skin through the immune system, implying that daily PHGG ingestion may be beneficial for suppressing AD symptoms across the gut-immune-skin axis.},
}
RevDate: 2025-06-13
Gut microbiome signatures predict 5-ASA efficacy in ulcerative colitis.
iScience, 28(6):112568.
Ulcerative colitis (UC) prevalence is rising globally, yet fewer than 50% of patients achieve mucosal healing (MH) with first-line 5-aminosalicylic acid (5-ASA) therapy. We aimed to identify microbial signatures that could predict the treatment efficacy of 5-ASA. Active UC patients on standardized 5-ASA treatment were prospectively enrolled. Shotgun metagenomic sequencing was performed to identify the taxonomic and functional profiles before and after treatment. Six species were enriched in the effective group and 3 species in the ineffective group at baseline. Faecalibacterium prausnitzii, Blautia massiliensis, and Phascolarctobacterium faecium were consistently depleted in the ineffective group at both time points. A random forest model based on these three species predicted ineffective 5-ASA treatment with area under the curve (AUC) = 0.80 (validation in the Inflammatory Bowel Disease Multi'omics Database [IBDMDB]: AUC = 0.82, specificity = 0.88, negative predictive value [NPV] = 0.70, and positive predictive value [PPV] = 0.80). Gut microbiome signatures have potential to serve as non-invasive predictors for ineffective 5-ASA treatment in UC.
Additional Links: PMID-40510115
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Citation:
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@article {pmid40510115,
year = {2025},
author = {Dang, Y and Xu, X and Ma, J and Zhou, M and Xu, C and Huang, X and Xu, F and Wang, Z and Shi, H and Zhang, S},
title = {Gut microbiome signatures predict 5-ASA efficacy in ulcerative colitis.},
journal = {iScience},
volume = {28},
number = {6},
pages = {112568},
pmid = {40510115},
issn = {2589-0042},
abstract = {Ulcerative colitis (UC) prevalence is rising globally, yet fewer than 50% of patients achieve mucosal healing (MH) with first-line 5-aminosalicylic acid (5-ASA) therapy. We aimed to identify microbial signatures that could predict the treatment efficacy of 5-ASA. Active UC patients on standardized 5-ASA treatment were prospectively enrolled. Shotgun metagenomic sequencing was performed to identify the taxonomic and functional profiles before and after treatment. Six species were enriched in the effective group and 3 species in the ineffective group at baseline. Faecalibacterium prausnitzii, Blautia massiliensis, and Phascolarctobacterium faecium were consistently depleted in the ineffective group at both time points. A random forest model based on these three species predicted ineffective 5-ASA treatment with area under the curve (AUC) = 0.80 (validation in the Inflammatory Bowel Disease Multi'omics Database [IBDMDB]: AUC = 0.82, specificity = 0.88, negative predictive value [NPV] = 0.70, and positive predictive value [PPV] = 0.80). Gut microbiome signatures have potential to serve as non-invasive predictors for ineffective 5-ASA treatment in UC.},
}
RevDate: 2025-06-13
CmpDate: 2025-06-13
[Changes of intestinal microflora in patients with colorectal benign and malignant tumors in high altitude area and comparison with the normal population in low altitude area].
Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences, 57(3):578-583.
OBJECTIVE: To analyze the changes of intestinal flora in patients with benign and malignant colorectal tumors in high altitude areas and to compare them with the normal population in low altitude areas.
METHODS: The clinical data of 61 patients who underwent colonoscopy in the People' s Hospital of Tibet Autonomous Region from 2020 to 2022 were collected as the high altitude group. According to the colonoscopy results, they were divided into control group (29 cases), non-adenomatous polyp group (12 cases), adenoma group (10 cases), colorectal cancer group (10 cases). 17 patients who had negative colonoscopy results in the Peking University Third Hospital during the same period were collected as the low altitude control group. Before bowel preparation for colonoscopy, the fecal samples were collected. Then the DNA of bacteria in the fecal samples was extracted. The V3-V4 variable region of the 16S rRNA gene was PCR amplified and high-throughput sequenced. The species diversity of fecal flora was analyzed.
RESULTS: Alpha diversity analysis showed that the species diversity of samples from the high altitude colorectal cancer group differed statistically from that of the high altitude non-adenomatous polyp group and the low altitude control group, and the species diversity of colorectal samples from the high altitude colorectal cancer group was higher than that of the other two groups. While beta diversity showed no significant difference among the five groups. Differences were found in phylum level analysis that the abundance of Actinobacteriota in the low altitude control group was significantly lower than those in each group of the high altitude area, while the abundance of Actinobacteriota in the colorectal cancer group was significantly lower than those in the other 3 groups of the high altitude area. Differences were found in genus level analysis that the abundance of Bacteroides, Phascclarctobacterium and Lachnoclostridium in the low altitude control group was significantly higher than those of all the groups in the high altitude area; the abundance of Blautia and Collinsella in the high altitude control group was the highest. Lactobacillus was not detected in the low altitude control group, while there was a highly significant difference (P < 0.05) in the level of Lactobacillus in the four groups of high altitude area, and the abundance of Lactobacillus was significantly higher in the control group than those of the other three groups. In the four groups of samples at high altitude, the abundance of Bifidobacterium decreased significantly, while the abundance of Christensenellaceae_R-7_group increased significantly.
CONCLUSION: Compared with the high and low altitude controls, the diversity and abundance of intestinal flora in patients with colorectal benign and malignant tumors at high altitudes are different. And the abundance of species are also diffe-rent at the phylum and genus levels, suggesting that altitude factors may have some influence on intestinal flora.
Additional Links: PMID-40509837
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Citation:
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@article {pmid40509837,
year = {2025},
author = {Han, D and Ciren, Y and Li, Q and Li, J},
title = {[Changes of intestinal microflora in patients with colorectal benign and malignant tumors in high altitude area and comparison with the normal population in low altitude area].},
journal = {Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences},
volume = {57},
number = {3},
pages = {578-583},
pmid = {40509837},
issn = {1671-167X},
mesh = {Humans ; *Altitude ; *Colorectal Neoplasms/microbiology ; *Gastrointestinal Microbiome ; Feces/microbiology ; Male ; Female ; Middle Aged ; Tibet ; RNA, Ribosomal, 16S/genetics ; Colonoscopy ; Adult ; Aged ; Adenoma/microbiology ; },
abstract = {OBJECTIVE: To analyze the changes of intestinal flora in patients with benign and malignant colorectal tumors in high altitude areas and to compare them with the normal population in low altitude areas.
METHODS: The clinical data of 61 patients who underwent colonoscopy in the People' s Hospital of Tibet Autonomous Region from 2020 to 2022 were collected as the high altitude group. According to the colonoscopy results, they were divided into control group (29 cases), non-adenomatous polyp group (12 cases), adenoma group (10 cases), colorectal cancer group (10 cases). 17 patients who had negative colonoscopy results in the Peking University Third Hospital during the same period were collected as the low altitude control group. Before bowel preparation for colonoscopy, the fecal samples were collected. Then the DNA of bacteria in the fecal samples was extracted. The V3-V4 variable region of the 16S rRNA gene was PCR amplified and high-throughput sequenced. The species diversity of fecal flora was analyzed.
RESULTS: Alpha diversity analysis showed that the species diversity of samples from the high altitude colorectal cancer group differed statistically from that of the high altitude non-adenomatous polyp group and the low altitude control group, and the species diversity of colorectal samples from the high altitude colorectal cancer group was higher than that of the other two groups. While beta diversity showed no significant difference among the five groups. Differences were found in phylum level analysis that the abundance of Actinobacteriota in the low altitude control group was significantly lower than those in each group of the high altitude area, while the abundance of Actinobacteriota in the colorectal cancer group was significantly lower than those in the other 3 groups of the high altitude area. Differences were found in genus level analysis that the abundance of Bacteroides, Phascclarctobacterium and Lachnoclostridium in the low altitude control group was significantly higher than those of all the groups in the high altitude area; the abundance of Blautia and Collinsella in the high altitude control group was the highest. Lactobacillus was not detected in the low altitude control group, while there was a highly significant difference (P < 0.05) in the level of Lactobacillus in the four groups of high altitude area, and the abundance of Lactobacillus was significantly higher in the control group than those of the other three groups. In the four groups of samples at high altitude, the abundance of Bifidobacterium decreased significantly, while the abundance of Christensenellaceae_R-7_group increased significantly.
CONCLUSION: Compared with the high and low altitude controls, the diversity and abundance of intestinal flora in patients with colorectal benign and malignant tumors at high altitudes are different. And the abundance of species are also diffe-rent at the phylum and genus levels, suggesting that altitude factors may have some influence on intestinal flora.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Altitude
*Colorectal Neoplasms/microbiology
*Gastrointestinal Microbiome
Feces/microbiology
Male
Female
Middle Aged
Tibet
RNA, Ribosomal, 16S/genetics
Colonoscopy
Adult
Aged
Adenoma/microbiology
RevDate: 2025-06-13
Skin microbiome analysis of a junctional epidermolysis bullosa patient treated with genetically modified stem cells.
Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG [Epub ahead of print].
BACKGROUND AND OBJECTIVE: Junctional epidermolysis bullosa (JEB) is a subtype of epidermolysis bullosa caused by mutations in the LAMB3 gene. We treated a patient with JEB using genetically corrected autologous epidermal cultures retrovirally transduced with the functional LAMB3 gene sequence. The objective of this study was to analyze the skin microbiome of this patient, with a particular focus on transgenic skin, and to compare the findings to the skin microbiome of healthy controls and patients with atopic dermatitis and well-documented microbial dysbiosis.
PATIENTS AND METHODS: Skin microbiome analysis was performed on a JEB patient 72 months after combined gene and stem cell therapy. Skin swabs from age-matched healthy controls and atopic dermatitis patients were included from the ProRaD study of CK-CARE.
RESULTS: The transgenic skin had comparably high relative and absolute Staphylococcus (S.) aureus abundance to blistering and non-blistering skin of the JEB patient, while the total bacterial load was lower. In blistering skin of the JEB patient, higher bacterial load was driven by S. aureus.
CONCLUSIONS: Our investigation confirms a unique microbiome composition in JEB, characterized by S. aureus driven bacterial overgrowth. The dysbiosis was not reversed in transgenic, non-blistering skin areas. However, the transgenic skin demonstrates stability in an environment of bacterial dysbiosis.
Additional Links: PMID-40509691
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@article {pmid40509691,
year = {2025},
author = {Dermietzel, A and Tosun, B and Nguyen, M and Wessel, K and Rauer, L and Neumann, AU and Hirsch, T and , and Traidl-Hoffmann, C and Reiger, M and Hülpüsch, C and Kueckelhaus, M},
title = {Skin microbiome analysis of a junctional epidermolysis bullosa patient treated with genetically modified stem cells.},
journal = {Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG},
volume = {},
number = {},
pages = {},
doi = {10.1111/ddg.15776},
pmid = {40509691},
issn = {1610-0387},
abstract = {BACKGROUND AND OBJECTIVE: Junctional epidermolysis bullosa (JEB) is a subtype of epidermolysis bullosa caused by mutations in the LAMB3 gene. We treated a patient with JEB using genetically corrected autologous epidermal cultures retrovirally transduced with the functional LAMB3 gene sequence. The objective of this study was to analyze the skin microbiome of this patient, with a particular focus on transgenic skin, and to compare the findings to the skin microbiome of healthy controls and patients with atopic dermatitis and well-documented microbial dysbiosis.
PATIENTS AND METHODS: Skin microbiome analysis was performed on a JEB patient 72 months after combined gene and stem cell therapy. Skin swabs from age-matched healthy controls and atopic dermatitis patients were included from the ProRaD study of CK-CARE.
RESULTS: The transgenic skin had comparably high relative and absolute Staphylococcus (S.) aureus abundance to blistering and non-blistering skin of the JEB patient, while the total bacterial load was lower. In blistering skin of the JEB patient, higher bacterial load was driven by S. aureus.
CONCLUSIONS: Our investigation confirms a unique microbiome composition in JEB, characterized by S. aureus driven bacterial overgrowth. The dysbiosis was not reversed in transgenic, non-blistering skin areas. However, the transgenic skin demonstrates stability in an environment of bacterial dysbiosis.},
}
RevDate: 2025-06-13
Protective Properties of the White Button Mushroom, Agaricus bisporus, in a Mouse Model of Colitis.
Molecular nutrition & food research [Epub ahead of print].
Previous work demonstrated the promising immunomodulatory potential of a naturally derived whole mushroom powder (WMP) from the white button mushroom, Agaricus bisporus. Here, we further investigate the protective properties of WMP in a mouse model of colitis. An in vitro digested WMP (IVD-WMP) reduced permeability of intestinal epithelial Caco-2 and HT-29-MTX cell monolayers to FITC dextran. In vivo, WMP orally administered to mice as a pretreatment before induction of dextran sulfate sodium (DSS)-induced colitis. Though statistically significant decreases in disease scores were not reported, we observed an antiinflammatory and antioxidative stress profile in the colon. Additionally, 16S ribosomal RNA (16S rRNA) microbiome analysis revealed differences in bacterial abundance associated with WMP pretreatment, including a decrease in Allobaculum species associated with inflammatory bowel disease. In a DSS-colitis recovery model, WMP promoted recovery as evidenced by improved weight gain, reduced stool scores, reduced IL-1β levels, and myeloperoxidase (MPO) activity in colonic tissue. This work demonstrates the health benefits associated with the consumption of the white button mushroom, including support of intestinal barrier integrity combined with antioxidant and antiinflammatory activity.
Additional Links: PMID-40509652
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@article {pmid40509652,
year = {2025},
author = {Dempsey, E and Walsh, AM and Yadav, S and Wilson, J and Sheedy, FJ and Corr, SC},
title = {Protective Properties of the White Button Mushroom, Agaricus bisporus, in a Mouse Model of Colitis.},
journal = {Molecular nutrition & food research},
volume = {},
number = {},
pages = {e70133},
doi = {10.1002/mnfr.70133},
pmid = {40509652},
issn = {1613-4133},
support = {EPSPD/2022/130//Irish Research Council Enterprise Partnership Scheme (Postdoctoral)/ ; 19/FFP/6499//Science Foundation Ireland Frontiers for the Future Programme/ ; },
abstract = {Previous work demonstrated the promising immunomodulatory potential of a naturally derived whole mushroom powder (WMP) from the white button mushroom, Agaricus bisporus. Here, we further investigate the protective properties of WMP in a mouse model of colitis. An in vitro digested WMP (IVD-WMP) reduced permeability of intestinal epithelial Caco-2 and HT-29-MTX cell monolayers to FITC dextran. In vivo, WMP orally administered to mice as a pretreatment before induction of dextran sulfate sodium (DSS)-induced colitis. Though statistically significant decreases in disease scores were not reported, we observed an antiinflammatory and antioxidative stress profile in the colon. Additionally, 16S ribosomal RNA (16S rRNA) microbiome analysis revealed differences in bacterial abundance associated with WMP pretreatment, including a decrease in Allobaculum species associated with inflammatory bowel disease. In a DSS-colitis recovery model, WMP promoted recovery as evidenced by improved weight gain, reduced stool scores, reduced IL-1β levels, and myeloperoxidase (MPO) activity in colonic tissue. This work demonstrates the health benefits associated with the consumption of the white button mushroom, including support of intestinal barrier integrity combined with antioxidant and antiinflammatory activity.},
}
RevDate: 2025-06-13
Nutrient Availability and Pathogen Clearance Impact Microbiome Composition in a Gnotobiotic Kimchi Model.
Foods (Basel, Switzerland), 14(11): pii:foods14111948.
Kimchi is a fermented Korean food typically made with napa cabbage, garlic, radish, ginger, and chili pepper. It is becoming increasingly popular due to its flavor, high fiber content, and purported probiotic benefits. The microbial ecology of the fermentation community has been extensively studied, though what's less understood is how its microbial community changes when nutrients or pathogens are introduced. To study this, we used gnotobiotic cabbage media inoculated with a kimchi starter culture as a model system. These inoculated samples were exposed to E. coli or Bacillus cereus, with or without added nutrients in the form of tryptic soy broth (TSB). We tracked pH, colony-forming units (CFUs), and community composition over time. We also used Oxford Nanopore sequencing to analyze the 16S rRNA gene (V4-V9), followed by use of the Emu algorithm for taxonomic assignments. As expected, LABs suppressed pathogens, but this effect was weaker early on in the nutrient-rich condition. Pathogen exposure changed the overall community-Lactobacillus species became more common, and Leuconostoc mesenteroides less so. Interestingly, adding nutrients alone caused similar microbial shifts to those seen with pathogen exposure. This could suggest that nutrient levels have a larger impact on the final microbiome structure than direct microbial competition. Together, these findings suggest that monitoring total microbial composition, and not just the presence of pathogens, may be important for ensuring kimchi fermentation reproducibility.
Additional Links: PMID-40509476
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PubMed:
Citation:
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@article {pmid40509476,
year = {2025},
author = {Bemis, DH and Camphausen, CE and Liu, E and Dantus, JJ and Navarro, JA and Dykstra, KL and Paltrowitz, LA and Dzhelmach, M and Joerg, M and Tamelessio, P and Belenky, P},
title = {Nutrient Availability and Pathogen Clearance Impact Microbiome Composition in a Gnotobiotic Kimchi Model.},
journal = {Foods (Basel, Switzerland)},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/foods14111948},
pmid = {40509476},
issn = {2304-8158},
abstract = {Kimchi is a fermented Korean food typically made with napa cabbage, garlic, radish, ginger, and chili pepper. It is becoming increasingly popular due to its flavor, high fiber content, and purported probiotic benefits. The microbial ecology of the fermentation community has been extensively studied, though what's less understood is how its microbial community changes when nutrients or pathogens are introduced. To study this, we used gnotobiotic cabbage media inoculated with a kimchi starter culture as a model system. These inoculated samples were exposed to E. coli or Bacillus cereus, with or without added nutrients in the form of tryptic soy broth (TSB). We tracked pH, colony-forming units (CFUs), and community composition over time. We also used Oxford Nanopore sequencing to analyze the 16S rRNA gene (V4-V9), followed by use of the Emu algorithm for taxonomic assignments. As expected, LABs suppressed pathogens, but this effect was weaker early on in the nutrient-rich condition. Pathogen exposure changed the overall community-Lactobacillus species became more common, and Leuconostoc mesenteroides less so. Interestingly, adding nutrients alone caused similar microbial shifts to those seen with pathogen exposure. This could suggest that nutrient levels have a larger impact on the final microbiome structure than direct microbial competition. Together, these findings suggest that monitoring total microbial composition, and not just the presence of pathogens, may be important for ensuring kimchi fermentation reproducibility.},
}
RevDate: 2025-06-13
Fermented Dairy Products as Precision Modulators of Gut Microbiota and Host Health: Mechanistic Insights, Clinical Evidence, and Future Directions.
Foods (Basel, Switzerland), 14(11): pii:foods14111946.
Dairy products-encompassing yogurt, kefir, cheese, and cultured milk beverages-are emerging as versatile, food-based modulators of gut microbiota and host physiology. This review synthesizes mechanistic insights demonstrating how live starter cultures and their fermentation-derived metabolites (short-chain fatty acids, bioactive peptides, and exopolysaccharides) act synergistically to enhance microbial diversity, reinforce epithelial barrier integrity via upregulation of tight-junction proteins, and modulate immune signaling. Clinical evidence supports significant improvements in metabolic parameters (fasting glucose, lipid profiles, blood pressure) and reductions in systemic inflammation across metabolic syndrome, hypertension, and IBS cohorts. We highlight critical modulatory factors-including strain specificity, host enterotypes and FUT2 genotype, fermentation parameters, and matrix composition-that govern probiotic engraftment, postbiotic yield, and therapeutic efficacy. Despite promising short-term outcomes, current studies are limited by heterogeneous designs and brief intervention periods, underscoring the need for long-term, adaptive trials and integrative multi-omics to establish durability and causality. Looking forward, precision nutrition frameworks that harness baseline microbiota profiling, host genetics, and data-driven fermentation design will enable bespoke fermented dairy formulations, transforming these traditional foods into next-generation functional matrices for targeted prevention and management of metabolic, inflammatory, and neuroimmune disorders.
Additional Links: PMID-40509473
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PubMed:
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@article {pmid40509473,
year = {2025},
author = {Gao, Y and Liu, Y and Ma, T and Liang, Q and Sun, J and Wu, X and Song, Y and Nie, H and Huang, J and Mu, G},
title = {Fermented Dairy Products as Precision Modulators of Gut Microbiota and Host Health: Mechanistic Insights, Clinical Evidence, and Future Directions.},
journal = {Foods (Basel, Switzerland)},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/foods14111946},
pmid = {40509473},
issn = {2304-8158},
support = {32302032//National Natural Science Foundation of China/ ; 2022YFD2101503//National Key Research and Development Program/ ; 2020GXNSFBA297083//Natural Science Foundation of Guangxi, China/ ; },
abstract = {Dairy products-encompassing yogurt, kefir, cheese, and cultured milk beverages-are emerging as versatile, food-based modulators of gut microbiota and host physiology. This review synthesizes mechanistic insights demonstrating how live starter cultures and their fermentation-derived metabolites (short-chain fatty acids, bioactive peptides, and exopolysaccharides) act synergistically to enhance microbial diversity, reinforce epithelial barrier integrity via upregulation of tight-junction proteins, and modulate immune signaling. Clinical evidence supports significant improvements in metabolic parameters (fasting glucose, lipid profiles, blood pressure) and reductions in systemic inflammation across metabolic syndrome, hypertension, and IBS cohorts. We highlight critical modulatory factors-including strain specificity, host enterotypes and FUT2 genotype, fermentation parameters, and matrix composition-that govern probiotic engraftment, postbiotic yield, and therapeutic efficacy. Despite promising short-term outcomes, current studies are limited by heterogeneous designs and brief intervention periods, underscoring the need for long-term, adaptive trials and integrative multi-omics to establish durability and causality. Looking forward, precision nutrition frameworks that harness baseline microbiota profiling, host genetics, and data-driven fermentation design will enable bespoke fermented dairy formulations, transforming these traditional foods into next-generation functional matrices for targeted prevention and management of metabolic, inflammatory, and neuroimmune disorders.},
}
RevDate: 2025-06-13
Characteristics and Functions of Different Intestinal Segments in Juvenile Greater Amberjack (Seriola dumerili).
Animals : an open access journal from MDPI, 15(11): pii:ani15111672.
The greater amberjack (Seriola dumerili), a key species in marine aquaculture, relies heavily on its intestine for nutrient absorption and immune function. However, the structural and functional specialization of its intestinal segments remains poorly understood. In this study, we divided the intestine of S. dumerili into foregut, midgut, and hindgut, and conducted a multi-omics analysis integrating histological staining (H&E/AB-PAS), digestive enzyme assays, transcriptome sequencing, and 16S rRNA microbiota profiling to characterize structural, functional, molecular, and microbial differences across intestinal segments. Histological examinations revealed that brush border microvillus length, muscle layer thickness, and folding height were significantly greater in the foregut and hindgut compared to the midgut, while mucus and goblet cell density was higher in the foregut and midgut. Digestive enzyme assays showed that lipase activity peaked in the foregut, α-amylase in the midgut, and protease in the midgut and hindgut. Alkaline phosphatase (AKP) and acid phosphatase (ACP) activities were highest in the foregut and midgut. Immune-related enzyme activities (SOD (Superoxide dismutase), GSH-Px (Glutathione peroxidase), T-AOC (Total Antioxidant Capacity)) were elevated and MDA levels were lower in the midgut, indicating its role as the primary immune site. Transcriptome analysis identified segment-specific expression of nutrient transporters, such as slc6a19b (hindgut, protein), apoa1b (foregut, lipid), and slc37a4 (midgut, carbohydrate). Microbiome analysis revealed Ruminococcus dominance in the foregut (lipid digestion) and Prevotella, Bifidobacterium, and Lactobacillus enrichment in the midgut (carbohydrate metabolism and immunity). These findings highlight functional zonation in S. dumerili: the foregut specializes in lipid digestion, the midgut in carbohydrate metabolism and immunity, and the hindgut in protein digestion. This study provides foundational insights for optimizing aquaculture practices and advancing research in nutrition, immunology, and disease modeling in S. dumerili.
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@article {pmid40509138,
year = {2025},
author = {Zhu, K and Jiang, M and Yan, M and Huang, Y and Yang, T and Zhu, C},
title = {Characteristics and Functions of Different Intestinal Segments in Juvenile Greater Amberjack (Seriola dumerili).},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {11},
pages = {},
doi = {10.3390/ani15111672},
pmid = {40509138},
issn = {2076-2615},
abstract = {The greater amberjack (Seriola dumerili), a key species in marine aquaculture, relies heavily on its intestine for nutrient absorption and immune function. However, the structural and functional specialization of its intestinal segments remains poorly understood. In this study, we divided the intestine of S. dumerili into foregut, midgut, and hindgut, and conducted a multi-omics analysis integrating histological staining (H&E/AB-PAS), digestive enzyme assays, transcriptome sequencing, and 16S rRNA microbiota profiling to characterize structural, functional, molecular, and microbial differences across intestinal segments. Histological examinations revealed that brush border microvillus length, muscle layer thickness, and folding height were significantly greater in the foregut and hindgut compared to the midgut, while mucus and goblet cell density was higher in the foregut and midgut. Digestive enzyme assays showed that lipase activity peaked in the foregut, α-amylase in the midgut, and protease in the midgut and hindgut. Alkaline phosphatase (AKP) and acid phosphatase (ACP) activities were highest in the foregut and midgut. Immune-related enzyme activities (SOD (Superoxide dismutase), GSH-Px (Glutathione peroxidase), T-AOC (Total Antioxidant Capacity)) were elevated and MDA levels were lower in the midgut, indicating its role as the primary immune site. Transcriptome analysis identified segment-specific expression of nutrient transporters, such as slc6a19b (hindgut, protein), apoa1b (foregut, lipid), and slc37a4 (midgut, carbohydrate). Microbiome analysis revealed Ruminococcus dominance in the foregut (lipid digestion) and Prevotella, Bifidobacterium, and Lactobacillus enrichment in the midgut (carbohydrate metabolism and immunity). These findings highlight functional zonation in S. dumerili: the foregut specializes in lipid digestion, the midgut in carbohydrate metabolism and immunity, and the hindgut in protein digestion. This study provides foundational insights for optimizing aquaculture practices and advancing research in nutrition, immunology, and disease modeling in S. dumerili.},
}
RevDate: 2025-06-13
A Preliminary Investigation of the Gastrointestinal Bacterial Microbiomes of Barred Owls (Strix varia) Admitted to a Wildlife Hospital.
Animals : an open access journal from MDPI, 15(11): pii:ani15111643.
Research on the gut microbiome, which includes microbial communities and genetic material in the gastrointestinal tract, has revealed essential roles beyond digestion, such as immune regulation, metabolism, and homeostasis. However, studies on birds-key ecosystem members-remain limited. Injured wild birds admitted to wildlife hospitals often receive antibiotics that can alter gut microbiota, leading to dysbiosis and promoting antimicrobial-resistant (AMR) bacteria. This study examined how hospitalization and antibiotics influence the cloacal microbiota of barred owls admitted for fracture repair. A total of 17 cloacal swab samples were analyzed using next-generation sequencing targeting 16S rRNA and AMR genes. Across all samples, Bacillota (Firmicutes), Actinomycetota (Actinobacteria), and Pseudomonadota (Proteobacteria) were the most abundant phyla. In non-antibiotic-treated owls, alpha and beta diversity showed no significant changes between admission and release; however, antibiotic-treated owls exhibited significant diversity shifts in these parameters at release. AMR genes were detected in most samples at admission, with some increasing significantly during hospitalization, suggesting an impact of antibiotic exposure. These findings provide insights into how antibiotics used in wildlife rehabilitation affect host microbiota and contribute to AMR gene dissemination.
Additional Links: PMID-40509108
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@article {pmid40509108,
year = {2025},
author = {Rhim, H and Aguilar, MG and Boykin, KL and Zapanta, K and Krumbeck, JA and Mitchell, MA},
title = {A Preliminary Investigation of the Gastrointestinal Bacterial Microbiomes of Barred Owls (Strix varia) Admitted to a Wildlife Hospital.},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {11},
pages = {},
doi = {10.3390/ani15111643},
pmid = {40509108},
issn = {2076-2615},
support = {PG007872//Louisiana State University/ ; Foundation//Fluker Farms/ ; },
abstract = {Research on the gut microbiome, which includes microbial communities and genetic material in the gastrointestinal tract, has revealed essential roles beyond digestion, such as immune regulation, metabolism, and homeostasis. However, studies on birds-key ecosystem members-remain limited. Injured wild birds admitted to wildlife hospitals often receive antibiotics that can alter gut microbiota, leading to dysbiosis and promoting antimicrobial-resistant (AMR) bacteria. This study examined how hospitalization and antibiotics influence the cloacal microbiota of barred owls admitted for fracture repair. A total of 17 cloacal swab samples were analyzed using next-generation sequencing targeting 16S rRNA and AMR genes. Across all samples, Bacillota (Firmicutes), Actinomycetota (Actinobacteria), and Pseudomonadota (Proteobacteria) were the most abundant phyla. In non-antibiotic-treated owls, alpha and beta diversity showed no significant changes between admission and release; however, antibiotic-treated owls exhibited significant diversity shifts in these parameters at release. AMR genes were detected in most samples at admission, with some increasing significantly during hospitalization, suggesting an impact of antibiotic exposure. These findings provide insights into how antibiotics used in wildlife rehabilitation affect host microbiota and contribute to AMR gene dissemination.},
}
RevDate: 2025-06-13
Postbiotic Lactiplantibacillus plantarum CECT 9161 Influences the Canine Oral Metagenome and Reduces Plaque Biofilm Formation.
Animals : an open access journal from MDPI, 15(11): pii:ani15111615.
Periodontal diseases are highly prevalent in dogs and intricately interconnected with the composition and functional attributes of the oral microbiota. The demand for non-invasive interventions to support oral health presents an opportunity for functional ingredients. The novel postbiotic heat-treated (HT) Lactiplantibacillus plantarum CECT 9161 inhibited growth and biofilm formation of oral microorganisms in vitro. The in vitro growth of saliva-derived biofilms was also inhibited and revealed microbiome modulation. Two doses of the postbiotic (LOW: 5 mg dog/day, HIGH: 25 mg/dog/day) were assessed in a placebo-controlled, double-blinded, 57-day clinical trial involving 60 dogs. Associations were found between the postbiotic, reduced plaque formation, and modulation of the oral microbiome, including increased abundance of genes involved in denitrification, heme and catechol biosynthesis, and oxidative stress reduction. The results suggest that HT Lactiplantibacillus plantarum CECT 9161 may support oral health in dogs by modifying the microbiome of supragingival plaque and reducing plaque formation.
Additional Links: PMID-40509083
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@article {pmid40509083,
year = {2025},
author = {Florit-Ruiz, A and Rago, L and Rojas, A and Guzelkhanova, B and Pont-Beltran, A and Lamelas, A and Solaz-Fuster, MC and Martinez-Blanch, JF and López, ME and García-Lainez, G and Rosier, BT and Day, R and Rubio, T and Batchelor, R and Nixon, SL},
title = {Postbiotic Lactiplantibacillus plantarum CECT 9161 Influences the Canine Oral Metagenome and Reduces Plaque Biofilm Formation.},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {11},
pages = {},
doi = {10.3390/ani15111615},
pmid = {40509083},
issn = {2076-2615},
support = {N/A//Archer Daniels Midland (United States)/ ; },
abstract = {Periodontal diseases are highly prevalent in dogs and intricately interconnected with the composition and functional attributes of the oral microbiota. The demand for non-invasive interventions to support oral health presents an opportunity for functional ingredients. The novel postbiotic heat-treated (HT) Lactiplantibacillus plantarum CECT 9161 inhibited growth and biofilm formation of oral microorganisms in vitro. The in vitro growth of saliva-derived biofilms was also inhibited and revealed microbiome modulation. Two doses of the postbiotic (LOW: 5 mg dog/day, HIGH: 25 mg/dog/day) were assessed in a placebo-controlled, double-blinded, 57-day clinical trial involving 60 dogs. Associations were found between the postbiotic, reduced plaque formation, and modulation of the oral microbiome, including increased abundance of genes involved in denitrification, heme and catechol biosynthesis, and oxidative stress reduction. The results suggest that HT Lactiplantibacillus plantarum CECT 9161 may support oral health in dogs by modifying the microbiome of supragingival plaque and reducing plaque formation.},
}
RevDate: 2025-06-13
Unlocking the Potential of Paper Mulberry Powder in Cherry Valley Ducks: Impacts on Growth, Serum Biochemistry, and Cecum Microbiome.
Animals : an open access journal from MDPI, 15(11): pii:ani15111602.
This study investigates the effects of incorporating paper mulberry (Broussonetia papyrifera L.) powder into the diets of Cherry Valley ducks on growth performance, serum biochemistry, and the gut microbiome. A total of 350 14-day-old male Cherry Valley ducks were randomly assigned to five groups receiving diets with 0%, 4%, 6%, 8%, and 10% paper mulberry powder for 42 days. Growth performance, meat quality, serum immunity, and cecal microbial composition were assessed. The results showed no significant differences in average daily feed intake and feed conversion ratio among treatments, with the 6% paper mulberry group showing the highest average daily gain (79.73 g) (p < 0.05). Meat quality parameters, including color, drip loss, cooking loss, and shear force, were not significantly affected by paper mulberry powder supplementation, while the 8% paper mulberry group showed the highest pH24 value (5.47) (p < 0.05). Serum biochemistry revealed increased total protein (G0, G4, G6, G8, and G10: 41.50, 44.47, 45.58, 45.67, and 45.85 g/L, respectively), albumin (G0, G4, G6, G8, and G10: 18.61, 19.56, 20.29, 20.2, and 20.39 g/L, respectively), total cholesterol (G0, G4, G6, G8, and G10: 5.31, 4.96, 5.37, 5.53, and 5.59 mmol/L, respectively), and high-density lipoprotein cholesterol (HDL) in ducks fed 6%, 8%, and 10% paper mulberry powder, with lower alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (TBI) in the 8% and 10% groups (p < 0.05). Cecal microbial diversity was enhanced with paper mulberry powder, particularly in the 6% group, which showed increased Bacteroides abundance (p < 0.05). Supplementing duck diets with 6% paper mulberry powder increased average daily gain, without adversely affecting meat quality and health, suggesting its potential as a sustainable feed ingredient in the duck meat industry.
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@article {pmid40509068,
year = {2025},
author = {Xiong, Y and Tang, C and Wang, X and Wang, Y and Yang, F},
title = {Unlocking the Potential of Paper Mulberry Powder in Cherry Valley Ducks: Impacts on Growth, Serum Biochemistry, and Cecum Microbiome.},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {11},
pages = {},
doi = {10.3390/ani15111602},
pmid = {40509068},
issn = {2076-2615},
support = {32201473//National Natural Science Foundation of China/ ; },
abstract = {This study investigates the effects of incorporating paper mulberry (Broussonetia papyrifera L.) powder into the diets of Cherry Valley ducks on growth performance, serum biochemistry, and the gut microbiome. A total of 350 14-day-old male Cherry Valley ducks were randomly assigned to five groups receiving diets with 0%, 4%, 6%, 8%, and 10% paper mulberry powder for 42 days. Growth performance, meat quality, serum immunity, and cecal microbial composition were assessed. The results showed no significant differences in average daily feed intake and feed conversion ratio among treatments, with the 6% paper mulberry group showing the highest average daily gain (79.73 g) (p < 0.05). Meat quality parameters, including color, drip loss, cooking loss, and shear force, were not significantly affected by paper mulberry powder supplementation, while the 8% paper mulberry group showed the highest pH24 value (5.47) (p < 0.05). Serum biochemistry revealed increased total protein (G0, G4, G6, G8, and G10: 41.50, 44.47, 45.58, 45.67, and 45.85 g/L, respectively), albumin (G0, G4, G6, G8, and G10: 18.61, 19.56, 20.29, 20.2, and 20.39 g/L, respectively), total cholesterol (G0, G4, G6, G8, and G10: 5.31, 4.96, 5.37, 5.53, and 5.59 mmol/L, respectively), and high-density lipoprotein cholesterol (HDL) in ducks fed 6%, 8%, and 10% paper mulberry powder, with lower alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (TBI) in the 8% and 10% groups (p < 0.05). Cecal microbial diversity was enhanced with paper mulberry powder, particularly in the 6% group, which showed increased Bacteroides abundance (p < 0.05). Supplementing duck diets with 6% paper mulberry powder increased average daily gain, without adversely affecting meat quality and health, suggesting its potential as a sustainable feed ingredient in the duck meat industry.},
}
RevDate: 2025-06-13
Characterisation of the Gastrointestinal Microbiome of Green Sea Turtles (Chelonia mydas): A Systematic Review.
Animals : an open access journal from MDPI, 15(11): pii:ani15111594.
The gut microbiome of sea turtles is essential for their ecological resilience and adaptation to environmental stressors. We hypothesised that different gut microbial profiles existed between green sea turtles kept in captivity and those in the wild. The aim of this systematic review was to determine dominant bacterial phyla in the gut microbiomes of wild and captive green sea turtles. Comparison of the top four bacterial phyla revealed that Bacillota was the most abundant phylum in captive turtles (40.9-87.5%), but it only ranked second (3.5-57.8%) in wild turtles. Bacteroidota had comparable relative abundance in captive (8.7-45.6%) and wild (3.6-43.1%) populations. By contrast, the relative abundance of Pseudomonadota was higher in wild turtles (6.2-68.1%) compared to the captive population (0.1-6.6%). Verrucomicrobiota was less prevalent in wild and captive populations, with relative abundances ranging from 0.28 to 5.4% and 2.3 to 7.2%, respectively. These findings highlight a putative gut microbial shift between wild and captive green sea turtle populations. This shift may be shaped by variations in environmental factors in captivity or the wild. Nonetheless, the significance of these putative changes is still unknown; the potential to use microbial shifts to guide management, rehabilitation, and conservation of green sea turtles is promising, but remains limited.
Additional Links: PMID-40509060
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@article {pmid40509060,
year = {2025},
author = {Ghafoor, D and Hayakijkosol, O and Ewels, C and Kinobe, R},
title = {Characterisation of the Gastrointestinal Microbiome of Green Sea Turtles (Chelonia mydas): A Systematic Review.},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {11},
pages = {},
doi = {10.3390/ani15111594},
pmid = {40509060},
issn = {2076-2615},
abstract = {The gut microbiome of sea turtles is essential for their ecological resilience and adaptation to environmental stressors. We hypothesised that different gut microbial profiles existed between green sea turtles kept in captivity and those in the wild. The aim of this systematic review was to determine dominant bacterial phyla in the gut microbiomes of wild and captive green sea turtles. Comparison of the top four bacterial phyla revealed that Bacillota was the most abundant phylum in captive turtles (40.9-87.5%), but it only ranked second (3.5-57.8%) in wild turtles. Bacteroidota had comparable relative abundance in captive (8.7-45.6%) and wild (3.6-43.1%) populations. By contrast, the relative abundance of Pseudomonadota was higher in wild turtles (6.2-68.1%) compared to the captive population (0.1-6.6%). Verrucomicrobiota was less prevalent in wild and captive populations, with relative abundances ranging from 0.28 to 5.4% and 2.3 to 7.2%, respectively. These findings highlight a putative gut microbial shift between wild and captive green sea turtle populations. This shift may be shaped by variations in environmental factors in captivity or the wild. Nonetheless, the significance of these putative changes is still unknown; the potential to use microbial shifts to guide management, rehabilitation, and conservation of green sea turtles is promising, but remains limited.},
}
RevDate: 2025-06-13
Acute Effect of Short-Term Benzocaine Anesthesia on the Skin Mucus Microbiome of Atlantic salmon (Salmo salar).
Animals : an open access journal from MDPI, 15(11): pii:ani15111566.
Routine aquaculture practices such as capture, transportation, and handling can disrupt the relationship between commensal and opportunistic bacteria in the fish skin microbiome. Anesthetic baths are a common welfare practice in aquaculture to reduce stress during handling. However, to date, no studies assessed the effect of anesthetics on bacterial communities in fish skin mucus. This study is the first to evaluate the influence of benzocaine, a widely used anesthetic, on the skin mucus bacterial microbiome of Atlantic salmon reared in a recirculating aquaculture system (RAS). Using Illumina high-throughput 16S rRNA gene sequencing, we found that bacterial richness and diversity were significantly reduced in skin mucus samples from fish with anesthesia (ANE) when compared with those without anesthesia (CTR). The predominant bacterial classes in both groups were Gammaproteobacteria (54.1-62.6%) and Betaproteobacteria (22.6-22.9%). However, significant dissimilarities in beta diversity were observed between the bacterial community structure of salmon skin mucus samples from ANE and CTR. These findings demonstrate that benzocaine exposure alters skin mucus microbiome of Atlantic salmon potentially leading to dysbiosis. This study also provides baseline information on the bacterial communities of Atlantic salmon skin mucus microbiome in an RAS. As no temporal resampling was performed, the duration and persistence of these changes remain unknown and warrant further investigation.
