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ESP: PubMed Auto Bibliography 12 Dec 2025 at 01:57 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: 2025-12-11
Ecological resilience of the rectal microbiome to environmental stressors in Hulunbuir grazing sheep: response to feed restriction and extreme cold challenge.
Journal of thermal biology, 134:104351 pii:S0306-4565(25)00308-0 [Epub ahead of print].
The gut microbiota is essential for helping animals to adapt to food shortages and extreme environments. In China's Hulunbuir region, local grazing sheep endure harsh winters characterized by intense cold and limited food supply. Uncovering the adaptive mechanisms that underpin their resilience is essential for improving their productivity, breeding practices, and management strategies. This research investigated the effects of feed restriction (set at 40 % of ad libitum intake) and extreme cold stress (temperature-humidity index set at 22.27) on the dynamics of gut microbiota in Hulunbuir sheep. We employed 16S rRNA gene sequencing to investigate alterations in rectal microbial diversity, community composition, and functional pathways in response to these stressors. Our findings revealed a significant reduction in bacterial diversity and microbial community structure in response to both stressors (P < 0.05), with cold stress exerting a more pronounced impact than feed restriction. Several key bacterial genera, including Akkermansia, Christensenellaceae, Monoglobus, Bacteroides, Alistipes, and Solibacillus, were identified as major contributors to the adaptive microbiota-drives responses of Hulunbuir sheep under environmental stress. A Spearman correlation analysis revealed strong associations between these genera and essential functional pathways such as fat digestion and absorption, quorum sensing, and mineral uptake, all of which were differentially regulated in response to stress (|r| > 0.6, Padj < 0.05). These findings offer novel insights into how the gut microbiota in Hulunbuir sheep supports physiological adaptation to extreme cold and nutritional stress, laying a robust foundation for creating microbiota-targeted strategies to enhance resilience, promote animal health, and improve productivity of grazing ruminants in harsh winter environments.
Additional Links: PMID-41380402
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@article {pmid41380402,
year = {2025},
author = {Huang, Q and Khan, NA and Tang, S and Zhou, C and He, Z and Tan, Z and Liu, Y},
title = {Ecological resilience of the rectal microbiome to environmental stressors in Hulunbuir grazing sheep: response to feed restriction and extreme cold challenge.},
journal = {Journal of thermal biology},
volume = {134},
number = {},
pages = {104351},
doi = {10.1016/j.jtherbio.2025.104351},
pmid = {41380402},
issn = {0306-4565},
abstract = {The gut microbiota is essential for helping animals to adapt to food shortages and extreme environments. In China's Hulunbuir region, local grazing sheep endure harsh winters characterized by intense cold and limited food supply. Uncovering the adaptive mechanisms that underpin their resilience is essential for improving their productivity, breeding practices, and management strategies. This research investigated the effects of feed restriction (set at 40 % of ad libitum intake) and extreme cold stress (temperature-humidity index set at 22.27) on the dynamics of gut microbiota in Hulunbuir sheep. We employed 16S rRNA gene sequencing to investigate alterations in rectal microbial diversity, community composition, and functional pathways in response to these stressors. Our findings revealed a significant reduction in bacterial diversity and microbial community structure in response to both stressors (P < 0.05), with cold stress exerting a more pronounced impact than feed restriction. Several key bacterial genera, including Akkermansia, Christensenellaceae, Monoglobus, Bacteroides, Alistipes, and Solibacillus, were identified as major contributors to the adaptive microbiota-drives responses of Hulunbuir sheep under environmental stress. A Spearman correlation analysis revealed strong associations between these genera and essential functional pathways such as fat digestion and absorption, quorum sensing, and mineral uptake, all of which were differentially regulated in response to stress (|r| > 0.6, Padj < 0.05). These findings offer novel insights into how the gut microbiota in Hulunbuir sheep supports physiological adaptation to extreme cold and nutritional stress, laying a robust foundation for creating microbiota-targeted strategies to enhance resilience, promote animal health, and improve productivity of grazing ruminants in harsh winter environments.},
}
RevDate: 2025-12-11
The impact of embryonic thermal manipulation on the microbiome of the jejunum and cecum in response to post-hatch acute heat stress.
Poultry science, 105(1):106212 pii:S0032-5791(25)01452-X [Epub ahead of print].
Thermal manipulation (TM) during embryogenesis has been proposed as a sustainable strategy to enhance thermotolerance and resilience in broiler chickens. However, its long-term Influence on gut microbiota composition, particularly under post-hatch acute heat stress (AHS), remains unclear. This study investigated the effects of TM on the jejunal and cecal microbiota of Ross broilers following AHS. Fertile eggs (n = 182) were incubated under standard conditions (37.8°C and 56 % relative humidity), while the thermally manipulated group (n = 182) was incubated at 38.5°C and 65 % relative humidity for 18 h/day during embryonic days 10-18. On day 35 post-hatch, birds were exposed to 35°C and 60-65 % RH for three hours to induce AHS, and jejunal and cecal contents were analyzed by 16S rRNA gene sequencing (V3-V4 region, Illumina MiSeq). Alpha diversity indices (Shannon, evenness) did not differ significantly between treatments (P > 0.05), although the cecum consistently exhibited higher richness and evenness than the jejunum (P < 0.05). Beta diversity analysis revealed strong separation between intestinal segments but no treatment-driven clustering. Firmicutes and Bacteroidota dominated all groups, with regional enrichment of Lactobacillus and Ligilactobacillus in the jejunum, and Faecalibacterium in the cecum. Differential abundance analysis revealed 30 taxa that differed significantly (q < 0.05) at the family level across intestinal segments. In contrast, comparing the TM, AHS, and control groups within any single segment yielded no significant taxonomic differences after false discovery rate (FDR) correction. These results indicate that anatomical location within the intestine exerts a more substantial influence on microbial community composition than either embryonic or post-hatch heat exposure. The stability of microbial diversity under acute thermal challenge suggests that the beneficial effects of TM on thermotolerance, as reported in the literature, are likely mediated through host physiological or epigenetic mechanisms rather than microbiome remodeling.