Additional Links: PMID-40509032
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@article {pmid40509032,
year = {2025},
author = {Martins, P and Pimentel, T and Ribeiro, N and Calado, R},
title = {Acute Effect of Short-Term Benzocaine Anesthesia on the Skin Mucus Microbiome of Atlantic salmon (Salmo salar).},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {11},
pages = {},
doi = {10.3390/ani15111566},
pmid = {40509032},
issn = {2076-2615},
support = {UIDP/50017/2020+UIDB/50017/2020+LA/P/0094/2020//Centro de Estudos Ambientais e Marinhos/ ; },
abstract = {Routine aquaculture practices such as capture, transportation, and handling can disrupt the relationship between commensal and opportunistic bacteria in the fish skin microbiome. Anesthetic baths are a common welfare practice in aquaculture to reduce stress during handling. However, to date, no studies assessed the effect of anesthetics on bacterial communities in fish skin mucus. This study is the first to evaluate the influence of benzocaine, a widely used anesthetic, on the skin mucus bacterial microbiome of Atlantic salmon reared in a recirculating aquaculture system (RAS). Using Illumina high-throughput 16S rRNA gene sequencing, we found that bacterial richness and diversity were significantly reduced in skin mucus samples from fish with anesthesia (ANE) when compared with those without anesthesia (CTR). The predominant bacterial classes in both groups were Gammaproteobacteria (54.1-62.6%) and Betaproteobacteria (22.6-22.9%). However, significant dissimilarities in beta diversity were observed between the bacterial community structure of salmon skin mucus samples from ANE and CTR. These findings demonstrate that benzocaine exposure alters skin mucus microbiome of Atlantic salmon potentially leading to dysbiosis. This study also provides baseline information on the bacterial communities of Atlantic salmon skin mucus microbiome in an RAS. As no temporal resampling was performed, the duration and persistence of these changes remain unknown and warrant further investigation.},
}
RevDate: 2025-06-13
Effects of Grazing in a Low Deciduous Forest on Rumen Microbiota and Volatile Fatty Acid Production in Lambs.
Animals : an open access journal from MDPI, 15(11): pii:ani15111565.
The aim of the present study was to evaluate the effect of grazing the low deciduous forest (LDF) vegetation on the diversity of the rumen microbiome in growing lambs and its relationship with volatile fatty acid (VFA) profiles. After a 35-day indoor acclimatization (stabilization period), the lambs were assigned to two groups: housed (CG, n = 4) and grazing (EG, n = 4). The grazing lambs had a 14-day habituation period in the LDF (4 h/day) and a further 30 grazing days when fodder intake was observed. Ruminal samples were collected at the end of the stabilization, on day 14 post-stabilization (14DPS), and on day 44 post-stabilization (44DPS). The ruminal butyrate concentration showed a progressive decrease of approximately 23% over the time (p = 0.0130). The qualitative composition (p = 0.001) and relative proportions of bacteria (p = 0.004) in EG-44DPS exhibited a greater diversity, with 107 total genera and 19 unique, significant abundances in 13 genera with a higher presence of Bacteroidales_RF16_group, Lachnospiraceae_ND3007_group, and WCHB1-41. Moreover, significant functional profiles are associated with key metabolic pathways in bacteria and are interconnected by the need to generate energy and biosynthetic precursors and to manage available nitrogen and carbon. Finally, eight bacterial genera were identified as biomarkers correlated with the increase in VFA in EG-44DPS.
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@article {pmid40509031,
year = {2025},
author = {Ávila-Cervantes, R and González-Pech, P and Sandoval-Castro, C and Torres-Acosta, F and Ramos-Zapata, J and Galicia-Jiménez, M and Pacheco-Arjona, R},
title = {Effects of Grazing in a Low Deciduous Forest on Rumen Microbiota and Volatile Fatty Acid Production in Lambs.},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {11},
pages = {},
doi = {10.3390/ani15111565},
pmid = {40509031},
issn = {2076-2615},
abstract = {The aim of the present study was to evaluate the effect of grazing the low deciduous forest (LDF) vegetation on the diversity of the rumen microbiome in growing lambs and its relationship with volatile fatty acid (VFA) profiles. After a 35-day indoor acclimatization (stabilization period), the lambs were assigned to two groups: housed (CG, n = 4) and grazing (EG, n = 4). The grazing lambs had a 14-day habituation period in the LDF (4 h/day) and a further 30 grazing days when fodder intake was observed. Ruminal samples were collected at the end of the stabilization, on day 14 post-stabilization (14DPS), and on day 44 post-stabilization (44DPS). The ruminal butyrate concentration showed a progressive decrease of approximately 23% over the time (p = 0.0130). The qualitative composition (p = 0.001) and relative proportions of bacteria (p = 0.004) in EG-44DPS exhibited a greater diversity, with 107 total genera and 19 unique, significant abundances in 13 genera with a higher presence of Bacteroidales_RF16_group, Lachnospiraceae_ND3007_group, and WCHB1-41. Moreover, significant functional profiles are associated with key metabolic pathways in bacteria and are interconnected by the need to generate energy and biosynthetic precursors and to manage available nitrogen and carbon. Finally, eight bacterial genera were identified as biomarkers correlated with the increase in VFA in EG-44DPS.},
}
RevDate: 2025-06-13
Soil-Gradient-Derived Bacterial Synthetic Communities Enhance Drought Tolerance in Quercus pubescens and Sorbus domestica Seedlings.
Plants (Basel, Switzerland), 14(11): pii:plants14111659.
Climate-change-induced drought threatens forest restoration by limiting seedling establishment. To address this, we developed synthetic bacterial communities (SynComs) tailored to support drought tolerance in two Mediterranean tree species, Quercus pubescens and Sorbus domestica. Bacteria were isolated from forest soil exposed to long-term drought, sampling across soil depths and root-associated compartments. We selected strains with key plant-beneficial traits, including exopolysaccharide (EPS) production, hormone synthesis (auxin, ABA), siderophore release, and osmotic tolerance. SynComs were assembled based on functional complementarity and ecological origin. Biofilm assays showed that even weak individual producers could enhance community-level performance. After initial screening on Arabidopsis thaliana, the most and least effective SynComs were tested on Q. pubescens and S. domestica seedlings. Compared to controls, the best-performing SynComs reduced the proportion of drought-symptomatic seedlings by 47% in Q. pubescens and 71% in S. domestica, outperforming single-strain inoculants. Notably, EPS-rich SynCom B aligned with the conservative root traits of Q. pubescens, while hormone-rich SynCom F matched the acquisitive strategy of S. domestica. Predictive modeling identified bacterial identity and symptom timing as key predictors of drought resilience. Our results highlight the value of matching microbial traits with plant strategies and drought context for climate-smart forest restoration.
Additional Links: PMID-40508333
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PubMed:
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@article {pmid40508333,
year = {2025},
author = {Aleksieienko, I and Fernandes Hertel, M and Reilhan, J and de Castro, M and Légeret, B and Caixeta Oliveira, H and Reiter, IM and Santaella, C},
title = {Soil-Gradient-Derived Bacterial Synthetic Communities Enhance Drought Tolerance in Quercus pubescens and Sorbus domestica Seedlings.},
journal = {Plants (Basel, Switzerland)},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/plants14111659},
pmid = {40508333},
issn = {2223-7747},
support = {101094587//HORIZON EUROPE INFRA-2022-TECH project 'PHENET'/ ; 88887.712065/2022-00//Coordenação de Aperfeicoamento de Pessoal de Nível Superior/ ; ANR-20-EBI5-0008-07//Agence Nationale de la Recherche/ ; ANR-20-EBI5-0008-07//2019-2020 BiodivERsA+ joint call, BiodivClim ERA-Net COFUND, Fundação Araucária/Secretaria de Estado da Ciência, Tecnologia e Ensino Superior do Paraná (NAPI Biodiversidade), FAPESP (BR), ANR (FR), Federal Ministry of Education and Research (DE)/ ; Sv 946/10 - 41880PL//CAPES-COFECUB/ ; },
abstract = {Climate-change-induced drought threatens forest restoration by limiting seedling establishment. To address this, we developed synthetic bacterial communities (SynComs) tailored to support drought tolerance in two Mediterranean tree species, Quercus pubescens and Sorbus domestica. Bacteria were isolated from forest soil exposed to long-term drought, sampling across soil depths and root-associated compartments. We selected strains with key plant-beneficial traits, including exopolysaccharide (EPS) production, hormone synthesis (auxin, ABA), siderophore release, and osmotic tolerance. SynComs were assembled based on functional complementarity and ecological origin. Biofilm assays showed that even weak individual producers could enhance community-level performance. After initial screening on Arabidopsis thaliana, the most and least effective SynComs were tested on Q. pubescens and S. domestica seedlings. Compared to controls, the best-performing SynComs reduced the proportion of drought-symptomatic seedlings by 47% in Q. pubescens and 71% in S. domestica, outperforming single-strain inoculants. Notably, EPS-rich SynCom B aligned with the conservative root traits of Q. pubescens, while hormone-rich SynCom F matched the acquisitive strategy of S. domestica. Predictive modeling identified bacterial identity and symptom timing as key predictors of drought resilience. Our results highlight the value of matching microbial traits with plant strategies and drought context for climate-smart forest restoration.},
}
RevDate: 2025-06-13
Application of a Synthetic Microbial Community to Enhance Pepper Resistance Against Phytophthora capsici.
Plants (Basel, Switzerland), 14(11): pii:plants14111625.
Pepper (Capsicum annuum) production faces significant challenges from soil-borne pathogens, particularly Phytophthora capsici, which induces root rot and damping-off diseases. Management of this pathogen remains challenging owing to the scarcity of resistant cultivars and the ineffectiveness of chemical control methods. A single strain has been used to prevent pathogenic disease, and this approach limits the exploration of consortia comprising different genera. In this study, we isolated five bacterial strains (Bacillus sp. T3, Flavobacterium anhuiense T4, Cytobacillus firmus T8, Streptomyces roseicoloratus T14, and Pseudomonas frederiksbergensis A6) from the rhizosphere of healthy pepper plants. We then applied this 5-isolate synthetic microbial community (SynCom) to Capsicum annuum to evaluate its efficacy in improving pepper resilience against P. capsici. The SynCom members exhibited phosphate solubilization, indole-3-acetic acid production, catalase activity, siderophore synthesis, and strong antagonism against P. capsici. The SynCom reduced disease severity and enhanced the growth of pepper plants. Furthermore, the beneficial genera such as Bacillus, Fusicolla, and Trichoderma, significantly increased in the rhizosphere of pepper after the application of the SynCom. Microbial functional prediction analysis revealed that these microbial shifts were associated with nitrogen cycling and pathogen suppression. Our SynCom approach demonstrates the effectiveness of microbial consortia in promoting the growth of pathogen-infected plants by reprogramming the microbial community in the rhizosphere.
Additional Links: PMID-40508300
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@article {pmid40508300,
year = {2025},
author = {Bashizi, TF and Kim, MJ and Lim, K and Lee, G and Tagele, SB and Shin, JH},
title = {Application of a Synthetic Microbial Community to Enhance Pepper Resistance Against Phytophthora capsici.},
journal = {Plants (Basel, Switzerland)},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/plants14111625},
pmid = {40508300},
issn = {2223-7747},
support = {2021R1A6C101A416//Korea Basic Science Institute/ ; },
abstract = {Pepper (Capsicum annuum) production faces significant challenges from soil-borne pathogens, particularly Phytophthora capsici, which induces root rot and damping-off diseases. Management of this pathogen remains challenging owing to the scarcity of resistant cultivars and the ineffectiveness of chemical control methods. A single strain has been used to prevent pathogenic disease, and this approach limits the exploration of consortia comprising different genera. In this study, we isolated five bacterial strains (Bacillus sp. T3, Flavobacterium anhuiense T4, Cytobacillus firmus T8, Streptomyces roseicoloratus T14, and Pseudomonas frederiksbergensis A6) from the rhizosphere of healthy pepper plants. We then applied this 5-isolate synthetic microbial community (SynCom) to Capsicum annuum to evaluate its efficacy in improving pepper resilience against P. capsici. The SynCom members exhibited phosphate solubilization, indole-3-acetic acid production, catalase activity, siderophore synthesis, and strong antagonism against P. capsici. The SynCom reduced disease severity and enhanced the growth of pepper plants. Furthermore, the beneficial genera such as Bacillus, Fusicolla, and Trichoderma, significantly increased in the rhizosphere of pepper after the application of the SynCom. Microbial functional prediction analysis revealed that these microbial shifts were associated with nitrogen cycling and pathogen suppression. Our SynCom approach demonstrates the effectiveness of microbial consortia in promoting the growth of pathogen-infected plants by reprogramming the microbial community in the rhizosphere.},
}
RevDate: 2025-06-13
Functional Roles of the Seagrass (Zostera marina) Holobiont Change with Plant Development.
Plants (Basel, Switzerland), 14(11): pii:plants14111584.
Seagrass meadows play a critical role in biogeochemical cycling, especially in nitrogen and sulphur processes, driven by their associated microbiome. This study provides a novel functional analysis of microbial communities in seagrass (Zostera marina) rhizosphere and endosphere, comparing seedlings and mature plants. While nitrogen-fixing bacteria are more abundant in seedlings, mature plants exhibit greater microbial diversity and stability. Sediment samples show higher microbial diversity than roots, suggesting distinct niche environments in seagrass roots. Key microbial taxa (sulphur-oxidizing and nitrogen-cycling bacteria) were observed across developmental stages, with rapid establishment in seedlings aiding survival in sulphide-rich, anoxic sediments. Chromatiales, which oxidize sulphur, are hypothesized to support juvenile plant growth by mitigating sulphide toxicity, a key stressor in early development. Additionally, sulfate-reducing bacteria (SRB), though potentially harmful due to H2S production, may also aid in nitrogen fixation by producing ammonium. The study underscores the dynamic relationship between seagrass and its microbiome, especially the differences in microbial community structure and function between juvenile and mature plants. The study emphasizes the need for a deeper understanding of microbial roles within the seagrass holobiont to aid with Blue Carbon stores and to improve restoration success, particularly for juvenile plants struggling to establish effective microbiomes.
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@article {pmid40508259,
year = {2025},
author = {Gorvel, S and Walter, B and Taylor, JD and Unsworth, RKF},
title = {Functional Roles of the Seagrass (Zostera marina) Holobiont Change with Plant Development.},
journal = {Plants (Basel, Switzerland)},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/plants14111584},
pmid = {40508259},
issn = {2223-7747},
abstract = {Seagrass meadows play a critical role in biogeochemical cycling, especially in nitrogen and sulphur processes, driven by their associated microbiome. This study provides a novel functional analysis of microbial communities in seagrass (Zostera marina) rhizosphere and endosphere, comparing seedlings and mature plants. While nitrogen-fixing bacteria are more abundant in seedlings, mature plants exhibit greater microbial diversity and stability. Sediment samples show higher microbial diversity than roots, suggesting distinct niche environments in seagrass roots. Key microbial taxa (sulphur-oxidizing and nitrogen-cycling bacteria) were observed across developmental stages, with rapid establishment in seedlings aiding survival in sulphide-rich, anoxic sediments. Chromatiales, which oxidize sulphur, are hypothesized to support juvenile plant growth by mitigating sulphide toxicity, a key stressor in early development. Additionally, sulfate-reducing bacteria (SRB), though potentially harmful due to H2S production, may also aid in nitrogen fixation by producing ammonium. The study underscores the dynamic relationship between seagrass and its microbiome, especially the differences in microbial community structure and function between juvenile and mature plants. The study emphasizes the need for a deeper understanding of microbial roles within the seagrass holobiont to aid with Blue Carbon stores and to improve restoration success, particularly for juvenile plants struggling to establish effective microbiomes.},
}
RevDate: 2025-06-13
CmpDate: 2025-06-13
α-Synuclein Pathology in Synucleinopathies: Mechanisms, Biomarkers, and Therapeutic Challenges.
International journal of molecular sciences, 26(11): pii:ijms26115405.
Parkinson's disease and related synucleinopathies, including dementia with Lewy bodies and multiple system atrophy, are characterised by the pathological aggregation of the α-synuclein (aSyn) protein in neuronal and glial cells, leading to cellular dysfunction and neurodegeneration. This review synthesizes knowledge of aSyn biology, including its structure, aggregation mechanisms, cellular interactions, and systemic influences. We highlight the structural diversity of aSyn aggregates, ranging from oligomers to fibrils, their strain-like properties, and their prion-like propagation. While the role of prion-like mechanisms in disease progression remains a topic of ongoing debate, these processes may contribute to the clinical heterogeneity of synucleinopathies. Dysregulation of protein clearance pathways, including chaperone-mediated autophagy and the ubiquitin-proteasome system, exacerbates aSyn accumulation, while post-translational modifications influence its toxicity and aggregation propensity. Emerging evidence suggests that immune responses and alterations in the gut microbiome are key modulators of aSyn pathology, linking peripheral processes-particularly those of intestinal origin-to central neurodegeneration. Advances in biomarker development, such as cerebrospinal fluid assays, post-translationally modified aSyn, and real-time quaking-induced conversion technology, hold promise for early diagnosis and disease monitoring. Furthermore, positron emission tomography imaging and conformation-specific antibodies offer innovative tools for visualising and targeting aSyn pathology in vivo. Despite significant progress, challenges remain in accurately modelling human synucleinopathies, as existing animal and cellular models capture only specific aspects of the disease. This review underscores the need for more reliable aSyn biomarkers to facilitate the development of effective treatments. Achieving this goal requires an interdisciplinary approach integrating genetic, epigenetic, and environmental insights.
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@article {pmid40508212,
year = {2025},
author = {Arias-Carrión, O and Guerra-Crespo, M and Padilla-Godínez, FJ and Soto-Rojas, LO and Manjarrez, E},
title = {α-Synuclein Pathology in Synucleinopathies: Mechanisms, Biomarkers, and Therapeutic Challenges.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115405},
pmid = {40508212},
issn = {1422-0067},
mesh = {Humans ; *alpha-Synuclein/metabolism/chemistry/genetics ; Biomarkers/metabolism ; *Synucleinopathies/metabolism/pathology/therapy/diagnosis ; Animals ; Parkinson Disease/metabolism/pathology ; Protein Aggregation, Pathological/metabolism ; },
abstract = {Parkinson's disease and related synucleinopathies, including dementia with Lewy bodies and multiple system atrophy, are characterised by the pathological aggregation of the α-synuclein (aSyn) protein in neuronal and glial cells, leading to cellular dysfunction and neurodegeneration. This review synthesizes knowledge of aSyn biology, including its structure, aggregation mechanisms, cellular interactions, and systemic influences. We highlight the structural diversity of aSyn aggregates, ranging from oligomers to fibrils, their strain-like properties, and their prion-like propagation. While the role of prion-like mechanisms in disease progression remains a topic of ongoing debate, these processes may contribute to the clinical heterogeneity of synucleinopathies. Dysregulation of protein clearance pathways, including chaperone-mediated autophagy and the ubiquitin-proteasome system, exacerbates aSyn accumulation, while post-translational modifications influence its toxicity and aggregation propensity. Emerging evidence suggests that immune responses and alterations in the gut microbiome are key modulators of aSyn pathology, linking peripheral processes-particularly those of intestinal origin-to central neurodegeneration. Advances in biomarker development, such as cerebrospinal fluid assays, post-translationally modified aSyn, and real-time quaking-induced conversion technology, hold promise for early diagnosis and disease monitoring. Furthermore, positron emission tomography imaging and conformation-specific antibodies offer innovative tools for visualising and targeting aSyn pathology in vivo. Despite significant progress, challenges remain in accurately modelling human synucleinopathies, as existing animal and cellular models capture only specific aspects of the disease. This review underscores the need for more reliable aSyn biomarkers to facilitate the development of effective treatments. Achieving this goal requires an interdisciplinary approach integrating genetic, epigenetic, and environmental insights.},
}
MeSH Terms:
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Humans
*alpha-Synuclein/metabolism/chemistry/genetics
Biomarkers/metabolism
*Synucleinopathies/metabolism/pathology/therapy/diagnosis
Animals
Parkinson Disease/metabolism/pathology
Protein Aggregation, Pathological/metabolism
RevDate: 2025-06-13
CmpDate: 2025-06-13
Colonizing Bacteria Aggravate Inflammation, Cytotoxicity and Immune Defense During Influenza A Virus Infection.
International journal of molecular sciences, 26(11): pii:ijms26115364.
A diverse bacterial community colonizes the respiratory system, including commensals such as Staphylococcus epidermidis (S. epidermidis) and Streptococcus salivarius (S. salivarius), as well as facultative pathogens like Staphylococcus aureus (S. aureus). This study aimed to establish a colonized cell culture model to investigate the impact of these bacteria on influenza A virus (IAV) infection. Respiratory epithelial cells were exposed to S. epidermidis, S. salivarius, or S. aureus, using either live or heat-inactivated bacteria, followed by IAV infection. Cell integrity was assessed microscopically, cytotoxicity was measured via LDH assay, and inflammatory responses were analyzed through cytokine expression. Additionally, macrophage function was examined in response to bacterial colonization and IAV infection. While commensals maintained epithelial integrity for 48 h, S. aureus induced severe cell damage and death. The most pronounced epithelial destruction was caused by coinfection with S. aureus and IAV. Notably, commensals did not confer protection against IAV but instead enhanced epithelial inflammation. These effects were dependent on live bacteria, as inactivated bacteria had no impact. However, prior exposure to S. epidermidis and S. salivarius improved macrophage-mediated immune responses against IAV. These findings suggest that while individual commensals do not directly protect epithelial cells, they may contribute to immune training and enhance lung defense mechanisms.
Additional Links: PMID-40508173
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@article {pmid40508173,
year = {2025},
author = {Giebeler, L and Ehrhardt, C and Häder, A and Lauf, T and Deinhardt-Emmer, S and Löffler, B},
title = {Colonizing Bacteria Aggravate Inflammation, Cytotoxicity and Immune Defense During Influenza A Virus Infection.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115364},
pmid = {40508173},
issn = {1422-0067},
support = {LPI-BT1 and BT2//BMBF/ ; EXC 2051-Project-ID 390713860 and SFB 1278/2, D02//Deutsche Forschungsgemeinschaft/ ; },
mesh = {Humans ; *Influenza A virus/immunology ; *Inflammation/microbiology/immunology ; Macrophages/immunology/microbiology ; Staphylococcus aureus/immunology ; Animals ; *Influenza, Human/immunology/microbiology/virology ; Epithelial Cells/microbiology/virology/immunology ; Staphylococcus epidermidis/immunology ; Cytokines/metabolism ; Coinfection/microbiology/immunology ; *Orthomyxoviridae Infections/immunology/microbiology ; A549 Cells ; },
abstract = {A diverse bacterial community colonizes the respiratory system, including commensals such as Staphylococcus epidermidis (S. epidermidis) and Streptococcus salivarius (S. salivarius), as well as facultative pathogens like Staphylococcus aureus (S. aureus). This study aimed to establish a colonized cell culture model to investigate the impact of these bacteria on influenza A virus (IAV) infection. Respiratory epithelial cells were exposed to S. epidermidis, S. salivarius, or S. aureus, using either live or heat-inactivated bacteria, followed by IAV infection. Cell integrity was assessed microscopically, cytotoxicity was measured via LDH assay, and inflammatory responses were analyzed through cytokine expression. Additionally, macrophage function was examined in response to bacterial colonization and IAV infection. While commensals maintained epithelial integrity for 48 h, S. aureus induced severe cell damage and death. The most pronounced epithelial destruction was caused by coinfection with S. aureus and IAV. Notably, commensals did not confer protection against IAV but instead enhanced epithelial inflammation. These effects were dependent on live bacteria, as inactivated bacteria had no impact. However, prior exposure to S. epidermidis and S. salivarius improved macrophage-mediated immune responses against IAV. These findings suggest that while individual commensals do not directly protect epithelial cells, they may contribute to immune training and enhance lung defense mechanisms.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Influenza A virus/immunology
*Inflammation/microbiology/immunology
Macrophages/immunology/microbiology
Staphylococcus aureus/immunology
Animals
*Influenza, Human/immunology/microbiology/virology
Epithelial Cells/microbiology/virology/immunology
Staphylococcus epidermidis/immunology
Cytokines/metabolism
Coinfection/microbiology/immunology
*Orthomyxoviridae Infections/immunology/microbiology
A549 Cells
RevDate: 2025-06-13
CmpDate: 2025-06-13
Microbiome Engineering for Biotherapeutic in Alzheimer's Disease Through the Gut-Brain Axis: Potentials and Limitations.
International journal of molecular sciences, 26(11): pii:ijms26115351.
Alzheimer's disease (AD) is a neurodegenerative condition characterized by considerable cognitive decline and functional impairment, primarily due to the progressive alteration of neurons, microglia, and astrocytes. Pathological manifestations of AD include the loss of synaptic plasticity, reduction in synaptic strength by amyloid-beta, aggregation, and neurotoxicity from tau protein post-translational modifications, all contributing to the disruption of neural networks. Despite its current pharmacological treatment for AD, different approaches to treat such disease are being developed, from a microbiome perspective. The microbiome encompasses a diverse microorganism, including beneficial bacteria that create a positive impact to diminish AD pathogenesis. Growing evidence suggests that probiotic, prebiotic, synbiotic, and postbiotics can positively modulate the gut-brain axis, reducing systemic inflammation, restoring neurotransmitter balance, and improving gut health, thereby possibly mitigating AD pathogenesis. Moreover, there is paraprobiotics as the most recently developed biotherapeutic with beneficial effects. This review explores the correlation between AD and gut-brain axis as a novel biotherapeutic target. The underlying mechanism of the microbiota-gut-brain axis in AD is examined. Novel insights into the current applications as potential treatment and its limitations are highlighted.
Additional Links: PMID-40508160
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PubMed:
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@article {pmid40508160,
year = {2025},
author = {Renesteen, E and Boyajian, JL and Islam, P and Kassab, A and Abosalha, A and Makhlouf, S and Santos, M and Chen, H and Shum-Tim, C and Prakash, S},
title = {Microbiome Engineering for Biotherapeutic in Alzheimer's Disease Through the Gut-Brain Axis: Potentials and Limitations.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115351},
pmid = {40508160},
issn = {1422-0067},
support = {252743//CIHR/ ; //Indonesia Endowment Fund for Education from the Ministry of Finance of the Republic of Indonesia/ ; 335999//Fonds de Recherche du Québec - Santé (FRQS)/ ; 2020-245622//Islamic Development Bank Scholarship/ ; //The Ministry of Higher Education of the Arab Republic of Egypt/ ; 504933//Canadian Graduate Scholarship-Masters from the Natural Sciences and Engineering Research Council (NSERC)/ ; 351337//Fonds de Recherche du Québec - Santé (FRQS)/ ; },
mesh = {Humans ; *Alzheimer Disease/therapy/microbiology/metabolism ; *Gastrointestinal Microbiome ; *Brain/metabolism ; Probiotics/therapeutic use ; Animals ; Prebiotics/administration & dosage ; *Brain-Gut Axis ; *Biological Therapy/methods ; },
abstract = {Alzheimer's disease (AD) is a neurodegenerative condition characterized by considerable cognitive decline and functional impairment, primarily due to the progressive alteration of neurons, microglia, and astrocytes. Pathological manifestations of AD include the loss of synaptic plasticity, reduction in synaptic strength by amyloid-beta, aggregation, and neurotoxicity from tau protein post-translational modifications, all contributing to the disruption of neural networks. Despite its current pharmacological treatment for AD, different approaches to treat such disease are being developed, from a microbiome perspective. The microbiome encompasses a diverse microorganism, including beneficial bacteria that create a positive impact to diminish AD pathogenesis. Growing evidence suggests that probiotic, prebiotic, synbiotic, and postbiotics can positively modulate the gut-brain axis, reducing systemic inflammation, restoring neurotransmitter balance, and improving gut health, thereby possibly mitigating AD pathogenesis. Moreover, there is paraprobiotics as the most recently developed biotherapeutic with beneficial effects. This review explores the correlation between AD and gut-brain axis as a novel biotherapeutic target. The underlying mechanism of the microbiota-gut-brain axis in AD is examined. Novel insights into the current applications as potential treatment and its limitations are highlighted.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Alzheimer Disease/therapy/microbiology/metabolism
*Gastrointestinal Microbiome
*Brain/metabolism
Probiotics/therapeutic use
Animals
Prebiotics/administration & dosage
*Brain-Gut Axis
*Biological Therapy/methods
RevDate: 2025-06-13
CmpDate: 2025-06-13
Quorum Signaling Molecules: Interactions Between Plants and Associated Pathogens.
International journal of molecular sciences, 26(11): pii:ijms26115235.
The morphogenesis and defense evolution of plants are intricately linked to soil microbial community dynamics, where beneficial and pathogenic bacteria regulate ecosystem stability through chemical signaling. A microbial communication mechanism known as quorum sensing (QS), which affects population density, virulence, and biofilm formation, substantially impacts plant development and immune responses. However, plants have developed strategies to detect and manipulate QS signals, enabling bidirectional interactions that influence both plant physiology and the balance of the microbiome. In this review, QS signals from bacteria, fungi, and nematodes are systematically examined, emphasizing their recognition by plant receptors, downstream signaling pathways, and the activation of defense responses. Most significantly, attention is given to the role of fungal and nematode QS molecules in modulating plant microbe interactions. By elucidating these communication networks, we highlight their potential applications in sustainable agriculture, offering novel insights into crop health management and ecosystem resilience.
Additional Links: PMID-40508052
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@article {pmid40508052,
year = {2025},
author = {Zheng, X and Liu, J and Wang, X},
title = {Quorum Signaling Molecules: Interactions Between Plants and Associated Pathogens.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115235},
pmid = {40508052},
issn = {1422-0067},
support = {202201BC070004//The Science and Technology Major Project from Yunnan Province/ ; 32370138//The National Natural Science Foundation of China/ ; 32260029//The National Natural Science Foundation of China/ ; 202201AT070089//The Applied Basic Research Foundation of Yunnan Province/ ; 2023YFD1400013//The National Key Research and Development Program/ ; },
mesh = {*Quorum Sensing ; *Plants/microbiology/metabolism/parasitology ; Signal Transduction ; Fungi/pathogenicity/metabolism ; Animals ; Bacteria/pathogenicity/metabolism ; Nematoda/physiology ; *Host-Pathogen Interactions ; Plant Diseases/microbiology ; Microbiota ; },
abstract = {The morphogenesis and defense evolution of plants are intricately linked to soil microbial community dynamics, where beneficial and pathogenic bacteria regulate ecosystem stability through chemical signaling. A microbial communication mechanism known as quorum sensing (QS), which affects population density, virulence, and biofilm formation, substantially impacts plant development and immune responses. However, plants have developed strategies to detect and manipulate QS signals, enabling bidirectional interactions that influence both plant physiology and the balance of the microbiome. In this review, QS signals from bacteria, fungi, and nematodes are systematically examined, emphasizing their recognition by plant receptors, downstream signaling pathways, and the activation of defense responses. Most significantly, attention is given to the role of fungal and nematode QS molecules in modulating plant microbe interactions. By elucidating these communication networks, we highlight their potential applications in sustainable agriculture, offering novel insights into crop health management and ecosystem resilience.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Quorum Sensing
*Plants/microbiology/metabolism/parasitology
Signal Transduction
Fungi/pathogenicity/metabolism
Animals
Bacteria/pathogenicity/metabolism
Nematoda/physiology
*Host-Pathogen Interactions
Plant Diseases/microbiology
Microbiota
RevDate: 2025-06-13
CmpDate: 2025-06-13
Impact of DNA Extraction and 16S rRNA Gene Amplification Strategy on Microbiota Profiling of Faecal Samples.
International journal of molecular sciences, 26(11): pii:ijms26115226.
High-throughput 16S rRNA metagenomic sequencing has advanced our understanding of the gut microbiome, but its reliability depends on upstream processes such as DNA extraction and bacterial library preparation. In this study, we evaluated the impact of three different DNA extraction methods (a manual method with an ad hoc-designed pre-extraction phase (PE-QIA), and two automated magnetic bead-based methods (T180H and TAT132H)) and two bacterial library preparation protocols (home brew and VeriFi) on the 16S rRNA-based metagenomic profiling of faecal samples. T180H and TAT132H produced significantly higher DNA concentrations than PE-QIA, whereas TAT132H yielded DNA of lower purity compared to the others. In the taxonomic analysis, PE-QIA provided a balanced recovery of Gram-positive and Gram-negative bacteria, TAT132H was enriched in Gram-positive taxa, and T180H was enriched in Gram-negative taxa. An analysis of Microbial Community Standard (MOCK) samples showed that PE-QIA and T180H were more accurate than TAT132H. Finally, the VeriFi method yielded higher amplicon concentrations and sequence counts than the home brew protocol, despite the high level of chimeras. In conclusion, a robust performance in terms of DNA yield, purity, and taxonomic representation was obtained by PE-QIA and T180H. Furthermore, it was found that the impact of PCR-based steps on gut microbiota profiling can be minimized by an accurate bioinformatic pipeline.
Additional Links: PMID-40508035
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PubMed:
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@article {pmid40508035,
year = {2025},
author = {Toto, F and Scanu, M and Gramegna, M and Putignani, L and Del Chierico, F},
title = {Impact of DNA Extraction and 16S rRNA Gene Amplification Strategy on Microbiota Profiling of Faecal Samples.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115226},
pmid = {40508035},
issn = {1422-0067},
support = {Current Research funds//Italian Ministry of Health/ ; n.a.//Technogenetics S.p.A./ ; },
mesh = {*RNA, Ribosomal, 16S/genetics ; *Feces/microbiology ; Humans ; *DNA, Bacterial/genetics/isolation & purification ; *Gastrointestinal Microbiome/genetics ; Metagenomics/methods ; High-Throughput Nucleotide Sequencing/methods ; *Microbiota/genetics ; Bacteria/genetics/classification ; Metagenome ; },
abstract = {High-throughput 16S rRNA metagenomic sequencing has advanced our understanding of the gut microbiome, but its reliability depends on upstream processes such as DNA extraction and bacterial library preparation. In this study, we evaluated the impact of three different DNA extraction methods (a manual method with an ad hoc-designed pre-extraction phase (PE-QIA), and two automated magnetic bead-based methods (T180H and TAT132H)) and two bacterial library preparation protocols (home brew and VeriFi) on the 16S rRNA-based metagenomic profiling of faecal samples. T180H and TAT132H produced significantly higher DNA concentrations than PE-QIA, whereas TAT132H yielded DNA of lower purity compared to the others. In the taxonomic analysis, PE-QIA provided a balanced recovery of Gram-positive and Gram-negative bacteria, TAT132H was enriched in Gram-positive taxa, and T180H was enriched in Gram-negative taxa. An analysis of Microbial Community Standard (MOCK) samples showed that PE-QIA and T180H were more accurate than TAT132H. Finally, the VeriFi method yielded higher amplicon concentrations and sequence counts than the home brew protocol, despite the high level of chimeras. In conclusion, a robust performance in terms of DNA yield, purity, and taxonomic representation was obtained by PE-QIA and T180H. Furthermore, it was found that the impact of PCR-based steps on gut microbiota profiling can be minimized by an accurate bioinformatic pipeline.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*RNA, Ribosomal, 16S/genetics
*Feces/microbiology
Humans
*DNA, Bacterial/genetics/isolation & purification
*Gastrointestinal Microbiome/genetics
Metagenomics/methods
High-Throughput Nucleotide Sequencing/methods
*Microbiota/genetics
Bacteria/genetics/classification
Metagenome
RevDate: 2025-06-13
CmpDate: 2025-06-13
Gut Microbiota Dysbiosis in Endometriosis: A Potential Link to Inflammation and Disease Progression.
International journal of molecular sciences, 26(11): pii:ijms26115144.
Endometriosis is a complex gynaecological disorder characterised by the presence of endometrial-like tissue outside the uterus, leading to chronic inflammation, pain, and infertility. Recent research suggests that gut microbiota may play a crucial role in the pathogenesis and progression of endometriosis by modulating immune responses and oestrogen metabolism. This study investigates the intestinal microbiota composition in women with endometriosis and its potential as a disease diagnosis and severity biomarker. Stool samples from nine patients diagnosed with endometriosis were analysed using the GI Effects[®] Comprehensive Stool Profile test. The tests revealed significant dysbiosis, particularly an altered Firmicutes/Bacteroidetes ratio and increased levels of Bacteroidetes. Inflammatory markers, including β-glucuronidase and secretory IgA, were also elevated, suggesting a potential link between gut microbiota and systemic inflammation in endometriosis. While our findings align with previous studies, further research with larger cohorts is necessary to validate these observations. Understanding the role of the microbiome in endometriosis could open new avenues for noninvasive diagnostic tools in endometriosis and microbiota-targeted therapies.
Additional Links: PMID-40507956
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PubMed:
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@article {pmid40507956,
year = {2025},
author = {Baușic, AIG and Scurtu, F and Manu, A and Matasariu, DR and Brătilă, E},
title = {Gut Microbiota Dysbiosis in Endometriosis: A Potential Link to Inflammation and Disease Progression.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115144},
pmid = {40507956},
issn = {1422-0067},
support = {"PUBLISH NOT PERISH" - 2025//Carol Davila University of Medicine and Pharmacy/ ; },
mesh = {Humans ; Female ; *Endometriosis/microbiology/pathology ; *Dysbiosis/microbiology/complications ; *Gastrointestinal Microbiome ; Adult ; Disease Progression ; *Inflammation/microbiology ; Biomarkers ; Feces/microbiology ; },
abstract = {Endometriosis is a complex gynaecological disorder characterised by the presence of endometrial-like tissue outside the uterus, leading to chronic inflammation, pain, and infertility. Recent research suggests that gut microbiota may play a crucial role in the pathogenesis and progression of endometriosis by modulating immune responses and oestrogen metabolism. This study investigates the intestinal microbiota composition in women with endometriosis and its potential as a disease diagnosis and severity biomarker. Stool samples from nine patients diagnosed with endometriosis were analysed using the GI Effects[®] Comprehensive Stool Profile test. The tests revealed significant dysbiosis, particularly an altered Firmicutes/Bacteroidetes ratio and increased levels of Bacteroidetes. Inflammatory markers, including β-glucuronidase and secretory IgA, were also elevated, suggesting a potential link between gut microbiota and systemic inflammation in endometriosis. While our findings align with previous studies, further research with larger cohorts is necessary to validate these observations. Understanding the role of the microbiome in endometriosis could open new avenues for noninvasive diagnostic tools in endometriosis and microbiota-targeted therapies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
*Endometriosis/microbiology/pathology
*Dysbiosis/microbiology/complications
*Gastrointestinal Microbiome
Adult
Disease Progression
*Inflammation/microbiology
Biomarkers
Feces/microbiology
RevDate: 2025-06-13
CmpDate: 2025-06-13
Synbiotic Supplementation Attenuates Doxorubicin-Induced Oxidative Stress and Inflammation in the Gut-Heart Axis of Chemotherapy-Treated Mice.
International journal of molecular sciences, 26(11): pii:ijms26115136.
The gut microbiome supports immune health and influences gut and heart functions through the gut-heart axis. Synbiotics (SBT), combining probiotics and prebiotics, help restore microbiome balance. Chemotherapy often disrupts this balance, leading to adverse effects on the gut and heart. This study explores the potential of SBT supplementation in reducing heart and gut inflammation caused by doxorubicin (DOX) chemotherapy. The gut microbiome plays a vital role in immune health, and metabolites produced by gut bacteria contribute to physiological functions through the gut-heart axis. Chemotherapy drugs often disrupt these processes, leading to adverse effects on internal organs. Using 24 ICR male mice divided into four groups, the experiment assessed the impact of SBT on DOX-induced damage. Results indicated that DOX treatment significantly worsened survival rates, physical performance, heart function, and gut microbiome stability. However, co-treatment with SBT improved these markers, suggesting that SBT may help mitigate chemotherapy-induced side effects in cancer patients.
Additional Links: PMID-40507947
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@article {pmid40507947,
year = {2025},
author = {Cheng, CF and Nguyen, TKN and Shen, SC and Chen, BY and Wu, YB and Liang, HJ and Wu, CH},
title = {Synbiotic Supplementation Attenuates Doxorubicin-Induced Oxidative Stress and Inflammation in the Gut-Heart Axis of Chemotherapy-Treated Mice.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115136},
pmid = {40507947},
issn = {1422-0067},
support = {N/A//This study was partly funded by Industry-Academic Cooperation Project from ARJIL Pharmaceu-ticals LLC, TTY Biopharm Co., Ltd., and Shiun Chao Biopharm Co., Ltd./ ; },
mesh = {Animals ; *Doxorubicin/adverse effects ; *Synbiotics/administration & dosage ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Oxidative Stress/drug effects ; Male ; *Inflammation/chemically induced/metabolism ; Mice, Inbred ICR ; *Heart/drug effects ; Dietary Supplements ; Probiotics ; },
abstract = {The gut microbiome supports immune health and influences gut and heart functions through the gut-heart axis. Synbiotics (SBT), combining probiotics and prebiotics, help restore microbiome balance. Chemotherapy often disrupts this balance, leading to adverse effects on the gut and heart. This study explores the potential of SBT supplementation in reducing heart and gut inflammation caused by doxorubicin (DOX) chemotherapy. The gut microbiome plays a vital role in immune health, and metabolites produced by gut bacteria contribute to physiological functions through the gut-heart axis. Chemotherapy drugs often disrupt these processes, leading to adverse effects on internal organs. Using 24 ICR male mice divided into four groups, the experiment assessed the impact of SBT on DOX-induced damage. Results indicated that DOX treatment significantly worsened survival rates, physical performance, heart function, and gut microbiome stability. However, co-treatment with SBT improved these markers, suggesting that SBT may help mitigate chemotherapy-induced side effects in cancer patients.},
}
MeSH Terms:
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Animals
*Doxorubicin/adverse effects
*Synbiotics/administration & dosage
*Gastrointestinal Microbiome/drug effects
Mice
*Oxidative Stress/drug effects
Male
*Inflammation/chemically induced/metabolism
Mice, Inbred ICR
*Heart/drug effects
Dietary Supplements
Probiotics
RevDate: 2025-06-13
CmpDate: 2025-06-13
Investigating the Role of Gut Microbiota in the Pathogenesis and Progression of Rheumatoid Arthritis in a Collagen-Induced Arthritis Mouse Model.
International journal of molecular sciences, 26(11): pii:ijms26115099.
Rheumatoid arthritis (RA) is a chronic systemic autoimmune disorder whose precise etiology remains unclear, though growing evidence implicates gut microbiota in its pathogenesis. This study aimed to investigate the role of gut microbiota in the onset and progression of RA by employing fecal microbiota transplantation (FMT) in a collagen-induced arthritis (CIA) mouse model using DBA/1J and Aire[-]/[-] strains. Mice received FMT from healthy donors, treatment-naïve RA patients, or treated RA patients in relapse, followed by assessment of microbiota composition via 16S rRNA sequencing, arthritis severity scoring, histological evaluations, and systemic inflammatory markers. The findings revealed distinct microbiota clustering patterns post-FMT across experimental groups, highlighting strain-specific colonization effects. Notably, genera such as Bifidobacterium and Paraprevotella correlated positively with arthritis severity in DBA/1J mice, whereas Corynebacterium, Enterorhabdus, and Odoribacter exhibited negative correlations, suggesting potential protective roles. Despite these microbial differences, minor variations in arthritis scores, paw inflammation, or systemic inflammation were observed among FMT groups. This indicates that although gut microbiota alterations are associated with RA pathogenesis, further investigation with larger cohorts and comprehensive sequencing approaches is essential to elucidate the therapeutic potential of microbiome modulation in autoimmune diseases.
Additional Links: PMID-40507919
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@article {pmid40507919,
year = {2025},
author = {Belvončíková, P and Macáková, K and Tóthová, N and Babál, P and Tarabčáková, L and Gardlík, R},
title = {Investigating the Role of Gut Microbiota in the Pathogenesis and Progression of Rheumatoid Arthritis in a Collagen-Induced Arthritis Mouse Model.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115099},
pmid = {40507919},
issn = {1422-0067},
support = {APVV-21-0370//Slovak Research and Development Agency/ ; VEGA 1/0706/25//Ministry of Education, Science, Research and Sport of the Slovak Republic/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Arthritis, Rheumatoid/microbiology/pathology/therapy/etiology ; *Arthritis, Experimental/microbiology/pathology/therapy ; Mice ; Disease Models, Animal ; RNA, Ribosomal, 16S/genetics ; Disease Progression ; Humans ; Mice, Inbred DBA ; Male ; Fecal Microbiota Transplantation ; Female ; },
abstract = {Rheumatoid arthritis (RA) is a chronic systemic autoimmune disorder whose precise etiology remains unclear, though growing evidence implicates gut microbiota in its pathogenesis. This study aimed to investigate the role of gut microbiota in the onset and progression of RA by employing fecal microbiota transplantation (FMT) in a collagen-induced arthritis (CIA) mouse model using DBA/1J and Aire[-]/[-] strains. Mice received FMT from healthy donors, treatment-naïve RA patients, or treated RA patients in relapse, followed by assessment of microbiota composition via 16S rRNA sequencing, arthritis severity scoring, histological evaluations, and systemic inflammatory markers. The findings revealed distinct microbiota clustering patterns post-FMT across experimental groups, highlighting strain-specific colonization effects. Notably, genera such as Bifidobacterium and Paraprevotella correlated positively with arthritis severity in DBA/1J mice, whereas Corynebacterium, Enterorhabdus, and Odoribacter exhibited negative correlations, suggesting potential protective roles. Despite these microbial differences, minor variations in arthritis scores, paw inflammation, or systemic inflammation were observed among FMT groups. This indicates that although gut microbiota alterations are associated with RA pathogenesis, further investigation with larger cohorts and comprehensive sequencing approaches is essential to elucidate the therapeutic potential of microbiome modulation in autoimmune diseases.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Gastrointestinal Microbiome
*Arthritis, Rheumatoid/microbiology/pathology/therapy/etiology
*Arthritis, Experimental/microbiology/pathology/therapy
Mice
Disease Models, Animal
RNA, Ribosomal, 16S/genetics
Disease Progression
Humans
Mice, Inbred DBA
Male
Fecal Microbiota Transplantation
Female
RevDate: 2025-06-13
CmpDate: 2025-06-13
Roseburia intestinalis Modulates Immune Responses by Inducing M1 Macrophage Polarization.
International journal of molecular sciences, 26(11): pii:ijms26115049.
In recent years, the gut microbiome has been recognized as one influential factor in cancer development. Particularly in colorectal cancer (CRC), several studies observed a major imbalance of the intestinal microbiota, marked by a reduction in beneficial bacterial species, such as Roseburia intestinalis, and an increase in opportunistic pathobionts, like Peptostreptococcus stomatis. We previously observed that specific Eubacteriales, including R. intestinalis, were significantly reduced in CRC patients and have a potent anti-tumor immune effect when applied as oral monotherapy in mice. Here, we investigate the molecular mechanism of R. intestinalis on various cell types in vitro, highlighting its potential therapeutic value in CRC. Co-culture experiments with macrophages demonstrated that R. intestinalis exposure induced an increase in the M1 phenotype and decreased the M2 phenotype, suggesting macrophage-polarizing properties of these bacteria. R. intestinalis also triggered a gene expression profile resembling M1 macrophages and led to distinct chemokine and cytokine secretion in cancer cells, suggesting an immune-activating environment. However, we did not observe direct cytotoxic effects in cancer cells. Our research provides insights into the potential of R. intestinalis to activate immune responses, supporting further investigation into its therapeutic role in CRC. These findings underscore the need for deeper studies on the bacterium's impact on CRC pathogenesis and treatment.
Additional Links: PMID-40507861
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PubMed:
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@article {pmid40507861,
year = {2025},
author = {Bircher, A and Katkeviciute, E and Morsy, Y and Lang, S and Montalban-Arques, A and Scharl, M},
title = {Roseburia intestinalis Modulates Immune Responses by Inducing M1 Macrophage Polarization.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115049},
pmid = {40507861},
issn = {1422-0067},
support = {KFS-5372-08-2021-R//Swiss Cancer Research Foundation/ ; NA//Fondazione San Salvatore/ ; NA//Holcim Foundation/ ; },
mesh = {*Macrophages/immunology/microbiology/metabolism ; Humans ; Animals ; Colorectal Neoplasms/immunology/microbiology ; *Clostridiales/immunology ; Mice ; Gastrointestinal Microbiome/immunology ; *Macrophage Activation/immunology ; Cytokines/metabolism ; Cell Line, Tumor ; Coculture Techniques ; },
abstract = {In recent years, the gut microbiome has been recognized as one influential factor in cancer development. Particularly in colorectal cancer (CRC), several studies observed a major imbalance of the intestinal microbiota, marked by a reduction in beneficial bacterial species, such as Roseburia intestinalis, and an increase in opportunistic pathobionts, like Peptostreptococcus stomatis. We previously observed that specific Eubacteriales, including R. intestinalis, were significantly reduced in CRC patients and have a potent anti-tumor immune effect when applied as oral monotherapy in mice. Here, we investigate the molecular mechanism of R. intestinalis on various cell types in vitro, highlighting its potential therapeutic value in CRC. Co-culture experiments with macrophages demonstrated that R. intestinalis exposure induced an increase in the M1 phenotype and decreased the M2 phenotype, suggesting macrophage-polarizing properties of these bacteria. R. intestinalis also triggered a gene expression profile resembling M1 macrophages and led to distinct chemokine and cytokine secretion in cancer cells, suggesting an immune-activating environment. However, we did not observe direct cytotoxic effects in cancer cells. Our research provides insights into the potential of R. intestinalis to activate immune responses, supporting further investigation into its therapeutic role in CRC. These findings underscore the need for deeper studies on the bacterium's impact on CRC pathogenesis and treatment.},
}
MeSH Terms:
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*Macrophages/immunology/microbiology/metabolism
Humans
Animals
Colorectal Neoplasms/immunology/microbiology
*Clostridiales/immunology
Mice
Gastrointestinal Microbiome/immunology
*Macrophage Activation/immunology
Cytokines/metabolism
Cell Line, Tumor
Coculture Techniques
RevDate: 2025-06-13
CmpDate: 2025-06-13
Exploring the Healing Powers of Histatins: From Oral Health to Therapeutics.
International journal of molecular sciences, 26(11): pii:ijms26115019.
Histatin peptides are a family of small histidine-rich cationic polypeptides produced by two genes, HTN1 and HTN3. They are found in salivary secretions from the parotid, sublingual, and submandibular salivary glands. These peptides undergo proteolytic cleavages to produce different histatin fragments which play multiple roles including wound healing, maintenance of enamel, and regulation of balance in the oral microbiome. In this review, we explored the expression, structural characteristics, and metal-ion-binding capacities of these peptides and how their functions are modulated by their structure. We also provide here an insight into the potential use of histatins as biomarkers and therapeutic peptides in the management of oral and non-oral diseases including cancer. Potential gaps in the current understanding of histatins that warrant further research have also been highlighted.
Additional Links: PMID-40507844
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@article {pmid40507844,
year = {2025},
author = {Usman, S and You, Y and Waseem, A},
title = {Exploring the Healing Powers of Histatins: From Oral Health to Therapeutics.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115019},
pmid = {40507844},
issn = {1422-0067},
mesh = {Humans ; *Histatins/chemistry/metabolism/therapeutic use/genetics/pharmacology ; *Wound Healing ; *Oral Health ; Animals ; },
abstract = {Histatin peptides are a family of small histidine-rich cationic polypeptides produced by two genes, HTN1 and HTN3. They are found in salivary secretions from the parotid, sublingual, and submandibular salivary glands. These peptides undergo proteolytic cleavages to produce different histatin fragments which play multiple roles including wound healing, maintenance of enamel, and regulation of balance in the oral microbiome. In this review, we explored the expression, structural characteristics, and metal-ion-binding capacities of these peptides and how their functions are modulated by their structure. We also provide here an insight into the potential use of histatins as biomarkers and therapeutic peptides in the management of oral and non-oral diseases including cancer. Potential gaps in the current understanding of histatins that warrant further research have also been highlighted.},
}
MeSH Terms:
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Humans
*Histatins/chemistry/metabolism/therapeutic use/genetics/pharmacology
*Wound Healing
*Oral Health
Animals
RevDate: 2025-06-13
CmpDate: 2025-06-13
A Comparison of the Effects of Milk, Yogurt, and Cheese on Insulin Sensitivity, Hepatic Steatosis, and Gut Microbiota in Diet-Induced Obese Male Mice.
International journal of molecular sciences, 26(11): pii:ijms26115026.
The effects of low-fat dairy products on insulin resistance (IR), hepatic steatosis, and gut microbiota composition in high-fat diet (HFD)-fed obese mice were examined. C57BL/6 male mice (n = 16/group) were fed a high-fat diet (HFD, 45% fat) or HFD supplemented with either fat-free milk (MILK), fat-free yogurt (YOG), or reduced-fat (19% milk fat) cheddar cheese (CHE) at 10% of the total energy intake for 8 weeks. Body weight, fat mass, liver lipids, and metabolic enzymes were evaluated. Compared with HFD, MILK reduced homeostatic assessment of insulin resistance along with increased hepatic insulin signaling and decreased hepatic gluconeogenic enzymes. YOG and MILK decreased hepatic triacylglycerol content and lipid droplet size, while CHE had no effect. In the liver, MILK and YOG downregulated de novo lipogenesis enzymes. In MILK, fat oxidation capacity was elevated. Compared with HFD, liver lipidomic analysis in MILK and YOG revealed unique profiles of decreased proinflammatory lipid species, including ceramides. Dairy feeding elicited an increase in beneficial bacteria, such as Streptococcus in YOG and Anaero-tignum in MILK, as shown by 16S rRNA sequencing of gut microbiota. In conclusion, the ability of milk and yogurt to reduce hepatic steatosis in HFD mice may be explained, at least in part, by the regulation of the gut microbiome and liver lipidome.
Additional Links: PMID-40507838
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PubMed:
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@article {pmid40507838,
year = {2025},
author = {Yuzbashian, E and Fernando, DN and Jacobs, RL and Lesker, TR and Strowig, T and Ussar, S and Chan, CB},
title = {A Comparison of the Effects of Milk, Yogurt, and Cheese on Insulin Sensitivity, Hepatic Steatosis, and Gut Microbiota in Diet-Induced Obese Male Mice.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115026},
pmid = {40507838},
issn = {1422-0067},
mesh = {Animals ; *Gastrointestinal Microbiome ; *Yogurt ; Male ; Mice ; *Milk ; Diet, High-Fat/adverse effects ; *Insulin Resistance ; *Cheese ; *Obesity/metabolism/etiology/microbiology ; Mice, Inbred C57BL ; Liver/metabolism ; *Fatty Liver/metabolism/etiology ; Mice, Obese ; Lipid Metabolism ; },
abstract = {The effects of low-fat dairy products on insulin resistance (IR), hepatic steatosis, and gut microbiota composition in high-fat diet (HFD)-fed obese mice were examined. C57BL/6 male mice (n = 16/group) were fed a high-fat diet (HFD, 45% fat) or HFD supplemented with either fat-free milk (MILK), fat-free yogurt (YOG), or reduced-fat (19% milk fat) cheddar cheese (CHE) at 10% of the total energy intake for 8 weeks. Body weight, fat mass, liver lipids, and metabolic enzymes were evaluated. Compared with HFD, MILK reduced homeostatic assessment of insulin resistance along with increased hepatic insulin signaling and decreased hepatic gluconeogenic enzymes. YOG and MILK decreased hepatic triacylglycerol content and lipid droplet size, while CHE had no effect. In the liver, MILK and YOG downregulated de novo lipogenesis enzymes. In MILK, fat oxidation capacity was elevated. Compared with HFD, liver lipidomic analysis in MILK and YOG revealed unique profiles of decreased proinflammatory lipid species, including ceramides. Dairy feeding elicited an increase in beneficial bacteria, such as Streptococcus in YOG and Anaero-tignum in MILK, as shown by 16S rRNA sequencing of gut microbiota. In conclusion, the ability of milk and yogurt to reduce hepatic steatosis in HFD mice may be explained, at least in part, by the regulation of the gut microbiome and liver lipidome.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Gastrointestinal Microbiome
*Yogurt
Male
Mice
*Milk
Diet, High-Fat/adverse effects
*Insulin Resistance
*Cheese
*Obesity/metabolism/etiology/microbiology
Mice, Inbred C57BL
Liver/metabolism
*Fatty Liver/metabolism/etiology
Mice, Obese
Lipid Metabolism
RevDate: 2025-06-13
CmpDate: 2025-06-13
Skin Microbiome and Radiation-Induced Skin Injury: Unraveling the Relationship, Mechanisms, and Therapeutic Implications.
International journal of molecular sciences, 26(11): pii:ijms26115022.
Radiotherapy (RT) is a treatment method commonly used in oncology. A vast majority of patients undergoing RT suffer from radiation-induced skin injury (RISI), which results from complex biochemical reactions in the irradiated skin. Current strategies for preventing and managing RISI are insufficient for achieving full skin regeneration. Multiple studies have shown that alterations in the skin microbiome correlate with the development and severity of RISI. These studies suggest that dysbiosis is a crucial factor in promoting radiation-associated dermatitis. Targeting the skin microbiota presents a potential therapeutic approach that could significantly improve the quality of life for patients undergoing RT. This review aims to present current findings on the interplay between the skin microbiome and radiation-induced skin damage as well as to discuss potential therapeutic strategies for preventing and mitigating this condition.
Additional Links: PMID-40507833
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PubMed:
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@article {pmid40507833,
year = {2025},
author = {Bratborska, AW and Głuszak, P and Joks, M and Kaźmierska, J and Pazdrowski, J and Polańska, A and Jain, S and Yadav, H and Masternak, MM and Dańczak-Pazdrowska, A},
title = {Skin Microbiome and Radiation-Induced Skin Injury: Unraveling the Relationship, Mechanisms, and Therapeutic Implications.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115022},
pmid = {40507833},
issn = {1422-0067},
mesh = {Humans ; *Skin/microbiology/radiation effects/pathology ; *Microbiota/radiation effects ; Animals ; *Radiodermatitis/microbiology/therapy/etiology ; Dysbiosis/microbiology ; *Radiation Injuries/microbiology ; Radiotherapy/adverse effects ; Skin Microbiome ; },
abstract = {Radiotherapy (RT) is a treatment method commonly used in oncology. A vast majority of patients undergoing RT suffer from radiation-induced skin injury (RISI), which results from complex biochemical reactions in the irradiated skin. Current strategies for preventing and managing RISI are insufficient for achieving full skin regeneration. Multiple studies have shown that alterations in the skin microbiome correlate with the development and severity of RISI. These studies suggest that dysbiosis is a crucial factor in promoting radiation-associated dermatitis. Targeting the skin microbiota presents a potential therapeutic approach that could significantly improve the quality of life for patients undergoing RT. This review aims to present current findings on the interplay between the skin microbiome and radiation-induced skin damage as well as to discuss potential therapeutic strategies for preventing and mitigating this condition.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Skin/microbiology/radiation effects/pathology
*Microbiota/radiation effects
Animals
*Radiodermatitis/microbiology/therapy/etiology
Dysbiosis/microbiology
*Radiation Injuries/microbiology
Radiotherapy/adverse effects
Skin Microbiome
RevDate: 2025-06-13
CmpDate: 2025-06-13
The MDA-MB-231 Breast Cancer Cell Secretomes Modify Metabolomes of Pseudomonas aeruginosa Breast Microbiome.
International journal of molecular sciences, 26(11): pii:ijms26115003.
Breast cancer (BC) is globally becoming a great challenge, being both the most diagnosed cancer and the leading cause of death in women. In addition to cancer cells, many bacteria co-inhabit BC, which differ in type and number from the resident microbiota found in healthy breast tissue. While many reports have demonstrated the ability of different bacteria to dysregulate BC's metabolites, the reciprocal effect of these metabolites on the bacterial microbiota has not yet been investigated. Herein, we assess the effect of conditioned media (CM) from a triple-negative BC cell line (MDA-MB-231) on the metabolic profile of Pseudomonas aeruginosa (P. aeruginosa), an important breast resident Gram-negative bacteria that influence oncogenesis. Optical density and scanning electron microscopes were used to assess the impact of MDA-MB-231-CM (BC-CM) on P. aeruginosa growth and morphological changes, respectively. In addition, liquid chromatography-high-resolution mass spectrometry was used to identify metabolic changes in P. aeruginosa and their secretomes in response to the BC-CM. The BC-CM significantly suppressed the growth of P. aeruginosa in the log phase and induced concentration-dependent cytopathological changes in their cell walls. The metabolites of P. aeruginosa were dysregulated considerably depending on the time of exposure to the BC-CM. When treated with the BC-CM, P. aeruginosa induced the purine alkaloid spliceostatin (FR901464), a prominent antitumor metabolite. The BC-CM also promoted other P. aeruginosa metabolites such as amino acids, phosphoribosyl-AMP, 2-aminoacetophenone, pyochelin I, guanosine monophosphate, riboflavin, and terpenoids, which are capable of interfering with oncogenesis. Nine of the significantly identified metabolites from the 0-3 h comparison and four of those identified from the 0-6 h comparison have potential roles in influencing cancer cell behavior. Our findings demonstrate the ability of triple-negative BC-CM not only to alter the growth and morphology of P. aeruginosa but also to modulate their metabolic profile. A better understanding of the influence of BC on certain resident breast microbiomes, such as P. aeruginosa, may open a new therapeutic intervention opportunity for the treatment of cancer.
Additional Links: PMID-40507816
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PubMed:
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@article {pmid40507816,
year = {2025},
author = {AlDawsari, M and Al-Ansari, MM and AlMalki, RH and Rahman, AMA and Al-Alwan, M},
title = {The MDA-MB-231 Breast Cancer Cell Secretomes Modify Metabolomes of Pseudomonas aeruginosa Breast Microbiome.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115003},
pmid = {40507816},
issn = {1422-0067},
support = {RAC#2240005 and 2220015//King Faisal Specialist Hospital & Research Centre/ ; },
mesh = {Humans ; *Pseudomonas aeruginosa/metabolism/drug effects/growth & development ; Female ; Cell Line, Tumor ; *Metabolome/drug effects ; *Breast Neoplasms/microbiology/metabolism ; *Microbiota ; Culture Media, Conditioned/pharmacology ; *Breast/microbiology ; },
abstract = {Breast cancer (BC) is globally becoming a great challenge, being both the most diagnosed cancer and the leading cause of death in women. In addition to cancer cells, many bacteria co-inhabit BC, which differ in type and number from the resident microbiota found in healthy breast tissue. While many reports have demonstrated the ability of different bacteria to dysregulate BC's metabolites, the reciprocal effect of these metabolites on the bacterial microbiota has not yet been investigated. Herein, we assess the effect of conditioned media (CM) from a triple-negative BC cell line (MDA-MB-231) on the metabolic profile of Pseudomonas aeruginosa (P. aeruginosa), an important breast resident Gram-negative bacteria that influence oncogenesis. Optical density and scanning electron microscopes were used to assess the impact of MDA-MB-231-CM (BC-CM) on P. aeruginosa growth and morphological changes, respectively. In addition, liquid chromatography-high-resolution mass spectrometry was used to identify metabolic changes in P. aeruginosa and their secretomes in response to the BC-CM. The BC-CM significantly suppressed the growth of P. aeruginosa in the log phase and induced concentration-dependent cytopathological changes in their cell walls. The metabolites of P. aeruginosa were dysregulated considerably depending on the time of exposure to the BC-CM. When treated with the BC-CM, P. aeruginosa induced the purine alkaloid spliceostatin (FR901464), a prominent antitumor metabolite. The BC-CM also promoted other P. aeruginosa metabolites such as amino acids, phosphoribosyl-AMP, 2-aminoacetophenone, pyochelin I, guanosine monophosphate, riboflavin, and terpenoids, which are capable of interfering with oncogenesis. Nine of the significantly identified metabolites from the 0-3 h comparison and four of those identified from the 0-6 h comparison have potential roles in influencing cancer cell behavior. Our findings demonstrate the ability of triple-negative BC-CM not only to alter the growth and morphology of P. aeruginosa but also to modulate their metabolic profile. A better understanding of the influence of BC on certain resident breast microbiomes, such as P. aeruginosa, may open a new therapeutic intervention opportunity for the treatment of cancer.},
}
MeSH Terms:
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Humans
*Pseudomonas aeruginosa/metabolism/drug effects/growth & development
Female
Cell Line, Tumor
*Metabolome/drug effects
*Breast Neoplasms/microbiology/metabolism
*Microbiota
Culture Media, Conditioned/pharmacology
*Breast/microbiology
RevDate: 2025-06-13
CmpDate: 2025-06-13
Biological Actions of Bile Acids via Cell Surface Receptors.
International journal of molecular sciences, 26(11): pii:ijms26115004.
Bile acids (BAs) are synthesized in the liver from cholesterol and are subsequently conjugated with glycine and taurine. In the intestine, bile acids undergo various modifications, such as deconjugation, dehydrogenation, oxidation, and epimerization by the gut microbiota. These bile acids are absorbed in the intestine and transported to the liver as well as the systemic circulation. BAs can activate many types of receptors, including nuclear receptors and cell surface receptors. By activating these receptors, BAs can exert various effects on the metabolic, immune, and nervous systems. Recently, the detailed structure of TGR5, the major plasma membrane receptor for BAs, was elucidated, revealing a putative second BA binding site along with the orthosteric binding site. Furthermore, BAs act as ligands for bitter taste receptors and the Leukemia inhibitory factor receptor. In addition, the Mas-related, G-protein-coupled receptor X4 interacts with receptor activity-modifying proteins. Thus, a variety of cell surface receptors are associated with BAs, and BAs are thought to have very complex activities. This review focuses on recent advances regarding cell surface receptors for bile acids and the biological actions they mediate.
Additional Links: PMID-40507815
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PubMed:
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@article {pmid40507815,
year = {2025},
author = {Kiriyama, Y and Tokumaru, H and Sadamoto, H and Nochi, H},
title = {Biological Actions of Bile Acids via Cell Surface Receptors.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115004},
pmid = {40507815},
issn = {1422-0067},
mesh = {*Bile Acids and Salts/metabolism/chemistry ; Humans ; Animals ; Receptors, G-Protein-Coupled/metabolism/chemistry ; *Receptors, Cell Surface/metabolism/chemistry ; },
abstract = {Bile acids (BAs) are synthesized in the liver from cholesterol and are subsequently conjugated with glycine and taurine. In the intestine, bile acids undergo various modifications, such as deconjugation, dehydrogenation, oxidation, and epimerization by the gut microbiota. These bile acids are absorbed in the intestine and transported to the liver as well as the systemic circulation. BAs can activate many types of receptors, including nuclear receptors and cell surface receptors. By activating these receptors, BAs can exert various effects on the metabolic, immune, and nervous systems. Recently, the detailed structure of TGR5, the major plasma membrane receptor for BAs, was elucidated, revealing a putative second BA binding site along with the orthosteric binding site. Furthermore, BAs act as ligands for bitter taste receptors and the Leukemia inhibitory factor receptor. In addition, the Mas-related, G-protein-coupled receptor X4 interacts with receptor activity-modifying proteins. Thus, a variety of cell surface receptors are associated with BAs, and BAs are thought to have very complex activities. This review focuses on recent advances regarding cell surface receptors for bile acids and the biological actions they mediate.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Bile Acids and Salts/metabolism/chemistry
Humans
Animals
Receptors, G-Protein-Coupled/metabolism/chemistry
*Receptors, Cell Surface/metabolism/chemistry
RevDate: 2025-06-13
CmpDate: 2025-06-13
SkinDuo[TM] as a Targeted Probiotic Therapy: Shifts in Skin Microbiota and Clinical Outcomes in Acne Patients.
International journal of molecular sciences, 26(11): pii:ijms26115000.
Acne vulgaris is a common dermatological condition strongly associated with disruptions in the skin microbiota, specifically involving key species such as Cutibacterium acnes and Staphylococcus epidermidis. This study investigates the efficacy of SkinDuo[TM], a topical probiotic containing Lactiplantibacillus plantarum, in modulating the skin microbiota and improving clinical outcomes in patients with acne vulgaris. Over a 4-week to 8-week observational study period, microbial composition and diversity shifts were analyzed using full-length 16S rRNA sequencing. Patient responses were categorized into "good" responders (showing significant clinical improvement) and "no_change" responders (with minimal or no improvement). SkinDuo[TM] treatment resulted in lower post-treatment Cutibacterium acnes abundance in the "good" group compared to the "no_change" group. The "good" group maintained a stable level of alpha diversity following treatment. In contrast, the "no_change" group exhibited a marked reduction in microbial diversity. Beta diversity analysis revealed distinct clustering patterns associated with improved clinical outcomes. These findings suggest that the preservation of microbial richness and evenness may serve as a potential biomarker for positive response to probiotic therapy. This study highlights the potential of SkinDuo[TM] to restore microbial balance and alleviate acne symptoms, contributing to the growing body of evidence supporting microbiome-based therapeutic strategies in dermatology.
Additional Links: PMID-40507814
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@article {pmid40507814,
year = {2025},
author = {Biazzo, M and Pinzauti, D and Podrini, C},
title = {SkinDuo[TM] as a Targeted Probiotic Therapy: Shifts in Skin Microbiota and Clinical Outcomes in Acne Patients.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115000},
pmid = {40507814},
issn = {1422-0067},
support = {R&I-2022-019L//Xjenza Malta/ ; },
mesh = {Humans ; *Probiotics/therapeutic use/administration & dosage ; *Acne Vulgaris/microbiology/therapy/drug therapy ; *Skin/microbiology ; *Microbiota/drug effects ; Male ; Female ; Treatment Outcome ; RNA, Ribosomal, 16S/genetics ; Adult ; Young Adult ; Adolescent ; Propionibacterium acnes ; Skin Microbiome ; },
abstract = {Acne vulgaris is a common dermatological condition strongly associated with disruptions in the skin microbiota, specifically involving key species such as Cutibacterium acnes and Staphylococcus epidermidis. This study investigates the efficacy of SkinDuo[TM], a topical probiotic containing Lactiplantibacillus plantarum, in modulating the skin microbiota and improving clinical outcomes in patients with acne vulgaris. Over a 4-week to 8-week observational study period, microbial composition and diversity shifts were analyzed using full-length 16S rRNA sequencing. Patient responses were categorized into "good" responders (showing significant clinical improvement) and "no_change" responders (with minimal or no improvement). SkinDuo[TM] treatment resulted in lower post-treatment Cutibacterium acnes abundance in the "good" group compared to the "no_change" group. The "good" group maintained a stable level of alpha diversity following treatment. In contrast, the "no_change" group exhibited a marked reduction in microbial diversity. Beta diversity analysis revealed distinct clustering patterns associated with improved clinical outcomes. These findings suggest that the preservation of microbial richness and evenness may serve as a potential biomarker for positive response to probiotic therapy. This study highlights the potential of SkinDuo[TM] to restore microbial balance and alleviate acne symptoms, contributing to the growing body of evidence supporting microbiome-based therapeutic strategies in dermatology.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Probiotics/therapeutic use/administration & dosage
*Acne Vulgaris/microbiology/therapy/drug therapy
*Skin/microbiology
*Microbiota/drug effects
Male
Female
Treatment Outcome
RNA, Ribosomal, 16S/genetics
Adult
Young Adult
Adolescent
Propionibacterium acnes
Skin Microbiome
RevDate: 2025-06-13
Corporal Composition and Gut Microbiome Modification Through Exclusion Dietary Intervention in Adult Patients with Crohn's Disease: Protocol for a Prospective, Interventional, Controlled, Randomized Clinical Trial.
Journal of clinical medicine, 14(11): pii:jcm14113998.
Background: Crohn's disease (CD) is an inflammatory bowel disease in which there is an alteration in the homeostasis and functionality of the intestinal mucosa accompanied by a dysbiosis of the commensal microbiota. The analysis of different dietary strategies to achieve CD remission and reduce gastrointestinal symptoms concludes that it is necessary to restrict the intake of ultra-processed products and to promote the consumption of those with anti-inflammatory effects that improve intestinal permeability and dysbiosis. Methods: Based on previous studies conducted in other cohorts, mainly pediatric, we propose an experimental, prospective, randomized study in patients with active CD who do not show improvement with conventional pharmacological treatment. The control group will receive standard nutritional recommendations while the intervention group will be prescribed an exclusion diet supplemented with enteral nutrition. Results: Patients in the intervention group are expected to exhibit increased lean body mass and reduced visceral fat, as measured by bioelectrical impedance analysis (BIA), alongside higher rates of clinical remission (CDAI), decreased inflammatory markers, and improved gut microbiota composition. Additionally, improvements in health-related quality of life are anticipated, as assessed by validated questionnaires. Conclusions: In the present project, we plan to conduct a detailed study to determine the potential of the exclusion diet for the treatment and remission of CD in adult patients, with the hypothesis that this nutritional intervention will be able to modify and improve intestinal dysbiosis, inflammatory status, and clinical and body composition markers in these patients.
Additional Links: PMID-40507757
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@article {pmid40507757,
year = {2025},
author = {Cano-Mármol, RP and Fernández-Ruiz, VE and Martínez-Pascual, C and Ros-Madrid, I and Martín-Pozuelo, G and Oliva-Bolarín, A and Martínez-Sánchez, MA and Egea-Valenzuela, J and Núñez-Sánchez, MÁ and Ramos-Molina, B and Ruiz-Alcaraz, AJ and Ferrer-Gómez, M},
title = {Corporal Composition and Gut Microbiome Modification Through Exclusion Dietary Intervention in Adult Patients with Crohn's Disease: Protocol for a Prospective, Interventional, Controlled, Randomized Clinical Trial.},
journal = {Journal of clinical medicine},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/jcm14113998},
pmid = {40507757},
issn = {2077-0383},
abstract = {Background: Crohn's disease (CD) is an inflammatory bowel disease in which there is an alteration in the homeostasis and functionality of the intestinal mucosa accompanied by a dysbiosis of the commensal microbiota. The analysis of different dietary strategies to achieve CD remission and reduce gastrointestinal symptoms concludes that it is necessary to restrict the intake of ultra-processed products and to promote the consumption of those with anti-inflammatory effects that improve intestinal permeability and dysbiosis. Methods: Based on previous studies conducted in other cohorts, mainly pediatric, we propose an experimental, prospective, randomized study in patients with active CD who do not show improvement with conventional pharmacological treatment. The control group will receive standard nutritional recommendations while the intervention group will be prescribed an exclusion diet supplemented with enteral nutrition. Results: Patients in the intervention group are expected to exhibit increased lean body mass and reduced visceral fat, as measured by bioelectrical impedance analysis (BIA), alongside higher rates of clinical remission (CDAI), decreased inflammatory markers, and improved gut microbiota composition. Additionally, improvements in health-related quality of life are anticipated, as assessed by validated questionnaires. Conclusions: In the present project, we plan to conduct a detailed study to determine the potential of the exclusion diet for the treatment and remission of CD in adult patients, with the hypothesis that this nutritional intervention will be able to modify and improve intestinal dysbiosis, inflammatory status, and clinical and body composition markers in these patients.},
}
RevDate: 2025-06-13
A Review of the Influence of Prebiotics, Probiotics, Synbiotics, and Postbiotics on the Human Gut Microbiome and Intestinal Integrity.
Journal of clinical medicine, 14(11): pii:jcm14113673.
OBJECTIVE: This review aims to comprehensively evaluate the current evidence on the role of prebiotics, probiotics, synbiotics, and postbiotics-collectively referred to as "biotics"-in modulating the human gut microbiota and enhancing intestinal epithelial integrity.
FINDINGS: Biotics exert their beneficial effects through several mechanisms, including by promoting the growth of beneficial microbes, producing short-chain fatty acids (SCFAs), strengthening the gut barrier, and regulating immune responses. Prebiotics selectively stimulate beneficial bacteria, probiotics introduce live microorganisms with therapeutic functions, synbiotics combine the strengths of both, and postbiotics offer non-viable microbial components and metabolites that mimic probiotic benefits with enhanced safety profiles. Each type of biotic demonstrates unique and complementary effects across a range of conditions, such as inflammatory bowel disease, irritable bowel syndrome, obesity, constipation, and antibiotic-associated diarrhea.
IMPLICATIONS: As disruptions in the gut microbiota and intestinal barrier are increasingly linked to chronic and immune-mediated diseases, leveraging biotics offers promising avenues for personalized nutrition, preventive healthcare, and adjunct therapies. The integration of biotics into clinical and dietary strategies may significantly contribute to improving gastrointestinal and systemic health.
Additional Links: PMID-40507435
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@article {pmid40507435,
year = {2025},
author = {Smolinska, S and Popescu, FD and Zemelka-Wiacek, M},
title = {A Review of the Influence of Prebiotics, Probiotics, Synbiotics, and Postbiotics on the Human Gut Microbiome and Intestinal Integrity.},
journal = {Journal of clinical medicine},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/jcm14113673},
pmid = {40507435},
issn = {2077-0383},
abstract = {OBJECTIVE: This review aims to comprehensively evaluate the current evidence on the role of prebiotics, probiotics, synbiotics, and postbiotics-collectively referred to as "biotics"-in modulating the human gut microbiota and enhancing intestinal epithelial integrity.
FINDINGS: Biotics exert their beneficial effects through several mechanisms, including by promoting the growth of beneficial microbes, producing short-chain fatty acids (SCFAs), strengthening the gut barrier, and regulating immune responses. Prebiotics selectively stimulate beneficial bacteria, probiotics introduce live microorganisms with therapeutic functions, synbiotics combine the strengths of both, and postbiotics offer non-viable microbial components and metabolites that mimic probiotic benefits with enhanced safety profiles. Each type of biotic demonstrates unique and complementary effects across a range of conditions, such as inflammatory bowel disease, irritable bowel syndrome, obesity, constipation, and antibiotic-associated diarrhea.
IMPLICATIONS: As disruptions in the gut microbiota and intestinal barrier are increasingly linked to chronic and immune-mediated diseases, leveraging biotics offers promising avenues for personalized nutrition, preventive healthcare, and adjunct therapies. The integration of biotics into clinical and dietary strategies may significantly contribute to improving gastrointestinal and systemic health.},
}
RevDate: 2025-06-13
Impaired Overall Survival of Melanoma Patients Due to Antibiotic Use Prior to Immune Checkpoint Inhibitor Therapy: Systematic Review and Meta-Analysis.
Cancers, 17(11): pii:cancers17111872.
Background: The gut microbiome plays a pivotal role in shaping systemic immunity and modulating anti-tumor responses. Preclinical and clinical studies have shown that higher gut microbial diversity and the presence of specific commensal taxa correlate with improved responses to immune checkpoint inhibitors (ICI) in melanoma. Conversely, broad-spectrum antibiotics can induce dysbiosis, reducing T cell activation and cytokine production, and have been linked to diminished ICI efficacy in several cancer types. Methods: We conducted a systematic review and meta-analysis of seven retrospective cohorts (total n = 5213) comparing overall survival in cutaneous melanoma (CM) patients who did or did not receive systemic antibiotics within six weeks before ICI initiation. From each study, we extracted hazard ratios (HRs) for death, antibiotic-to-ICI interval, ICI regimen (PD-1 monotherapy vs. PD-1 + CTLA-4 combination), cohort size, and country. Pooled log-HRs were estimated under fixed-effect and random-effects (REML) models. Statistical heterogeneity was quantified by Cochran's Q and I[2] statistics, and τ[2]. We performed leave-one-out sensitivity analyses, generated a Baujat plot to identify influential studies, applied trim-and-fill to assess publication bias, and ran meta-regressions for regimen, antibiotic timing, sample size, and geography. Results: Under the fixed-effect model, antibiotic exposure corresponded to a pooled HR of 1.26 (95% CI 1.13-1.41; p < 0.001). The random-effects model yielded a pooled HR of 1.55 (95% CI 1.21-1.98; p = 0.0005) with substantial heterogeneity (Q = 25.1; I[2] = 76%). Prediction intervals (0.78-3.06) underscored between-study variability. Leave-one-out analyses produced HRs from 1.50 to 1.75, confirming robustness, and the Baujat plot highlighted two cohorts as primary heterogeneity drivers. Trim-and-fill adjusted the HR to 1.46 (95% CI 1.08-1.97). In subgroup analyses, combination therapy studies (k = 4) showed a pooled HR of ~1.9 (I[2] = 58%) versus ~1.3 (I[2] = 79%) for monotherapy. Meta-regression attributed the largest variance to the regimen (R[2] = 32%; β(monotherapy) = -0.35; p = 0.13). Conclusions: Pre-ICI antibiotic use in CM is consistently associated with a 26-55% increase in mortality risk, particularly with PD-1 + CTLA-4 combinations, reinforcing the mechanistic link between microbiome integrity and ICI success. Looking ahead, integrating prospective microbiome profiling into clinical trials will be critical to personalize ICI therapy, clarify causality, and identify microbial biomarkers for optimal treatment selection. Prospective, microbiome-integrated trials promise to refine melanoma immunotherapy by tailoring antibiotic stewardship and microbial interventions to enhance patient outcomes.