Additional Links: PMID-41380320
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@article {pmid41380320,
year = {2025},
author = {Hundam, S and Al-Zghoul, MB and Almaasfeh, M},
title = {The impact of embryonic thermal manipulation on the microbiome of the jejunum and cecum in response to post-hatch acute heat stress.},
journal = {Poultry science},
volume = {105},
number = {1},
pages = {106212},
doi = {10.1016/j.psj.2025.106212},
pmid = {41380320},
issn = {1525-3171},
abstract = {Thermal manipulation (TM) during embryogenesis has been proposed as a sustainable strategy to enhance thermotolerance and resilience in broiler chickens. However, its long-term Influence on gut microbiota composition, particularly under post-hatch acute heat stress (AHS), remains unclear. This study investigated the effects of TM on the jejunal and cecal microbiota of Ross broilers following AHS. Fertile eggs (n = 182) were incubated under standard conditions (37.8°C and 56 % relative humidity), while the thermally manipulated group (n = 182) was incubated at 38.5°C and 65 % relative humidity for 18 h/day during embryonic days 10-18. On day 35 post-hatch, birds were exposed to 35°C and 60-65 % RH for three hours to induce AHS, and jejunal and cecal contents were analyzed by 16S rRNA gene sequencing (V3-V4 region, Illumina MiSeq). Alpha diversity indices (Shannon, evenness) did not differ significantly between treatments (P > 0.05), although the cecum consistently exhibited higher richness and evenness than the jejunum (P < 0.05). Beta diversity analysis revealed strong separation between intestinal segments but no treatment-driven clustering. Firmicutes and Bacteroidota dominated all groups, with regional enrichment of Lactobacillus and Ligilactobacillus in the jejunum, and Faecalibacterium in the cecum. Differential abundance analysis revealed 30 taxa that differed significantly (q < 0.05) at the family level across intestinal segments. In contrast, comparing the TM, AHS, and control groups within any single segment yielded no significant taxonomic differences after false discovery rate (FDR) correction. These results indicate that anatomical location within the intestine exerts a more substantial influence on microbial community composition than either embryonic or post-hatch heat exposure. The stability of microbial diversity under acute thermal challenge suggests that the beneficial effects of TM on thermotolerance, as reported in the literature, are likely mediated through host physiological or epigenetic mechanisms rather than microbiome remodeling.},
}
RevDate: 2025-12-11
Metagenomic insights into rhizosphere microbiome dynamics of Oenanthe javanica in ecological floating beds under different hydrodynamic regimes.
Journal of contaminant hydrology, 277:104795 pii:S0169-7722(25)00300-6 [Epub ahead of print].
Ecological floating beds (EFBs) are a cost-effective and sustainable technology that utilizes macrophyte to remove nutrients from aquatic ecosystems, where rhizosphere bacterial degradation and assimilation play a key role in nutrient removal. However, the current knowledge about how hydrodynamic regimes impact the rhizosphere bacterial community on EFB systems remains limited. Here, we investigated the effects of different hydrodynamic regimes (i.e., stagnant water, pulsed water, and flowing water conditions) on the rhizosphere bacterial community structure and function of Oenanthe javanica in an experimental EFB system based on metagenomic sequencing. We observed that bacterial community compositions on the roots of O. javanica were significantly differed across the three hydrodynamic regimes, with the highest bacterial biodiversity captured from the flowing water condition. Moreover, a total of 65 nitrogen functional genes (NFGs) were identified in the rhizosphere bacterial community, with nitrate reduction pathways dominating the nitrogen cycling processes. In contrast, totally 139 phosphorus functional genes (PFGs) were detected, primarily involved in purine metabolism, which drove the phosphorus cycling dynamics. We found the distinct nitrogen and phosphorus metabolic strategies of rhizosphere bacterial communities in response to hydrodynamic regime changes. Specifically, the relative abundances of NFGs like nasB, narl, and ansB were significantly increased under the pulsed water condition, whereas gdh_K00262 were relative abundant under the flowing condition. Moreover, pulsed water condition promoted the relative abundances of PFGs such asas phnC, phoD, and pgtP in rhizosphere bacterial communities, in contrast to the stagnant condition, which favored genes like ugpC, purK, phoH, and purA. Our study offers technical support for regulating plant degradation of pollutants to improve EFB's performance in engineering applications.
Additional Links: PMID-41380282
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@article {pmid41380282,
year = {2025},
author = {Xu, X and Wang, J and Deng, C and Yu, X and Nie, R and Wang, S and Huang, W},
title = {Metagenomic insights into rhizosphere microbiome dynamics of Oenanthe javanica in ecological floating beds under different hydrodynamic regimes.},
journal = {Journal of contaminant hydrology},
volume = {277},
number = {},
pages = {104795},
doi = {10.1016/j.jconhyd.2025.104795},
pmid = {41380282},
issn = {1873-6009},
abstract = {Ecological floating beds (EFBs) are a cost-effective and sustainable technology that utilizes macrophyte to remove nutrients from aquatic ecosystems, where rhizosphere bacterial degradation and assimilation play a key role in nutrient removal. However, the current knowledge about how hydrodynamic regimes impact the rhizosphere bacterial community on EFB systems remains limited. Here, we investigated the effects of different hydrodynamic regimes (i.e., stagnant water, pulsed water, and flowing water conditions) on the rhizosphere bacterial community structure and function of Oenanthe javanica in an experimental EFB system based on metagenomic sequencing. We observed that bacterial community compositions on the roots of O. javanica were significantly differed across the three hydrodynamic regimes, with the highest bacterial biodiversity captured from the flowing water condition. Moreover, a total of 65 nitrogen functional genes (NFGs) were identified in the rhizosphere bacterial community, with nitrate reduction pathways dominating the nitrogen cycling processes. In contrast, totally 139 phosphorus functional genes (PFGs) were detected, primarily involved in purine metabolism, which drove the phosphorus cycling dynamics. We found the distinct nitrogen and phosphorus metabolic strategies of rhizosphere bacterial communities in response to hydrodynamic regime changes. Specifically, the relative abundances of NFGs like nasB, narl, and ansB were significantly increased under the pulsed water condition, whereas gdh_K00262 were relative abundant under the flowing condition. Moreover, pulsed water condition promoted the relative abundances of PFGs such asas phnC, phoD, and pgtP in rhizosphere bacterial communities, in contrast to the stagnant condition, which favored genes like ugpC, purK, phoH, and purA. Our study offers technical support for regulating plant degradation of pollutants to improve EFB's performance in engineering applications.},
}
RevDate: 2025-12-11
The effect of maternal exposure to Tris(n-butyl) phosphate on the gut microbiome of SD rats and offspring.
Journal of hazardous materials, 501:140763 pii:S0304-3894(25)03683-0 [Epub ahead of print].
Tris (n-butyl) phosphate (TnBP), a heavily utilized organophosphate ester, remains poorly characterized with respect to its long-term effects on the structure and metabolic capacity of the gut microbiota. The purpose of this study is to explore how TnBP exposure affects the intestinal microbiota of maternal Sprague-Dawley (SD) rats and their corresponding progeny, as well as the impact of its metabolite, dibutyl phosphate (DBP), in the human population. A cross-sectional analysis revealed a significant positive correlation between DBP concentrations and the C-reactive protein/albumin ratio (CAR) in the United States population. Results of 16S rRNA gene sequencing revealed that maternal TnBP exposure significantly increased gut bacterial α-diversity in both dams and their F1-generation offspring (Shannon index, P < 0.05). Principal-coordinate analysis (PCoA) based on Bray-Curtis dissimilarity showed distinct clustering of the microbial communities, and PERMANOVA confirmed significant differences between the exposed and control groupsAt the phylum level, TnBP exposure elicited a proportional expansion of Proteobacteria coupled with concomitant reductions in Bacillota and Bacteroidetes in both dams and their F1 offspring. Genus-level profiling further revealed a selective enrichment of Bifidobacterium and significant perturbations in Lactobacillus, Limosilactobacillus, Muribaculum, Turicibacter, Allobaculum, and Clostridium.Furthermore, TnBP exposure significantly elevated total short-chain fatty acid (SCFA) levels in the offspring, indicating a functional shift in microbial metabolism. Correlation analysis further revealed that under TnBP treatment the relative abundances of Allobaculum and Collinsella were positively associated with the concentrations of acetate, propionate, and butyrate (P < 0.05 for each). Quantitative PCR and histopathological examination collectively demonstrated a pronounced inflammatory signature in the colons of juvenile offspring exposed to TnBP. These observations underscore the potential for persistent adverse health outcomes following developmental exposure and warrant comprehensive mechanistic and epidemiological investigations.
Additional Links: PMID-41380257
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PubMed:
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@article {pmid41380257,
year = {2025},
author = {Zeng, C and Wu, D and Yang, J and Chen, J and Tan, C and Wang, D and Zhang, G},
title = {The effect of maternal exposure to Tris(n-butyl) phosphate on the gut microbiome of SD rats and offspring.},
journal = {Journal of hazardous materials},
volume = {501},
number = {},
pages = {140763},
doi = {10.1016/j.jhazmat.2025.140763},
pmid = {41380257},
issn = {1873-3336},
abstract = {Tris (n-butyl) phosphate (TnBP), a heavily utilized organophosphate ester, remains poorly characterized with respect to its long-term effects on the structure and metabolic capacity of the gut microbiota. The purpose of this study is to explore how TnBP exposure affects the intestinal microbiota of maternal Sprague-Dawley (SD) rats and their corresponding progeny, as well as the impact of its metabolite, dibutyl phosphate (DBP), in the human population. A cross-sectional analysis revealed a significant positive correlation between DBP concentrations and the C-reactive protein/albumin ratio (CAR) in the United States population. Results of 16S rRNA gene sequencing revealed that maternal TnBP exposure significantly increased gut bacterial α-diversity in both dams and their F1-generation offspring (Shannon index, P < 0.05). Principal-coordinate analysis (PCoA) based on Bray-Curtis dissimilarity showed distinct clustering of the microbial communities, and PERMANOVA confirmed significant differences between the exposed and control groupsAt the phylum level, TnBP exposure elicited a proportional expansion of Proteobacteria coupled with concomitant reductions in Bacillota and Bacteroidetes in both dams and their F1 offspring. Genus-level profiling further revealed a selective enrichment of Bifidobacterium and significant perturbations in Lactobacillus, Limosilactobacillus, Muribaculum, Turicibacter, Allobaculum, and Clostridium.Furthermore, TnBP exposure significantly elevated total short-chain fatty acid (SCFA) levels in the offspring, indicating a functional shift in microbial metabolism. Correlation analysis further revealed that under TnBP treatment the relative abundances of Allobaculum and Collinsella were positively associated with the concentrations of acetate, propionate, and butyrate (P < 0.05 for each). Quantitative PCR and histopathological examination collectively demonstrated a pronounced inflammatory signature in the colons of juvenile offspring exposed to TnBP. These observations underscore the potential for persistent adverse health outcomes following developmental exposure and warrant comprehensive mechanistic and epidemiological investigations.},
}
RevDate: 2025-12-11
The Gut Microbiome and Butyrate Differentiate Clostridioides difficile Colonization and Infection in Children.
The Journal of infectious diseases pii:8377423 [Epub ahead of print].
BACKGROUND AND AIMS: Symptomatic Clostridioides difficile infection (CDI) can cause significant morbidity and mortality. Conversely, patients can be colonized with toxigenic C. difficile in the absence of symptoms, termed asymptomatic colonization. We previously demonstrated that the presence and function of C. difficile toxins do not differentiate between asymptomatic colonization and CDI in children, suggesting the influence of other factors. This study aimed to interrogate the intestinal microbiome and butyrate in stool samples from children with CDI and asymptomatic colonization.
METHODS: Design: Case-control studySetting: Tertiary care children's hospitalParticipants and measures: Asymptomatic children had stool tested for C. difficile by nucleic-acid amplification-based testing (NAAT) and were considered colonized if positive (N=50). Residual stool was also obtained from symptomatic children who tested positive for C. difficile by NAAT (N=55). The microbiome was assessed via 16S rRNA sequencing and butyrate via liquid chromatography-mass spectrometry.
RESULTS: Compared to clinical co-variates and comorbidities, C. difficile symptom status (i.e., asymptomatic colonization versus symptomatic CDI) demonstrated the strongest differential abundance association on gut microbes. Symptomatic CDI was associated with increased abundance of Escherichia/Shigella (Benjamini-Hochberg adjusted q=3.94x10-5), Haemophilus (q=0.022), and Gemella (q=0.085), and depleted abundance of gut commensals such as Faecalibacterium (q=0.041), Blautia (q=0.041), and Bifidobacterium (q=0.063). We also observed depletion in the abundance of microbial butyrate producers and fecal butyrate in participants with symptomatic CDI versus asymptomatic colonization.
CONCLUSION: The gut microbiota and butyrate differ between participants with asymptomatic C. difficile colonization and symptomatic CDI, suggesting their potential role in symptom development.
Additional Links: PMID-41379981
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@article {pmid41379981,
year = {2025},
author = {Nicholson, MR and Ma, S and Strickland, BA and Cecala, M and Zhang, L and Reasoner, S and Guiberson, ER and Munneke, MJ and Shilts, MH and Skaar, EP and Das, SR},
title = {The Gut Microbiome and Butyrate Differentiate Clostridioides difficile Colonization and Infection in Children.},
journal = {The Journal of infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/infdis/jiaf631},
pmid = {41379981},
issn = {1537-6613},
abstract = {BACKGROUND AND AIMS: Symptomatic Clostridioides difficile infection (CDI) can cause significant morbidity and mortality. Conversely, patients can be colonized with toxigenic C. difficile in the absence of symptoms, termed asymptomatic colonization. We previously demonstrated that the presence and function of C. difficile toxins do not differentiate between asymptomatic colonization and CDI in children, suggesting the influence of other factors. This study aimed to interrogate the intestinal microbiome and butyrate in stool samples from children with CDI and asymptomatic colonization.