Additional Links: PMID-40507352
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PubMed:
Citation:
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@article {pmid40507352,
year = {2025},
author = {Gambichler, T and Weyer-Fahlbusch, SS and Overbeck, J and Abu Rached, N and Becker, JC and Susok, L},
title = {Impaired Overall Survival of Melanoma Patients Due to Antibiotic Use Prior to Immune Checkpoint Inhibitor Therapy: Systematic Review and Meta-Analysis.},
journal = {Cancers},
volume = {17},
number = {11},
pages = {},
doi = {10.3390/cancers17111872},
pmid = {40507352},
issn = {2072-6694},
abstract = {Background: The gut microbiome plays a pivotal role in shaping systemic immunity and modulating anti-tumor responses. Preclinical and clinical studies have shown that higher gut microbial diversity and the presence of specific commensal taxa correlate with improved responses to immune checkpoint inhibitors (ICI) in melanoma. Conversely, broad-spectrum antibiotics can induce dysbiosis, reducing T cell activation and cytokine production, and have been linked to diminished ICI efficacy in several cancer types. Methods: We conducted a systematic review and meta-analysis of seven retrospective cohorts (total n = 5213) comparing overall survival in cutaneous melanoma (CM) patients who did or did not receive systemic antibiotics within six weeks before ICI initiation. From each study, we extracted hazard ratios (HRs) for death, antibiotic-to-ICI interval, ICI regimen (PD-1 monotherapy vs. PD-1 + CTLA-4 combination), cohort size, and country. Pooled log-HRs were estimated under fixed-effect and random-effects (REML) models. Statistical heterogeneity was quantified by Cochran's Q and I[2] statistics, and τ[2]. We performed leave-one-out sensitivity analyses, generated a Baujat plot to identify influential studies, applied trim-and-fill to assess publication bias, and ran meta-regressions for regimen, antibiotic timing, sample size, and geography. Results: Under the fixed-effect model, antibiotic exposure corresponded to a pooled HR of 1.26 (95% CI 1.13-1.41; p < 0.001). The random-effects model yielded a pooled HR of 1.55 (95% CI 1.21-1.98; p = 0.0005) with substantial heterogeneity (Q = 25.1; I[2] = 76%). Prediction intervals (0.78-3.06) underscored between-study variability. Leave-one-out analyses produced HRs from 1.50 to 1.75, confirming robustness, and the Baujat plot highlighted two cohorts as primary heterogeneity drivers. Trim-and-fill adjusted the HR to 1.46 (95% CI 1.08-1.97). In subgroup analyses, combination therapy studies (k = 4) showed a pooled HR of ~1.9 (I[2] = 58%) versus ~1.3 (I[2] = 79%) for monotherapy. Meta-regression attributed the largest variance to the regimen (R[2] = 32%; β(monotherapy) = -0.35; p = 0.13). Conclusions: Pre-ICI antibiotic use in CM is consistently associated with a 26-55% increase in mortality risk, particularly with PD-1 + CTLA-4 combinations, reinforcing the mechanistic link between microbiome integrity and ICI success. Looking ahead, integrating prospective microbiome profiling into clinical trials will be critical to personalize ICI therapy, clarify causality, and identify microbial biomarkers for optimal treatment selection. Prospective, microbiome-integrated trials promise to refine melanoma immunotherapy by tailoring antibiotic stewardship and microbial interventions to enhance patient outcomes.},
}
RevDate: 2025-06-13
The Knowledge Gap in Gut Microbiome Characterization in Early-Onset Colorectal Cancer Patients: A Systematic Scoping Review.
Cancers, 17(11): pii:cancers17111863.
BACKGROUND/OBJECTIVES: Over the past two decades, the incidence of early-onset colorectal cancer (EoCRC) has been increasing, although its underlying causes remain unclear. Gut microbiome is known to play a role in carcinogenesis of colorectal cancer. This scoping review aims to systematically map and synthetize current evidence on gut microbiome characterization in EoCRC (vs. late-onset colorectal cancer (LoCRC) and healthy individuals), describe the methodology used, and identify knowledge gaps to inform and guide future research.
METHODS: This systematic scoping review followed the Joanna Briggs Institute (JBI) methodology for scoping reviews. Searches were conducted in PubMed, Web of Science, and Scopus between January and February 2025. Two reviewers independently screened and selected the studies. One reviewer extracted the relevant information, using an adapted version of the JBI template.
RESULTS: Seven studies met eligibility criteria. Compared to healthy young adults, EoCRC patients had a predominance of lower α diversity, different β diversity, and greater abundance of Flavonifractor plautii, Akkermansia muciniphila, Bacteroides, and Fusobacteria. Comparisons with LoCRC showed that EoCRC had distinct β diversity and a higher abundance in Fusobacterium, Akkermansia, Bacteroides, and Actinomyces. Only three studies correlated the microbiota composition of EoCRC with clinicopathology features and suggested positive associations between Fusobacterium abundance, rectal tumors and lower survival and Akkermansia abundance with body mass index (BMI) ≥ 25 kg/m[2], rectal EoCRC, and better survival.
CONCLUSIONS: There is a lack of large, methodologically robust studies linking gut microbiota with clinicopathological, lifestyle, and tumor molecular features in EoCRC. Our review highlights critical knowledge gaps, the need for standardized methodologies, and key areas for future investigation.
Additional Links: PMID-40507344
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@article {pmid40507344,
year = {2025},
author = {Gomes de Sousa, R and Guerreiro, CS and Santos, I and Cravo, M},
title = {The Knowledge Gap in Gut Microbiome Characterization in Early-Onset Colorectal Cancer Patients: A Systematic Scoping Review.},
journal = {Cancers},
volume = {17},
number = {11},
pages = {},
doi = {10.3390/cancers17111863},
pmid = {40507344},
issn = {2072-6694},
abstract = {BACKGROUND/OBJECTIVES: Over the past two decades, the incidence of early-onset colorectal cancer (EoCRC) has been increasing, although its underlying causes remain unclear. Gut microbiome is known to play a role in carcinogenesis of colorectal cancer. This scoping review aims to systematically map and synthetize current evidence on gut microbiome characterization in EoCRC (vs. late-onset colorectal cancer (LoCRC) and healthy individuals), describe the methodology used, and identify knowledge gaps to inform and guide future research.
METHODS: This systematic scoping review followed the Joanna Briggs Institute (JBI) methodology for scoping reviews. Searches were conducted in PubMed, Web of Science, and Scopus between January and February 2025. Two reviewers independently screened and selected the studies. One reviewer extracted the relevant information, using an adapted version of the JBI template.
RESULTS: Seven studies met eligibility criteria. Compared to healthy young adults, EoCRC patients had a predominance of lower α diversity, different β diversity, and greater abundance of Flavonifractor plautii, Akkermansia muciniphila, Bacteroides, and Fusobacteria. Comparisons with LoCRC showed that EoCRC had distinct β diversity and a higher abundance in Fusobacterium, Akkermansia, Bacteroides, and Actinomyces. Only three studies correlated the microbiota composition of EoCRC with clinicopathology features and suggested positive associations between Fusobacterium abundance, rectal tumors and lower survival and Akkermansia abundance with body mass index (BMI) ≥ 25 kg/m[2], rectal EoCRC, and better survival.
CONCLUSIONS: There is a lack of large, methodologically robust studies linking gut microbiota with clinicopathological, lifestyle, and tumor molecular features in EoCRC. Our review highlights critical knowledge gaps, the need for standardized methodologies, and key areas for future investigation.},
}
RevDate: 2025-06-13
CmpDate: 2025-06-13
Function of Yogurt Fermented with the Lactococcus lactis 11/19-B1 Strain in Improving the Lipid Profile and Intestinal Microbiome in Hemodialysis Patients.
Nutrients, 17(11): pii:nu17111931.
BACKGROUND/OBJECTIVES: The number of chronic kidney disease (CKD) patients is increasing in Japan, and this population is at high risk of death from cardiovascular and cerebrovascular diseases. Therefore, prevention of arteriosclerosis as a common underlying cause of these diseases is required. In this study, we examined whether 11/19-B1 yogurt, which has been proven to reduce serum low-density lipoprotein (LDL) levels, can decrease the serum levels of indoxylsulfate and trimethylamine-N-oxide (TMAO), which are produced by intestinal microbiota and known to cause arteriosclerosis, through improving dysbiosis in hemodialysis patients.
METHODS: Nineteen dialysis patients consumed 50 g of 11/19-B1 yogurt daily for 8 weeks, and changes in serum lipid profile and uremic toxin levels, intestinal microbiome, as well as the frequency of bowel movement and stool characteristics were observed.
RESULTS: The results demonstrated that an intake of yogurt decreased serum LDL 99.3 to 88.5 (p = 0.049) and indoxylsulfate in seven of nine subjects with previously high concentrations, and improved stool characteristics as estimated by the Bristle stool score, although decreased HDL and no beneficial effect on serum TMAO was observed.
CONCLUSIONS: These results may suggest that the ingestion of 11/19-B1 yogurt provides a preventative effect against the progression of atherosclerosis and renal dysfunction.
Additional Links: PMID-40507200
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PubMed:
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@article {pmid40507200,
year = {2025},
author = {Suzuki, Y and Ishioka, K and Nakamura, T and Miyazaki, N and Marubashi, S and Suzutani, T},
title = {Function of Yogurt Fermented with the Lactococcus lactis 11/19-B1 Strain in Improving the Lipid Profile and Intestinal Microbiome in Hemodialysis Patients.},
journal = {Nutrients},
volume = {17},
number = {11},
pages = {},
doi = {10.3390/nu17111931},
pmid = {40507200},
issn = {2072-6643},
mesh = {Humans ; *Yogurt/microbiology ; *Gastrointestinal Microbiome ; *Renal Dialysis ; Male ; Female ; Middle Aged ; Aged ; *Renal Insufficiency, Chronic/therapy/blood ; *Fermentation ; *Lipids/blood ; Indican/blood ; Methylamines/blood ; Dysbiosis ; Probiotics ; },
abstract = {BACKGROUND/OBJECTIVES: The number of chronic kidney disease (CKD) patients is increasing in Japan, and this population is at high risk of death from cardiovascular and cerebrovascular diseases. Therefore, prevention of arteriosclerosis as a common underlying cause of these diseases is required. In this study, we examined whether 11/19-B1 yogurt, which has been proven to reduce serum low-density lipoprotein (LDL) levels, can decrease the serum levels of indoxylsulfate and trimethylamine-N-oxide (TMAO), which are produced by intestinal microbiota and known to cause arteriosclerosis, through improving dysbiosis in hemodialysis patients.
METHODS: Nineteen dialysis patients consumed 50 g of 11/19-B1 yogurt daily for 8 weeks, and changes in serum lipid profile and uremic toxin levels, intestinal microbiome, as well as the frequency of bowel movement and stool characteristics were observed.
RESULTS: The results demonstrated that an intake of yogurt decreased serum LDL 99.3 to 88.5 (p = 0.049) and indoxylsulfate in seven of nine subjects with previously high concentrations, and improved stool characteristics as estimated by the Bristle stool score, although decreased HDL and no beneficial effect on serum TMAO was observed.
CONCLUSIONS: These results may suggest that the ingestion of 11/19-B1 yogurt provides a preventative effect against the progression of atherosclerosis and renal dysfunction.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Yogurt/microbiology
*Gastrointestinal Microbiome
*Renal Dialysis
Male
Female
Middle Aged
Aged
*Renal Insufficiency, Chronic/therapy/blood
*Fermentation
*Lipids/blood
Indican/blood
Methylamines/blood
Dysbiosis
Probiotics
RevDate: 2025-06-13
CmpDate: 2025-06-13
Potential Therapeutic Targets for Androgenetic Alopecia (AGA) in Obese Individuals as Revealed by a Gut Microbiome Analysis: A Mendelian Randomization Study.
Nutrients, 17(11): pii:nu17111892.
Objective: This study aimed to investigate the role of the gut microbiome in androgenetic alopecia (AGA) among obese individuals using Mendelian randomization (MR), and to identify potential therapeutic targets for mitigating AGA in this population. Methods: Genomic data for 412 gut microbiomes, AGA, and obesity were obtained from genome-wide association studies (GWAS). Bidirectional MR was performed using inverse variance weighted (IVW) as the primary analysis method, complemented by sensitivity analyses. Potential therapeutic targets within the gut microbiome associated with AGA in obese individuals were identified. Results: Two gut microbiomes were identified as having a significant impact on obese individuals with AGA. Specifically, the abundance of the sulfoglycolysis pathway in gut bacteria was found to significantly increase the risk of both obesity and AGA. In contrast, the abundance of the de novo biosynthesis of the adenosine ribonucleotide pathway in gut bacteria was associated with a significant increase in the risk of obesity but a significant decrease in the risk of AGA. Conclusions: The abundance of gut bacterial pathways, including sulfoglycolysis and the de novo biosynthesis of adenosine ribonucleotides, can serve as potential therapeutic targets for managing obesity-associated AGA. These findings offer a novel research direction for the development of innovative diagnostic and treatment strategies for patients with obesity and AGA.
Additional Links: PMID-40507161
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@article {pmid40507161,
year = {2025},
author = {Li, Y and Liao, X and Tang, S and Wang, Q and Lin, H and Yu, X and Xiao, Y and Tao, X and Zhong, T},
title = {Potential Therapeutic Targets for Androgenetic Alopecia (AGA) in Obese Individuals as Revealed by a Gut Microbiome Analysis: A Mendelian Randomization Study.},
journal = {Nutrients},
volume = {17},
number = {11},
pages = {},
doi = {10.3390/nu17111892},
pmid = {40507161},
issn = {2072-6643},
mesh = {Humans ; *Gastrointestinal Microbiome/genetics ; *Alopecia/microbiology/genetics/therapy ; Mendelian Randomization Analysis ; *Obesity/complications/microbiology/genetics ; Genome-Wide Association Study ; Male ; Female ; Adult ; },
abstract = {Objective: This study aimed to investigate the role of the gut microbiome in androgenetic alopecia (AGA) among obese individuals using Mendelian randomization (MR), and to identify potential therapeutic targets for mitigating AGA in this population. Methods: Genomic data for 412 gut microbiomes, AGA, and obesity were obtained from genome-wide association studies (GWAS). Bidirectional MR was performed using inverse variance weighted (IVW) as the primary analysis method, complemented by sensitivity analyses. Potential therapeutic targets within the gut microbiome associated with AGA in obese individuals were identified. Results: Two gut microbiomes were identified as having a significant impact on obese individuals with AGA. Specifically, the abundance of the sulfoglycolysis pathway in gut bacteria was found to significantly increase the risk of both obesity and AGA. In contrast, the abundance of the de novo biosynthesis of the adenosine ribonucleotide pathway in gut bacteria was associated with a significant increase in the risk of obesity but a significant decrease in the risk of AGA. Conclusions: The abundance of gut bacterial pathways, including sulfoglycolysis and the de novo biosynthesis of adenosine ribonucleotides, can serve as potential therapeutic targets for managing obesity-associated AGA. These findings offer a novel research direction for the development of innovative diagnostic and treatment strategies for patients with obesity and AGA.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Gastrointestinal Microbiome/genetics
*Alopecia/microbiology/genetics/therapy
Mendelian Randomization Analysis
*Obesity/complications/microbiology/genetics
Genome-Wide Association Study
Male
Female
Adult
RevDate: 2025-06-13
CmpDate: 2025-06-13
The Influence of Dietary Factors on Melanoma Development and Progression: A Comprehensive Review.
Nutrients, 17(11): pii:nu17111891.
Melanoma is an aggressive cutaneous malignancy with increasing global incidence and high metastatic potential. While ultraviolet (UV) radiation remains the primary environmental risk factor, emerging evidence suggests that dietary factors may influence melanoma risk, progression, and treatment outcomes. This comprehensive review examines the impact of dietary components, including fats, vitamins, minerals, antioxidants, bioactive compounds, and the gut microbiome, on melanoma pathogenesis. The current literature indicates that diets rich in polyunsaturated fatty acids (PUFAs), antioxidants, and plant-based bioactive compounds may confer protective effects against melanoma by modulating oxidative stress, inflammation, and immune response. Additionally, the gut microbiome plays a critical role in melanoma progression and immunotherapy response, with dietary patterns influencing microbial composition and, consequently, host immunity. Despite these promising associations, research remains limited, and findings across studies are inconsistent, preventing the establishment of definitive dietary guidelines for melanoma prevention and management. Future research should focus on large-scale prospective studies to elucidate the mechanisms underlying the dietary influences on melanoma and determine evidence-based nutritional strategies. Understanding the interplay between diet, immune modulation, and gut microbiome composition represents a promising avenue for advancing melanoma prevention and treatment strategies.
Additional Links: PMID-40507159
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@article {pmid40507159,
year = {2025},
author = {Watson, AE and Yusuf, N},
title = {The Influence of Dietary Factors on Melanoma Development and Progression: A Comprehensive Review.},
journal = {Nutrients},
volume = {17},
number = {11},
pages = {},
doi = {10.3390/nu17111891},
pmid = {40507159},
issn = {2072-6643},
mesh = {Humans ; *Melanoma/etiology/prevention & control/pathology ; Gastrointestinal Microbiome ; *Diet/adverse effects ; Disease Progression ; *Skin Neoplasms/etiology/prevention & control/pathology ; Antioxidants/administration & dosage ; Risk Factors ; Oxidative Stress ; },
abstract = {Melanoma is an aggressive cutaneous malignancy with increasing global incidence and high metastatic potential. While ultraviolet (UV) radiation remains the primary environmental risk factor, emerging evidence suggests that dietary factors may influence melanoma risk, progression, and treatment outcomes. This comprehensive review examines the impact of dietary components, including fats, vitamins, minerals, antioxidants, bioactive compounds, and the gut microbiome, on melanoma pathogenesis. The current literature indicates that diets rich in polyunsaturated fatty acids (PUFAs), antioxidants, and plant-based bioactive compounds may confer protective effects against melanoma by modulating oxidative stress, inflammation, and immune response. Additionally, the gut microbiome plays a critical role in melanoma progression and immunotherapy response, with dietary patterns influencing microbial composition and, consequently, host immunity. Despite these promising associations, research remains limited, and findings across studies are inconsistent, preventing the establishment of definitive dietary guidelines for melanoma prevention and management. Future research should focus on large-scale prospective studies to elucidate the mechanisms underlying the dietary influences on melanoma and determine evidence-based nutritional strategies. Understanding the interplay between diet, immune modulation, and gut microbiome composition represents a promising avenue for advancing melanoma prevention and treatment strategies.},
}
MeSH Terms:
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Humans
*Melanoma/etiology/prevention & control/pathology
Gastrointestinal Microbiome
*Diet/adverse effects
Disease Progression
*Skin Neoplasms/etiology/prevention & control/pathology
Antioxidants/administration & dosage
Risk Factors
Oxidative Stress
RevDate: 2025-06-13
CmpDate: 2025-06-13
In Search of Healthy Ageing: A Microbiome-Based Precision Nutrition Approach for Type 2 Diabetes Prevention.
Nutrients, 17(11): pii:nu17111877.
Background/Objectives: Type 2 diabetes (T2D) is a leading cause of morbidity and mortality worldwide and in Spain, particularly in the elderly population, affecting healthy ageing. Nutritional strategies are key to its prevention. The gut microbiota is also implicated in T2D and can be modulated by nutrition. We hypothesize that precision nutrition through microbiota modulation may help prevent T2D. This article aims to (1) describe a gut microbiota bacterial profile associated with T2D prevention, (2) provide precision nutrition tools to optimize this profile, (3) analyze how overweight influences the microbiota composition and precision nutrition response, and (4) address the technical challenges of microbiome-based precision nutrition clinical implementation to prevent T2D. Methods: A review of gut microbiota associated with T2D prevention was conducted. 13 healthy Spanish participants over 62 with optimal blood glucose levels (7 normal weight and 6 overweight) underwent a 3-month precision nutrition intervention to optimize T2D-preventive gut microbiota using a bioinformatics food recommendation system, Phymofood (EP22382095). Fecal microbiota was analyzed pre- and post-intervention using full-length 16S rRNA gene amplification, MinION sequencing, and NCBI taxonomic classification. Results: 31 potentially preventive bacteria against T2D were selected. The intervention increased the relative abundance of beneficial genera (Butyrivibrio and Faecalibacterium) and species (Eshraghiella crossota, and Faecalibacterium prausnitzii). The overweight influenced microbiota composition and intervention response. Conclusions: A gut microbiota profile associated with T2D prevention was identified, and precision nutrition could increase the relative abundance of beneficial bacteria. Confounding factors such as overweight should be considered when designing microbiome-based precision nutrition interventions. These results contribute to a better understanding of the microbiota associated with T2D prevention and address technical challenges for clinical implementation in future healthy ageing strategies.
Additional Links: PMID-40507144
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PubMed:
Citation:
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@article {pmid40507144,
year = {2025},
author = {González, A and Fullaondo, A and Odriozola, A},
title = {In Search of Healthy Ageing: A Microbiome-Based Precision Nutrition Approach for Type 2 Diabetes Prevention.},
journal = {Nutrients},
volume = {17},
number = {11},
pages = {},
doi = {10.3390/nu17111877},
pmid = {40507144},
issn = {2072-6643},
support = {IT1547-22//Basque Government, Department of Education/ ; },
mesh = {Humans ; *Diabetes Mellitus, Type 2/prevention & control/microbiology ; *Gastrointestinal Microbiome/physiology ; Aged ; Female ; Middle Aged ; Male ; *Healthy Aging ; *Precision Medicine/methods ; Spain ; Feces/microbiology ; Overweight/microbiology ; },
abstract = {Background/Objectives: Type 2 diabetes (T2D) is a leading cause of morbidity and mortality worldwide and in Spain, particularly in the elderly population, affecting healthy ageing. Nutritional strategies are key to its prevention. The gut microbiota is also implicated in T2D and can be modulated by nutrition. We hypothesize that precision nutrition through microbiota modulation may help prevent T2D. This article aims to (1) describe a gut microbiota bacterial profile associated with T2D prevention, (2) provide precision nutrition tools to optimize this profile, (3) analyze how overweight influences the microbiota composition and precision nutrition response, and (4) address the technical challenges of microbiome-based precision nutrition clinical implementation to prevent T2D. Methods: A review of gut microbiota associated with T2D prevention was conducted. 13 healthy Spanish participants over 62 with optimal blood glucose levels (7 normal weight and 6 overweight) underwent a 3-month precision nutrition intervention to optimize T2D-preventive gut microbiota using a bioinformatics food recommendation system, Phymofood (EP22382095). Fecal microbiota was analyzed pre- and post-intervention using full-length 16S rRNA gene amplification, MinION sequencing, and NCBI taxonomic classification. Results: 31 potentially preventive bacteria against T2D were selected. The intervention increased the relative abundance of beneficial genera (Butyrivibrio and Faecalibacterium) and species (Eshraghiella crossota, and Faecalibacterium prausnitzii). The overweight influenced microbiota composition and intervention response. Conclusions: A gut microbiota profile associated with T2D prevention was identified, and precision nutrition could increase the relative abundance of beneficial bacteria. Confounding factors such as overweight should be considered when designing microbiome-based precision nutrition interventions. These results contribute to a better understanding of the microbiota associated with T2D prevention and address technical challenges for clinical implementation in future healthy ageing strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Diabetes Mellitus, Type 2/prevention & control/microbiology
*Gastrointestinal Microbiome/physiology
Aged
Female
Middle Aged
Male
*Healthy Aging
*Precision Medicine/methods
Spain
Feces/microbiology
Overweight/microbiology
RevDate: 2025-06-13
CmpDate: 2025-06-13
Cooked Bean (Phaseolus vulgaris L.) Consumption Alters Bile Acid Metabolism in a Mouse Model of Diet-Induced Metabolic Dysfunction: Proof-of-Concept Investigation.
Nutrients, 17(11): pii:nu17111827.
Background/Objectives: Metabolic dysregulation underlies a myriad of chronic diseases, including metabolic dysfunction-associated steatotic liver disease (MASLD) and obesity, and bile acids emerge as an important mediator in their etiology. Weight control by improving diet quality is the standard of care in prevention and control of these metabolic diseases. Inclusion of pulses, such as common bean, is an affordable yet neglected approach to improving diet quality and metabolic outcomes. Thus, this study evaluated the possibility that common bean alters bile acid metabolism in a health-beneficial manner. Methods: Using biospecimens from several similarly designed studies, cecal content, feces, liver tissue, and plasma samples from C57BL/6 mice fed an obesogenic diet lacking (control) or containing cooked common bean were subjected to total bile acid analysis and untargeted metabolomics. RNA-seq, qPCR, and Western blot assays of liver tissue complemented the bile acid analyses. Microbial composition and predicted function in the cecal contents were evaluated using 16S rRNA gene amplicon and shotgun metagenomic sequencing. Results: Bean-fed mice had increased cecal bile acid content and excreted more bile acids per gram of feces. Consistent with these effects, increased synthesis of bile acids in the liver was observed. Microbial composition and capacity to metabolize bile acids were markedly altered by bean, with greater prominence of secondary bile acid metabolites in bean-fed mice, i.e., microbial metabolites of chenodeoxycholate/lithocholate increased while metabolites of hyocholate were reduced. Conclusions: In rendering mice resistant to obesogenic diet-induced MASLD and obesity, cooked bean consumption sequesters bile acids, increasing their hepatic synthesis and enhancing their diversity through microbial metabolism. Bean-induced changes in bile acid metabolism have potential to improve dyslipidemia.
Additional Links: PMID-40507096
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PubMed:
Citation:
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@article {pmid40507096,
year = {2025},
author = {Lutsiv, T and Fitzgerald, VK and Neil, ES and McGinley, JN and Hussan, H and Thompson, HJ},
title = {Cooked Bean (Phaseolus vulgaris L.) Consumption Alters Bile Acid Metabolism in a Mouse Model of Diet-Induced Metabolic Dysfunction: Proof-of-Concept Investigation.},
journal = {Nutrients},
volume = {17},
number = {11},
pages = {},
doi = {10.3390/nu17111827},
pmid = {40507096},
issn = {2072-6643},
support = {58-3060-8-031//USDA ARS/ ; 2020-05206//National Institute for Food and Agriculture:/ ; },
mesh = {Animals ; *Bile Acids and Salts/metabolism ; Mice, Inbred C57BL ; *Phaseolus ; Mice ; Male ; Liver/metabolism ; Disease Models, Animal ; Feces/chemistry ; Cecum/microbiology/metabolism ; Gastrointestinal Microbiome ; Cooking ; Obesity/metabolism ; Metabolomics ; *Diet ; *Metabolic Diseases/etiology/metabolism ; Diet, High-Fat/adverse effects ; },
abstract = {Background/Objectives: Metabolic dysregulation underlies a myriad of chronic diseases, including metabolic dysfunction-associated steatotic liver disease (MASLD) and obesity, and bile acids emerge as an important mediator in their etiology. Weight control by improving diet quality is the standard of care in prevention and control of these metabolic diseases. Inclusion of pulses, such as common bean, is an affordable yet neglected approach to improving diet quality and metabolic outcomes. Thus, this study evaluated the possibility that common bean alters bile acid metabolism in a health-beneficial manner. Methods: Using biospecimens from several similarly designed studies, cecal content, feces, liver tissue, and plasma samples from C57BL/6 mice fed an obesogenic diet lacking (control) or containing cooked common bean were subjected to total bile acid analysis and untargeted metabolomics. RNA-seq, qPCR, and Western blot assays of liver tissue complemented the bile acid analyses. Microbial composition and predicted function in the cecal contents were evaluated using 16S rRNA gene amplicon and shotgun metagenomic sequencing. Results: Bean-fed mice had increased cecal bile acid content and excreted more bile acids per gram of feces. Consistent with these effects, increased synthesis of bile acids in the liver was observed. Microbial composition and capacity to metabolize bile acids were markedly altered by bean, with greater prominence of secondary bile acid metabolites in bean-fed mice, i.e., microbial metabolites of chenodeoxycholate/lithocholate increased while metabolites of hyocholate were reduced. Conclusions: In rendering mice resistant to obesogenic diet-induced MASLD and obesity, cooked bean consumption sequesters bile acids, increasing their hepatic synthesis and enhancing their diversity through microbial metabolism. Bean-induced changes in bile acid metabolism have potential to improve dyslipidemia.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Bile Acids and Salts/metabolism
Mice, Inbred C57BL
*Phaseolus
Mice
Male
Liver/metabolism
Disease Models, Animal
Feces/chemistry
Cecum/microbiology/metabolism
Gastrointestinal Microbiome
Cooking
Obesity/metabolism
Metabolomics
*Diet
*Metabolic Diseases/etiology/metabolism
Diet, High-Fat/adverse effects
RevDate: 2025-06-13
CmpDate: 2025-06-13
The Effect of Probiotics on Health in Pregnancy and Infants: A Randomized, Double-Blind, Placebo-Controlled Trial.
Nutrients, 17(11): pii:nu17111825.
Background/Objectives: There is growing interest in the benefits of probiotic supplementation during pregnancy and lactation, but evidence supporting the beneficial effects for mother-infant dyads remains scarce. This study assessed the effects of probiotic supplementation on infection frequency and immunity in pregnant women and infants, and on microbiome establishment during the first month of life. Methods: At 28 weeks of gestation, 180 healthy pregnant women were randomized to receive either a placebo (n = 90) or a probiotic supplement (n = 90), Prenatis™, containing 5 billion CFU/day of Lacticaseibacillus rhamnosus Rosell[®]-11 and Bifidobacterium bifidum HA-132. Results: There was a significantly lower number of women with one or more infections during the study in the probiotics group (8 vs. 18, p = 0.05) and a trend for a lower number of infections during pregnancy (primary outcome) in the probiotics group (p = 0.07). Regarding infants, a lower number of days with infections during the first month of life was observed in the probiotics group (4.7 days on average vs. 10.5 days, p = 0.03). The vaginal microbiota composition during pregnancy and after childbirth showed no significant differences between groups while the infants' gut microbiome demonstrated a significantly higher abundance/prevalence of beneficial taxa in the probiotics group. The benefits conferred by probiotics were especially notable when considering birth by C-section. Probiotics promoted the vertical transmission of beneficial species and the induction of a highly interconnected microbiota, structured around key species. Conclusions: Probiotic supplementation during the third trimester of pregnancy and lactation is a valid strategy for conferring benefits to mothers and infants.
Additional Links: PMID-40507094
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PubMed:
Citation:
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@article {pmid40507094,
year = {2025},
author = {Binda, S and Chow-Shi-Yée, M and El Salti, S and Auclair-Ouellet, N and Oula, ML and Carton, T and Leuillet, S and Tomassi, D and Hemmings, R and Kadoch, IJ},
title = {The Effect of Probiotics on Health in Pregnancy and Infants: A Randomized, Double-Blind, Placebo-Controlled Trial.},
journal = {Nutrients},
volume = {17},
number = {11},
pages = {},
doi = {10.3390/nu17111825},
pmid = {40507094},
issn = {2072-6643},
mesh = {Humans ; Female ; *Probiotics/administration & dosage ; Pregnancy ; Double-Blind Method ; Adult ; Infant, Newborn ; Gastrointestinal Microbiome ; Infant ; Lacticaseibacillus rhamnosus ; Vagina/microbiology ; Dietary Supplements ; Bifidobacterium bifidum ; Young Adult ; },
abstract = {Background/Objectives: There is growing interest in the benefits of probiotic supplementation during pregnancy and lactation, but evidence supporting the beneficial effects for mother-infant dyads remains scarce. This study assessed the effects of probiotic supplementation on infection frequency and immunity in pregnant women and infants, and on microbiome establishment during the first month of life. Methods: At 28 weeks of gestation, 180 healthy pregnant women were randomized to receive either a placebo (n = 90) or a probiotic supplement (n = 90), Prenatis™, containing 5 billion CFU/day of Lacticaseibacillus rhamnosus Rosell[®]-11 and Bifidobacterium bifidum HA-132. Results: There was a significantly lower number of women with one or more infections during the study in the probiotics group (8 vs. 18, p = 0.05) and a trend for a lower number of infections during pregnancy (primary outcome) in the probiotics group (p = 0.07). Regarding infants, a lower number of days with infections during the first month of life was observed in the probiotics group (4.7 days on average vs. 10.5 days, p = 0.03). The vaginal microbiota composition during pregnancy and after childbirth showed no significant differences between groups while the infants' gut microbiome demonstrated a significantly higher abundance/prevalence of beneficial taxa in the probiotics group. The benefits conferred by probiotics were especially notable when considering birth by C-section. Probiotics promoted the vertical transmission of beneficial species and the induction of a highly interconnected microbiota, structured around key species. Conclusions: Probiotic supplementation during the third trimester of pregnancy and lactation is a valid strategy for conferring benefits to mothers and infants.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
*Probiotics/administration & dosage
Pregnancy
Double-Blind Method
Adult
Infant, Newborn
Gastrointestinal Microbiome
Infant
Lacticaseibacillus rhamnosus
Vagina/microbiology
Dietary Supplements
Bifidobacterium bifidum
Young Adult
RevDate: 2025-06-13
CmpDate: 2025-06-13
A Comprehensive Scoping Review on Diet and Nutrition in Relation to Long COVID-19 Symptoms and Recovery.
Nutrients, 17(11): pii:nu17111802.
Background/Objectives: Long COVID-19 is characterized by persistent symptoms lasting three months or more following SARS-CoV-2 infection. Nutrition has emerged as a modifiable factor influencing recovery trajectories and symptom burden; however, existing evidence remains fragmented across diverse study designs and populations. This scoping review synthesized global evidence on the role of diet and nutrition in managing long COVID-19 symptoms and supporting recovery. Methods: Following PRISMA-ScR and Joanna Briggs Institute guidelines for scoping reviews, we searched major biomedical databases for studies published between 2020 and 2025. Eligible studies examined dietary intake, nutritional status, or nutrition-related interventions in adults with long COVID-19. Results: After duplicates were removed, 1808 records were screened, resulting in 50 studies that met the inclusion criteria-27 intervention studies and 23 observational studies. Nutritional exposures included micronutrients (e.g., vitamins D, K2), amino acids (e.g., L-arginine), multinutrient formulations, microbiota-targeted therapies (e.g., probiotics, synbiotics), nutritional status, diet quality, and whole-diet patterns (e.g., the Mediterranean diet). Approximately 76% of studies reported improvements in long COVID-19-related symptoms such as fatigue, mood disturbances, physical function, and markers of inflammation. Conclusions: Diet and nutrition may support long COVID-19 recovery by targeting inflammation and the gut microbiome to alleviate symptoms and improve functional outcomes. Well-powered trials of whole-diet approaches, combined with targeted supplementation, are needed to confirm their potential as scalable, accessible tools for post-COVID-19 recovery and management.
Additional Links: PMID-40507071
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PubMed:
Citation:
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@article {pmid40507071,
year = {2025},
author = {Bigman, G and Rusu, ME and Shelawala, N and Sorkin, JD and Beamer, BA and Ryan, AS},
title = {A Comprehensive Scoping Review on Diet and Nutrition in Relation to Long COVID-19 Symptoms and Recovery.},
journal = {Nutrients},
volume = {17},
number = {11},
pages = {},
doi = {10.3390/nu17111802},
pmid = {40507071},
issn = {2072-6643},
mesh = {Humans ; *COVID-19/complications/physiopathology/diet therapy ; *Nutritional Status ; *Diet ; SARS-CoV-2 ; Post-Acute COVID-19 Syndrome ; Adult ; },
abstract = {Background/Objectives: Long COVID-19 is characterized by persistent symptoms lasting three months or more following SARS-CoV-2 infection. Nutrition has emerged as a modifiable factor influencing recovery trajectories and symptom burden; however, existing evidence remains fragmented across diverse study designs and populations. This scoping review synthesized global evidence on the role of diet and nutrition in managing long COVID-19 symptoms and supporting recovery. Methods: Following PRISMA-ScR and Joanna Briggs Institute guidelines for scoping reviews, we searched major biomedical databases for studies published between 2020 and 2025. Eligible studies examined dietary intake, nutritional status, or nutrition-related interventions in adults with long COVID-19. Results: After duplicates were removed, 1808 records were screened, resulting in 50 studies that met the inclusion criteria-27 intervention studies and 23 observational studies. Nutritional exposures included micronutrients (e.g., vitamins D, K2), amino acids (e.g., L-arginine), multinutrient formulations, microbiota-targeted therapies (e.g., probiotics, synbiotics), nutritional status, diet quality, and whole-diet patterns (e.g., the Mediterranean diet). Approximately 76% of studies reported improvements in long COVID-19-related symptoms such as fatigue, mood disturbances, physical function, and markers of inflammation. Conclusions: Diet and nutrition may support long COVID-19 recovery by targeting inflammation and the gut microbiome to alleviate symptoms and improve functional outcomes. Well-powered trials of whole-diet approaches, combined with targeted supplementation, are needed to confirm their potential as scalable, accessible tools for post-COVID-19 recovery and management.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*COVID-19/complications/physiopathology/diet therapy
*Nutritional Status
*Diet
SARS-CoV-2
Post-Acute COVID-19 Syndrome
Adult
RevDate: 2025-06-13
CmpDate: 2025-06-13
Cultural and Molecular Factors Predisposed to Non-Alcoholic Fatty Liver Disease and Type 2 Diabetes Mellitus.
Nutrients, 17(11): pii:nu17111797.
There is an exponential increase in the global prevalence of non-alcoholic fatty liver disease (NAFLD) in all populations. The objective of this review is to examine how different cultures and molecular entities influence the progression of NAFLD. Research databases, including PubMed, Scopus, the American Diabetes Association, the American Liver Foundation, and Diabetes UK, were used to retrieve information. Our data analysis showed that cultural norms shape the perceptions of health, illness, and mortality, thus influencing how individuals view themselves and express their experiences and may also affect decisions related to treatment and healthcare. Cultural competence, the ability to understand and navigate cultural differences, is essential for eliciting patient and practitioner perspectives and integrating this understanding into diagnostic and treatment plans. By acknowledging and respecting a patient's cultural background, healthcare providers can foster trust, improve care quality, enhance acceptance of diagnoses, and boost treatment adherence. Although cultural factors play a crucial role in the progression of NAFLD, the disease is also shaped by genetic predispositions, molecular mechanisms, and comorbidities. Molecular pathways involved in the development and progression of NAFLD include alterations in lipid metabolism, insulin signaling, insulin resistance, oxidative stress, defective gut microbiome, and inflammation. This study concludes that a combination of cultural preferences and molecular factors has contributed to the worldwide exponential rise in the prevalence of NAFLD, which in turn has led to an increase in the prevalence of comorbidities such as cardiovascular diseases, diabetes mellitus, and metabolic syndrome.
Additional Links: PMID-40507067
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PubMed:
Citation:
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@article {pmid40507067,
year = {2025},
author = {George, H and Permata, FS and D'Souza, CM and Adeghate, EA},
title = {Cultural and Molecular Factors Predisposed to Non-Alcoholic Fatty Liver Disease and Type 2 Diabetes Mellitus.},
journal = {Nutrients},
volume = {17},
number = {11},
pages = {},
doi = {10.3390/nu17111797},
pmid = {40507067},
issn = {2072-6643},
support = {G00003388; G00002809; G00003627, 31M374//United Arab Emirates University/ ; },
mesh = {Humans ; *Non-alcoholic Fatty Liver Disease/epidemiology/ethnology/genetics/etiology ; *Diabetes Mellitus, Type 2/ethnology/epidemiology/etiology ; Prevalence ; *Culture ; Insulin Resistance ; Genetic Predisposition to Disease ; },
abstract = {There is an exponential increase in the global prevalence of non-alcoholic fatty liver disease (NAFLD) in all populations. The objective of this review is to examine how different cultures and molecular entities influence the progression of NAFLD. Research databases, including PubMed, Scopus, the American Diabetes Association, the American Liver Foundation, and Diabetes UK, were used to retrieve information. Our data analysis showed that cultural norms shape the perceptions of health, illness, and mortality, thus influencing how individuals view themselves and express their experiences and may also affect decisions related to treatment and healthcare. Cultural competence, the ability to understand and navigate cultural differences, is essential for eliciting patient and practitioner perspectives and integrating this understanding into diagnostic and treatment plans. By acknowledging and respecting a patient's cultural background, healthcare providers can foster trust, improve care quality, enhance acceptance of diagnoses, and boost treatment adherence. Although cultural factors play a crucial role in the progression of NAFLD, the disease is also shaped by genetic predispositions, molecular mechanisms, and comorbidities. Molecular pathways involved in the development and progression of NAFLD include alterations in lipid metabolism, insulin signaling, insulin resistance, oxidative stress, defective gut microbiome, and inflammation. This study concludes that a combination of cultural preferences and molecular factors has contributed to the worldwide exponential rise in the prevalence of NAFLD, which in turn has led to an increase in the prevalence of comorbidities such as cardiovascular diseases, diabetes mellitus, and metabolic syndrome.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Non-alcoholic Fatty Liver Disease/epidemiology/ethnology/genetics/etiology
*Diabetes Mellitus, Type 2/ethnology/epidemiology/etiology
Prevalence
*Culture
Insulin Resistance
Genetic Predisposition to Disease
RevDate: 2025-06-13
CmpDate: 2025-06-13
Age-Dependent Gut Microbiome Dysbiosis in Autism Spectrum Disorder and the Role of Key Bacterial Ratios.