METHODS: Design: Case-control studySetting: Tertiary care children's hospitalParticipants and measures: Asymptomatic children had stool tested for C. difficile by nucleic-acid amplification-based testing (NAAT) and were considered colonized if positive (N=50). Residual stool was also obtained from symptomatic children who tested positive for C. difficile by NAAT (N=55). The microbiome was assessed via 16S rRNA sequencing and butyrate via liquid chromatography-mass spectrometry.
RESULTS: Compared to clinical co-variates and comorbidities, C. difficile symptom status (i.e., asymptomatic colonization versus symptomatic CDI) demonstrated the strongest differential abundance association on gut microbes. Symptomatic CDI was associated with increased abundance of Escherichia/Shigella (Benjamini-Hochberg adjusted q=3.94x10-5), Haemophilus (q=0.022), and Gemella (q=0.085), and depleted abundance of gut commensals such as Faecalibacterium (q=0.041), Blautia (q=0.041), and Bifidobacterium (q=0.063). We also observed depletion in the abundance of microbial butyrate producers and fecal butyrate in participants with symptomatic CDI versus asymptomatic colonization.
CONCLUSION: The gut microbiota and butyrate differ between participants with asymptomatic C. difficile colonization and symptomatic CDI, suggesting their potential role in symptom development.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Microbial dysbiosis and host-microbe interactions in proliferative verrucous leukoplakia: insights into carcinogenic potential.
Archives of microbiology, 208(1):65.
Proliferative verrucous leukoplakia (PVL) is a rare and aggressive oral potentially malignant disorder (OPMD) characterized by multifocal keratotic plaques, progressive expansion, high recurrence, and a strong risk of malignant transformation. Although its etiology remains unclear, recent evidence emphasizes the role of the oral microbiome as a key factor in disease progression. Alterations in microbial diversity and ecological balance create a shift toward dysbiosis, supporting a chronic inflammatory microenvironment that favors epithelial transformation. Specific taxa, including Fusobacterium and Porphyromonas, have been implicated in biofilm formation, immune evasion, and modulation of epithelial signaling pathways. These interactions highlight the potential of microbial communities to drive oncogenic processes through host-microbe crosstalk. Advanced methodological approaches such as metagenomics, functional microbiome profiling, and multi-omics integration provide novel opportunities to unravel the mechanisms of dysbiosis in PVL. Beyond pathogenesis, microbiome research opens perspectives for the identification of predictive biomarkers, targeted prevention, and microbiome-based therapeutics. This review synthesizes current insights into the microbial basis of PVL and outlines future directions aimed at improving understanding of host-microbe interactions and their role in oral carcinogenesis. Relevant literature was identified through PubMed and Web of Science searches (1985-2025) using terms related to PVL, oral leukoplakia, OPMD, oral microbiome, and oral squamous cell carcinoma. In conclusion, current evidence suggests that while microbial dysbiosis is not an isolated driver, it likely synergizes with genetic, epigenetic, and immunological factors in PVL progression, offering opportunities for biomarker discovery and novel therapeutic strategies. This study also provides a potential direction for the early diagnosis of PVL and the development of microecologically targeted interventions.
Additional Links: PMID-41379255
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@article {pmid41379255,
year = {2025},
author = {Špiljak, B and Ozretić, P and Brailo, V and Škrinjar, I and Lončar Brzak, B and Andabak Rogulj, A and Butić, I and Tambić Andrašević, A and Vidović Juras, D},
title = {Microbial dysbiosis and host-microbe interactions in proliferative verrucous leukoplakia: insights into carcinogenic potential.},
journal = {Archives of microbiology},
volume = {208},
number = {1},
pages = {65},
pmid = {41379255},
issn = {1432-072X},
mesh = {Humans ; *Dysbiosis/microbiology ; *Leukoplakia, Oral/microbiology/pathology ; Microbiota ; *Host Microbial Interactions ; Carcinogenesis ; Mouth Neoplasms/microbiology/pathology ; },
abstract = {Proliferative verrucous leukoplakia (PVL) is a rare and aggressive oral potentially malignant disorder (OPMD) characterized by multifocal keratotic plaques, progressive expansion, high recurrence, and a strong risk of malignant transformation. Although its etiology remains unclear, recent evidence emphasizes the role of the oral microbiome as a key factor in disease progression. Alterations in microbial diversity and ecological balance create a shift toward dysbiosis, supporting a chronic inflammatory microenvironment that favors epithelial transformation. Specific taxa, including Fusobacterium and Porphyromonas, have been implicated in biofilm formation, immune evasion, and modulation of epithelial signaling pathways. These interactions highlight the potential of microbial communities to drive oncogenic processes through host-microbe crosstalk. Advanced methodological approaches such as metagenomics, functional microbiome profiling, and multi-omics integration provide novel opportunities to unravel the mechanisms of dysbiosis in PVL. Beyond pathogenesis, microbiome research opens perspectives for the identification of predictive biomarkers, targeted prevention, and microbiome-based therapeutics. This review synthesizes current insights into the microbial basis of PVL and outlines future directions aimed at improving understanding of host-microbe interactions and their role in oral carcinogenesis. Relevant literature was identified through PubMed and Web of Science searches (1985-2025) using terms related to PVL, oral leukoplakia, OPMD, oral microbiome, and oral squamous cell carcinoma. In conclusion, current evidence suggests that while microbial dysbiosis is not an isolated driver, it likely synergizes with genetic, epigenetic, and immunological factors in PVL progression, offering opportunities for biomarker discovery and novel therapeutic strategies. This study also provides a potential direction for the early diagnosis of PVL and the development of microecologically targeted interventions.},
}
MeSH Terms:
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Humans
*Dysbiosis/microbiology
*Leukoplakia, Oral/microbiology/pathology
Microbiota
*Host Microbial Interactions
Carcinogenesis
Mouth Neoplasms/microbiology/pathology
RevDate: 2025-12-11
CmpDate: 2025-12-11
Comparative metagenomic analysis of bacterial communities associated with two mealybug species, Phenacoccus saccharifolii and Dysmicoccus carens infesting sugarcane in Tamil Nadu, India.
World journal of microbiology & biotechnology, 41(12):504.