Nutrients, 17(11): pii:nu17111775.
Background/Objectives: Autism spectrum disorder (ASD) has a wide-ranging impact on individuals' quality of life and development, and there is a critical need for greater awareness, early intervention, and comprehensive support strategies to effectively address the unique needs of those affected by ASD. Recent studies highlight the gut microbiome's potential role in modulating ASD symptoms via the gut-brain axis, but specific microbial biomarkers remain unclear. This study aims to investigate differences in gut microbiota composition between ASD patients and neurotypical controls in a novel approach, specifically assessing ratios of Firmicutes/Bacteroidetes (F/B), Actinobacteria/Proteobacteria (A/P), and Prevotella/Bacteroides (P/B) as potential biomarkers. Methods: We analyzed gut microbiome samples from 302 Bulgarian children and adolescents diagnosed with ASD (aged 2-19 years). Microbial ratios (F/B, A/P, and P/B) were calculated and compared against previously reported reference meta-analytic means from European neurotypical populations. The statistical significance of deviations was assessed using parametric (t-tests), non-parametric (Wilcoxon signed-rank tests), and proportion-based (binomial tests) methods. Effect sizes were quantified using Cohen's d. Significant differences between ASD cases and neurotypical reference values were observed across several age groups. Results: Notably, children with ASD demonstrated significantly lower F/B and A/P ratios, with the youngest cohort (0-4 years) exhibiting the greatest differences. Deviations in the P/B ratio varied across age groups, with a significant elevation in the oldest group (≥10 years). Collectively, ASD cases consistently exhibited microbiota profiles indicative of dysbiosis. Conclusions: Our findings support gut microbiome dysbiosis as a potential biomarker for ASD, highlighting significantly altered bacterial ratios compared to neurotypical controls. These microbiome shifts could reflect early-life disruptions influencing neurodevelopment. Future studies should adopt longitudinal and mechanistic approaches to elucidate causal relationships and evaluate therapeutic microbiome modulation strategies.
Additional Links: PMID-40507042
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PubMed:
Citation:
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@article {pmid40507042,
year = {2025},
author = {Kadiyska, T and Vassilev, D and Tourtourikov, I and Ciurinskiene, S and Madzharova, D and Savcheva, M and Stoynev, N and Mileva-Popova, R and Tafradjiiska-Hadjiolova, R and Mitev, V},
title = {Age-Dependent Gut Microbiome Dysbiosis in Autism Spectrum Disorder and the Role of Key Bacterial Ratios.},
journal = {Nutrients},
volume = {17},
number = {11},
pages = {},
doi = {10.3390/nu17111775},
pmid = {40507042},
issn = {2072-6643},
support = {D-116/29.05.2024//Medical University of Sofia/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; *Autism Spectrum Disorder/microbiology ; *Dysbiosis/microbiology ; Child ; Adolescent ; Child, Preschool ; Male ; Female ; Young Adult ; Age Factors ; Feces/microbiology ; Biomarkers ; Case-Control Studies ; },
abstract = {Background/Objectives: Autism spectrum disorder (ASD) has a wide-ranging impact on individuals' quality of life and development, and there is a critical need for greater awareness, early intervention, and comprehensive support strategies to effectively address the unique needs of those affected by ASD. Recent studies highlight the gut microbiome's potential role in modulating ASD symptoms via the gut-brain axis, but specific microbial biomarkers remain unclear. This study aims to investigate differences in gut microbiota composition between ASD patients and neurotypical controls in a novel approach, specifically assessing ratios of Firmicutes/Bacteroidetes (F/B), Actinobacteria/Proteobacteria (A/P), and Prevotella/Bacteroides (P/B) as potential biomarkers. Methods: We analyzed gut microbiome samples from 302 Bulgarian children and adolescents diagnosed with ASD (aged 2-19 years). Microbial ratios (F/B, A/P, and P/B) were calculated and compared against previously reported reference meta-analytic means from European neurotypical populations. The statistical significance of deviations was assessed using parametric (t-tests), non-parametric (Wilcoxon signed-rank tests), and proportion-based (binomial tests) methods. Effect sizes were quantified using Cohen's d. Significant differences between ASD cases and neurotypical reference values were observed across several age groups. Results: Notably, children with ASD demonstrated significantly lower F/B and A/P ratios, with the youngest cohort (0-4 years) exhibiting the greatest differences. Deviations in the P/B ratio varied across age groups, with a significant elevation in the oldest group (≥10 years). Collectively, ASD cases consistently exhibited microbiota profiles indicative of dysbiosis. Conclusions: Our findings support gut microbiome dysbiosis as a potential biomarker for ASD, highlighting significantly altered bacterial ratios compared to neurotypical controls. These microbiome shifts could reflect early-life disruptions influencing neurodevelopment. Future studies should adopt longitudinal and mechanistic approaches to elucidate causal relationships and evaluate therapeutic microbiome modulation strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome
*Autism Spectrum Disorder/microbiology
*Dysbiosis/microbiology
Child
Adolescent
Child, Preschool
Male
Female
Young Adult
Age Factors
Feces/microbiology
Biomarkers
Case-Control Studies
RevDate: 2025-06-13
The Lung Microbiome and Its Impact on Obstructive Sleep Apnea: A Diagnostic Frontier.
Diagnostics (Basel, Switzerland), 15(11): pii:diagnostics15111431.
Obstructive sleep apnea (OSA), a prevalent disorder characterized by recurrent upper airway collapse, is increasingly recognized as a systemic inflammatory condition influenced by microbial dysregulation. Emerging evidence underscores the lung microbiome as a mediator in OSA pathophysiology, where dysbiotic shifts driven by intermittent hypoxia, oxidative stress and mechanical airway trauma amplify inflammatory cascades and perpetuate respiratory instability. This review synthesizes current knowledge on the bidirectional interplay between OSA and lung microbial communities. It aims to highlight how hypoxia-induced alterations in microbial ecology disrupt immune homeostasis, while inflammation-driven mucosal injury fosters pathogenic colonization. Clinical correlations between specific taxa like Streptococcus and Prevotella, and disease severity, suggest microbial signatures as novel biomarkers for OSA progression and treatment response. Furthermore, oxidative stress markers and pro-inflammatory cytokines emerge as potential diagnostic tools that bridge microbial dysbiosis with sleep-related outcomes. However, challenges persist in sampling standardization of the low-biomass lower airways, as well as in causative mechanisms linking microbial dysbiosis to OSA pathophysiology. By integrating microbial ecology with precision sleep medicine, this paradigm shift promises to transform OSA management from mechanical stabilization to holistic ecosystem restoration.
Additional Links: PMID-40507003
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PubMed:
Citation:
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@article {pmid40507003,
year = {2025},
author = {Karkala, A and Kotoulas, SC and Tzinas, A and Massa, E and Mouloudi, E and Gkakou, F and Pataka, A},
title = {The Lung Microbiome and Its Impact on Obstructive Sleep Apnea: A Diagnostic Frontier.},
journal = {Diagnostics (Basel, Switzerland)},
volume = {15},
number = {11},
pages = {},
doi = {10.3390/diagnostics15111431},
pmid = {40507003},
issn = {2075-4418},
abstract = {Obstructive sleep apnea (OSA), a prevalent disorder characterized by recurrent upper airway collapse, is increasingly recognized as a systemic inflammatory condition influenced by microbial dysregulation. Emerging evidence underscores the lung microbiome as a mediator in OSA pathophysiology, where dysbiotic shifts driven by intermittent hypoxia, oxidative stress and mechanical airway trauma amplify inflammatory cascades and perpetuate respiratory instability. This review synthesizes current knowledge on the bidirectional interplay between OSA and lung microbial communities. It aims to highlight how hypoxia-induced alterations in microbial ecology disrupt immune homeostasis, while inflammation-driven mucosal injury fosters pathogenic colonization. Clinical correlations between specific taxa like Streptococcus and Prevotella, and disease severity, suggest microbial signatures as novel biomarkers for OSA progression and treatment response. Furthermore, oxidative stress markers and pro-inflammatory cytokines emerge as potential diagnostic tools that bridge microbial dysbiosis with sleep-related outcomes. However, challenges persist in sampling standardization of the low-biomass lower airways, as well as in causative mechanisms linking microbial dysbiosis to OSA pathophysiology. By integrating microbial ecology with precision sleep medicine, this paradigm shift promises to transform OSA management from mechanical stabilization to holistic ecosystem restoration.},
}
RevDate: 2025-06-12
CmpDate: 2025-06-12
The gut microbiome and metabolomic alterations underlying colitis-induced encephalopathy in mice: mechanistic insight.
Behavioral and brain functions : BBF, 21(1):17.
BACKGROUND: In addition to classical gastrointestinal symptoms, patients with inflammatory bowel disease (IBD) often exhibit neurological manifestations, such as mood disorders and cognitive dysfunctions, which are frequently overlooked. However, the potential pathogenesis of IBD-related encephalopathy remains unclear, and few studies have explored the influence of interactions between the gut microbiota and the host gut-brain metabolome on the emergence of brain diseases in IBD mice. In this study, we conducted a comprehensive analysis of gut microbiome and metabolome alterations in dextran sulfate sodium salt (DSS)-induced IBD mice compared to control mice, focusing on colonic contents and hippocampal tissue. Our aim was to investigate the putative mechanisms underlying the microbiota-gut-brain axis in IBD-induced encephalopathy.
RESULTS: IBD mice showed depression-like behaviors and cognitive deficits. Metabolic profiling revealed distinct patterns in the colonic contents and hippocampal areas of IBD mice, marked by decreased energy metabolism, amino acid levels, short-chain fatty acids (SCFAs), and choline metabolism. These metabolic changes were negatively associated with the abundance of Bacteroides, Turicibacter, Ruminococcus, and Akkermansia, while Desulfovibrio and Lactobacillus showed positive correlations.
CONCLUSIONS: This study identifies unique microbial and gut-brain metabolite signatures associated with DSS-induced changes and offers new metabolic insights into the microbiota-gut-brain axis in IBD-related brain disorders. It highlights the potential of targeting gut microbiota to modulate host metabolism as a therapeutic approach for IBD-related neurological complications.
Additional Links: PMID-40506791
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Citation:
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@article {pmid40506791,
year = {2025},
author = {Cai, A and Shen, D and Xiong, Q and Li, S and Qiu, C and Li, L and Chen, Z and Lin, X and Yao, Q and Zhang, Y and Chen, R and Kou, L},
title = {The gut microbiome and metabolomic alterations underlying colitis-induced encephalopathy in mice: mechanistic insight.},
journal = {Behavioral and brain functions : BBF},
volume = {21},
number = {1},
pages = {17},
pmid = {40506791},
issn = {1744-9081},
support = {Y20210133//Wenzhou Science and Technology Bureau/ ; 2024ZYC-A10//Zhejiang Medical Association Clinical Medical Research special fund project/ ; 2023KY907//Zhejiang Medical and Health Science and Technology Program/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; Mice ; *Colitis/metabolism/complications/chemically induced/microbiology ; Male ; Hippocampus/metabolism ; *Metabolome/physiology ; *Brain Diseases/metabolism/microbiology/etiology ; Dextran Sulfate ; Colon/metabolism ; *Inflammatory Bowel Diseases/metabolism/complications/microbiology ; Disease Models, Animal ; Mice, Inbred C57BL ; Brain/metabolism ; Metabolomics ; Fatty Acids, Volatile/metabolism ; Brain-Gut Axis/physiology ; },
abstract = {BACKGROUND: In addition to classical gastrointestinal symptoms, patients with inflammatory bowel disease (IBD) often exhibit neurological manifestations, such as mood disorders and cognitive dysfunctions, which are frequently overlooked. However, the potential pathogenesis of IBD-related encephalopathy remains unclear, and few studies have explored the influence of interactions between the gut microbiota and the host gut-brain metabolome on the emergence of brain diseases in IBD mice. In this study, we conducted a comprehensive analysis of gut microbiome and metabolome alterations in dextran sulfate sodium salt (DSS)-induced IBD mice compared to control mice, focusing on colonic contents and hippocampal tissue. Our aim was to investigate the putative mechanisms underlying the microbiota-gut-brain axis in IBD-induced encephalopathy.
RESULTS: IBD mice showed depression-like behaviors and cognitive deficits. Metabolic profiling revealed distinct patterns in the colonic contents and hippocampal areas of IBD mice, marked by decreased energy metabolism, amino acid levels, short-chain fatty acids (SCFAs), and choline metabolism. These metabolic changes were negatively associated with the abundance of Bacteroides, Turicibacter, Ruminococcus, and Akkermansia, while Desulfovibrio and Lactobacillus showed positive correlations.
CONCLUSIONS: This study identifies unique microbial and gut-brain metabolite signatures associated with DSS-induced changes and offers new metabolic insights into the microbiota-gut-brain axis in IBD-related brain disorders. It highlights the potential of targeting gut microbiota to modulate host metabolism as a therapeutic approach for IBD-related neurological complications.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Gastrointestinal Microbiome/physiology
Mice
*Colitis/metabolism/complications/chemically induced/microbiology
Male
Hippocampus/metabolism
*Metabolome/physiology
*Brain Diseases/metabolism/microbiology/etiology
Dextran Sulfate
Colon/metabolism
*Inflammatory Bowel Diseases/metabolism/complications/microbiology
Disease Models, Animal
Mice, Inbred C57BL
Brain/metabolism
Metabolomics
Fatty Acids, Volatile/metabolism
Brain-Gut Axis/physiology
RevDate: 2025-06-12
CmpDate: 2025-06-12
Underground guardians: how collagen and chitin amendments shape soil microbiome structure and function for Meloidogyne enterolobii control.
Microbiome, 13(1):141.
BACKGROUND: The emergence of the guava root-knot nematode (Meloidogyne enterolobii) poses a significant threat to tomato yields globally. This study evaluated the impact of collagen and chitin soil amendments on soil microbial composition and function (fungal and bacterial communities) and their effects on tomato plant health and M. enterolobii infection under standard (5000 eggs plant[-1]) and high (50,000 eggs plant[-1]) inoculum pressure. Conducted in a greenhouse setting, the study investigated the effectiveness of these amendments in nurturing beneficial microbial communities across both native and agricultural soils.
RESULTS: Both collagen and chitin were effective in reducing nematode egg counts by up to 66% and 84% under standard and high inoculum pressure, respectively, and enhanced plant health parameters (biomass and chlorophyll content). Moreover, a microbiome shift led to an increase in bacterial (Kitasatospora, Bacillus, and Streptomyces) and fungal (Phialemonium) genera, known for their chitinase, collagenase, and plant-parasitic nematode control. Among the microbes, Streptomyces spp. were found among the core microbiome and associated with a lower disease incidence assessed through a phenotype-OTU network analysis (PhONA). Under standard inoculum, higher metabolite expression was observed with amino acids representing a majority among the metabolite groups.
CONCLUSIONS: The findings highlight the potential of collagen and chitin to mitigate M. enterolobii infection by fostering beneficial soil microbial communities. Video Abstract.
Additional Links: PMID-40506747
PubMed:
Citation:
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@article {pmid40506747,
year = {2025},
author = {Pasche, JM and Sawlani, R and Buttrós, VH and Desaeger, J and Garrett, KA and Martins, SJ},
title = {Underground guardians: how collagen and chitin amendments shape soil microbiome structure and function for Meloidogyne enterolobii control.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {141},
pmid = {40506747},
issn = {2049-2618},
support = {2021-68013-33758//National Institute of Food and Agriculture/ ; },
mesh = {*Chitin/pharmacology ; Animals ; *Soil Microbiology ; *Tylenchoidea/drug effects/pathogenicity ; Solanum lycopersicum/parasitology/growth & development/microbiology ; *Collagen/pharmacology ; Soil/chemistry ; *Microbiota/drug effects ; *Plant Diseases/parasitology/prevention & control ; Bacteria/classification/genetics/isolation & purification ; Fungi/classification/isolation & purification/genetics ; Plant Roots/parasitology ; },
abstract = {BACKGROUND: The emergence of the guava root-knot nematode (Meloidogyne enterolobii) poses a significant threat to tomato yields globally. This study evaluated the impact of collagen and chitin soil amendments on soil microbial composition and function (fungal and bacterial communities) and their effects on tomato plant health and M. enterolobii infection under standard (5000 eggs plant[-1]) and high (50,000 eggs plant[-1]) inoculum pressure. Conducted in a greenhouse setting, the study investigated the effectiveness of these amendments in nurturing beneficial microbial communities across both native and agricultural soils.
RESULTS: Both collagen and chitin were effective in reducing nematode egg counts by up to 66% and 84% under standard and high inoculum pressure, respectively, and enhanced plant health parameters (biomass and chlorophyll content). Moreover, a microbiome shift led to an increase in bacterial (Kitasatospora, Bacillus, and Streptomyces) and fungal (Phialemonium) genera, known for their chitinase, collagenase, and plant-parasitic nematode control. Among the microbes, Streptomyces spp. were found among the core microbiome and associated with a lower disease incidence assessed through a phenotype-OTU network analysis (PhONA). Under standard inoculum, higher metabolite expression was observed with amino acids representing a majority among the metabolite groups.
CONCLUSIONS: The findings highlight the potential of collagen and chitin to mitigate M. enterolobii infection by fostering beneficial soil microbial communities. Video Abstract.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Chitin/pharmacology
Animals
*Soil Microbiology
*Tylenchoidea/drug effects/pathogenicity
Solanum lycopersicum/parasitology/growth & development/microbiology
*Collagen/pharmacology
Soil/chemistry
*Microbiota/drug effects
*Plant Diseases/parasitology/prevention & control
Bacteria/classification/genetics/isolation & purification
Fungi/classification/isolation & purification/genetics
Plant Roots/parasitology
RevDate: 2025-06-12
Selective recruitment of beneficial microbes in the rhizosphere of maize affected by microbial inoculants, farming practice, and seasonal variations.
Environmental microbiome, 20(1):69.
BACKGROUND: Plant beneficial microorganisms as inoculants can improve crop performance, but factors affecting their impact on plant performance under field conditions remain unclear, thereby limiting their use in farming. Here, we investigated how farming practices (e.g., tillage and N-fertilization intensity) and growing seasons influenced the impact of a beneficial microorganism consortium (BMc: Trichoderma, Bacillus, and Pseudomonas strains) in maize and affected the rhizosphere competence of each BMc strain. In addition, we tested whether the consortium affects the resident rhizosphere microbiome and crop performance. In two growing seasons (2020 and 2021), we assessed how BMc inoculation affects maize growth, nutritional status, gene expression, and rhizosphere microbiome under different farming practices at the flowering stage.
RESULTS: Inoculated strains successfully colonized the maize rhizosphere independently of farming practice. BMc inoculation improved plant growth and iron uptake in 2020, regardless of farming practice. These effects co-occurred with lower precipitation levels in 2020 compared to 2021. BMc inoculation reduced the expression of several stress-related genes in maize in 2020 under drought. An increased iron uptake by the BMc-inoculated plants was observed in 2020 and was associated with the upregulation of the gene ZmNAS3, which is linked to iron uptake. Therefore, BMc inoculation mitigated the drought impact on maize. The microbial rhizosphere communities were altered by BMc inoculation in both years, but patterns of responder taxa differed between seasons. Metagenome analysis revealed that more genes (e.g., genes encoding biosurfactants and siderophores) were enriched in the rhizosphere of BMc-inoculated plants in 2020 than in 2021. Moreover, we identified bacterial and fungal taxa positively associated with maize iron uptake. The relative abundance of these iron uptake-associated bacterial and fungal taxa significantly increased due to BMc inoculation in 2020, while they showed overall higher relative abundances in 2021, independently of BMc inoculation. We mapped the sequences of these iron-associated taxa to publicly available genomes and verified the occurrence of various plant beneficial traits in several mapped genomes.
CONCLUSIONS: Overall, we show that the growing season determined the effect of BMc inoculation on maize plants by shaping microbiome composition and function in the maize rhizosphere more than farming practice. These findings highlight the importance of the complex interplay between microbial inoculants and the resident rhizosphere microorganisms under abiotic stress conditions.
Additional Links: PMID-40506735
PubMed:
Citation:
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@article {pmid40506735,
year = {2025},
author = {Kampouris, ID and Kuhl-Nagel, T and Behr, JH and Sommermann, L and Babin, D and Francioli, D and Zrenner, R and Kublik, S and Schloter, M and Ludewig, U and Smalla, K and Neumann, G and Grosch, R and Geistlinger, J},
title = {Selective recruitment of beneficial microbes in the rhizosphere of maize affected by microbial inoculants, farming practice, and seasonal variations.},
journal = {Environmental microbiome},
volume = {20},
number = {1},
pages = {69},
pmid = {40506735},
issn = {2524-6372},
abstract = {BACKGROUND: Plant beneficial microorganisms as inoculants can improve crop performance, but factors affecting their impact on plant performance under field conditions remain unclear, thereby limiting their use in farming. Here, we investigated how farming practices (e.g., tillage and N-fertilization intensity) and growing seasons influenced the impact of a beneficial microorganism consortium (BMc: Trichoderma, Bacillus, and Pseudomonas strains) in maize and affected the rhizosphere competence of each BMc strain. In addition, we tested whether the consortium affects the resident rhizosphere microbiome and crop performance. In two growing seasons (2020 and 2021), we assessed how BMc inoculation affects maize growth, nutritional status, gene expression, and rhizosphere microbiome under different farming practices at the flowering stage.
RESULTS: Inoculated strains successfully colonized the maize rhizosphere independently of farming practice. BMc inoculation improved plant growth and iron uptake in 2020, regardless of farming practice. These effects co-occurred with lower precipitation levels in 2020 compared to 2021. BMc inoculation reduced the expression of several stress-related genes in maize in 2020 under drought. An increased iron uptake by the BMc-inoculated plants was observed in 2020 and was associated with the upregulation of the gene ZmNAS3, which is linked to iron uptake. Therefore, BMc inoculation mitigated the drought impact on maize. The microbial rhizosphere communities were altered by BMc inoculation in both years, but patterns of responder taxa differed between seasons. Metagenome analysis revealed that more genes (e.g., genes encoding biosurfactants and siderophores) were enriched in the rhizosphere of BMc-inoculated plants in 2020 than in 2021. Moreover, we identified bacterial and fungal taxa positively associated with maize iron uptake. The relative abundance of these iron uptake-associated bacterial and fungal taxa significantly increased due to BMc inoculation in 2020, while they showed overall higher relative abundances in 2021, independently of BMc inoculation. We mapped the sequences of these iron-associated taxa to publicly available genomes and verified the occurrence of various plant beneficial traits in several mapped genomes.
CONCLUSIONS: Overall, we show that the growing season determined the effect of BMc inoculation on maize plants by shaping microbiome composition and function in the maize rhizosphere more than farming practice. These findings highlight the importance of the complex interplay between microbial inoculants and the resident rhizosphere microorganisms under abiotic stress conditions.},
}
RevDate: 2025-06-12
CmpDate: 2025-06-12
Metagenomic insight into the vaginal microbiome in women infected with HPV 16 and 18.
NPJ biofilms and microbiomes, 11(1):105.
Human papillomavirus (HPV) 16 and 18 (HPV 16/18) account for over 70% of cervical cancer (CC) cases, yet their interaction with the vaginal microbiome (VM) remains unclear. This study explored the association between high-risk HPV types (HR-HPVs), VM composition and bacterial function using shotgun metagenomic sequencing. In early-stage cervical lesions, the HPV 16/18 group showed reduced Lactobacillus-dominant community state types compared to other HR-HPVs, while invasive CC exhibited increased pathogenic bacteria, including Streptococcus agalactiae, Fannyhessea vaginae, and Sneathia vaginalis. The VM associated with HPV 16/18 was enriched in immune response and inflammation pathways, whereas other HR-HPVs were linked to cellular metabolism and hormonal signaling. Notably, HPV 16/18 exhibited stronger bacterial-fungal correlations, indicating shifts in the microbial community. Furthermore, 137 metagenome-assembled genomes provided insights into unique microbial genomic signatures. Our study links VM differences with HPV 16/18 oncogenic potential across cervical lesion stages, urging further research for better diagnostics and treatments.
Additional Links: PMID-40506497
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Citation:
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@article {pmid40506497,
year = {2025},
author = {Jung, DR and Choi, Y and Jeong, M and Singh, V and Jeon, SY and Seo, I and Park, NJ and Lee, YH and Park, JY and Han, HS and Shin, JH and Chong, GO},
title = {Metagenomic insight into the vaginal microbiome in women infected with HPV 16 and 18.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {105},
pmid = {40506497},
issn = {2055-5008},
mesh = {Female ; Humans ; *Vagina/microbiology/virology ; *Human papillomavirus 16/genetics/isolation & purification ; *Papillomavirus Infections/virology/microbiology ; *Microbiota/genetics ; Metagenomics ; *Human papillomavirus 18/genetics/isolation & purification ; *Bacteria/classification/genetics/isolation & purification ; Uterine Cervical Neoplasms/virology/microbiology ; Metagenome ; Adult ; Middle Aged ; },
abstract = {Human papillomavirus (HPV) 16 and 18 (HPV 16/18) account for over 70% of cervical cancer (CC) cases, yet their interaction with the vaginal microbiome (VM) remains unclear. This study explored the association between high-risk HPV types (HR-HPVs), VM composition and bacterial function using shotgun metagenomic sequencing. In early-stage cervical lesions, the HPV 16/18 group showed reduced Lactobacillus-dominant community state types compared to other HR-HPVs, while invasive CC exhibited increased pathogenic bacteria, including Streptococcus agalactiae, Fannyhessea vaginae, and Sneathia vaginalis. The VM associated with HPV 16/18 was enriched in immune response and inflammation pathways, whereas other HR-HPVs were linked to cellular metabolism and hormonal signaling. Notably, HPV 16/18 exhibited stronger bacterial-fungal correlations, indicating shifts in the microbial community. Furthermore, 137 metagenome-assembled genomes provided insights into unique microbial genomic signatures. Our study links VM differences with HPV 16/18 oncogenic potential across cervical lesion stages, urging further research for better diagnostics and treatments.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Female
Humans
*Vagina/microbiology/virology
*Human papillomavirus 16/genetics/isolation & purification
*Papillomavirus Infections/virology/microbiology
*Microbiota/genetics
Metagenomics
*Human papillomavirus 18/genetics/isolation & purification
*Bacteria/classification/genetics/isolation & purification
Uterine Cervical Neoplasms/virology/microbiology
Metagenome
Adult
Middle Aged
RevDate: 2025-06-12
Detection of Volatile Organic Compounds as an emerging strategy for Parkinson's disease diagnosis and monitoring.
NPJ Parkinson's disease, 11(1):161.
Growing evidence suggests that specific volatile organic compound (VOC) profiles may reflect key pathophysiological processes in Parkinson's disease (PD), including alterations in the microbiome, metabolism, and oxidative stress. Identifying reliable VOC biomarkers could enable non-invasive tests for early diagnosis, disease monitoring, and therapy evaluation. This review examines VOC analysis in biological matrices such as breath, skin, and stool, outlining current research and future applications in PD. We evaluate analytical techniques based on sensitivity, specificity, and clinical applicability. Additionally, we classify VOCs identified in previous studies alongside their proposed biological origins. Special attention is given to short-chain fatty acids, produced by the gut microbiome, a novel target in PD research. Our findings highlight the need for larger cohort studies and standardized protocols to advance VOC-based diagnostics in PD. Understanding the interplay between VOCs and PD may facilitate biomarker discovery, enhancing non-invasive diagnostic strategies and personalized disease management.
Additional Links: PMID-40506424
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Citation:
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@article {pmid40506424,
year = {2025},
author = {Belluomo, I and Tarazi, M and Lao-Kaim, NP and Tai, YF and Spanel, P and Hanna, GB},
title = {Detection of Volatile Organic Compounds as an emerging strategy for Parkinson's disease diagnosis and monitoring.},
journal = {NPJ Parkinson's disease},
volume = {11},
number = {1},
pages = {161},
pmid = {40506424},
issn = {2373-8057},
abstract = {Growing evidence suggests that specific volatile organic compound (VOC) profiles may reflect key pathophysiological processes in Parkinson's disease (PD), including alterations in the microbiome, metabolism, and oxidative stress. Identifying reliable VOC biomarkers could enable non-invasive tests for early diagnosis, disease monitoring, and therapy evaluation. This review examines VOC analysis in biological matrices such as breath, skin, and stool, outlining current research and future applications in PD. We evaluate analytical techniques based on sensitivity, specificity, and clinical applicability. Additionally, we classify VOCs identified in previous studies alongside their proposed biological origins. Special attention is given to short-chain fatty acids, produced by the gut microbiome, a novel target in PD research. Our findings highlight the need for larger cohort studies and standardized protocols to advance VOC-based diagnostics in PD. Understanding the interplay between VOCs and PD may facilitate biomarker discovery, enhancing non-invasive diagnostic strategies and personalized disease management.},
}
RevDate: 2025-06-12
Potential role of intratumoral Fusobacterium nucleatum and interleukin-1 beta in breast cancer cell growth.
Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi pii:S1684-1182(25)00119-7 [Epub ahead of print].
BACKGROUND: It has been shown that the human breast harbors a rich and diverse microbiome, with significant differences observed between tumor tissue and normal breast tissue. Recently, Fusobacterium nucleatum (F. nucleatum) has been shown to affect breast cancer growth, but the underlying mechanism remains enigmatic.
METHODS: Breast cancer tissues were obtained from clinical patients and analyzed for the microbiome composition using 16S rDNA sequencing and qPCR. Both serum and intratumoral cytokine levels were measured to assess their correlation with intratumoral F. nucleatum. Breast cancer cell lines and patient-derived cancer cells were infected with different strains of F. nucleatum, followed by different analyses. Additionally, peripheral blood mononuclear cells (PBMCs) were isolated from healthy individuals to investigate the immunoregulatory effect of F. nucleatum.
RESULTS: Our results identified a higher abundance of F. nucleatum in breast cancer tissue compared to adjacent normal breast tissue, which strongly correlated with intratumoral IL-1β levels. In vitro studies confirmed this correlation, demonstrating that infection of breast cancer cells with F. nucleatum promotes tumor growth. Further investigation suggested that F. nucleatum induces IL-1β secretion in both breast cancer cells and PBMCs, but only IL-1β secreted by breast cancer cells stimulates cancer cell growth. Inhibition of NLRP3 reversed the growth-promoting effect of F. nucleatum on breast cancer cells.
CONCLUSION: Our results demonstrate the role of F. nucleatum in stimulating breast cancer cell growth. Therefore, targeting intratumoral F. nucleatum could provide a promising therapeutic approach to combat breast cancer.
Additional Links: PMID-40506319
Publisher:
PubMed:
Citation:
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@article {pmid40506319,
year = {2025},
author = {Chang, CM and Lam, LY and Lam, HYP and Kao, PY and Hsu, ST and Wu, WJ and Chang, KC and Huang, CY},
title = {Potential role of intratumoral Fusobacterium nucleatum and interleukin-1 beta in breast cancer cell growth.},
journal = {Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jmii.2025.05.008},
pmid = {40506319},
issn = {1995-9133},
abstract = {BACKGROUND: It has been shown that the human breast harbors a rich and diverse microbiome, with significant differences observed between tumor tissue and normal breast tissue. Recently, Fusobacterium nucleatum (F. nucleatum) has been shown to affect breast cancer growth, but the underlying mechanism remains enigmatic.
METHODS: Breast cancer tissues were obtained from clinical patients and analyzed for the microbiome composition using 16S rDNA sequencing and qPCR. Both serum and intratumoral cytokine levels were measured to assess their correlation with intratumoral F. nucleatum. Breast cancer cell lines and patient-derived cancer cells were infected with different strains of F. nucleatum, followed by different analyses. Additionally, peripheral blood mononuclear cells (PBMCs) were isolated from healthy individuals to investigate the immunoregulatory effect of F. nucleatum.
RESULTS: Our results identified a higher abundance of F. nucleatum in breast cancer tissue compared to adjacent normal breast tissue, which strongly correlated with intratumoral IL-1β levels. In vitro studies confirmed this correlation, demonstrating that infection of breast cancer cells with F. nucleatum promotes tumor growth. Further investigation suggested that F. nucleatum induces IL-1β secretion in both breast cancer cells and PBMCs, but only IL-1β secreted by breast cancer cells stimulates cancer cell growth. Inhibition of NLRP3 reversed the growth-promoting effect of F. nucleatum on breast cancer cells.
CONCLUSION: Our results demonstrate the role of F. nucleatum in stimulating breast cancer cell growth. Therefore, targeting intratumoral F. nucleatum could provide a promising therapeutic approach to combat breast cancer.},
}
RevDate: 2025-06-12
Cystic Fibrosis Microbiome-directed Antibiotic Therapy Trial in Exacerbations Results Stratified (CFMATTERS): Results of a multi-centre randomised controlled trial.
The European respiratory journal pii:13993003.02443-2024 [Epub ahead of print].
BACKGROUND: This study explores the effectiveness and safety of microbiome-directed-antimicrobial-therapy versus usual-antimicrobial-therapy in adult cystic fibrosis pulmonary exacerbations.
METHODS: A multi-centre two-arm parallel randomised control trial conducted across Europe/North-America enrolled 223 participants (January 2015 - August 2017). All participants were chronically colonised with Pseudomonas aeruginosa and were randomised 1:1 into two study-arms. The "usual-therapy group" received 2-weeks of IV ceftazidime 3g thrice-daily (for allergies: aztreonam 2g thrice-daily) and tobramycin 5-10mg·kg[-1] once-daily. The "microbiome-directed group" received the same usual-therapy plus an additional antibiotic with greatest presumed activity against the 2nd, 3rd and 4th most abundant genera present in the sputum microbiome, selected by a Consensus Expert Treatment Panel. The primary outcome was change in percentage of predicted FEV1 (ppFEV1) at 14 days post initiation of antibiotics. Secondary outcomes examined ppFEV1 at 7 days, 28 days, and 3 months; time-to-next exacerbation; symptom burden at 7 days; Health Related Quality of Life (HRQoL) at 28 days; and number of exacerbations and IV antibiotic days at 12 months.
RESULTS: 149 participants had an eligible exacerbation (usual-therapy n=83, microbiome-directed therapy n=66). There was no difference between the groups for ppFEV1 at day 14 (-1.1%, 95%CI -3.9 to 1.7; p=0.46), or ppFEV1 measured at other time-points, or for time-to-next exacerbation (microbiome-directed versus usual-therapy Hazard Ratio 0.91 [95%CI 0.60 to 1.38; p=0.66]). The microbiome-directed group trended to have more IV days (median 42 versus 28; p=0.08) and more subsequent exacerbations (median 3 versus 2; p=0.044) the following year. There were no appreciable differences in symptom burden; however, HRQoL sub-scores were consistently worse in the microbiome-directed group (-4.3 points versus usual therapy (95%CI -8.3 to -0.3, p=0.033).
CONCLUSION: The addition of a third antibiotic based on sputum microbiome sequencing analysis did not result in improved clinical outcomes.
Additional Links: PMID-40506211
Publisher:
PubMed:
Citation:
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@article {pmid40506211,
year = {2025},
author = {Plant, BJ and Einarsson, GG and Deasy, KF and Dahly, D and Singh, PK and Barry, PJ and Goss, CH and Fajac, I and Vagg, T and Durieu, I and Flanagan, E and O'Callaghan, G and Martin, C and Burgel, PR and Haworth, CS and Floto, RA and Downey, DG and Dupont, LJ and Jones, AM and Elborn, JS and Eustace, JA and Mall, MA and Tunney, MM},
title = {Cystic Fibrosis Microbiome-directed Antibiotic Therapy Trial in Exacerbations Results Stratified (CFMATTERS): Results of a multi-centre randomised controlled trial.},
journal = {The European respiratory journal},
volume = {},
number = {},
pages = {},
doi = {10.1183/13993003.02443-2024},
pmid = {40506211},
issn = {1399-3003},
abstract = {BACKGROUND: This study explores the effectiveness and safety of microbiome-directed-antimicrobial-therapy versus usual-antimicrobial-therapy in adult cystic fibrosis pulmonary exacerbations.
METHODS: A multi-centre two-arm parallel randomised control trial conducted across Europe/North-America enrolled 223 participants (January 2015 - August 2017). All participants were chronically colonised with Pseudomonas aeruginosa and were randomised 1:1 into two study-arms. The "usual-therapy group" received 2-weeks of IV ceftazidime 3g thrice-daily (for allergies: aztreonam 2g thrice-daily) and tobramycin 5-10mg·kg[-1] once-daily. The "microbiome-directed group" received the same usual-therapy plus an additional antibiotic with greatest presumed activity against the 2nd, 3rd and 4th most abundant genera present in the sputum microbiome, selected by a Consensus Expert Treatment Panel. The primary outcome was change in percentage of predicted FEV1 (ppFEV1) at 14 days post initiation of antibiotics. Secondary outcomes examined ppFEV1 at 7 days, 28 days, and 3 months; time-to-next exacerbation; symptom burden at 7 days; Health Related Quality of Life (HRQoL) at 28 days; and number of exacerbations and IV antibiotic days at 12 months.
RESULTS: 149 participants had an eligible exacerbation (usual-therapy n=83, microbiome-directed therapy n=66). There was no difference between the groups for ppFEV1 at day 14 (-1.1%, 95%CI -3.9 to 1.7; p=0.46), or ppFEV1 measured at other time-points, or for time-to-next exacerbation (microbiome-directed versus usual-therapy Hazard Ratio 0.91 [95%CI 0.60 to 1.38; p=0.66]). The microbiome-directed group trended to have more IV days (median 42 versus 28; p=0.08) and more subsequent exacerbations (median 3 versus 2; p=0.044) the following year. There were no appreciable differences in symptom burden; however, HRQoL sub-scores were consistently worse in the microbiome-directed group (-4.3 points versus usual therapy (95%CI -8.3 to -0.3, p=0.033).
CONCLUSION: The addition of a third antibiotic based on sputum microbiome sequencing analysis did not result in improved clinical outcomes.},
}
RevDate: 2025-06-12
Milk Composition Changes and Alterations in Bacteria, Serum, and Gut Metabolome Over Time in Lactating Naks and Simmental Cows.
Animal bioscience pii:ab.25.0109 [Epub ahead of print].
OBJECTIVE: This study aimed to elucidate the mechanisms underlying milk composition divergence between naks (female yaks) and Simmental cows (S-cows) by integrating longitudinal multi-omics analyses of gut microbiota and metabolomes.
METHODS: We determined the gut microbiota and metabolites of both species over a 54-day period (day 26 to 80 of lactation), with ten naks and ten S-cows. Gut microbiota dynamics were assessed via 16S rRNA sequencing, while serum and fecal metabolomes were profiled using UHPLC-MS/MS. Statistical analyses included Wilcoxon rank-sum tests, LEfSe (LDA > 2, p < 0.05), and Spearman correlations (r > 0.70).
RESULTS: Milk yield was lesser (0.53-0.91 vs. 2.07-3.88 kg/d) but concentrations of fat (5.63-6.30% vs. 3.30-3.74%), protein (5.66-6.30% vs. 3.39-3.74%), and conjugated linoleic acid(CLA) (1.74-2.35% vs. 1.40-1.75%) were greater (p < 0.001) in nak than S-cow milk. Species-specific microbial signatures emerged. In naks, the g-Family-XIII-AD3011-group and g-norank-Ruminococcaceae were correlated with bile acid metabolism and CLA synthesis via 13-hydroxyoctadecadienoic acid transport. Additionally, the naks gut had a greater concentration of 13-hydroxyoctadecadienoic acid, a precursor of CLA, which may be transported to mammary cells via phosphatidylcholine and converted to CLA under the catalysis of fatty acid desaturase2(FADS2). S-cows harbored g-Succinivibrio and g-Eubacterium-ruminantium-group, which are linked to galactose utilization and mTOR-mediated amino acid allocation. Metabolomics revealed naks-enriched steroid biosynthesis and taurine pathways (FDR < 0.05), while S-cows exhibited a lactating network associated with greater milk yield.
CONCLUSIONS: Host-specific gut microbiota mediated nutrient allocation trade-offs. Naks optimized lipid-rich milk through bile acid and CLA metabolic networks, whereas S-cows enhanced yield via microbial-galactose synergies. This research underscores the pivotal role of the gut microbiome in mediating milk composition and suggests that microbiome manipulation could be a promising strategy to enhance milk quality in ruminants.
Additional Links: PMID-40506032
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PubMed:
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@article {pmid40506032,
year = {2025},
author = {Wang, R and Yunxiang, X and Degen, A and Han, X and Zhao, X and Zhang, Q and Huang, Y and Bai, B and Yang, Y and Liu, S and Xue, Y and Hao, L},
title = {Milk Composition Changes and Alterations in Bacteria, Serum, and Gut Metabolome Over Time in Lactating Naks and Simmental Cows.},
journal = {Animal bioscience},
volume = {},
number = {},
pages = {},
doi = {10.5713/ab.25.0109},
pmid = {40506032},
issn = {2765-0189},
abstract = {OBJECTIVE: This study aimed to elucidate the mechanisms underlying milk composition divergence between naks (female yaks) and Simmental cows (S-cows) by integrating longitudinal multi-omics analyses of gut microbiota and metabolomes.