This study presents a comparative metagenomic analysis of the gut bacterial communities of two sugarcane-infesting mealybug species, Phenacoccus saccharifolii (WR) and Dysmicoccus carens (RR), from Tamil Nadu, India. Using Oxford Nanopore sequencing of the 16s rRNA gene spanning the hypervariable regions V1 - V9 and predictive metagenomics, differences in microbial diversity, taxonomy, and functional potential were assessed to explore the ecological adaptations of the gut microbiota in mealybugs. The D. carens gut microbiome showed higher species richness than P. saccharifolii (WR) (125 vs. 45 species, p < 0.05) but lower community evenness (0.43 vs. 0.61, p < 0.05), resulting in similar overall Shannon diversity (2.08 vs. 2.30) despite markedly different community structures, which may be influenced by their different feeding niches, including the sugarcane crown region, leaf sheath tissues, and basal stem and root portions. Both mealybug species exhibited contrasting bacterial community structures. D. carens (RR) harbored high abundances of endosymbionts (43.8%), Gilliamella (22.3%), Enterobacter (18.3%), and Candidatus Tremblaya (9.3%), representing a symbiont-dominated microbiome typical of many hemipteran insects. P. saccharifolii (WR) displayed a distinct profile with Serratia as the dominant genus (43.2%), followed by Enterobacter (20.1%), Klebsiella (14.6%), and substantially reduced endosymbiont abundances (14.8%). Beta diversity analysis revealed distinct community clustering of species, highlighting the variation driven by feeding habitat and host genotype. Functional profiling indicated largely conserved metabolic capabilities dominated by amino acid and carbohydrate metabolism, which was a key to compensate the nutrient-poor phloem sap diet. The core microbiome identified several genera that form complex ecological networks, emphasizing their importance in community stability. These findings provide insights into the role of symbiotic bacteria in mealybug adaptation to different ecological niches within the sugarcane agroecosystem. Understanding these host-microbiome interactions may facilitate the development of targeted, microbiome-based biocontrol strategies for sustainable mealybug management in sugarcane cultivation.
Additional Links: PMID-41379245
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@article {pmid41379245,
year = {2025},
author = {Namadara, S and Pragadeesh, ARU and Uthandi, S and Rangasamy, A and Malaichamy, K and Venkatesan, M and Narayanan, MB and Murugaiyan, S},
title = {Comparative metagenomic analysis of bacterial communities associated with two mealybug species, Phenacoccus saccharifolii and Dysmicoccus carens infesting sugarcane in Tamil Nadu, India.},
journal = {World journal of microbiology & biotechnology},
volume = {41},
number = {12},
pages = {504},
pmid = {41379245},
issn = {1573-0972},
support = {DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; DABC/CPN001/ Kothari sugars-AGM,DNRM,CBE/2024//kothari sugars/ ; },
mesh = {*Saccharum/parasitology ; Animals ; India ; *Bacteria/classification/genetics/isolation & purification ; *Hemiptera/microbiology ; RNA, Ribosomal, 16S/genetics ; *Metagenomics/methods ; *Gastrointestinal Microbiome/genetics ; Phylogeny ; DNA, Bacterial/genetics ; },
abstract = {This study presents a comparative metagenomic analysis of the gut bacterial communities of two sugarcane-infesting mealybug species, Phenacoccus saccharifolii (WR) and Dysmicoccus carens (RR), from Tamil Nadu, India. Using Oxford Nanopore sequencing of the 16s rRNA gene spanning the hypervariable regions V1 - V9 and predictive metagenomics, differences in microbial diversity, taxonomy, and functional potential were assessed to explore the ecological adaptations of the gut microbiota in mealybugs. The D. carens gut microbiome showed higher species richness than P. saccharifolii (WR) (125 vs. 45 species, p < 0.05) but lower community evenness (0.43 vs. 0.61, p < 0.05), resulting in similar overall Shannon diversity (2.08 vs. 2.30) despite markedly different community structures, which may be influenced by their different feeding niches, including the sugarcane crown region, leaf sheath tissues, and basal stem and root portions. Both mealybug species exhibited contrasting bacterial community structures. D. carens (RR) harbored high abundances of endosymbionts (43.8%), Gilliamella (22.3%), Enterobacter (18.3%), and Candidatus Tremblaya (9.3%), representing a symbiont-dominated microbiome typical of many hemipteran insects. P. saccharifolii (WR) displayed a distinct profile with Serratia as the dominant genus (43.2%), followed by Enterobacter (20.1%), Klebsiella (14.6%), and substantially reduced endosymbiont abundances (14.8%). Beta diversity analysis revealed distinct community clustering of species, highlighting the variation driven by feeding habitat and host genotype. Functional profiling indicated largely conserved metabolic capabilities dominated by amino acid and carbohydrate metabolism, which was a key to compensate the nutrient-poor phloem sap diet. The core microbiome identified several genera that form complex ecological networks, emphasizing their importance in community stability. These findings provide insights into the role of symbiotic bacteria in mealybug adaptation to different ecological niches within the sugarcane agroecosystem. Understanding these host-microbiome interactions may facilitate the development of targeted, microbiome-based biocontrol strategies for sustainable mealybug management in sugarcane cultivation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Saccharum/parasitology
Animals
India
*Bacteria/classification/genetics/isolation & purification
*Hemiptera/microbiology
RNA, Ribosomal, 16S/genetics
*Metagenomics/methods
*Gastrointestinal Microbiome/genetics
Phylogeny
DNA, Bacterial/genetics
RevDate: 2025-12-11
CmpDate: 2025-12-11
EFFICACY OF PROBIOTICS IN PREVENTING CHEMOTHERAPY-INDUCED DIARRHEA IN GASTROINTESTINAL CANCER PATIENTS.
Arquivos de gastroenterologia, 62:e25020 pii:S0004-28032025000100211.
BACKGROUND: Chemotherapy-induced diarrhea is a common and distressing side effect experienced by patients undergoing cancer treatment, particularly those with gastrointestinal cancer. It can lead to significant health complications, including dehydration, electrolyte imbalances, and treatment interruptions. Recent studies have shown that the gut microbiome plays an important role in the development and severity of chemotherapy-induced diarrhea. Modulating the gut microbiome with probiotics has emerged as a potential strategy for preventing and managing chemotherapy-induced diarrhea.
OBJECTIVE: In this study we aimed to evaluate the efficacy of one probiotic containing a mixture of several strains of Lactobacillus and Bifidobacterium species in prevention of chemotherapy induced diarrhea among patients with gastrointestinal cancer.
METHODS: Between April 2022 and June 2024, a total of 28 patients diagnosed with gastrointestinal cancer who were intended to receive chemotherapy based on fluoropyrimidine, oxaliplatin, and/or irinotecan were randomized in a ratio 1:1 to receive either a placebo or 20 billion colony-forming units (CFU) of a mixture containing five viable strains including 335 mg of Lactobacillus acidophilus NCFM®, Lactobacillus paracasei Lpc-37TM, Bifidobacterium lactis Bi-04TM, Bifidobacterium lactis Bi-07TM, and Bifidobacterium bifidum Bb-02TM. Patients were instructed to take the product orally once daily for 90 days and to record their bowel habits in a diary using the Bristol stool scale.
RESULTS: The use of probiotics, compared to placebo, did not result in reduction of grade 2/3 diarrhea episodes (placebo arm 55.56% vs probiotic arm 44.44%; P=1). Likewise, no statistically significant difference was observed in the overall incidence of diarrhea between the two groups (71.43% vs 64.29%; P=1). The median number of diarrhea episodes during the 90-day follow-up tended to be lower in the probiotic group (eight episodes) compared to the placebo group (9 episodes) (P=0.639) Subgroup analyses failed to identify any specific patient characteristics that associated any benefit from the probiotic use, regardless of diarrhea grade. Also, no infections related to the probiotic strains administered in this study were detected.
CONCLUSION: Probiotic in comparison to a placebo did not result in a statistically significant effect, suggesting a lack of benefit of administered probiotic for prevention of chemotherapy induced diarrhea among patients with gastrointestinal cancer.
Additional Links: PMID-41379184
Publisher:
PubMed:
Citation:
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@article {pmid41379184,
year = {2025},
author = {DE Souza, GC and Araujo Filho, HB and DE Oliveira, CZ and Paiotti, APR and Forones, NM},
title = {EFFICACY OF PROBIOTICS IN PREVENTING CHEMOTHERAPY-INDUCED DIARRHEA IN GASTROINTESTINAL CANCER PATIENTS.},
journal = {Arquivos de gastroenterologia},
volume = {62},
number = {},
pages = {e25020},
doi = {10.1590/S0004-2803.24612025-020},
pmid = {41379184},
issn = {1678-4219},
mesh = {Humans ; *Probiotics/therapeutic use ; *Diarrhea/prevention & control/chemically induced ; Female ; Male ; Middle Aged ; *Gastrointestinal Neoplasms/drug therapy ; Aged ; Treatment Outcome ; *Antineoplastic Agents/adverse effects ; Bifidobacterium ; Lactobacillus ; Gastrointestinal Microbiome/drug effects ; Adult ; Double-Blind Method ; },
abstract = {BACKGROUND: Chemotherapy-induced diarrhea is a common and distressing side effect experienced by patients undergoing cancer treatment, particularly those with gastrointestinal cancer. It can lead to significant health complications, including dehydration, electrolyte imbalances, and treatment interruptions. Recent studies have shown that the gut microbiome plays an important role in the development and severity of chemotherapy-induced diarrhea. Modulating the gut microbiome with probiotics has emerged as a potential strategy for preventing and managing chemotherapy-induced diarrhea.
OBJECTIVE: In this study we aimed to evaluate the efficacy of one probiotic containing a mixture of several strains of Lactobacillus and Bifidobacterium species in prevention of chemotherapy induced diarrhea among patients with gastrointestinal cancer.
METHODS: Between April 2022 and June 2024, a total of 28 patients diagnosed with gastrointestinal cancer who were intended to receive chemotherapy based on fluoropyrimidine, oxaliplatin, and/or irinotecan were randomized in a ratio 1:1 to receive either a placebo or 20 billion colony-forming units (CFU) of a mixture containing five viable strains including 335 mg of Lactobacillus acidophilus NCFM®, Lactobacillus paracasei Lpc-37TM, Bifidobacterium lactis Bi-04TM, Bifidobacterium lactis Bi-07TM, and Bifidobacterium bifidum Bb-02TM. Patients were instructed to take the product orally once daily for 90 days and to record their bowel habits in a diary using the Bristol stool scale.
RESULTS: The use of probiotics, compared to placebo, did not result in reduction of grade 2/3 diarrhea episodes (placebo arm 55.56% vs probiotic arm 44.44%; P=1). Likewise, no statistically significant difference was observed in the overall incidence of diarrhea between the two groups (71.43% vs 64.29%; P=1). The median number of diarrhea episodes during the 90-day follow-up tended to be lower in the probiotic group (eight episodes) compared to the placebo group (9 episodes) (P=0.639) Subgroup analyses failed to identify any specific patient characteristics that associated any benefit from the probiotic use, regardless of diarrhea grade. Also, no infections related to the probiotic strains administered in this study were detected.
CONCLUSION: Probiotic in comparison to a placebo did not result in a statistically significant effect, suggesting a lack of benefit of administered probiotic for prevention of chemotherapy induced diarrhea among patients with gastrointestinal cancer.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Probiotics/therapeutic use
*Diarrhea/prevention & control/chemically induced
Female
Male
Middle Aged
*Gastrointestinal Neoplasms/drug therapy
Aged
Treatment Outcome
*Antineoplastic Agents/adverse effects
Bifidobacterium
Lactobacillus
Gastrointestinal Microbiome/drug effects
Adult
Double-Blind Method
RevDate: 2025-12-11
CmpDate: 2025-12-11
Community Modeling Reveals Disrupted Gut Microbial Secretion in Autism Associated With Redox and Neurometabolic Alterations.
Biotechnology journal, 20(12):e70164.
Emerging evidence suggests that disruptions in the gut microbiome may influence autism spectrum disorder (ASD) through altered microbial metabolism and gut-brain communication. However, the specific metabolic impacts of these microbial changes remain unclear. Community-scale metabolic modeling was applied to shotgun metagenomics data from children with ASD and neurotypical controls to predict secretion of host-impacting metabolites. Modeled ASD-associated communities exhibited altered predicted secretion of metabolites related to redox balance and neurotransmission, including increased 2-ketobutyrate and GABA and reduced riboflavin and inositol, with microbiota transfer therapy (MTT) shifting these profiles toward NT. Empirical fecal metabolomics data showed generally consistent directional trends with model predictions. Reductions in autism severity scores following MTT were associated with increased predicted secretion potentials for inositol and arginine. Taxonomic analysis revealed a depletion of beneficial and an enrichment of pro-inflammatory species, such as Escherichia and Flavonifractor, in ASD. Associations between microbial taxa (e.g., Bacteroides, Bifidobacterium) and neuroactive metabolites highlight microbial modulation as a promising therapeutic strategy in ASD. These results emphasize microbial metabolism as a contributor to ASD traits and a target for therapeutic intervention.