METHODS: We determined the gut microbiota and metabolites of both species over a 54-day period (day 26 to 80 of lactation), with ten naks and ten S-cows. Gut microbiota dynamics were assessed via 16S rRNA sequencing, while serum and fecal metabolomes were profiled using UHPLC-MS/MS. Statistical analyses included Wilcoxon rank-sum tests, LEfSe (LDA > 2, p < 0.05), and Spearman correlations (r > 0.70).
RESULTS: Milk yield was lesser (0.53-0.91 vs. 2.07-3.88 kg/d) but concentrations of fat (5.63-6.30% vs. 3.30-3.74%), protein (5.66-6.30% vs. 3.39-3.74%), and conjugated linoleic acid(CLA) (1.74-2.35% vs. 1.40-1.75%) were greater (p < 0.001) in nak than S-cow milk. Species-specific microbial signatures emerged. In naks, the g-Family-XIII-AD3011-group and g-norank-Ruminococcaceae were correlated with bile acid metabolism and CLA synthesis via 13-hydroxyoctadecadienoic acid transport. Additionally, the naks gut had a greater concentration of 13-hydroxyoctadecadienoic acid, a precursor of CLA, which may be transported to mammary cells via phosphatidylcholine and converted to CLA under the catalysis of fatty acid desaturase2(FADS2). S-cows harbored g-Succinivibrio and g-Eubacterium-ruminantium-group, which are linked to galactose utilization and mTOR-mediated amino acid allocation. Metabolomics revealed naks-enriched steroid biosynthesis and taurine pathways (FDR < 0.05), while S-cows exhibited a lactating network associated with greater milk yield.
CONCLUSIONS: Host-specific gut microbiota mediated nutrient allocation trade-offs. Naks optimized lipid-rich milk through bile acid and CLA metabolic networks, whereas S-cows enhanced yield via microbial-galactose synergies. This research underscores the pivotal role of the gut microbiome in mediating milk composition and suggests that microbiome manipulation could be a promising strategy to enhance milk quality in ruminants.},
}
RevDate: 2025-06-12
Investigating acupuncture therapy in depression: mechanisms of synaptic plasticity regulation.
Neuroscience pii:S0306-4522(25)00687-6 [Epub ahead of print].
Depression is a severe heterogeneous mental illness that is highly co-morbid with other mental and somatic disorders. It poses a significant healthcare burden on both individuals and society. Currently, the use of single-target antidepressants exhibits suboptimal efficacy with significant adverse effects. Acupuncture has been advocated as a practical and effective treatment for depression, due to its low adverse effects rate compared to antidepressant medication. Currently, several studies have shown that acupuncture treatment for depression primarily involves multiple therapeutic mechanisms, including the regulation of specific gene expression, neuropeptide and neurotransmitter release, increasing the expression of neurotrophic factors, suppressing hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, attenuating inflammatory responses, and restoring gut microbiota balance. These therapeutic effects involve the regulation of critical signaling pathways, including the cAMP-responsive element binding protein (CREB) signaling pathway, mitogen-activated protein kinases (MAPK) signaling pathway, mechanistic target of rapamycin (mTOR) signaling pathway, and toll-like receptors (TLR) signaling pathway. Notably, depression-associated molecular mechanisms and signaling pathway dysregulations are closely linked to impaired neural and synaptic plasticity. Acupuncture synergistically modulates the neuro-immune-microbiome multidimensional network and integrates crosstalk among key pathways such as CREB, thereby systemically restoring synaptic plasticity. This multi-dimensional integrative mechanism likely underlies its therapeutic superiority over single-target antidepressants. This review aims to elucidate how acupuncture restores cerebral synaptic plasticity by rectifying depression-related systemic dysfunctions and signaling pathway abnormalities, which will advance our understanding of its regulatory potential in depression treatment and inform the development of precision therapeutic strategies.
Additional Links: PMID-40506009
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PubMed:
Citation:
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@article {pmid40506009,
year = {2025},
author = {Si, Y and Ma, W and Zhang, Q and Zhang, Y and An, J and Zhang, M and Fu, Y and Yu, Y and Zhang, H and Fang, Y and Zhang, D},
title = {Investigating acupuncture therapy in depression: mechanisms of synaptic plasticity regulation.},
journal = {Neuroscience},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.neuroscience.2025.06.005},
pmid = {40506009},
issn = {1873-7544},
abstract = {Depression is a severe heterogeneous mental illness that is highly co-morbid with other mental and somatic disorders. It poses a significant healthcare burden on both individuals and society. Currently, the use of single-target antidepressants exhibits suboptimal efficacy with significant adverse effects. Acupuncture has been advocated as a practical and effective treatment for depression, due to its low adverse effects rate compared to antidepressant medication. Currently, several studies have shown that acupuncture treatment for depression primarily involves multiple therapeutic mechanisms, including the regulation of specific gene expression, neuropeptide and neurotransmitter release, increasing the expression of neurotrophic factors, suppressing hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, attenuating inflammatory responses, and restoring gut microbiota balance. These therapeutic effects involve the regulation of critical signaling pathways, including the cAMP-responsive element binding protein (CREB) signaling pathway, mitogen-activated protein kinases (MAPK) signaling pathway, mechanistic target of rapamycin (mTOR) signaling pathway, and toll-like receptors (TLR) signaling pathway. Notably, depression-associated molecular mechanisms and signaling pathway dysregulations are closely linked to impaired neural and synaptic plasticity. Acupuncture synergistically modulates the neuro-immune-microbiome multidimensional network and integrates crosstalk among key pathways such as CREB, thereby systemically restoring synaptic plasticity. This multi-dimensional integrative mechanism likely underlies its therapeutic superiority over single-target antidepressants. This review aims to elucidate how acupuncture restores cerebral synaptic plasticity by rectifying depression-related systemic dysfunctions and signaling pathway abnormalities, which will advance our understanding of its regulatory potential in depression treatment and inform the development of precision therapeutic strategies.},
}
RevDate: 2025-06-12
Gut Microbiota and Behavioral Ontogeny in Autism Spectrum Disorder: A Pathway to Therapeutic Innovations.
Physiology & behavior pii:S0031-9384(25)00190-8 [Epub ahead of print].
Autism Spectrum Disorder (ASD) is a multifaceted neurodevelopmental condition characterized by deficits in social communication, repetitive behaviors, and restricted interests. Emerging evidence suggests that gut-brain axis a dynamic, bidirectional communication network between gut microbiota and central nervous system, is critical in shaping behavioral ontogeny in ASD. Dysbiosis of gut microbiota, commonly observed in individuals with ASD, has been associated with alterations in neurodevelopmental trajectories and symptom severity. Furthermore, disturbances in maternal microbiome during pregnancy are increasingly recognized as key factors influencing fetal brain development, potentially heightening risk of ASD and behavioral manifestations. Mechanistic research reveals that gut-derived metabolites modulate blood-brain barrier integrity, neuroinflammatory processes, and neuronal circuit formation, contributing to behavioral outcomes. These findings emphasize gut microbiota's profound influence on emergence and progression of ASD-related behaviors. Promising therapeutic strategies, including probiotics, prebiotics, fecal microbiota transplantation, and dietary interventions, have demonstrated potential in modulating the gut microbiome and improving behavioral symptoms in ASD. However, challenges such as individual variability in microbiome composition, limited clinical evidence, and an incomplete understanding of causative mechanisms remain significant barriers to clinical translation. This review explores the interplay between gut microbiota and ASD-associated behaviors, focusing on key mechanisms such as microbial regulation of neurotransmitter production, immune signaling, and neuroinflammation. It further highlights gut microbiota's potential as a modifiable factor influencing neurodevelopmental and behavioral outcomes in ASD. By advancing our understanding of gut-brain axis, we can pave the way for personalized and targeted interventions aimed at improving behavioral ontogeny and developmental trajectories in individuals with ASD.
Additional Links: PMID-40505847
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PubMed:
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@article {pmid40505847,
year = {2025},
author = {Yadav, A and Tadas, M and Kale, M and Wankhede, N and Umekar, M and Kotagale, N and Taksande, B},
title = {Gut Microbiota and Behavioral Ontogeny in Autism Spectrum Disorder: A Pathway to Therapeutic Innovations.},
journal = {Physiology & behavior},
volume = {},
number = {},
pages = {114989},
doi = {10.1016/j.physbeh.2025.114989},
pmid = {40505847},
issn = {1873-507X},
abstract = {Autism Spectrum Disorder (ASD) is a multifaceted neurodevelopmental condition characterized by deficits in social communication, repetitive behaviors, and restricted interests. Emerging evidence suggests that gut-brain axis a dynamic, bidirectional communication network between gut microbiota and central nervous system, is critical in shaping behavioral ontogeny in ASD. Dysbiosis of gut microbiota, commonly observed in individuals with ASD, has been associated with alterations in neurodevelopmental trajectories and symptom severity. Furthermore, disturbances in maternal microbiome during pregnancy are increasingly recognized as key factors influencing fetal brain development, potentially heightening risk of ASD and behavioral manifestations. Mechanistic research reveals that gut-derived metabolites modulate blood-brain barrier integrity, neuroinflammatory processes, and neuronal circuit formation, contributing to behavioral outcomes. These findings emphasize gut microbiota's profound influence on emergence and progression of ASD-related behaviors. Promising therapeutic strategies, including probiotics, prebiotics, fecal microbiota transplantation, and dietary interventions, have demonstrated potential in modulating the gut microbiome and improving behavioral symptoms in ASD. However, challenges such as individual variability in microbiome composition, limited clinical evidence, and an incomplete understanding of causative mechanisms remain significant barriers to clinical translation. This review explores the interplay between gut microbiota and ASD-associated behaviors, focusing on key mechanisms such as microbial regulation of neurotransmitter production, immune signaling, and neuroinflammation. It further highlights gut microbiota's potential as a modifiable factor influencing neurodevelopmental and behavioral outcomes in ASD. By advancing our understanding of gut-brain axis, we can pave the way for personalized and targeted interventions aimed at improving behavioral ontogeny and developmental trajectories in individuals with ASD.},
}
RevDate: 2025-06-12
Gut microbiome contributes to 6PPD-Quinone induced cognitive impairment through PI3K/Akt signaling.
Toxicology pii:S0300-483X(25)00176-3 [Epub ahead of print].
Studies show that N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-Q) accumulates in the central nervous system, but its role in cognitive impairment and underlying mechanisms remain unclear. Morris water maze assay revealed that 6-PPDQ significantly impairs cognitive function, particularly learning and memory. HE staining revealed alterations in the hippocampal DG and CA3 regions of exposed mice, including sparse cell arrangement, blurred boundaries, nuclear condensation, and a reduction in Nissl bodies. Fecal microbiota transplantation from 6-PPDQ-exposed mice to normal mice induced cognitive deficits and hippocampal pathological damage. Western Blot assay showed that 6-PPDQ exposure resulted in inhibition of PI3K/AKT signaling. Moreover, blunted PI3K/AKT signaling was observed in mice transplanted with 6-PPDQ-associated mice fecal microbiota. Further analysis of 16S rDNA assay identified a total of 30 differential bacteria at the genus level, including 8 upregulated bacteria such as g_Helicobacter and 22 downregulated bacteria such as g_Prevotellaceae_NK3B31_group. In conclusion, this study uncovers gut microbiome mediates 6PPD-Q-induced cognitive impairment through inhibiting of PI3K/Akt signaling, and provides a basis for further investigation into gut microbiome's protective effects on 6-PPDQ-induced nervous system injury.
Additional Links: PMID-40505719
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PubMed:
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@article {pmid40505719,
year = {2025},
author = {Zhu, X and Xu, Y},
title = {Gut microbiome contributes to 6PPD-Quinone induced cognitive impairment through PI3K/Akt signaling.},
journal = {Toxicology},
volume = {},
number = {},
pages = {154217},
doi = {10.1016/j.tox.2025.154217},
pmid = {40505719},
issn = {1879-3185},
abstract = {Studies show that N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-Q) accumulates in the central nervous system, but its role in cognitive impairment and underlying mechanisms remain unclear. Morris water maze assay revealed that 6-PPDQ significantly impairs cognitive function, particularly learning and memory. HE staining revealed alterations in the hippocampal DG and CA3 regions of exposed mice, including sparse cell arrangement, blurred boundaries, nuclear condensation, and a reduction in Nissl bodies. Fecal microbiota transplantation from 6-PPDQ-exposed mice to normal mice induced cognitive deficits and hippocampal pathological damage. Western Blot assay showed that 6-PPDQ exposure resulted in inhibition of PI3K/AKT signaling. Moreover, blunted PI3K/AKT signaling was observed in mice transplanted with 6-PPDQ-associated mice fecal microbiota. Further analysis of 16S rDNA assay identified a total of 30 differential bacteria at the genus level, including 8 upregulated bacteria such as g_Helicobacter and 22 downregulated bacteria such as g_Prevotellaceae_NK3B31_group. In conclusion, this study uncovers gut microbiome mediates 6PPD-Q-induced cognitive impairment through inhibiting of PI3K/Akt signaling, and provides a basis for further investigation into gut microbiome's protective effects on 6-PPDQ-induced nervous system injury.},
}
RevDate: 2025-06-12
CmpDate: 2025-06-12
Microbiome-facilitated plant nutrient acquisition.
Cell host & microbe, 33(6):869-881.
Plants and microbiomes have co-evolved for millennia. Through this co-evolution, microbiomes have become essential for plant nutrient acquisition, which involves plant signaling, microbial sensing, and acquiring and sharing nutrients. In this review, we synthesize recent advancements in the complex associations of molecular, physiological, and eco-evolutionary mechanisms that underpin microbe-facilitated plant nutrient uptake. Focusing on emerging insights in plant-microbial communication and metabolic pathways, we evaluate potential opportunities to harness plant microbiomes to sustainably supply nutrients in agricultural and natural ecosystems. However, further progress is constrained by key knowledge gaps. We propose an amended conceptual framework for advancement that includes a holistic understanding of eco-evolutionary relationships with explicit consideration of signaling and sensing mechanisms. Finally, we argue that advancing fundamental science by utilizing emerging analytical approaches in an integrated way is critical to develop effective microbiome-informed tools that can enhance plant nutrient acquisition and promote long-term food security and environmental sustainability.
Additional Links: PMID-40505623
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PubMed:
Citation:
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@article {pmid40505623,
year = {2025},
author = {Singh, BK and Hu, HW and Macdonald, CA and Xiong, C},
title = {Microbiome-facilitated plant nutrient acquisition.},
journal = {Cell host & microbe},
volume = {33},
number = {6},
pages = {869-881},
doi = {10.1016/j.chom.2025.05.005},
pmid = {40505623},
issn = {1934-6069},
mesh = {*Microbiota/physiology ; *Plants/microbiology/metabolism ; *Nutrients/metabolism ; Ecosystem ; Bacteria/metabolism ; Symbiosis ; Biological Evolution ; },
abstract = {Plants and microbiomes have co-evolved for millennia. Through this co-evolution, microbiomes have become essential for plant nutrient acquisition, which involves plant signaling, microbial sensing, and acquiring and sharing nutrients. In this review, we synthesize recent advancements in the complex associations of molecular, physiological, and eco-evolutionary mechanisms that underpin microbe-facilitated plant nutrient uptake. Focusing on emerging insights in plant-microbial communication and metabolic pathways, we evaluate potential opportunities to harness plant microbiomes to sustainably supply nutrients in agricultural and natural ecosystems. However, further progress is constrained by key knowledge gaps. We propose an amended conceptual framework for advancement that includes a holistic understanding of eco-evolutionary relationships with explicit consideration of signaling and sensing mechanisms. Finally, we argue that advancing fundamental science by utilizing emerging analytical approaches in an integrated way is critical to develop effective microbiome-informed tools that can enhance plant nutrient acquisition and promote long-term food security and environmental sustainability.},
}
MeSH Terms:
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*Microbiota/physiology
*Plants/microbiology/metabolism
*Nutrients/metabolism
Ecosystem
Bacteria/metabolism
Symbiosis
Biological Evolution
RevDate: 2025-06-12
CmpDate: 2025-06-12
Unlocking the power of human milk and infant feeding: Understanding how nutrition and early microbiota interaction shapes health programming.
Cell host & microbe, 33(6):820-835.
Human milk represents a highly evolved bioactive system that promotes colonization by infant microbial pioneers, supports immune maturation, and fosters infant development. Beyond providing nutrition, human milk contains key bioactive components, such as microbes, metabolites, human milk oligosaccharides, immunoglobulins, lactoferrin, and antimicrobial peptides. These factors influence colonization of the infant gut microbiome and facilitate immune development and metabolic health, with implications for health outcomes and risk of non-communicable diseases. In this review, we highlight the impact of infant feeding, human milk constituents (especially bioactive compounds), and weaning on infant microbial trajectories. By understanding how early-life nutrition influences microbial colonization and nutrient sensing, i.e., "how we feed our microbes," we can develop targeted interventions and personalized diets to support proper gut maturation and disease prevention from infancy to adulthood, as well as explore the therapeutic potential of human milk bioactives beyond infancy, offering new strategies for disease prevention and treatment.
Additional Links: PMID-40505621
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PubMed:
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@article {pmid40505621,
year = {2025},
author = {Zhernakova, A and Yassour, M and Hall, LJ and Collado, MC},
title = {Unlocking the power of human milk and infant feeding: Understanding how nutrition and early microbiota interaction shapes health programming.},
journal = {Cell host & microbe},
volume = {33},
number = {6},
pages = {820-835},
doi = {10.1016/j.chom.2025.05.014},
pmid = {40505621},
issn = {1934-6069},
mesh = {Humans ; *Milk, Human/chemistry/microbiology ; Infant ; *Gastrointestinal Microbiome/physiology ; *Infant Nutritional Physiological Phenomena ; Infant, Newborn ; Breast Feeding ; Oligosaccharides ; Weaning ; },
abstract = {Human milk represents a highly evolved bioactive system that promotes colonization by infant microbial pioneers, supports immune maturation, and fosters infant development. Beyond providing nutrition, human milk contains key bioactive components, such as microbes, metabolites, human milk oligosaccharides, immunoglobulins, lactoferrin, and antimicrobial peptides. These factors influence colonization of the infant gut microbiome and facilitate immune development and metabolic health, with implications for health outcomes and risk of non-communicable diseases. In this review, we highlight the impact of infant feeding, human milk constituents (especially bioactive compounds), and weaning on infant microbial trajectories. By understanding how early-life nutrition influences microbial colonization and nutrient sensing, i.e., "how we feed our microbes," we can develop targeted interventions and personalized diets to support proper gut maturation and disease prevention from infancy to adulthood, as well as explore the therapeutic potential of human milk bioactives beyond infancy, offering new strategies for disease prevention and treatment.},
}
MeSH Terms:
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Humans
*Milk, Human/chemistry/microbiology
Infant
*Gastrointestinal Microbiome/physiology
*Infant Nutritional Physiological Phenomena
Infant, Newborn
Breast Feeding
Oligosaccharides
Weaning
RevDate: 2025-06-12
CmpDate: 2025-06-12
Origins and functions of microbiome rhythms.
Cell host & microbe, 33(6):808-819.
Daily oscillations in microbiota composition and function are emerging as an important element in host-microbiota interactions. Here, we summarize features of the microbiota that undergo diurnal rhythms, their development, their impact on the biology of the host, and their relevance to human health and disease. In particular, we focus on the intrinsic and extrinsic factors that regulate microbiota oscillations and the multifaceted roles that microbiota rhythmicity plays in host physiology, immunity, and metabolism. Given the pervasive impact of intestinal microorganisms on host health, understanding the origins and functions of microbiota rhythms is a critical aspect of the circadian biology of the meta-organism.
Additional Links: PMID-40505620
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PubMed:
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@article {pmid40505620,
year = {2025},
author = {Kiessling, S and Liu, S and Haller, D and Thaiss, CA},
title = {Origins and functions of microbiome rhythms.},
journal = {Cell host & microbe},
volume = {33},
number = {6},
pages = {808-819},
doi = {10.1016/j.chom.2025.05.017},
pmid = {40505620},
issn = {1934-6069},
mesh = {Humans ; *Circadian Rhythm/physiology ; *Gastrointestinal Microbiome/physiology ; Animals ; *Host Microbial Interactions ; *Microbiota/physiology ; },
abstract = {Daily oscillations in microbiota composition and function are emerging as an important element in host-microbiota interactions. Here, we summarize features of the microbiota that undergo diurnal rhythms, their development, their impact on the biology of the host, and their relevance to human health and disease. In particular, we focus on the intrinsic and extrinsic factors that regulate microbiota oscillations and the multifaceted roles that microbiota rhythmicity plays in host physiology, immunity, and metabolism. Given the pervasive impact of intestinal microorganisms on host health, understanding the origins and functions of microbiota rhythms is a critical aspect of the circadian biology of the meta-organism.},
}
MeSH Terms:
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Humans
*Circadian Rhythm/physiology
*Gastrointestinal Microbiome/physiology
Animals
*Host Microbial Interactions
*Microbiota/physiology
RevDate: 2025-06-12
CmpDate: 2025-06-12
Metabolic ecology of microbiomes: Nutrient competition, host benefits, and community engineering.
Cell host & microbe, 33(6):790-807.
Many plants and animals, including humans, host diverse communities of microbes that provide many benefits. A key challenge in understanding microbiomes is that the species composition often differs among individuals, which can thwart generalization. Here, we argue that the key to identifying general principles for microbiome science lies in microbial metabolism. In the human microbiome and in other systems, every microbial species must find ways to harvest nutrients to thrive. The available nutrients in a microbiome interact with microbial metabolism to define which species have the potential to persist in a host. The resulting nutrient competition shapes other mechanisms, including bacterial warfare and cross-feeding, to define microbiome composition and properties. We discuss impacts on ecological stability, colonization resistance, nutrient provision for the host, and evolution. A focus on the metabolic ecology of microbiomes offers a powerful way to understand and engineer microbiomes in health, agriculture, and the environment.
Additional Links: PMID-40505619
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PubMed:
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@article {pmid40505619,
year = {2025},
author = {Bakkeren, E and Piskovsky, V and Foster, KR},
title = {Metabolic ecology of microbiomes: Nutrient competition, host benefits, and community engineering.},
journal = {Cell host & microbe},
volume = {33},
number = {6},
pages = {790-807},
doi = {10.1016/j.chom.2025.05.013},
pmid = {40505619},
issn = {1934-6069},
mesh = {*Microbiota/physiology ; Humans ; *Nutrients/metabolism ; Animals ; *Bacteria/metabolism/genetics ; *Host Microbial Interactions ; Plants/microbiology ; },
abstract = {Many plants and animals, including humans, host diverse communities of microbes that provide many benefits. A key challenge in understanding microbiomes is that the species composition often differs among individuals, which can thwart generalization. Here, we argue that the key to identifying general principles for microbiome science lies in microbial metabolism. In the human microbiome and in other systems, every microbial species must find ways to harvest nutrients to thrive. The available nutrients in a microbiome interact with microbial metabolism to define which species have the potential to persist in a host. The resulting nutrient competition shapes other mechanisms, including bacterial warfare and cross-feeding, to define microbiome composition and properties. We discuss impacts on ecological stability, colonization resistance, nutrient provision for the host, and evolution. A focus on the metabolic ecology of microbiomes offers a powerful way to understand and engineer microbiomes in health, agriculture, and the environment.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Microbiota/physiology
Humans
*Nutrients/metabolism
Animals
*Bacteria/metabolism/genetics
*Host Microbial Interactions
Plants/microbiology
RevDate: 2025-06-12
CmpDate: 2025-06-12
The microbiome: An actor or stage for the beneficial action of probiotics, prebiotics, synbiotics, and postbiotics?.
Cell host & microbe, 33(6):777-789.
Probiotics, prebiotics, synbiotics, and postbiotics are required, by definition, to confer a health benefit on the host. It is often presumed the host microbiome plays a central role in the mechanism of action of these substances, collectively referred to here as "biotics." However, the definitions of both probiotics and postbiotics do not include an associated mechanism nor the involvement of the microbiome. The definitions of prebiotics and synbiotics require evidence of selective utilization by the host microbiome, but do not state that confirmatory evidence must be provided that this utilization causes the associated health benefit. In this perspective, we discuss evidence supporting a role for the microbiome in delivering these health benefits and whether or not measuring microbiome alterations can serve as important readouts of efficacy. We also discuss the possibility of expanding the biotics family with substances such as bacteriophage, fermented foods, and live dietary microbes.
Additional Links: PMID-40505618
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PubMed:
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@article {pmid40505618,
year = {2025},
author = {Sanders, ME and Hill, C},
title = {The microbiome: An actor or stage for the beneficial action of probiotics, prebiotics, synbiotics, and postbiotics?.},
journal = {Cell host & microbe},
volume = {33},
number = {6},
pages = {777-789},
doi = {10.1016/j.chom.2025.04.017},
pmid = {40505618},
issn = {1934-6069},
mesh = {*Probiotics/administration & dosage ; *Prebiotics/administration & dosage ; *Synbiotics/administration & dosage ; Humans ; *Microbiota/physiology ; *Gastrointestinal Microbiome ; Animals ; },
abstract = {Probiotics, prebiotics, synbiotics, and postbiotics are required, by definition, to confer a health benefit on the host. It is often presumed the host microbiome plays a central role in the mechanism of action of these substances, collectively referred to here as "biotics." However, the definitions of both probiotics and postbiotics do not include an associated mechanism nor the involvement of the microbiome. The definitions of prebiotics and synbiotics require evidence of selective utilization by the host microbiome, but do not state that confirmatory evidence must be provided that this utilization causes the associated health benefit. In this perspective, we discuss evidence supporting a role for the microbiome in delivering these health benefits and whether or not measuring microbiome alterations can serve as important readouts of efficacy. We also discuss the possibility of expanding the biotics family with substances such as bacteriophage, fermented foods, and live dietary microbes.},
}
MeSH Terms:
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*Probiotics/administration & dosage
*Prebiotics/administration & dosage
*Synbiotics/administration & dosage
Humans
*Microbiota/physiology
*Gastrointestinal Microbiome
Animals
RevDate: 2025-06-12
CmpDate: 2025-06-12
Precision nutrition and the gut microbiome: Harnessing AI to revolutionize cancer prevention and therapy.
Cell host & microbe, 33(6):766-776.
The gut microbiome plays a pivotal role in human health, particularly in cancer prevention and treatment. Diet can significantly influence microbiome composition, but individual variability complicates intervention outcomes. We review the microbiome's influence on cancer development and therapy outcomes and evaluate dietary strategies that modulate microbial composition and metabolites. To address these complexities, we propose the digital gut twin: an artificial intelligence (AI)-driven, dynamically updated simulation that integrates nutrient databases, multi-omic microbiome profiles, host genomics, and clinical data to predict personalized responses to dietary interventions. While significant data and regulatory challenges exist that currently limit clinical implementation, emerging solutions-including pre-trained microbiome models, mechanistic simulators, automated knowledge graphs, and privacy-preserving training-provide a promising pathway toward establishing personalized diet-microbiome modulation as a core component of precision oncology.
Additional Links: PMID-40505617
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PubMed:
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@article {pmid40505617,
year = {2025},
author = {Greathouse, KL and Choudhury, A},
title = {Precision nutrition and the gut microbiome: Harnessing AI to revolutionize cancer prevention and therapy.},
journal = {Cell host & microbe},
volume = {33},
number = {6},
pages = {766-776},
doi = {10.1016/j.chom.2025.05.011},
pmid = {40505617},
issn = {1934-6069},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Neoplasms/prevention & control/therapy/microbiology/diet therapy ; *Precision Medicine/methods ; *Artificial Intelligence ; Diet ; },
abstract = {The gut microbiome plays a pivotal role in human health, particularly in cancer prevention and treatment. Diet can significantly influence microbiome composition, but individual variability complicates intervention outcomes. We review the microbiome's influence on cancer development and therapy outcomes and evaluate dietary strategies that modulate microbial composition and metabolites. To address these complexities, we propose the digital gut twin: an artificial intelligence (AI)-driven, dynamically updated simulation that integrates nutrient databases, multi-omic microbiome profiles, host genomics, and clinical data to predict personalized responses to dietary interventions. While significant data and regulatory challenges exist that currently limit clinical implementation, emerging solutions-including pre-trained microbiome models, mechanistic simulators, automated knowledge graphs, and privacy-preserving training-provide a promising pathway toward establishing personalized diet-microbiome modulation as a core component of precision oncology.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/physiology
*Neoplasms/prevention & control/therapy/microbiology/diet therapy
*Precision Medicine/methods
*Artificial Intelligence
Diet
RevDate: 2025-06-12
CmpDate: 2025-06-12
Human milk as a microbial pacemaker.
Cell host & microbe, 33(6):762-765.
A Nature Medicine paper by Sawhney et al.[1] presents a strain-resolved analysis of the gut microbiome from infancy through eight years of age, identifying weaning as an evolutionary trigger for microbial adaptation. Their findings refine the timeline of microbiome development and highlight human milk as a pacemaker of microbial succession.
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@article {pmid40505616,
year = {2025},
author = {Shenhav, L and Azad, MB and Silverman, MA},
title = {Human milk as a microbial pacemaker.},
journal = {Cell host & microbe},
volume = {33},
number = {6},
pages = {762-765},
doi = {10.1016/j.chom.2025.05.018},
pmid = {40505616},
issn = {1934-6069},
mesh = {Humans ; *Milk, Human/microbiology ; *Gastrointestinal Microbiome/physiology ; Infant ; Weaning ; Child ; Female ; },
abstract = {A Nature Medicine paper by Sawhney et al.[1] presents a strain-resolved analysis of the gut microbiome from infancy through eight years of age, identifying weaning as an evolutionary trigger for microbial adaptation. Their findings refine the timeline of microbiome development and highlight human milk as a pacemaker of microbial succession.},
}
MeSH Terms:
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Humans
*Milk, Human/microbiology
*Gastrointestinal Microbiome/physiology
Infant
Weaning
Child
Female
RevDate: 2025-06-12
Microbial regulation of interoception.
Current opinion in neurobiology, 93:103064 pii:S0959-4388(25)00095-9 [Epub ahead of print].
Interoceptive pathways communicate between the body and the brain to coordinate behavioral responses to changes in the internal milieu. An important contributor to the internal milieu of the body is the gastrointestinal microbiome. Here, we conceptualize the role of the microbiome and microbiome-derived metabolites in interoceptive processes that enable homeostasis maintenance. We highlight four key features that make the microbiome a valuable sensory source for interoceptive processes: its capacity to engage canonical sensory pathways, dynamic responsiveness to environmental perturbations, diurnal oscillations aligned with host circadian rhythms, and the selective gating of sensory information through the intestinal barrier. We further explore how microbiome-derived sensory information contributes to homeostasis, imparts valence to events and cues, and serves as a substrate for memory. Collectively, we present a framework for understanding interoceptive dysfunction through the lens of microbiome-host interactions.
Additional Links: PMID-40505513
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@article {pmid40505513,
year = {2025},
author = {Subramanian, M and Thaiss, CA},
title = {Microbial regulation of interoception.},
journal = {Current opinion in neurobiology},
volume = {93},
number = {},
pages = {103064},
doi = {10.1016/j.conb.2025.103064},
pmid = {40505513},
issn = {1873-6882},
abstract = {Interoceptive pathways communicate between the body and the brain to coordinate behavioral responses to changes in the internal milieu. An important contributor to the internal milieu of the body is the gastrointestinal microbiome. Here, we conceptualize the role of the microbiome and microbiome-derived metabolites in interoceptive processes that enable homeostasis maintenance. We highlight four key features that make the microbiome a valuable sensory source for interoceptive processes: its capacity to engage canonical sensory pathways, dynamic responsiveness to environmental perturbations, diurnal oscillations aligned with host circadian rhythms, and the selective gating of sensory information through the intestinal barrier. We further explore how microbiome-derived sensory information contributes to homeostasis, imparts valence to events and cues, and serves as a substrate for memory. Collectively, we present a framework for understanding interoceptive dysfunction through the lens of microbiome-host interactions.},
}
RevDate: 2025-06-12
Does schistosome infection affect behavior through the gut-brain axis?.
PLoS neglected tropical diseases, 19(6):e0013088 pii:PNTD-D-24-01627 [Epub ahead of print].
Parasitic helminths infect over 2 billion people, primarily those living in poverty. Helminth infections typically establish in early childhood and persist through critical periods of growth and development, leading to cognitive deficits and/or behavioral changes. These deficits could result from the helminths themselves or due to dysbiosis of the gut microbiota and its influence on the gut-brain axis. Using two cohorts of 3-week-old female mice, we measured levels of anxiety, fear, compulsion, spatial learning, and spatial memory, between schistosome-infected and sham-exposed mice. Additionally, we compared their fecal microbiomes using 16S rRNA gene sequencing at two time points during the chronic stage of infection. Schistosome-infected mice showed higher levels of anxiety in the open field test, reduced spatial learning in the Morris water maze task, and enhanced memory retention in the novel object task. All mice performed equally on the marble bury task. Each cohort started with unique microbiota which showed marked changes in the beta diversity of their microbiota after exposure. In both cohorts, at 7- weeks post exposure, infected mice had more Alistipes sp. and Bacteroides thetaiotaomicron and less Turicibacter sp. and Ligilactobacillus sp. than uninfected mice. At 10 weeks, infected mice had more Alistipes sp. and fewer Muribaculaceae sp. Interestingly, taxon shifts in infected mice were those typically associated with protective effects on liver disease and IL-10 gut conditions, suggesting a possible protective role of the shifted microbiome. Our analyses did not indicate associations between behavioral measures and microbiome composition; however, this could be due to the strong impact of infection on the microbiome composition. Findings here uncover behavioral and cognitive impacts of schistosome infection and shed light on the complex interplay between schistosome infection, behavioral changes, and host microbiome composition, which could ultimately support future global health efforts.
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PubMed:
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@article {pmid40504882,
year = {2025},
author = {Combrink, L and Spaan, JM and Perret, A and Maehara, T and Hyun, B and Parker, D and Johns, JL and Blouin, MS and Magnusson, K and Steinauer, ML},
title = {Does schistosome infection affect behavior through the gut-brain axis?.},
journal = {PLoS neglected tropical diseases},
volume = {19},
number = {6},
pages = {e0013088},
doi = {10.1371/journal.pntd.0013088},
pmid = {40504882},
issn = {1935-2735},
abstract = {Parasitic helminths infect over 2 billion people, primarily those living in poverty. Helminth infections typically establish in early childhood and persist through critical periods of growth and development, leading to cognitive deficits and/or behavioral changes. These deficits could result from the helminths themselves or due to dysbiosis of the gut microbiota and its influence on the gut-brain axis. Using two cohorts of 3-week-old female mice, we measured levels of anxiety, fear, compulsion, spatial learning, and spatial memory, between schistosome-infected and sham-exposed mice. Additionally, we compared their fecal microbiomes using 16S rRNA gene sequencing at two time points during the chronic stage of infection. Schistosome-infected mice showed higher levels of anxiety in the open field test, reduced spatial learning in the Morris water maze task, and enhanced memory retention in the novel object task. All mice performed equally on the marble bury task. Each cohort started with unique microbiota which showed marked changes in the beta diversity of their microbiota after exposure. In both cohorts, at 7- weeks post exposure, infected mice had more Alistipes sp. and Bacteroides thetaiotaomicron and less Turicibacter sp. and Ligilactobacillus sp. than uninfected mice. At 10 weeks, infected mice had more Alistipes sp. and fewer Muribaculaceae sp. Interestingly, taxon shifts in infected mice were those typically associated with protective effects on liver disease and IL-10 gut conditions, suggesting a possible protective role of the shifted microbiome. Our analyses did not indicate associations between behavioral measures and microbiome composition; however, this could be due to the strong impact of infection on the microbiome composition. Findings here uncover behavioral and cognitive impacts of schistosome infection and shed light on the complex interplay between schistosome infection, behavioral changes, and host microbiome composition, which could ultimately support future global health efforts.},
}
RevDate: 2025-06-12
Enterohemorrhagic E. coli (EHEC) and the microbiome.
PLoS pathogens, 21(6):e1013224 pii:PPATHOGENS-D-25-00690.
Additional Links: PMID-40504797
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@article {pmid40504797,
year = {2025},
author = {Perraud, Q and Sperandio, V},
title = {Enterohemorrhagic E. coli (EHEC) and the microbiome.},
journal = {PLoS pathogens},
volume = {21},
number = {6},
pages = {e1013224},
doi = {10.1371/journal.ppat.1013224},
pmid = {40504797},
issn = {1553-7374},
}
RevDate: 2025-06-12
The Overlooked Hazard: Clostridioides difficile in Preterm Infants and Immature Immune Systems-Harnessing Postbiotics for Safer Therapeutic Strategies.
Letters in applied microbiology pii:8161042 [Epub ahead of print].
Clostridioides difficile is a potentially harmful bacterium that can affect preterm infants more seriously than full-term infants, largely due to their immature immune systems and underdeveloped gut microbiota. Although colonization with C. difficile is often harmless in healthy babies, preterm infants are more likely to develop infections, which can lead to serious health problems. This review looks at how an immature immune system and an imbalanced gut microbiome increase the risk of C. difficile infection (CDI) in early life. To reduce this risk, researchers are exploring postbiotics-non-living bacterial products or byproducts-as a safer alternative to traditional treatments like antibiotics. Postbiotics can help by strengthening the gut barrier, reducing inflammation, and supporting the growth of beneficial bacteria. They are also considered safe for use in vulnerable populations, including infants. This review discusses the types of postbiotics, their functions, and how they may help prevent or manage CDI. It also highlights their potential for use in infant formula as a preventative strategy. Overall, postbiotics may offer a promising new way to protect preterm infants from C. difficile and support healthier immune and gut development.
Additional Links: PMID-40504562
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@article {pmid40504562,
year = {2025},
author = {Soleimani, RA and Milani, PG and Khani, N and Homayouni-Rad, A},
title = {The Overlooked Hazard: Clostridioides difficile in Preterm Infants and Immature Immune Systems-Harnessing Postbiotics for Safer Therapeutic Strategies.},
journal = {Letters in applied microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/lambio/ovaf083},
pmid = {40504562},
issn = {1472-765X},
abstract = {Clostridioides difficile is a potentially harmful bacterium that can affect preterm infants more seriously than full-term infants, largely due to their immature immune systems and underdeveloped gut microbiota. Although colonization with C. difficile is often harmless in healthy babies, preterm infants are more likely to develop infections, which can lead to serious health problems. This review looks at how an immature immune system and an imbalanced gut microbiome increase the risk of C. difficile infection (CDI) in early life. To reduce this risk, researchers are exploring postbiotics-non-living bacterial products or byproducts-as a safer alternative to traditional treatments like antibiotics. Postbiotics can help by strengthening the gut barrier, reducing inflammation, and supporting the growth of beneficial bacteria. They are also considered safe for use in vulnerable populations, including infants. This review discusses the types of postbiotics, their functions, and how they may help prevent or manage CDI. It also highlights their potential for use in infant formula as a preventative strategy. Overall, postbiotics may offer a promising new way to protect preterm infants from C. difficile and support healthier immune and gut development.},
}
RevDate: 2025-06-12
Typical skin and oral bacterial species present in human milk are not the result of contamination during the sampling process.
Letters in applied microbiology pii:8161044 [Epub ahead of print].
Human milk has a low microbial biomass with a microbiome dominated by typical skin and oral taxa, raising concerns about contamination during sample collection. However, to date, no study has directly compared samples collected with and without aseptic technique, leaving questions related to potential contamination within the field. To address this, we compared the microbiota of hand-expressed milk samples collected from 23 mothers before and after cleansing of the hands and breast. Metataxonomic analysis showed that taxonomic profiles were largely unaffected by cleansing, with only Rothia mucilaginosa significantly more abundant in non-aseptically collected samples (P = 0.007). Although aseptically and non-aseptically collected samples were taxonomically similar, there was a higher level of bacterial richness (P = 0.003) and evenness (Shannon diversity, P = 0.0002) in non-aseptically collected samples, suggesting that multiple low-abundance taxa are introduced via skin contamination. These findings support the use of aseptic collection methods to minimise external contamination and accurately assess milk microbial diversity. Importantly, they also suggest that common skin and oral taxa detected in human milk are likely true members of the mammary microbiome.