Additional Links: PMID-41379027
Publisher:
PubMed:
Citation:
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@article {pmid41379027,
year = {2025},
author = {Esvap, E and Ulgen, KO},
title = {Community Modeling Reveals Disrupted Gut Microbial Secretion in Autism Associated With Redox and Neurometabolic Alterations.},
journal = {Biotechnology journal},
volume = {20},
number = {12},
pages = {e70164},
doi = {10.1002/biot.70164},
pmid = {41379027},
issn = {1860-7314},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology/genetics ; Oxidation-Reduction ; Child ; Male ; Feces/microbiology ; *Autism Spectrum Disorder/microbiology/metabolism ; Female ; Child, Preschool ; Metagenomics ; Metabolomics ; Bacteria/metabolism/classification/genetics ; *Autistic Disorder/microbiology/metabolism ; },
abstract = {Emerging evidence suggests that disruptions in the gut microbiome may influence autism spectrum disorder (ASD) through altered microbial metabolism and gut-brain communication. However, the specific metabolic impacts of these microbial changes remain unclear. Community-scale metabolic modeling was applied to shotgun metagenomics data from children with ASD and neurotypical controls to predict secretion of host-impacting metabolites. Modeled ASD-associated communities exhibited altered predicted secretion of metabolites related to redox balance and neurotransmission, including increased 2-ketobutyrate and GABA and reduced riboflavin and inositol, with microbiota transfer therapy (MTT) shifting these profiles toward NT. Empirical fecal metabolomics data showed generally consistent directional trends with model predictions. Reductions in autism severity scores following MTT were associated with increased predicted secretion potentials for inositol and arginine. Taxonomic analysis revealed a depletion of beneficial and an enrichment of pro-inflammatory species, such as Escherichia and Flavonifractor, in ASD. Associations between microbial taxa (e.g., Bacteroides, Bifidobacterium) and neuroactive metabolites highlight microbial modulation as a promising therapeutic strategy in ASD. These results emphasize microbial metabolism as a contributor to ASD traits and a target for therapeutic intervention.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology/genetics
Oxidation-Reduction
Child
Male
Feces/microbiology
*Autism Spectrum Disorder/microbiology/metabolism
Female
Child, Preschool
Metagenomics
Metabolomics
Bacteria/metabolism/classification/genetics
*Autistic Disorder/microbiology/metabolism
RevDate: 2025-12-11
Analysis of gut microbiota in Restless Legs Syndrome: searching for a metagenomic signature.
Sleep pii:8377255 [Epub ahead of print].
STUDY OBJECTIVES: We aim to analyse the microbiota composition in RLS patients and its relationship with the different RLS phenotypes.
METHODS: We recruited idiopathic RLS (RLS) and insomnia (INS) patients and healthy subjects (CTRL). Validated questionnaires (PSQI, IRLS, ISI, BDI-II) were administered in the RLS and INS. Fecal microbiota was analysed by 16S rRNA gene sequencing according to Illumina metagenomics standard procedure on MiSeq Platform. Dada2 pipeline was used to process sequencing data, while DESeq2 and Aldex2 tools were used to calculate differential abundance taxa, correcting for age, sex, Body Mass Index, sequencing run and presence of mood disorders.
RESULTS: The sample included 37 RLS (28 females, mean age 64.78 years), 31 INS (22 females, mean age 60.64 years) and 33 CTRL (24 females, mean age 62.54 years). Differential abundance analysis revealed a statistically significant decrease in the abundance of Lachnoclostridium and Flavonifractor genera in RLS compared to CTRL and INS, but not in the INS compared to CTRL. Lachnoclostridium abundance tended to decrease with long disease duration and a predominant motor phenotype. In the RLS group, several genera were identified as significantly associated with IRLS and PSQI scores.
CONCLUSIONS: Although only a few previous studies have reported the presence of small intestinal bacterial overgrowth (SIBO) in RLS, to the best of our knowledge this is the first study to highlight significant differences in the gut microbiota composition of RLS compared to both CTRL and INS, identifying a specific RLS metagenomic signature.
Additional Links: PMID-41378921
Publisher:
PubMed:
Citation:
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@article {pmid41378921,
year = {2025},
author = {Montini, A and Pellegrini, C and Loddo, G and Ravaioli, F and Baldelli, L and Mainieri, G and Pirazzini, C and Mazzotta, E and Carano, F and Sala, C and De Fanti, S and Bacalini, MG and Provini, F},
title = {Analysis of gut microbiota in Restless Legs Syndrome: searching for a metagenomic signature.},
journal = {Sleep},
volume = {},
number = {},
pages = {},
doi = {10.1093/sleep/zsaf383},
pmid = {41378921},
issn = {1550-9109},
abstract = {STUDY OBJECTIVES: We aim to analyse the microbiota composition in RLS patients and its relationship with the different RLS phenotypes.
METHODS: We recruited idiopathic RLS (RLS) and insomnia (INS) patients and healthy subjects (CTRL). Validated questionnaires (PSQI, IRLS, ISI, BDI-II) were administered in the RLS and INS. Fecal microbiota was analysed by 16S rRNA gene sequencing according to Illumina metagenomics standard procedure on MiSeq Platform. Dada2 pipeline was used to process sequencing data, while DESeq2 and Aldex2 tools were used to calculate differential abundance taxa, correcting for age, sex, Body Mass Index, sequencing run and presence of mood disorders.
RESULTS: The sample included 37 RLS (28 females, mean age 64.78 years), 31 INS (22 females, mean age 60.64 years) and 33 CTRL (24 females, mean age 62.54 years). Differential abundance analysis revealed a statistically significant decrease in the abundance of Lachnoclostridium and Flavonifractor genera in RLS compared to CTRL and INS, but not in the INS compared to CTRL. Lachnoclostridium abundance tended to decrease with long disease duration and a predominant motor phenotype. In the RLS group, several genera were identified as significantly associated with IRLS and PSQI scores.
CONCLUSIONS: Although only a few previous studies have reported the presence of small intestinal bacterial overgrowth (SIBO) in RLS, to the best of our knowledge this is the first study to highlight significant differences in the gut microbiota composition of RLS compared to both CTRL and INS, identifying a specific RLS metagenomic signature.},
}
RevDate: 2025-12-11
Dormancy and reactivation of the seed and its microbiome: a holobiont perspective.
mSystems [Epub ahead of print].
Desiccation-tolerant seeds provide an intriguing system for studying microbial dormancy, which includes reversible inactivation and reactivation in response to stress. Focusing on bacterial responses to desiccation and rehydration, we offer a holistic interpretation of dormancy and quiescence within the seed holobiont, highlighting both parallels and distinctions between microbes and their plant host. Based on pilot evidence, we propose that microbial dormancy supports persistence throughout the life cycle of desiccation-tolerant seeds. Transcriptomic analyses of seed-transmitted bacteria have identified genes implicated in inactivation and the viable-but-nonculturable state. Our analysis of Xanthomonas citri pv. fuscans illustrates this during seed maturation. However, the signals triggering microbial reactivation and the potential reciprocal interactions between seed dormancy and quiescence, and microbial dormancy, remain unknown. Elucidating this interplay within the seed holobiont could enhance plant growth and health either by promoting seed germination through microbial inoculation or by enabling early detection of seed-transmitted phytopathogens.