Additional Links: PMID-40504523
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Citation:
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@article {pmid40504523,
year = {2025},
author = {Stinson, LF and Geddes, DT},
title = {Typical skin and oral bacterial species present in human milk are not the result of contamination during the sampling process.},
journal = {Letters in applied microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/lambio/ovaf084},
pmid = {40504523},
issn = {1472-765X},
abstract = {Human milk has a low microbial biomass with a microbiome dominated by typical skin and oral taxa, raising concerns about contamination during sample collection. However, to date, no study has directly compared samples collected with and without aseptic technique, leaving questions related to potential contamination within the field. To address this, we compared the microbiota of hand-expressed milk samples collected from 23 mothers before and after cleansing of the hands and breast. Metataxonomic analysis showed that taxonomic profiles were largely unaffected by cleansing, with only Rothia mucilaginosa significantly more abundant in non-aseptically collected samples (P = 0.007). Although aseptically and non-aseptically collected samples were taxonomically similar, there was a higher level of bacterial richness (P = 0.003) and evenness (Shannon diversity, P = 0.0002) in non-aseptically collected samples, suggesting that multiple low-abundance taxa are introduced via skin contamination. These findings support the use of aseptic collection methods to minimise external contamination and accurately assess milk microbial diversity. Importantly, they also suggest that common skin and oral taxa detected in human milk are likely true members of the mammary microbiome.},
}
RevDate: 2025-06-12
Host-microbiome interactions as moderators of host quality and biodiversity-disease relationships.
Integrative and comparative biology pii:8161039 [Epub ahead of print].
Biodiversity-disease studies typically focus on how changes in community composition (e.g., species richness, abundance, and functional or phylogenetic metrics of biodiversity) affect disease risk. In doing so, these studies tend to overlook intraspecific variation in the organisms comprising the community. Yet, intraspecific variation, which occurs to varying degrees both within and between communities, could also modulate biodiversity-disease relationships. One important driver of intraspecific variation is the microbiome. By directly and indirectly influencing health and susceptibility to infection and disease, microbiomes are integral to organismal functioning. Thus, the microbiome plays a crucial role in host quality. We define host quality as an integration of host traits related to parasite exposure, establishment, growth, and infectivity, which ultimately shape parasite fitness. The microbiome can impact host quality via a variety of mechanisms including host size and developmental stage, immune function, reproduction, nutrient acquisition, and behavior. However, the potential for such microbiome-driven changes in host quality to trigger cascading effects on community-level processes, specifically by altering parasite transmission dynamics and community competence, has not been well explored. Here, we examine and illustrate a pathway by which the microbiome may influence variation in organismal biology (i.e., host quality) of hosts in communities. Furthermore, we consider how major anthropogenic drivers of microbiome shifts, such as climate change, pollution, land use change, and domestication, might influence this pathway and thereby alter outcomes. Future studies bridging microbiome and disease ecology research will provide opportunities to unify these concepts across scales and between the plant and animal domains. To date, most microbiome research has focused on humans, crops, and laboratory animals. However, to better understand the potential for knock-on ecological effects of microbiomes, more attention must be paid to the microbiomes of wild plants and animals. Ultimately, more experimental and theoretical data are needed to clarify how the microbiome impacts host quality and disease dynamics, as well as how anthropogenic factors continuously reshape these relationships.
Additional Links: PMID-40504492
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@article {pmid40504492,
year = {2025},
author = {Rosamond, KM and Esser, HJ and Assink, RB and Jaramillo-Ortiz, L and Rowe, M and Kirke, EC and Matson, KD},
title = {Host-microbiome interactions as moderators of host quality and biodiversity-disease relationships.},
journal = {Integrative and comparative biology},
volume = {},
number = {},
pages = {},
doi = {10.1093/icb/icaf091},
pmid = {40504492},
issn = {1557-7023},
abstract = {Biodiversity-disease studies typically focus on how changes in community composition (e.g., species richness, abundance, and functional or phylogenetic metrics of biodiversity) affect disease risk. In doing so, these studies tend to overlook intraspecific variation in the organisms comprising the community. Yet, intraspecific variation, which occurs to varying degrees both within and between communities, could also modulate biodiversity-disease relationships. One important driver of intraspecific variation is the microbiome. By directly and indirectly influencing health and susceptibility to infection and disease, microbiomes are integral to organismal functioning. Thus, the microbiome plays a crucial role in host quality. We define host quality as an integration of host traits related to parasite exposure, establishment, growth, and infectivity, which ultimately shape parasite fitness. The microbiome can impact host quality via a variety of mechanisms including host size and developmental stage, immune function, reproduction, nutrient acquisition, and behavior. However, the potential for such microbiome-driven changes in host quality to trigger cascading effects on community-level processes, specifically by altering parasite transmission dynamics and community competence, has not been well explored. Here, we examine and illustrate a pathway by which the microbiome may influence variation in organismal biology (i.e., host quality) of hosts in communities. Furthermore, we consider how major anthropogenic drivers of microbiome shifts, such as climate change, pollution, land use change, and domestication, might influence this pathway and thereby alter outcomes. Future studies bridging microbiome and disease ecology research will provide opportunities to unify these concepts across scales and between the plant and animal domains. To date, most microbiome research has focused on humans, crops, and laboratory animals. However, to better understand the potential for knock-on ecological effects of microbiomes, more attention must be paid to the microbiomes of wild plants and animals. Ultimately, more experimental and theoretical data are needed to clarify how the microbiome impacts host quality and disease dynamics, as well as how anthropogenic factors continuously reshape these relationships.},
}
RevDate: 2025-06-12
Exploring the trimethylamine-degrading genes in the human gut microbiome.
AMB Express, 15(1):91.
Trimethylamine (TMA), produced by gut microbes, is a precursor to a risk factor for cardiovascular diseases. Currently, TMA-degrading bacteria in the human gut have rarely been studied. This study combined TMA-enriched cultures (from 104 young male stool samples) with metagenomic profiling to identify key microbial players of TMA degradation. The results showed that the contribution of Enterococcus to methane metabolism was significantly higher in TMA-enriched culture samples. The 68.58% up-regulation of dmd-tmd (dimethylamine/trimethylamine dehydrogenase) in the TMA-enriched group indicated that the anaerobic dehydrogenase pathway participated in TMA metabolism. Notably, we first identified that taxa containing dmd-tmd belonged to Christensenella timonensis. The up-regulation of genes involved in methanogenesis (M00563) as well as the significant enrichment of M00563 (Reporter Score = 2.223) indicated that the methanogenesis pathway may play a role. We constructed gene databases for genes involved in the anaerobic dehydrogenase pathway (1526 sequences for dmd-tmd, 1319 sequences for mauA, and 326 sequences for mauB, respectively) and the aerobic oxidation pathway (2146 sequences for tmm, 1445 sequences for tdm, and 1519 sequences for dmm, respectively) based on genomes from the Integrated Microbial Genome (IMG) database, most of which belong to Pseudomonadota. Screening gut metagenomes with these databases revealed low sequence identity (< 70%), possibly because of the underrepresentation of gut-specific genomes from IMG. This study links Christensenella timonensis to TMA degradation, providing potential targets for microbiota modulation and a gene-centric framework to advance the characterization of gut microbial TMA metabolism.
Additional Links: PMID-40504464
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@article {pmid40504464,
year = {2025},
author = {Chen, YR and Chen, LD and Zheng, LJ},
title = {Exploring the trimethylamine-degrading genes in the human gut microbiome.},
journal = {AMB Express},
volume = {15},
number = {1},
pages = {91},
pmid = {40504464},
issn = {2191-0855},
support = {32100082//National Natural Science Foundation of China/ ; 2023A03J0696//Science and Technology Program of Guangzhou/ ; },
abstract = {Trimethylamine (TMA), produced by gut microbes, is a precursor to a risk factor for cardiovascular diseases. Currently, TMA-degrading bacteria in the human gut have rarely been studied. This study combined TMA-enriched cultures (from 104 young male stool samples) with metagenomic profiling to identify key microbial players of TMA degradation. The results showed that the contribution of Enterococcus to methane metabolism was significantly higher in TMA-enriched culture samples. The 68.58% up-regulation of dmd-tmd (dimethylamine/trimethylamine dehydrogenase) in the TMA-enriched group indicated that the anaerobic dehydrogenase pathway participated in TMA metabolism. Notably, we first identified that taxa containing dmd-tmd belonged to Christensenella timonensis. The up-regulation of genes involved in methanogenesis (M00563) as well as the significant enrichment of M00563 (Reporter Score = 2.223) indicated that the methanogenesis pathway may play a role. We constructed gene databases for genes involved in the anaerobic dehydrogenase pathway (1526 sequences for dmd-tmd, 1319 sequences for mauA, and 326 sequences for mauB, respectively) and the aerobic oxidation pathway (2146 sequences for tmm, 1445 sequences for tdm, and 1519 sequences for dmm, respectively) based on genomes from the Integrated Microbial Genome (IMG) database, most of which belong to Pseudomonadota. Screening gut metagenomes with these databases revealed low sequence identity (< 70%), possibly because of the underrepresentation of gut-specific genomes from IMG. This study links Christensenella timonensis to TMA degradation, providing potential targets for microbiota modulation and a gene-centric framework to advance the characterization of gut microbial TMA metabolism.},
}
RevDate: 2025-06-12
Unravelling the gut-skin axis: the role of gut microbiota in pathogenesis and management of psoriasis.
Inflammopharmacology [Epub ahead of print].
Psoriasis is a chronic, multifactorial, inflammatory skin disease, increasingly recognized as a systemic disorder influenced by the gut-skin axis, which is a dynamic bidirectional communication between intestinal microbiome and cutaneous immune response. This narrative review explores the understanding of the gut-skin axis with the latest evidence on how gut dysbiosis occurs in psoriasis, characterized by reduced microbial diversity and its shifts, and how it contributes to pathogenesis and exacerbation of psoriasis. Notably, recent scientific literature evidence suggests that the alteration of gut microbiome in psoriasis includes a decreased level of beneficial species like Faecalibacterium prausnitzii and a rise in the level of proinflammatory bacterial species like Prevotella copri. Mechanistic insights reveal that gut-derived metabolites, impaired barrier functions, and immune signaling, particularly involving IL-23 and Th17 cells, play a pivotal role in this axis, linking intestinal health to cutaneous manifestations. Both animal and human trials underscore the therapeutic potential of interventions targeting the gut microbiota, including prebiotics, probiotics, dietary modifications, and FMT, demonstrating some promising but variable effects on disease severity and systemic inflammation. Despite these advances, translating the gut-skin axis into clinical practice presents a notable challenge due to limited scientific evidence, a lack of standardised microbiome profiling, and the absence of universally accepted biomarkers to monitor and stratify therapeutic outcomes. These limitations hinder the development of personalised care approaches and the integration of the gut-skin axis as a promising frontier in many autoimmune diseases, where the gut-skin axis and the intestinal microbiome play a crucial role.
Additional Links: PMID-40504322
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@article {pmid40504322,
year = {2025},
author = {Pachauri, A and Sharma, S},
title = {Unravelling the gut-skin axis: the role of gut microbiota in pathogenesis and management of psoriasis.},
journal = {Inflammopharmacology},
volume = {},
number = {},
pages = {},
pmid = {40504322},
issn = {1568-5608},
abstract = {Psoriasis is a chronic, multifactorial, inflammatory skin disease, increasingly recognized as a systemic disorder influenced by the gut-skin axis, which is a dynamic bidirectional communication between intestinal microbiome and cutaneous immune response. This narrative review explores the understanding of the gut-skin axis with the latest evidence on how gut dysbiosis occurs in psoriasis, characterized by reduced microbial diversity and its shifts, and how it contributes to pathogenesis and exacerbation of psoriasis. Notably, recent scientific literature evidence suggests that the alteration of gut microbiome in psoriasis includes a decreased level of beneficial species like Faecalibacterium prausnitzii and a rise in the level of proinflammatory bacterial species like Prevotella copri. Mechanistic insights reveal that gut-derived metabolites, impaired barrier functions, and immune signaling, particularly involving IL-23 and Th17 cells, play a pivotal role in this axis, linking intestinal health to cutaneous manifestations. Both animal and human trials underscore the therapeutic potential of interventions targeting the gut microbiota, including prebiotics, probiotics, dietary modifications, and FMT, demonstrating some promising but variable effects on disease severity and systemic inflammation. Despite these advances, translating the gut-skin axis into clinical practice presents a notable challenge due to limited scientific evidence, a lack of standardised microbiome profiling, and the absence of universally accepted biomarkers to monitor and stratify therapeutic outcomes. These limitations hinder the development of personalised care approaches and the integration of the gut-skin axis as a promising frontier in many autoimmune diseases, where the gut-skin axis and the intestinal microbiome play a crucial role.},
}
RevDate: 2025-06-12
Periodontitis Accelerates Progression of Heart Failure With Preserved Ejection Fraction in Mice.
JACC. Basic to translational science pii:S2452-302X(25)00122-6 [Epub ahead of print].
Chronic low-grade inflammation and nitric oxide (NO) depletion are important contributors to heart failure with preserved ejection fraction (HFpEF) pathophysiology. Periodontitis (PD) is a common inflammatory disease implicated in dysregulation of NO hemostasis. Epidemiological studies have shown an association between PD and increased risk of cardiovascular disease, including heart failure. However, a causative relationship between the 2 diseases has not yet been proven. In this study, we sought to investigate the direct effect of PD induction on HFpEF progression in a mouse model. Induction of PD in HFpEF mice resulted in significant oral microbial dysbiosis, accelerated progression of diastolic dysfunction by echocardiography, and increased myocardial inflammation and fibrosis. These deleterious effects seen with PD were shown to be mediated by increased systemic blood pressure, increased systemic inflammation, and NO depletion. Our study provides evidence of potential mechanistic links between PD and HFpEF progression and suggests PD as a new therapeutic target for HFpEF.
Additional Links: PMID-40504059
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@article {pmid40504059,
year = {2025},
author = {Daana, S and Rokach, Y and Abedat, S and Nachman, D and Mohsen, H and Karram, S and Zandberg, Y and Tzach-Nachman, R and Cohen, J and Amir, O and Houri-Haddad, Y and Rabea Asleh, },
title = {Periodontitis Accelerates Progression of Heart Failure With Preserved Ejection Fraction in Mice.},
journal = {JACC. Basic to translational science},
volume = {},
number = {},
pages = {101270},
doi = {10.1016/j.jacbts.2025.03.002},
pmid = {40504059},
issn = {2452-302X},
abstract = {Chronic low-grade inflammation and nitric oxide (NO) depletion are important contributors to heart failure with preserved ejection fraction (HFpEF) pathophysiology. Periodontitis (PD) is a common inflammatory disease implicated in dysregulation of NO hemostasis. Epidemiological studies have shown an association between PD and increased risk of cardiovascular disease, including heart failure. However, a causative relationship between the 2 diseases has not yet been proven. In this study, we sought to investigate the direct effect of PD induction on HFpEF progression in a mouse model. Induction of PD in HFpEF mice resulted in significant oral microbial dysbiosis, accelerated progression of diastolic dysfunction by echocardiography, and increased myocardial inflammation and fibrosis. These deleterious effects seen with PD were shown to be mediated by increased systemic blood pressure, increased systemic inflammation, and NO depletion. Our study provides evidence of potential mechanistic links between PD and HFpEF progression and suggests PD as a new therapeutic target for HFpEF.},
}
RevDate: 2025-06-12
Pharmacological inhibitors of the gamma-secretase enzyme complex disrupt epithelial cell function triggering colitis in mice.
Journal of Crohn's & colitis pii:8160927 [Epub ahead of print].
BACKGROUND AND AIMS: Inhibiting γ-secretase mediated Notch signaling has been explored as a potential treatment for Alzheimer's disease and cancer. However, clinical trials have revealed that this approach can lead to side effects, such as gut inflammation. Notch signaling has been shown to be a key mediator of intestinal epithelial homeostasis. We aimed to investigate the molecular mechanisms of γ-secretase inhibition-associated colitis.
METHODS: Mice and small intestinal organoids were treated with γ-secretase inhibitors and analyzed for IEC differentiation and inflammation-associated markers using different molecular and histological approaches, along with transcriptomic and proteomic analyses. To evaluate the role of the microbiome in colitis development, mice undergoing pharmacological γ-secretase inhibition were treated with antibiotics. Additionally, inflammatory bowel disease (IBD) patient samples and control samples were analyzed to assess the expression of Notch signaling pathway components in IECs.
RESULTS: This study shows that pharmacological γ-secretase inhibition induces inflammation in both the small and large intestine of mice, a phenotype that could be rescued upon microbiota depletion. Inhibiting the γ-secretase induced structural disruption of the epithelium and inflammatory cytokine release. On a molecular level, epithelial organoids exhibited disrupted IEC differentiation and impaired proliferation, associated with defective Notch signaling. Finally, analysis of IBD patients revealed deregulation of Notch pathway components within IECs.
CONCLUSIONS: In conclusion, systemic use of γ-secretase inhibitors disrupts epithelial cell function by impairing IEC differentiation and triggering gut inflammation in mice. These findings should be considered when designing future therapeutic interventions involving γ-secretase inhibitors.
Additional Links: PMID-40503970
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@article {pmid40503970,
year = {2025},
author = {Erkert, L and Kabisch, M and Gamez-Belmonte, R and Gonzalez-Acera, M and Patankar, JV and Schödel, L and Hofmann, K and Wagner, Y and Plattner, C and Spath, EM and Distler, U and Tenzer, S and , and Neufert, C and Neurath, MF and Becker, C},
title = {Pharmacological inhibitors of the gamma-secretase enzyme complex disrupt epithelial cell function triggering colitis in mice.},
journal = {Journal of Crohn's & colitis},
volume = {},
number = {},
pages = {},
doi = {10.1093/ecco-jcc/jjaf096},
pmid = {40503970},
issn = {1876-4479},
abstract = {BACKGROUND AND AIMS: Inhibiting γ-secretase mediated Notch signaling has been explored as a potential treatment for Alzheimer's disease and cancer. However, clinical trials have revealed that this approach can lead to side effects, such as gut inflammation. Notch signaling has been shown to be a key mediator of intestinal epithelial homeostasis. We aimed to investigate the molecular mechanisms of γ-secretase inhibition-associated colitis.
METHODS: Mice and small intestinal organoids were treated with γ-secretase inhibitors and analyzed for IEC differentiation and inflammation-associated markers using different molecular and histological approaches, along with transcriptomic and proteomic analyses. To evaluate the role of the microbiome in colitis development, mice undergoing pharmacological γ-secretase inhibition were treated with antibiotics. Additionally, inflammatory bowel disease (IBD) patient samples and control samples were analyzed to assess the expression of Notch signaling pathway components in IECs.
RESULTS: This study shows that pharmacological γ-secretase inhibition induces inflammation in both the small and large intestine of mice, a phenotype that could be rescued upon microbiota depletion. Inhibiting the γ-secretase induced structural disruption of the epithelium and inflammatory cytokine release. On a molecular level, epithelial organoids exhibited disrupted IEC differentiation and impaired proliferation, associated with defective Notch signaling. Finally, analysis of IBD patients revealed deregulation of Notch pathway components within IECs.
CONCLUSIONS: In conclusion, systemic use of γ-secretase inhibitors disrupts epithelial cell function by impairing IEC differentiation and triggering gut inflammation in mice. These findings should be considered when designing future therapeutic interventions involving γ-secretase inhibitors.},
}
RevDate: 2025-06-12
Evaluating the effect of amoxicillin treatment on the microbiome of Orbicella faveolata with Caribbean yellow band disease.
Applied and environmental microbiology [Epub ahead of print].
Host microbiomes play a key role in coral disease dynamics; thus, it is essential to characterize microbial communities of diseased tissues and identify how they are altered by potential treatments, especially as coral reef populations continue to decline globally. The abundance of Orbicella faveolata, a major reef-building Caribbean coral species, has significantly declined due to several stressors, including infectious disease. Caribbean yellow band disease (CYBD) often results in complete colony mortality. We applied an amoxicillin-laced Base2B ointment to CYBD lesion areas on O. faveolata within Buck Island Reef National Monument, St. Croix, USVI, trying to halt disease progression. Another CYBD lesion area on the same colony served as a paired untreated control. Microbiomes of the apparently healthy tissue adjacent to the treatment were characterized pretreatment and 2 days post-treatment, along with the paired untreated CYBD controls and nearby healthy colonies. Both microbiomes of untreated CYBD lesions and apparently healthy tissue on CYBD colonies had a significantly higher alpha diversity and significantly differed from those of nearby healthy colonies, suggesting potential systemic effects of CYBD. Amoxicillin treatment significantly changed the microbial community composition of tissues adjacent to the treatment site. The relative abundance of the bacterial family Vibrionaceae, a putative pathogen for CYBD and often associated with other coral diseases, was enriched post-treatment. However, the lesion progression rates of treated and untreated lesion areas were similar. Our results suggest that amoxicillin may disrupt the microbiome of adjacent tissue on O. faveolata, allowing for opportunistic Vibrio sp. bacteria to colonize, and may not be an effective treatment for CYBD.IMPORTANCEOrbicella faveolata, a primary reef-building coral species in the Caribbean, has been severely impacted by Caribbean yellow band disease. This disease causes tissue loss, which often culminates in the complete loss of the colony since recovery is rarely observed. The present study is significant because the development of an effective long-term treatment for Caribbean yellow band disease and understanding how the microbial partners contribute to pathogenesis are essential for conserving Caribbean coral reefs. While treatment with amoxicillin was not effective, our study uncovered valuable insights into the microbial composition of Caribbean yellow band disease in O. faveolata. In addition, this study highlights the possible unintended negative effects of treatment with amoxicillin and casts doubt on Vibrionaceae as the culprit of this disease.
Additional Links: PMID-40503883
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@article {pmid40503883,
year = {2025},
author = {Pearson-Lund, AS and Williams, SD and Eaton, KR and Clark, AS and Holloway, NH and Ewen, KA and Muller, EM},
title = {Evaluating the effect of amoxicillin treatment on the microbiome of Orbicella faveolata with Caribbean yellow band disease.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0240724},
doi = {10.1128/aem.02407-24},
pmid = {40503883},
issn = {1098-5336},
abstract = {Host microbiomes play a key role in coral disease dynamics; thus, it is essential to characterize microbial communities of diseased tissues and identify how they are altered by potential treatments, especially as coral reef populations continue to decline globally. The abundance of Orbicella faveolata, a major reef-building Caribbean coral species, has significantly declined due to several stressors, including infectious disease. Caribbean yellow band disease (CYBD) often results in complete colony mortality. We applied an amoxicillin-laced Base2B ointment to CYBD lesion areas on O. faveolata within Buck Island Reef National Monument, St. Croix, USVI, trying to halt disease progression. Another CYBD lesion area on the same colony served as a paired untreated control. Microbiomes of the apparently healthy tissue adjacent to the treatment were characterized pretreatment and 2 days post-treatment, along with the paired untreated CYBD controls and nearby healthy colonies. Both microbiomes of untreated CYBD lesions and apparently healthy tissue on CYBD colonies had a significantly higher alpha diversity and significantly differed from those of nearby healthy colonies, suggesting potential systemic effects of CYBD. Amoxicillin treatment significantly changed the microbial community composition of tissues adjacent to the treatment site. The relative abundance of the bacterial family Vibrionaceae, a putative pathogen for CYBD and often associated with other coral diseases, was enriched post-treatment. However, the lesion progression rates of treated and untreated lesion areas were similar. Our results suggest that amoxicillin may disrupt the microbiome of adjacent tissue on O. faveolata, allowing for opportunistic Vibrio sp. bacteria to colonize, and may not be an effective treatment for CYBD.IMPORTANCEOrbicella faveolata, a primary reef-building coral species in the Caribbean, has been severely impacted by Caribbean yellow band disease. This disease causes tissue loss, which often culminates in the complete loss of the colony since recovery is rarely observed. The present study is significant because the development of an effective long-term treatment for Caribbean yellow band disease and understanding how the microbial partners contribute to pathogenesis are essential for conserving Caribbean coral reefs. While treatment with amoxicillin was not effective, our study uncovered valuable insights into the microbial composition of Caribbean yellow band disease in O. faveolata. In addition, this study highlights the possible unintended negative effects of treatment with amoxicillin and casts doubt on Vibrionaceae as the culprit of this disease.},
}
RevDate: 2025-06-12
The rumen microbiota and metabolism of dairy cows are affected by the dietary rate of inclusion of Yucca schidigera extract.
Microbiology spectrum [Epub ahead of print].
Natural plant compounds can be used to supplement livestock diets, improving feed efficiency, production, and health, while also reducing environmental impact. In the present study, a Yucca schidigera (Mohave Yucca) extract was added at four rates of inclusion (ROI) of 0, 5, 15, or 30 g/day to a ryegrass and maize silage-based diet and fed to dairy cows in a 4 × 4 Latin square experimental design. Each period was 28 days in duration, with sampling undertaken during the final week of each period. Solid phase digesta (SPD) and liquid phase digesta (LPD) samples were collected via a rumen cannula and analyzed for volatile fatty acids (VFAs), ammonia N, and microbiome using 16S rRNA gene sequencing. Total fecal and urine collection was undertaken over a 3-day period. Rumen microbial diversity was not affected by ROI (LPD: P = 0.180; SPD: P = 0.059). However, discriminant analysis found a decrease in Methanobrevibacter millerae (linear discriminant analysis, LDA = 2.15) and an increase in an unclassified species of Proteobacteria (LDA = 2.10) associated with ROI. Univariate analysis also revealed differential abundance of operational taxonomic units classified as Prevotellaceae and Fibrobacteraceae by ROI (P < 0.05). Maximum rumen ammonia N concentration decreased linearly from 228 to 109 mg/L with ROI (P = 0.044). Rumen VFA concentration was unaffected with the exception of propionate, which showed a linear increase with ROI (P = 0.010). The diurnal rumen pH range (maximum-minimum) also decreased with ROI (P = 0.004). Dry matter intake and milk yield were not affected (P > 0.05) by ROI; however, there was a linear increase in milk fat content from 38.9 to 42.0 g/kg with ROI (P < 0.05).IMPORTANCEDomestic livestock such as dairy cows are inefficient utilizers of dietary nitrogen. This increases feed costs and reduces animal production efficiency. Excreted nitrogenous compounds are also an environmental hazard, such as when they enter water courses as nitrate or are lost to the atmosphere as ammonia or nitrous oxide. Dietary protein is degraded in the rumen via the activity of the microbial population, mainly into ammonia, which may then be utilized by the microbial population to synthesize microbial protein or absorbed into the blood and potentially excreted. Manipulation of the diet or altering the microbial population may increase the utilization of dietary protein, increasing animal performance, decreasing feed costs, and reducing the environmental impact of milk production. This study examines the effect of Yucca schidigera extract on the rumen microbiome and nitrogen utilization in dairy cows.
Additional Links: PMID-40503824
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@article {pmid40503824,
year = {2025},
author = {Snelling, TJ and Condren, M and Huntington, JA and Warren, HE and Taylor-Pickard, J and Sinclair, LA},
title = {The rumen microbiota and metabolism of dairy cows are affected by the dietary rate of inclusion of Yucca schidigera extract.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0064125},
doi = {10.1128/spectrum.00641-25},
pmid = {40503824},
issn = {2165-0497},
abstract = {Natural plant compounds can be used to supplement livestock diets, improving feed efficiency, production, and health, while also reducing environmental impact. In the present study, a Yucca schidigera (Mohave Yucca) extract was added at four rates of inclusion (ROI) of 0, 5, 15, or 30 g/day to a ryegrass and maize silage-based diet and fed to dairy cows in a 4 × 4 Latin square experimental design. Each period was 28 days in duration, with sampling undertaken during the final week of each period. Solid phase digesta (SPD) and liquid phase digesta (LPD) samples were collected via a rumen cannula and analyzed for volatile fatty acids (VFAs), ammonia N, and microbiome using 16S rRNA gene sequencing. Total fecal and urine collection was undertaken over a 3-day period. Rumen microbial diversity was not affected by ROI (LPD: P = 0.180; SPD: P = 0.059). However, discriminant analysis found a decrease in Methanobrevibacter millerae (linear discriminant analysis, LDA = 2.15) and an increase in an unclassified species of Proteobacteria (LDA = 2.10) associated with ROI. Univariate analysis also revealed differential abundance of operational taxonomic units classified as Prevotellaceae and Fibrobacteraceae by ROI (P < 0.05). Maximum rumen ammonia N concentration decreased linearly from 228 to 109 mg/L with ROI (P = 0.044). Rumen VFA concentration was unaffected with the exception of propionate, which showed a linear increase with ROI (P = 0.010). The diurnal rumen pH range (maximum-minimum) also decreased with ROI (P = 0.004). Dry matter intake and milk yield were not affected (P > 0.05) by ROI; however, there was a linear increase in milk fat content from 38.9 to 42.0 g/kg with ROI (P < 0.05).IMPORTANCEDomestic livestock such as dairy cows are inefficient utilizers of dietary nitrogen. This increases feed costs and reduces animal production efficiency. Excreted nitrogenous compounds are also an environmental hazard, such as when they enter water courses as nitrate or are lost to the atmosphere as ammonia or nitrous oxide. Dietary protein is degraded in the rumen via the activity of the microbial population, mainly into ammonia, which may then be utilized by the microbial population to synthesize microbial protein or absorbed into the blood and potentially excreted. Manipulation of the diet or altering the microbial population may increase the utilization of dietary protein, increasing animal performance, decreasing feed costs, and reducing the environmental impact of milk production. This study examines the effect of Yucca schidigera extract on the rumen microbiome and nitrogen utilization in dairy cows.},
}
RevDate: 2025-06-12
CmpDate: 2025-06-12
Dupilumab treatment has no effect on the nasal microbiome in patients with NSAID-exacerbated respiratory disease: a longitudinal pilot study.
Frontiers in immunology, 16:1508500.
BACKGROUND: Non-steroidal anti-inflammatory drugs-exacerbated respiratory disease (N-ERD) affects up to 10% of patients suffering from nasal polyps and has a severe impact on quality of life. Dupilumab, a monoclonal antibody targeting the IL-4 receptor α chain, leads to symptom relief and reduction in nasal type 2 mediator levels. Here, we investigated the impact of dupilumab treatment on the composition and diversity of the nasal microbiome.
METHODOLOGY: Nasal microbiome was analyzed by 16s rRNA gene amplicon sequencing in 28 patients before, 4, 12, and 24 weeks after dupilumab therapy.
RESULTS: After stringent decontamination and removal of patients whose samples contained less than 500 reads at ≥ one of the four visits, full datasets from 8 out of 28 patients remained for downstream analysis of microbiome data. All 8 patients showed significant reduction in TPS (total polyp score; p=0.0078) and an improvement in SNOT-22 (Sino-nasal outcome test-22, a quality of life questionnaire; p=0.0781) after dupilumab therapy. During 24 weeks of dupilumab therapy, there were no major changes in microbiome diversity or composition observed (Shannon index: V1-V4:p-adj=0.25, Chao 1 Index V1-V4:p-adj=0.31), and only 2 out of 8 patients showed a decrease in staphylococci abundance.
CONCLUSIONS: More than 70% of the samples did not pass quality control, this warrants further refinement of nasal microbiome sampling techniques and mandatory guidelines on stringent quality control for analysis of this low biomass data in future. Furthermore, dupilumab did not have an impact on microbiome diversity or composition.
Additional Links: PMID-40503236
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@article {pmid40503236,
year = {2025},
author = {Bartosik, T and Pjevac, P and Séneca, J and Morgenstern, C and Arnoldner, T and Gangl, K and Sinz, C and Campion, NJ and Tu, A and Stanek, V and Bangert, C and Schneider, S and Eckl-Dorna, J},
title = {Dupilumab treatment has no effect on the nasal microbiome in patients with NSAID-exacerbated respiratory disease: a longitudinal pilot study.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1508500},
pmid = {40503236},
issn = {1664-3224},
mesh = {Humans ; *Antibodies, Monoclonal, Humanized/therapeutic use ; Male ; Middle Aged ; *Microbiota/drug effects ; Pilot Projects ; Female ; Longitudinal Studies ; Aged ; Adult ; *Anti-Inflammatory Agents, Non-Steroidal/adverse effects ; Quality of Life ; RNA, Ribosomal, 16S/genetics ; Nasal Polyps/drug therapy/microbiology ; Treatment Outcome ; },
abstract = {BACKGROUND: Non-steroidal anti-inflammatory drugs-exacerbated respiratory disease (N-ERD) affects up to 10% of patients suffering from nasal polyps and has a severe impact on quality of life. Dupilumab, a monoclonal antibody targeting the IL-4 receptor α chain, leads to symptom relief and reduction in nasal type 2 mediator levels. Here, we investigated the impact of dupilumab treatment on the composition and diversity of the nasal microbiome.
METHODOLOGY: Nasal microbiome was analyzed by 16s rRNA gene amplicon sequencing in 28 patients before, 4, 12, and 24 weeks after dupilumab therapy.
RESULTS: After stringent decontamination and removal of patients whose samples contained less than 500 reads at ≥ one of the four visits, full datasets from 8 out of 28 patients remained for downstream analysis of microbiome data. All 8 patients showed significant reduction in TPS (total polyp score; p=0.0078) and an improvement in SNOT-22 (Sino-nasal outcome test-22, a quality of life questionnaire; p=0.0781) after dupilumab therapy. During 24 weeks of dupilumab therapy, there were no major changes in microbiome diversity or composition observed (Shannon index: V1-V4:p-adj=0.25, Chao 1 Index V1-V4:p-adj=0.31), and only 2 out of 8 patients showed a decrease in staphylococci abundance.
CONCLUSIONS: More than 70% of the samples did not pass quality control, this warrants further refinement of nasal microbiome sampling techniques and mandatory guidelines on stringent quality control for analysis of this low biomass data in future. Furthermore, dupilumab did not have an impact on microbiome diversity or composition.},
}
MeSH Terms:
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Humans
*Antibodies, Monoclonal, Humanized/therapeutic use
Male
Middle Aged
*Microbiota/drug effects
Pilot Projects
Female
Longitudinal Studies
Aged
Adult
*Anti-Inflammatory Agents, Non-Steroidal/adverse effects
Quality of Life
RNA, Ribosomal, 16S/genetics
Nasal Polyps/drug therapy/microbiology
Treatment Outcome
RevDate: 2025-06-12
Huangqin decoction inhibits colorectal inflammatory cancer transformation by improving gut microbiome-mediated metabolic dysfunction.
Journal of pharmaceutical analysis, 15(5):101138.
Colorectal inflammatory cancer transformation poses a major risk to patients with colitis. Patients with chronic intestinal inflammation have an approximately 2-3 folds increased risk of developing colorectal cancer (CRC). Unfortunately, there is currently no effective intervention available. Huangqin decoction (HQD), a well-known traditional Chinese medicine (TCM) formula, is frequently clinically prescribed for treating patients with colitis, and its active ingredients have effective antitumour efficacy. Nonetheless, the mechanism of HQD-mediated prevention of colorectal inflammatory cancer transformation remains unclear. A strategy integrating metagenomic, lipidomic, and messenger RNA (mRNA) sequencing analysis was used to investigate the regulatory effects of HQD on the gut microbiome, metabolism and potential mechanisms involved in colorectal inflammatory cancer transformation. Our study revealed that HQD suppressed colorectal inflammatory cancer transformation, which was associated with enhanced intestinal barrier function, decreased the inflammatory response, and regulation of the gut microbiome. Notably, cohousing experiments revealed that the transfer of the gut microbiome from HQD-treated mice largely inhibited the pathological transformation of colitis. Moreover, gut microbiome transfer from HQD-treated mice primarily resulted in the altered regulation of fatty acid metabolism, especially the remodeling of arachidonic acid metabolism, which was associated with the amelioration of pathological transformation. Arachidonic acid metabolism and the key metabolic enzyme arachidonic acid 12-lipoxygenase (ALOX12) were affected by HQD treatment, and no obvious protective effect of HQD was observed in Alox 12 [-/-] mice, which revealed that ALOX12 was a critical mediator of HQD protection against colorectal inflammatory cancer transformation. In summary, multiple omics analyses were applied to produce valuable data and theoretical support for the application of HQD as a promising intervention for the transformation of inflammatory CRC.
Additional Links: PMID-40502641
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Citation:
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@article {pmid40502641,
year = {2025},
author = {Lu, L and Li, Y and Su, H and Ren, S and Liu, Y and Shao, G and Liu, W and Ji, G and Xu, H},
title = {Huangqin decoction inhibits colorectal inflammatory cancer transformation by improving gut microbiome-mediated metabolic dysfunction.},
journal = {Journal of pharmaceutical analysis},
volume = {15},
number = {5},
pages = {101138},
pmid = {40502641},
issn = {2214-0883},
abstract = {Colorectal inflammatory cancer transformation poses a major risk to patients with colitis. Patients with chronic intestinal inflammation have an approximately 2-3 folds increased risk of developing colorectal cancer (CRC). Unfortunately, there is currently no effective intervention available. Huangqin decoction (HQD), a well-known traditional Chinese medicine (TCM) formula, is frequently clinically prescribed for treating patients with colitis, and its active ingredients have effective antitumour efficacy. Nonetheless, the mechanism of HQD-mediated prevention of colorectal inflammatory cancer transformation remains unclear. A strategy integrating metagenomic, lipidomic, and messenger RNA (mRNA) sequencing analysis was used to investigate the regulatory effects of HQD on the gut microbiome, metabolism and potential mechanisms involved in colorectal inflammatory cancer transformation. Our study revealed that HQD suppressed colorectal inflammatory cancer transformation, which was associated with enhanced intestinal barrier function, decreased the inflammatory response, and regulation of the gut microbiome. Notably, cohousing experiments revealed that the transfer of the gut microbiome from HQD-treated mice largely inhibited the pathological transformation of colitis. Moreover, gut microbiome transfer from HQD-treated mice primarily resulted in the altered regulation of fatty acid metabolism, especially the remodeling of arachidonic acid metabolism, which was associated with the amelioration of pathological transformation. Arachidonic acid metabolism and the key metabolic enzyme arachidonic acid 12-lipoxygenase (ALOX12) were affected by HQD treatment, and no obvious protective effect of HQD was observed in Alox 12 [-/-] mice, which revealed that ALOX12 was a critical mediator of HQD protection against colorectal inflammatory cancer transformation. In summary, multiple omics analyses were applied to produce valuable data and theoretical support for the application of HQD as a promising intervention for the transformation of inflammatory CRC.},
}
RevDate: 2025-06-12
Modulating effects of environmental enrichment on stress-induced changes in the gut microbiome.
Brain, behavior, & immunity - health, 46:101023.
Environmental enrichment (EE) involves adding non-standard stimuli, such as running wheels, mazes, and cage mates, to standard animal living conditions to facilitate physical activity, cognitive stimulation, and socialization. Interestingly, exposure to EE can modulate stress and immune responses. However, it is unclear whether housing environments can modulate the effects of stress on the gut microbiome. This study aimed to explore the effects of three different housing conditions-deprived (DH), social (SH), and enriched (EE)-on the central and peripheral immune responses, the HPA axis, and the gut microbiome in 180 male and female mice. Mice were housed in either the DH, SH, or EE condition for 3 weeks starting from post-natal day 21. At 6 weeks of age, during the pubertal stress-sensitive period, mice were treated with either saline or lipopolysaccharide (LPS), a bacterial endotoxin. Eight hours post-treatment, mice were euthanized, and brain, fecal samples, and trunk blood were collected to examine peripheral and central cytokine levels, glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) expressions, along with diversity in the gut microbiome. Contrary to expectations, EE and SH mice showed higher plasma concentrations of TNFα, IL6, and IL12 cytokines than DH mice following LPS treatment, with male mice exhibiting significantly higher levels of these cytokines than their female counterparts. Moreover, EE mice exhibited significantly greater hypothalamic and hippocampal expressions of GR and MR compared to DH mice. The gut microbiome analysis revealed sex-specific beta diversity patterns post-LPS treatment, with male EE and SH mice displaying a more diverse microbiome compared to female counterparts. These findings enhance our understanding of how housing conditions influence the acute immune and stress responses and modulate their effects on the gut microbiome during puberty.
Additional Links: PMID-40502530
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@article {pmid40502530,
year = {2025},
author = {Smith, KB and Murack, M and Butcher, J and Hinterberger, A and Stintzi, A and Liang, J and Tata, DA and Ismail, N},
title = {Modulating effects of environmental enrichment on stress-induced changes in the gut microbiome.},
journal = {Brain, behavior, & immunity - health},
volume = {46},
number = {},
pages = {101023},
pmid = {40502530},
issn = {2666-3546},
abstract = {Environmental enrichment (EE) involves adding non-standard stimuli, such as running wheels, mazes, and cage mates, to standard animal living conditions to facilitate physical activity, cognitive stimulation, and socialization. Interestingly, exposure to EE can modulate stress and immune responses. However, it is unclear whether housing environments can modulate the effects of stress on the gut microbiome. This study aimed to explore the effects of three different housing conditions-deprived (DH), social (SH), and enriched (EE)-on the central and peripheral immune responses, the HPA axis, and the gut microbiome in 180 male and female mice. Mice were housed in either the DH, SH, or EE condition for 3 weeks starting from post-natal day 21. At 6 weeks of age, during the pubertal stress-sensitive period, mice were treated with either saline or lipopolysaccharide (LPS), a bacterial endotoxin. Eight hours post-treatment, mice were euthanized, and brain, fecal samples, and trunk blood were collected to examine peripheral and central cytokine levels, glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) expressions, along with diversity in the gut microbiome. Contrary to expectations, EE and SH mice showed higher plasma concentrations of TNFα, IL6, and IL12 cytokines than DH mice following LPS treatment, with male mice exhibiting significantly higher levels of these cytokines than their female counterparts. Moreover, EE mice exhibited significantly greater hypothalamic and hippocampal expressions of GR and MR compared to DH mice. The gut microbiome analysis revealed sex-specific beta diversity patterns post-LPS treatment, with male EE and SH mice displaying a more diverse microbiome compared to female counterparts. These findings enhance our understanding of how housing conditions influence the acute immune and stress responses and modulate their effects on the gut microbiome during puberty.},
}
RevDate: 2025-06-12
Searching for bacteria within acute cholecystitis using next-generation sequencers.
Surgery open science, 26:113-118.
INTRODUCTION: A biliary microbiome comprising flora within normal gallbladders was recently uncovered through analyses targeting the bacterial 16S ribosomal RNA (16S rRNA) gene, despite the gallbladder previously being regarded as a sterile environment. In the present study, we subjected bile samples from patients with acute cholecystitis to gene analysis targeting bacterial flora.
METHODS: We targeted patients diagnosed as having Grade I or Grade II acute cholecystitis (in accordance with the Tokyo Guidelines 2018 established by the Japanese Society of Hepato-Biliary-Pancreatic Surgery) who underwent laparoscopic cholecystectomy within 24 h of diagnosis at Juntendo University Urayasu Hospital between July 2021 and January 2024 for evaluation. We drew bile sample from the gallbladder of each patient to confirm the presence of biliary bacterial flora, using both standard bacteriology (culture test) and 16S rRNA gene sequence.
RESULTS: Of the 29 samples, 15 yielded cultures positive for bacterial flora, and gene analysis revealed the presence of bacterial biliary flora in all 14 samples that had tested negative in standard bacteriology. Considering the bacterial flora of a normal gallbladder without lesions as "normal flora," bacteria other than normal flora-Propionibacterium spp., Coprococcus spp., Prevotella spp., Sediminibacterium spp., and Collinesella spp.-were detected in 25 of the 29 cases (86 %).
CONCLUSIONS: Bacteria not detected in non-inflammatory gallbladders such as Propiobacterium spp., Coprococcus spp., Prevotella spp., Sediminibacterium spp., and Collinesella spp. may play a role in the mechanism underlying development of acute cholecystitis.
Additional Links: PMID-40502457
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@article {pmid40502457,
year = {2025},
author = {Otsuka, T and Ishizaki, Y and Yoshimoto, J and Takamori, K and Watanabe, S},
title = {Searching for bacteria within acute cholecystitis using next-generation sequencers.},
journal = {Surgery open science},
volume = {26},
number = {},
pages = {113-118},
pmid = {40502457},
issn = {2589-8450},
abstract = {INTRODUCTION: A biliary microbiome comprising flora within normal gallbladders was recently uncovered through analyses targeting the bacterial 16S ribosomal RNA (16S rRNA) gene, despite the gallbladder previously being regarded as a sterile environment. In the present study, we subjected bile samples from patients with acute cholecystitis to gene analysis targeting bacterial flora.
METHODS: We targeted patients diagnosed as having Grade I or Grade II acute cholecystitis (in accordance with the Tokyo Guidelines 2018 established by the Japanese Society of Hepato-Biliary-Pancreatic Surgery) who underwent laparoscopic cholecystectomy within 24 h of diagnosis at Juntendo University Urayasu Hospital between July 2021 and January 2024 for evaluation. We drew bile sample from the gallbladder of each patient to confirm the presence of biliary bacterial flora, using both standard bacteriology (culture test) and 16S rRNA gene sequence.
RESULTS: Of the 29 samples, 15 yielded cultures positive for bacterial flora, and gene analysis revealed the presence of bacterial biliary flora in all 14 samples that had tested negative in standard bacteriology. Considering the bacterial flora of a normal gallbladder without lesions as "normal flora," bacteria other than normal flora-Propionibacterium spp., Coprococcus spp., Prevotella spp., Sediminibacterium spp., and Collinesella spp.-were detected in 25 of the 29 cases (86 %).
CONCLUSIONS: Bacteria not detected in non-inflammatory gallbladders such as Propiobacterium spp., Coprococcus spp., Prevotella spp., Sediminibacterium spp., and Collinesella spp. may play a role in the mechanism underlying development of acute cholecystitis.},
}
RevDate: 2025-06-12
[The Relationship of Dysbiosis of Duodenal Microbiome and Functional Dyspepsia].
The Korean journal of helicobacter and upper gastrointestinal research, 24(4):327-338.
Functional dyspepsia (FD) is a common gastrointestinal disorder characterized by chronic or recurrent epigastric pain or discomfort and postprandial fullness, without a definite organic cause. Despite the importance of FD in terms of decreased quality of life and recurrence, treatment modalities have been unsatisfactory, mainly because of their complex and heterogeneous nature. A link between microbiome dysbiosis and low-grade inflammation, along with mucosal barrier disruption of the duodenal mucosa, has been suggested and may be a potential target for FD treatment. This link supports the gut-brain (overactive visceral signaling and pain modulation) and the brain-gut (abnormal central processing) axes in FD. A definite increase in Streptococcus and a reduced abundance of Prevotella, Veillonella, and Actinomyces have also been observed. In addition, bacterial overgrowth is frequently observed in the small intestine, and rifaximin treatment improves the symptoms of FD, especially in women. This evidence highlights the importance of bacterial ecology in the development of FD symptoms. However, further research is necessary to prove the causal relationship between duodenal mucosal microbiota dysbiosis and FD.
Additional Links: PMID-40502320
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@article {pmid40502320,
year = {2024},
author = {Kim, N},
title = {[The Relationship of Dysbiosis of Duodenal Microbiome and Functional Dyspepsia].},
journal = {The Korean journal of helicobacter and upper gastrointestinal research},
volume = {24},
number = {4},
pages = {327-338},
pmid = {40502320},
issn = {2671-826X},
abstract = {Functional dyspepsia (FD) is a common gastrointestinal disorder characterized by chronic or recurrent epigastric pain or discomfort and postprandial fullness, without a definite organic cause. Despite the importance of FD in terms of decreased quality of life and recurrence, treatment modalities have been unsatisfactory, mainly because of their complex and heterogeneous nature. A link between microbiome dysbiosis and low-grade inflammation, along with mucosal barrier disruption of the duodenal mucosa, has been suggested and may be a potential target for FD treatment. This link supports the gut-brain (overactive visceral signaling and pain modulation) and the brain-gut (abnormal central processing) axes in FD. A definite increase in Streptococcus and a reduced abundance of Prevotella, Veillonella, and Actinomyces have also been observed. In addition, bacterial overgrowth is frequently observed in the small intestine, and rifaximin treatment improves the symptoms of FD, especially in women. This evidence highlights the importance of bacterial ecology in the development of FD symptoms. However, further research is necessary to prove the causal relationship between duodenal mucosal microbiota dysbiosis and FD.},
}
RevDate: 2025-06-12
A missense mutation in Muc2 promotes gut microbiome- and metabolome-dependent colitis-associated tumorigenesis.
bioRxiv : the preprint server for biology pii:2025.05.31.657160.
UNLABELLED: Colitis-associated cancer (CAC) arises from a complex interplay between host and environmental factors, including the gut microbiome. Since ulcerative colitis (UC), a significant risk factor for CAC, is rising in prevalence worldwide, an integrative approach is essential to identify potential triggers linking inflammation to cancer. In the present study, we investigated the role of the gut microbiome using Winnie mice, a UC-like model with a relevant missense mutation in the Muc2 gene. Upon transfer from a conventional (CONV) to a specific-pathogen-free (SPF) facility, Winnie mice exhibited a more severe colitis phenotype, and notably, spontaneous CAC as early as four weeks of age, which progressively worsened over time. In contrast, CONV Winnie developed only mild colitis but with no overt signs of tumorigenesis. Notably, when rederived into germ-free (GF) conditions, SPF Winnie mice were protected from colitis or colon tumor development, indicating an essential role for the gut microbiome in the initiation and progression of CAC in these mice. Using shotgun metagenomics, metabolomics, and lipidomics, we identified a distinct pro-inflammatory microbial and metabolic signature that potentially drives the transition from colitis to CAC. Fecal microbiota transplantation (FMT), using either SPF Winnie or WT (Bl/6) donors into GF Winnie recipients, demonstrated that while colitis developed regardless of donor, only FMT from SPF Winnie donors resulted in CAC, revealing a microbiota-driven, host-specific susceptibility to tumorigenesis in Winnie mice. Our studies present a novel and relevant model of CAC, providing further evidence that the microbiome plays a key role in the pathogenesis of CAC, thereby challenging the concept of colon cancer as a strictly non-transmissible disease.
LAY SUMMARY: This study reveals a distinct metagenomic, metabolomic, and lipidomic profile associated with tumorigenesis in a murine model of ulcerative colitis, highlighting the risks of specific intestinal dysbiosis in genetically predisposed subjects.
WHAT YOU NEED TO KNOW: Background and context: Colitis-associated colorectal cancer arises from complex host-environment interactions, including gut microbiome influences, driving chronic inflammation, with the intestinal lumen environment remaining a largely unexplored potential risk factor in cancer development.New findings: Winnie mice in specific pathogen-free conditions developed severe colitis, and a novel juvenile colon dysplasia and cancer, with gut microbiome changes driving colitis-associated cancer initiation and progression.Limitations: We identified a pro-inflammatory microbial/metabolic signature promoting colitis-to-CAC transition in Winnie mice, with FMT confirming microbiota-driven tumor susceptibility. However, further research is needed to pinpoint the key bacteria-metabolite-lipid combination driving CAC.Clinical research relevance: This newly characterized microbiota-metabolome-based model of CAC, challenges the dogma of cancer as a non-transmittable disease, providing a foundation for developing microbiota-based strategies for CAC prevention and treatment.Basic research relevance: Unlike genetic or chemically induced models, the Winnie mouse model uniquely serves as a dual model for spontaneous colitis and juvenile CAC, offering a fast, 100% penetrant phenotype that enhances reliability, accelerates research, and provides valuable insights into IBD and CAC.
Additional Links: PMID-40502184
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@article {pmid40502184,
year = {2025},
author = {Verna, G and De Santis, S and Islam, B and Sommella, EM and Licastro, D and Zhang, L and De Almeida Celio, F and Merciai, F and Caponigro, V and Campiglia, P and Pizarro, TT and Chieppa, M and Cominelli, F},
title = {A missense mutation in Muc2 promotes gut microbiome- and metabolome-dependent colitis-associated tumorigenesis.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.05.31.657160},
pmid = {40502184},
issn = {2692-8205},
abstract = {UNLABELLED: Colitis-associated cancer (CAC) arises from a complex interplay between host and environmental factors, including the gut microbiome. Since ulcerative colitis (UC), a significant risk factor for CAC, is rising in prevalence worldwide, an integrative approach is essential to identify potential triggers linking inflammation to cancer. In the present study, we investigated the role of the gut microbiome using Winnie mice, a UC-like model with a relevant missense mutation in the Muc2 gene. Upon transfer from a conventional (CONV) to a specific-pathogen-free (SPF) facility, Winnie mice exhibited a more severe colitis phenotype, and notably, spontaneous CAC as early as four weeks of age, which progressively worsened over time. In contrast, CONV Winnie developed only mild colitis but with no overt signs of tumorigenesis. Notably, when rederived into germ-free (GF) conditions, SPF Winnie mice were protected from colitis or colon tumor development, indicating an essential role for the gut microbiome in the initiation and progression of CAC in these mice. Using shotgun metagenomics, metabolomics, and lipidomics, we identified a distinct pro-inflammatory microbial and metabolic signature that potentially drives the transition from colitis to CAC. Fecal microbiota transplantation (FMT), using either SPF Winnie or WT (Bl/6) donors into GF Winnie recipients, demonstrated that while colitis developed regardless of donor, only FMT from SPF Winnie donors resulted in CAC, revealing a microbiota-driven, host-specific susceptibility to tumorigenesis in Winnie mice. Our studies present a novel and relevant model of CAC, providing further evidence that the microbiome plays a key role in the pathogenesis of CAC, thereby challenging the concept of colon cancer as a strictly non-transmissible disease.
LAY SUMMARY: This study reveals a distinct metagenomic, metabolomic, and lipidomic profile associated with tumorigenesis in a murine model of ulcerative colitis, highlighting the risks of specific intestinal dysbiosis in genetically predisposed subjects.
WHAT YOU NEED TO KNOW: Background and context: Colitis-associated colorectal cancer arises from complex host-environment interactions, including gut microbiome influences, driving chronic inflammation, with the intestinal lumen environment remaining a largely unexplored potential risk factor in cancer development.New findings: Winnie mice in specific pathogen-free conditions developed severe colitis, and a novel juvenile colon dysplasia and cancer, with gut microbiome changes driving colitis-associated cancer initiation and progression.Limitations: We identified a pro-inflammatory microbial/metabolic signature promoting colitis-to-CAC transition in Winnie mice, with FMT confirming microbiota-driven tumor susceptibility. However, further research is needed to pinpoint the key bacteria-metabolite-lipid combination driving CAC.Clinical research relevance: This newly characterized microbiota-metabolome-based model of CAC, challenges the dogma of cancer as a non-transmittable disease, providing a foundation for developing microbiota-based strategies for CAC prevention and treatment.Basic research relevance: Unlike genetic or chemically induced models, the Winnie mouse model uniquely serves as a dual model for spontaneous colitis and juvenile CAC, offering a fast, 100% penetrant phenotype that enhances reliability, accelerates research, and provides valuable insights into IBD and CAC.},
}
RevDate: 2025-06-12
Gut microbiota of Brazilian Melipona stingless bees: dominant members and their localization in different gut regions.
bioRxiv : the preprint server for biology pii:2025.06.03.657762.
The gut microbiome of eusocial corbiculate bees, which include honeybees, bumblebees, and stingless bees, consists of anciently associated, host-specific bacteria that are vital for bee health. Two symbionts, Snodgrassella and Gilliamella , are ubiquitous in honeybees and bumblebees. However, their presence varies in the stingless bee clade (Meliponini), a group with pantropical distribution. They are absent or rare in the diverse genus Melipona , indicating a shift in microbiota composition in this lineage. To identify the main members of the Melipona microbiota, we combined newly collected and published data from field-collected individuals of several species. Additionally, we identified the localization of the dominant microbiota members within the gut regions of Melipona quadrifasciata anthidioides . The dominant microbiota of Melipona species includes members of the genera Bifidobacterium, Lactobacillus, Apilactobacillus, Floricoccus , and Bombella . Among these, Apilactobacillus and Bombella dominate in the crop, whereas Apilactobacillus and other members of the Lactobacillaceae dominate the ventriculus. The ileum lacks Snodgrassella or Gilliamella but contains a putative new symbiont close to Floricoccus , as well as strains of Bifidobacterium , Lactobacillaceae (including Apilactobacillus), and Bombella . The rectum is dominated by Bifidobacterium and Lactobacillus . In summary, the Melipona microbiota is compositionally distinct but shows spatial organization paralleling that of other eusocial corbiculate bees.
Additional Links: PMID-40502178
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@article {pmid40502178,
year = {2025},
author = {Tristao Santini, A and Cerqueira, AES and Moran, NA and Resende, HC and Santana, WC and de Paula, SO and da Silva, CC},
title = {Gut microbiota of Brazilian Melipona stingless bees: dominant members and their localization in different gut regions.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.06.03.657762},
pmid = {40502178},
issn = {2692-8205},
abstract = {The gut microbiome of eusocial corbiculate bees, which include honeybees, bumblebees, and stingless bees, consists of anciently associated, host-specific bacteria that are vital for bee health. Two symbionts, Snodgrassella and Gilliamella , are ubiquitous in honeybees and bumblebees. However, their presence varies in the stingless bee clade (Meliponini), a group with pantropical distribution. They are absent or rare in the diverse genus Melipona , indicating a shift in microbiota composition in this lineage. To identify the main members of the Melipona microbiota, we combined newly collected and published data from field-collected individuals of several species. Additionally, we identified the localization of the dominant microbiota members within the gut regions of Melipona quadrifasciata anthidioides . The dominant microbiota of Melipona species includes members of the genera Bifidobacterium, Lactobacillus, Apilactobacillus, Floricoccus , and Bombella . Among these, Apilactobacillus and Bombella dominate in the crop, whereas Apilactobacillus and other members of the Lactobacillaceae dominate the ventriculus. The ileum lacks Snodgrassella or Gilliamella but contains a putative new symbiont close to Floricoccus , as well as strains of Bifidobacterium , Lactobacillaceae (including Apilactobacillus), and Bombella . The rectum is dominated by Bifidobacterium and Lactobacillus . In summary, the Melipona microbiota is compositionally distinct but shows spatial organization paralleling that of other eusocial corbiculate bees.},
}
RevDate: 2025-06-12
Single-cell transcriptomics reveals probiotic reversal of neonatal morphine-induced gene disruptions underlying adolescent pain hypersensitivity.
bioRxiv : the preprint server for biology pii:2025.05.30.657034.
Neonatal morphine is commonly administered in the Neonatal Intensive Care Unit (NICU) to manage pain. However, its long-term effects on neurodevelopment of pain pathways, remain a significant concern. The midbrain is a core region that plays a central role in pain processing and opioid-mediated analgesia. Here, we performed single-cell RNA sequencing to study gene expression in 107,427 midbrain single cells from adolescent mice neonatally exposed to either saline, morphine, or morphine with the probiotic Bifidobacterium infantis (B. infantis). We found broad alterations in transcriptomics within neurons, astrocytes, oligodendrocytes, and microglial cells. Analysis of differentially regulated genes revealed down regulation of HOX genes and upregulation of pathways related to neurotransmitter signaling and pain in adolescence that were neonatally treated with morphine. Interestingly, neonatal probiotic supplementation mitigated these morphine-induced alterations on the transcriptome. This study presents the first single-cell RNA sequencing dataset of the adolescent midbrain following neonatal morphine exposure and probiotic intervention. These findings offer new insights into the neurodevelopmental impact of early opioid exposure and highlight the therapeutic potential of microbiome-targeted interventions.
Additional Links: PMID-40502161
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@article {pmid40502161,
year = {2025},
author = {Tao, J and Antoine, D and Jalodia, R and Valdes, E and Boyles, SM and Hulme, W and Roy, S},
title = {Single-cell transcriptomics reveals probiotic reversal of neonatal morphine-induced gene disruptions underlying adolescent pain hypersensitivity.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.05.30.657034},
pmid = {40502161},
issn = {2692-8205},
abstract = {Neonatal morphine is commonly administered in the Neonatal Intensive Care Unit (NICU) to manage pain. However, its long-term effects on neurodevelopment of pain pathways, remain a significant concern. The midbrain is a core region that plays a central role in pain processing and opioid-mediated analgesia. Here, we performed single-cell RNA sequencing to study gene expression in 107,427 midbrain single cells from adolescent mice neonatally exposed to either saline, morphine, or morphine with the probiotic Bifidobacterium infantis (B. infantis). We found broad alterations in transcriptomics within neurons, astrocytes, oligodendrocytes, and microglial cells. Analysis of differentially regulated genes revealed down regulation of HOX genes and upregulation of pathways related to neurotransmitter signaling and pain in adolescence that were neonatally treated with morphine. Interestingly, neonatal probiotic supplementation mitigated these morphine-induced alterations on the transcriptome. This study presents the first single-cell RNA sequencing dataset of the adolescent midbrain following neonatal morphine exposure and probiotic intervention. These findings offer new insights into the neurodevelopmental impact of early opioid exposure and highlight the therapeutic potential of microbiome-targeted interventions.},
}
RevDate: 2025-06-12
Gut microbe-derived lactic acid optimizes host energy metabolism during starvation.
bioRxiv : the preprint server for biology pii:2025.05.27.656452.
Gut microbes convert dietary compounds into an array of metabolites that can directly provide energy to their host and indirectly impact host metabolism as systemic endocrine signals. Here, we show that gut microbe-derived metabolites can extend Drosophila melanogaster survival during starvation, despite minimal alteration of dietary energy intake. Combining survival assays with mathematical modeling and untargeted metabolomics, we identify a single, dominant mediator of starvation resilience: lactic acid produced by the commensal bacterium Lactiplantibacillus plantarum . We discover that the basis of starvation resilience is not catabolism of lactic acid using lactate dehydrogenase, but rather increased dietary energy yield through lactic acid-driven promotion of oxidative phosphorylation. Our findings emphasize the role of the microbiome as a source of endocrine cues coordinating host metabolism and underscore the potential of microbiome-derived metabolites as therapeutic molecules for manipulating metabolic health and preventing disease.
Additional Links: PMID-40502158
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@article {pmid40502158,
year = {2025},
author = {Millington, JW and Lopez, JA and Sajjadian, AM and Scheffler, RJ and DeFelice, BC and Ludington, WB and Good, BH and O'Brien, LE and Huang, KC},
title = {Gut microbe-derived lactic acid optimizes host energy metabolism during starvation.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.05.27.656452},
pmid = {40502158},
issn = {2692-8205},
abstract = {Gut microbes convert dietary compounds into an array of metabolites that can directly provide energy to their host and indirectly impact host metabolism as systemic endocrine signals. Here, we show that gut microbe-derived metabolites can extend Drosophila melanogaster survival during starvation, despite minimal alteration of dietary energy intake. Combining survival assays with mathematical modeling and untargeted metabolomics, we identify a single, dominant mediator of starvation resilience: lactic acid produced by the commensal bacterium Lactiplantibacillus plantarum . We discover that the basis of starvation resilience is not catabolism of lactic acid using lactate dehydrogenase, but rather increased dietary energy yield through lactic acid-driven promotion of oxidative phosphorylation. Our findings emphasize the role of the microbiome as a source of endocrine cues coordinating host metabolism and underscore the potential of microbiome-derived metabolites as therapeutic molecules for manipulating metabolic health and preventing disease.},
}
RevDate: 2025-06-12
Endothelial c-IAP2 Loss Amplifies P2X7 Receptor-Driven Inflammation and Worsens Infection-Associated Pulmonary Hypertension.
bioRxiv : the preprint server for biology pii:2025.05.22.655387.
Schistosomiasis-associated Pulmonary Hypertension (Sch-PH) is the most common form of group I PH worldwide. Recently, data revealed that the preclinical animal model of Sch-PH exhibited gut and lung microbiome dysbiosis linked to significant endothelial dysfunction and microvascular apoptosis, but the role of pro/anti-apoptosis sensors, such as the inhibitor of apoptosis protein 2 (c-IAP2) and purinergic receptor P2X7 (P2X7R), remained unclear. Using a novel Cdh5cre-ER [T2] ;cIAP1 [-/-] ;cIAP2 [fl/fl] animal model, this study investigated the contribution of endothelial c-IAP2 in this process, revealing P2X7R overexpression as a putative target in the onset of Sch-PH. Pharmacologically, inhibition of P2X7R function confirmed its role in promoting lung endothelial death and disease progression. Moreover, data suggest that microbiome-associated metabolic alterations in Sch-PH seem linked to microvascular endothelial apoptosis driven by ATP/P2X7R overactivation and suppressed c-IAP2 expression. Indeed, genetic ablation of endothelial c-IAP2 expression was sufficient to induce PH-like features in mice, with echocardiography indicating a higher pulmonary acceleration time (PAT), PAT/pulmonary ejection time (PET), and right ventricular free wall thickness after IP/IV-Egg challenge compared to controls. These findings suggest a significant contribution of lung endothelial P2X7R activation and c-IAP2 suppression to Sch-PH pathology, highlighting them as promising novel therapeutic targets for this life-threatening illness.
Additional Links: PMID-40502111
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@article {pmid40502111,
year = {2025},
author = {Villarreal, ES and Marinho, Y and Loya, O and Aboagye, SY and Williams, DL and Sun, J and Erzurum, S and de Jesus Perez, V and Oliveira, SD},
title = {Endothelial c-IAP2 Loss Amplifies P2X7 Receptor-Driven Inflammation and Worsens Infection-Associated Pulmonary Hypertension.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.05.22.655387},
pmid = {40502111},
issn = {2692-8205},
abstract = {Schistosomiasis-associated Pulmonary Hypertension (Sch-PH) is the most common form of group I PH worldwide. Recently, data revealed that the preclinical animal model of Sch-PH exhibited gut and lung microbiome dysbiosis linked to significant endothelial dysfunction and microvascular apoptosis, but the role of pro/anti-apoptosis sensors, such as the inhibitor of apoptosis protein 2 (c-IAP2) and purinergic receptor P2X7 (P2X7R), remained unclear. Using a novel Cdh5cre-ER [T2] ;cIAP1 [-/-] ;cIAP2 [fl/fl] animal model, this study investigated the contribution of endothelial c-IAP2 in this process, revealing P2X7R overexpression as a putative target in the onset of Sch-PH. Pharmacologically, inhibition of P2X7R function confirmed its role in promoting lung endothelial death and disease progression. Moreover, data suggest that microbiome-associated metabolic alterations in Sch-PH seem linked to microvascular endothelial apoptosis driven by ATP/P2X7R overactivation and suppressed c-IAP2 expression. Indeed, genetic ablation of endothelial c-IAP2 expression was sufficient to induce PH-like features in mice, with echocardiography indicating a higher pulmonary acceleration time (PAT), PAT/pulmonary ejection time (PET), and right ventricular free wall thickness after IP/IV-Egg challenge compared to controls. These findings suggest a significant contribution of lung endothelial P2X7R activation and c-IAP2 suppression to Sch-PH pathology, highlighting them as promising novel therapeutic targets for this life-threatening illness.},
}
RevDate: 2025-06-12
The Spinal Cord-Gut Axis Regulates Gut Microbial Homeostasis: Insights from a New Murine Metagenomic Catalog.
bioRxiv : the preprint server for biology pii:2025.05.27.656368.
The spinal cord, a nexus for brain-body crosstalk, controls gut physiology and microbial homeostasis. Here, >6,500 microbial metagenome-assembled genomes were recovered de novo , from male and female C57BL/6 mice gut metagenomes before and up to 6 months after disrupting the "spinal cord-gut axis". This "Mouse B6 Gut Catalog" improved or doubled species- and strain-level representation in other published catalogs. Analyses showed that breaking the spinal cord-gut axis caused persistent microbial changes that varied by sex, spinal lesion level, and time. A key bacterium, Lactobacillus johnsonii , was consistently reduced, and feeding this to mice with a clinically relevant spinal cord injury improved host health. Genome-resolved, community-contextualized metabolic profiling showed that spinal-dependent effects on microbe-encoded carbohydrate metabolism explain the reduction of L. johnsonii . These data improve murine microbiome catalogs and emphasize that mammalian health and gut ecosystem function depend on a functional spinal cord-gut axis.
Additional Links: PMID-40502000
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@article {pmid40502000,
year = {2025},
author = {Mohssen, M and Zayed, AA and Kigerl, KA and Du, J and Smith, GJ and Schwab, JM and Sullivan, MB and Popovich, PG},
title = {The Spinal Cord-Gut Axis Regulates Gut Microbial Homeostasis: Insights from a New Murine Metagenomic Catalog.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.05.27.656368},
pmid = {40502000},
issn = {2692-8205},
abstract = {The spinal cord, a nexus for brain-body crosstalk, controls gut physiology and microbial homeostasis. Here, >6,500 microbial metagenome-assembled genomes were recovered de novo , from male and female C57BL/6 mice gut metagenomes before and up to 6 months after disrupting the "spinal cord-gut axis". This "Mouse B6 Gut Catalog" improved or doubled species- and strain-level representation in other published catalogs. Analyses showed that breaking the spinal cord-gut axis caused persistent microbial changes that varied by sex, spinal lesion level, and time. A key bacterium, Lactobacillus johnsonii , was consistently reduced, and feeding this to mice with a clinically relevant spinal cord injury improved host health. Genome-resolved, community-contextualized metabolic profiling showed that spinal-dependent effects on microbe-encoded carbohydrate metabolism explain the reduction of L. johnsonii . These data improve murine microbiome catalogs and emphasize that mammalian health and gut ecosystem function depend on a functional spinal cord-gut axis.},
}
RevDate: 2025-06-12
Episymbiotic Saccharibacteria suppresses epithelial immunoactivation through Type IV pili and TLR2 dependent endocytosis.
bioRxiv : the preprint server for biology pii:2025.05.30.656655.
Saccharibacteria are episymbionts that require host-bacteria to grow. They are positively associated with inflammatory diseases within the human microbiome, yet their mechanisms for interacting with the human host and contributing to diseases remain unknown. This study investigated interactions between a Saccharibacterium (Nanosynbacter lyticus), its host-bacteria (Schaalia odontolytica), and oral epithelial cells. The host-bacteria induced proinflammatory cytokines in epithelial cells, while Saccharibacteria were immune silent. Remarkably, Saccharibacteria dampened cytokine responses to host-bacteria during coinfection. This effect was driven by Saccharibacteria-induced clustering of TLR2 receptors, a process likely facilitated by type IV, ultimately leading to reduced TLR2-mediated cytokine signalling. High resolution imaging showed that Saccharibacteria were endocytosed by oral epithelial cells, and colocalized with endosome markers, eventually trafficking to lysosomes. Moreover, a subset of the Saccharibacteria survive endocytosis long-term, and retains their capability to reinfect host-bacteria, highlighting a mechanism for persistence in the oral microbiome and a vital role in mammalian immune system modulation.
Additional Links: PMID-40501963
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@article {pmid40501963,
year = {2025},
author = {Chouhan, D and Grossman, AS and Kerns, KA and Stocke, KS and Kim, M and Dong, PT and Kumar, A and Lei, L and Lamont, RJ and McLean, JS and He, X and Bor, B},
title = {Episymbiotic Saccharibacteria suppresses epithelial immunoactivation through Type IV pili and TLR2 dependent endocytosis.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.05.30.656655},
pmid = {40501963},
issn = {2692-8205},
abstract = {Saccharibacteria are episymbionts that require host-bacteria to grow. They are positively associated with inflammatory diseases within the human microbiome, yet their mechanisms for interacting with the human host and contributing to diseases remain unknown. This study investigated interactions between a Saccharibacterium (Nanosynbacter lyticus), its host-bacteria (Schaalia odontolytica), and oral epithelial cells. The host-bacteria induced proinflammatory cytokines in epithelial cells, while Saccharibacteria were immune silent. Remarkably, Saccharibacteria dampened cytokine responses to host-bacteria during coinfection. This effect was driven by Saccharibacteria-induced clustering of TLR2 receptors, a process likely facilitated by type IV, ultimately leading to reduced TLR2-mediated cytokine signalling. High resolution imaging showed that Saccharibacteria were endocytosed by oral epithelial cells, and colocalized with endosome markers, eventually trafficking to lysosomes. Moreover, a subset of the Saccharibacteria survive endocytosis long-term, and retains their capability to reinfect host-bacteria, highlighting a mechanism for persistence in the oral microbiome and a vital role in mammalian immune system modulation.},
}
RevDate: 2025-06-12
Biomni: A General-Purpose Biomedical AI Agent.
bioRxiv : the preprint server for biology pii:2025.05.30.656746.
Biomedical research underpins progress in our understanding of human health and disease, drug discovery, and clinical care. However, with the growth of complex lab experiments, large datasets, many analytical tools, and expansive literature, biomedical research is increasingly constrained by repetitive and fragmented workflows that slow discovery and limit innovation, underscoring the need for a fundamentally new way to scale scientific expertise. Here, we introduce Biomni, a general-purpose biomedical AI agent designed to autonomously execute a wide spectrum of research tasks across diverse biomedical subfields. To systematically map the biomedical action space, Biomni first employs an action discovery agent to create the first unified agentic environment - mining essential tools, databases, and protocols from tens of thousands of publications across 25 biomedical domains. Built on this foundation, Biomni features a generalist agentic architecture that integrates large language model (LLM) reasoning with retrieval-augmented planning and code-based execution, enabling it to dynamically compose and carry out complex biomedical workflows - entirely without relying on predefined templates or rigid task flows. Systematic benchmarking demonstrates that Biomni achieves strong generalization across heterogeneous biomedical tasks - including causal gene prioritization, drug repurposing, rare disease diagnosis, micro-biome analysis, and molecular cloning - without any task-specific prompt tuning. Real-world case studies further showcase Biomni's ability to interpret complex, multi-modal biomedical datasets and autonomously generate experimentally testable protocols. Biomni envisions a future where virtual AI biologists operate alongside and augment human scientists to dramatically enhance research productivity, clinical insight, and healthcare. Biomni is ready to use at https://biomni.stanford.edu , and we invite scientists to explore its capabilities, stress-test its limits, and co-create the next era of biomedical discoveries.
Additional Links: PMID-40501924
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@article {pmid40501924,
year = {2025},
author = {Huang, K and Zhang, S and Wang, H and Qu, Y and Lu, Y and Roohani, Y and Li, R and Qiu, L and Li, G and Zhang, J and Yin, D and Marwaha, S and Carter, JN and Zhou, X and Wheeler, M and Bernstein, JA and Wang, M and He, P and Zhou, J and Snyder, M and Cong, L and Regev, A and Leskovec, J},
title = {Biomni: A General-Purpose Biomedical AI Agent.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.05.30.656746},
pmid = {40501924},
issn = {2692-8205},
abstract = {Biomedical research underpins progress in our understanding of human health and disease, drug discovery, and clinical care. However, with the growth of complex lab experiments, large datasets, many analytical tools, and expansive literature, biomedical research is increasingly constrained by repetitive and fragmented workflows that slow discovery and limit innovation, underscoring the need for a fundamentally new way to scale scientific expertise. Here, we introduce Biomni, a general-purpose biomedical AI agent designed to autonomously execute a wide spectrum of research tasks across diverse biomedical subfields. To systematically map the biomedical action space, Biomni first employs an action discovery agent to create the first unified agentic environment - mining essential tools, databases, and protocols from tens of thousands of publications across 25 biomedical domains. Built on this foundation, Biomni features a generalist agentic architecture that integrates large language model (LLM) reasoning with retrieval-augmented planning and code-based execution, enabling it to dynamically compose and carry out complex biomedical workflows - entirely without relying on predefined templates or rigid task flows. Systematic benchmarking demonstrates that Biomni achieves strong generalization across heterogeneous biomedical tasks - including causal gene prioritization, drug repurposing, rare disease diagnosis, micro-biome analysis, and molecular cloning - without any task-specific prompt tuning. Real-world case studies further showcase Biomni's ability to interpret complex, multi-modal biomedical datasets and autonomously generate experimentally testable protocols. Biomni envisions a future where virtual AI biologists operate alongside and augment human scientists to dramatically enhance research productivity, clinical insight, and healthcare. Biomni is ready to use at https://biomni.stanford.edu , and we invite scientists to explore its capabilities, stress-test its limits, and co-create the next era of biomedical discoveries.},
}
RevDate: 2025-06-12
Deep Coverage and Extended Sequence Reads Obtained with a Single Archaeal Protease Expedite de novo Protein Sequencing by Mass Spectrometry.
bioRxiv : the preprint server for biology pii:2025.05.26.656138.
The ability to sequence proteins without reliance on a genomic template defines a critical frontier in modern proteomics. This approach, known as de novo protein sequencing, is essential for applications such as antibody sequencing, microbiome proteomics, and antigen discovery, which require accurate reconstruction of peptide and protein sequences. While trypsin remains the gold-standard protease in proteomics, its restricted cleavage specificity limits peptide diversity. This constraint is especially problematic in antibody sequencing, where the functionally critical regions often lack canonical tryptic sites. As a result, exclusively trypsin-based approaches yield sparse reads, leading to sequence gaps. Multi-protease and hybrid-fragmentation strategies can improve the sequence coverage, but they add complexity, compromise scalability and reproducibility. Here, we explore two HyperThermoacidic Archaeal (HTA)-proteases as single-enzyme solutions for de novo antibody sequencing. Each HTA-protease generated about five times more unique peptide reads than trypsin or chymotrypsin, providing high redundancy across all CDRs. Combined with EAciD fragmentation on a ZenoTOF 7600 system, this approach enabled complete, unambiguous antibody sequencing. De novo analysis using PEAKS/DeepNovo and Stitch showed up to fourfold higher alignment scores and reduced the sequence errors within the HTA-generated data. Additionally, the HTA-EAciD approach offers short digestion times, eliminates extensive cleanup, and enables analysis in a single LC-MS/MS run. This streamlined, single-protease approach delivers therefore performance comparable to multi-enzyme workflows, offering a scalable and efficient strategy for de novo protein sequencing across diverse applications.
Additional Links: PMID-40501842
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@article {pmid40501842,
year = {2025},
author = {Shamorkina, TM and Pañeda, LP and Kadavá, T and Schulte, D and Pribil, P and Heidelberger, S and Narlock-Brand, AM and Yannone, SM and Snijder, J and Heck, AJR},
title = {Deep Coverage and Extended Sequence Reads Obtained with a Single Archaeal Protease Expedite de novo Protein Sequencing by Mass Spectrometry.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.05.26.656138},
pmid = {40501842},
issn = {2692-8205},
abstract = {The ability to sequence proteins without reliance on a genomic template defines a critical frontier in modern proteomics. This approach, known as de novo protein sequencing, is essential for applications such as antibody sequencing, microbiome proteomics, and antigen discovery, which require accurate reconstruction of peptide and protein sequences. While trypsin remains the gold-standard protease in proteomics, its restricted cleavage specificity limits peptide diversity. This constraint is especially problematic in antibody sequencing, where the functionally critical regions often lack canonical tryptic sites. As a result, exclusively trypsin-based approaches yield sparse reads, leading to sequence gaps. Multi-protease and hybrid-fragmentation strategies can improve the sequence coverage, but they add complexity, compromise scalability and reproducibility. Here, we explore two HyperThermoacidic Archaeal (HTA)-proteases as single-enzyme solutions for de novo antibody sequencing. Each HTA-protease generated about five times more unique peptide reads than trypsin or chymotrypsin, providing high redundancy across all CDRs. Combined with EAciD fragmentation on a ZenoTOF 7600 system, this approach enabled complete, unambiguous antibody sequencing. De novo analysis using PEAKS/DeepNovo and Stitch showed up to fourfold higher alignment scores and reduced the sequence errors within the HTA-generated data. Additionally, the HTA-EAciD approach offers short digestion times, eliminates extensive cleanup, and enables analysis in a single LC-MS/MS run. This streamlined, single-protease approach delivers therefore performance comparable to multi-enzyme workflows, offering a scalable and efficient strategy for de novo protein sequencing across diverse applications.},
}
RevDate: 2025-06-12
Linkage of nucleotide and functional diversity varies across gut bacteria.
bioRxiv : the preprint server for biology pii:2025.06.06.658399.
Understanding the forces shaping genomic diversity within bacterial species is essential for interpreting microbiome evolution, ecology, and host associations. Here, we analyze over one hundred prevalent gut bacterial species using the Unified Human Gut Genome (UHGG) collection to characterize patterns of intra-specific genomic variability. Gene content divergence scales predictably with divergence in core genome single nucleotide polymorphisms (SNPs), though there is substantial variability in evolutionary dynamics across species. Overall, accessory genes exhibit consistently faster linkage decay compared to core SNPs, highlighting the fluidity of functional repertoires within species boundaries. This signal is strongest for mobile genetic elements, which show minimal linkage to core genome SNPs. Together, our findings reveal species-specific recombination regimes in the gut microbiome, underscoring the importance of accounting for horizontal gene transfer and genome plasticity in microbiome-wide association studies and evolutionary models.
Additional Links: PMID-40501780
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@article {pmid40501780,
year = {2025},
author = {Dubinkina, V and Smith, B and Zhao, C and Pino, C and Pollard, KS},
title = {Linkage of nucleotide and functional diversity varies across gut bacteria.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.06.06.658399},
pmid = {40501780},
issn = {2692-8205},
abstract = {Understanding the forces shaping genomic diversity within bacterial species is essential for interpreting microbiome evolution, ecology, and host associations. Here, we analyze over one hundred prevalent gut bacterial species using the Unified Human Gut Genome (UHGG) collection to characterize patterns of intra-specific genomic variability. Gene content divergence scales predictably with divergence in core genome single nucleotide polymorphisms (SNPs), though there is substantial variability in evolutionary dynamics across species. Overall, accessory genes exhibit consistently faster linkage decay compared to core SNPs, highlighting the fluidity of functional repertoires within species boundaries. This signal is strongest for mobile genetic elements, which show minimal linkage to core genome SNPs. Together, our findings reveal species-specific recombination regimes in the gut microbiome, underscoring the importance of accounting for horizontal gene transfer and genome plasticity in microbiome-wide association studies and evolutionary models.},
}
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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.
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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.
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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.
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