Additional Links: PMID-41378889
Publisher:
PubMed:
Citation:
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@article {pmid41378889,
year = {2025},
author = {Gerna, D and Chadelaud, T and Lamouche, F and Barret, M and Darrasse, A and Simonin, M},
title = {Dormancy and reactivation of the seed and its microbiome: a holobiont perspective.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0114025},
doi = {10.1128/msystems.01140-25},
pmid = {41378889},
issn = {2379-5077},
abstract = {Desiccation-tolerant seeds provide an intriguing system for studying microbial dormancy, which includes reversible inactivation and reactivation in response to stress. Focusing on bacterial responses to desiccation and rehydration, we offer a holistic interpretation of dormancy and quiescence within the seed holobiont, highlighting both parallels and distinctions between microbes and their plant host. Based on pilot evidence, we propose that microbial dormancy supports persistence throughout the life cycle of desiccation-tolerant seeds. Transcriptomic analyses of seed-transmitted bacteria have identified genes implicated in inactivation and the viable-but-nonculturable state. Our analysis of Xanthomonas citri pv. fuscans illustrates this during seed maturation. However, the signals triggering microbial reactivation and the potential reciprocal interactions between seed dormancy and quiescence, and microbial dormancy, remain unknown. Elucidating this interplay within the seed holobiont could enhance plant growth and health either by promoting seed germination through microbial inoculation or by enabling early detection of seed-transmitted phytopathogens.},
}
RevDate: 2025-12-11
Inhibition of PFKFB3 in macrophages ameliorates intestinal inflammation by modulating gut microbiota in DSS-induced colitis.
mSystems [Epub ahead of print].
UNLABELLED: Phosphofructo-2-kinase/fructose-2,6-biophosphatase 3 (PFKFB3), a key glycolytic enzyme, has attracted increasing attention for its essential roles in various inflammatory responses and immune-related diseases. But the functional relevance and mechanistic basis of the PFKFB3 on ulcerative colitis (UC) remain unclear. Immunohistochemical staining and publicly available data sets were used to analyze PFKFB3 expression in healthy controls (HCs) and UC patients. The role of PFKFB3 on colitis and gut microbiota was investigated by deficiency of PFKFB3 in macrophages (PFKFB3[fl/fl]Lyz2-Cre) mice. In silico meta- and Spearman's correlation analysis of published high-throughput transcriptomic data analyzed the correlation between PFKFB3 and microbiome-associated genes. The expression of PFKFB3 was significantly upregulated in the colon of both human UC cohorts and colitis mice. Pharmacological inhibition of PFKFB3 by 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO) diminished the severity of colitis. Single-cell RNA sequencing and flow analysis revealed that the upregulated PFKFB3 was predominantly contributed by colonic macrophages. PFKFB3[fl/fl]Lyz2-Cre mice alleviated experimental colitis in contrast to littermate control (PFKFB3[fl/fl]). Concomitantly, PFKFB3[fl/fl]Lyz2-Cre mice exhibited a remarkably Faecalibaculum genus-enhanced microenvironment, which can be horizontally transmitted to co-housed wild-type mice, leading to an attenuation of DSS-induced colitis. However, when antibiotics were administered to PFKFB3[fl/fl]Lyz2-Cre mice, the transmission effect was lost. By analyzing the UC patient cohort, Spearman's correlation provided additional evidence for a significant positive correlation between PFKFB3 and microbiota-associated genes expression. This study demonstrated that PFKFB3 deficiency in macrophages could effectively ameliorate colonic inflammation, providing the first evidence that gut microbiota from PFKFB3-deficient mice may represent a novel therapeutic strategy for UC.
IMPORTANCE: PFKFB3 expression was upregulated in the colon of both ulcerative colitis (UC) patients and colitis mice, and this differential expression was predominantly contributed by colonic lamina propria macrophages. Knockout of PFKFB3 in macrophages significantly alleviated DSS-induced colitis. Knockout of PFKFB3 in macrophage mice exhibited a remarkably Faecalibaculum genus-enhanced microenvironment, which can be horizontally transmitted to co-housed wild-type mice, leading to an attenuation of DSS-induced colitis; however, when administered to antibiotics, the transmission effect was lost. By analyzing the UC patient cohort, we demonstrated significant positive correlation between PFKFB3 and microbiota-associated gene expression. Our study first elucidates the relationship of PFKFB3 in macrophages with intestinal inflammation and gut microbiota in UC, which may provide a new strategy for the treatment.
Additional Links: PMID-41378888
Publisher:
PubMed:
Citation:
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@article {pmid41378888,
year = {2025},
author = {Gao, J-H and Li, L-X and Li, W-J and Wang, X and Lyu, D-p and Xie, X-R and Li, S-Y and Zuo, X-L and Li, Y-Q},
title = {Inhibition of PFKFB3 in macrophages ameliorates intestinal inflammation by modulating gut microbiota in DSS-induced colitis.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0063225},
doi = {10.1128/msystems.00632-25},
pmid = {41378888},
issn = {2379-5077},
abstract = {UNLABELLED: Phosphofructo-2-kinase/fructose-2,6-biophosphatase 3 (PFKFB3), a key glycolytic enzyme, has attracted increasing attention for its essential roles in various inflammatory responses and immune-related diseases. But the functional relevance and mechanistic basis of the PFKFB3 on ulcerative colitis (UC) remain unclear. Immunohistochemical staining and publicly available data sets were used to analyze PFKFB3 expression in healthy controls (HCs) and UC patients. The role of PFKFB3 on colitis and gut microbiota was investigated by deficiency of PFKFB3 in macrophages (PFKFB3[fl/fl]Lyz2-Cre) mice. In silico meta- and Spearman's correlation analysis of published high-throughput transcriptomic data analyzed the correlation between PFKFB3 and microbiome-associated genes. The expression of PFKFB3 was significantly upregulated in the colon of both human UC cohorts and colitis mice. Pharmacological inhibition of PFKFB3 by 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO) diminished the severity of colitis. Single-cell RNA sequencing and flow analysis revealed that the upregulated PFKFB3 was predominantly contributed by colonic macrophages. PFKFB3[fl/fl]Lyz2-Cre mice alleviated experimental colitis in contrast to littermate control (PFKFB3[fl/fl]). Concomitantly, PFKFB3[fl/fl]Lyz2-Cre mice exhibited a remarkably Faecalibaculum genus-enhanced microenvironment, which can be horizontally transmitted to co-housed wild-type mice, leading to an attenuation of DSS-induced colitis. However, when antibiotics were administered to PFKFB3[fl/fl]Lyz2-Cre mice, the transmission effect was lost. By analyzing the UC patient cohort, Spearman's correlation provided additional evidence for a significant positive correlation between PFKFB3 and microbiota-associated genes expression. This study demonstrated that PFKFB3 deficiency in macrophages could effectively ameliorate colonic inflammation, providing the first evidence that gut microbiota from PFKFB3-deficient mice may represent a novel therapeutic strategy for UC.
IMPORTANCE: PFKFB3 expression was upregulated in the colon of both ulcerative colitis (UC) patients and colitis mice, and this differential expression was predominantly contributed by colonic lamina propria macrophages. Knockout of PFKFB3 in macrophages significantly alleviated DSS-induced colitis. Knockout of PFKFB3 in macrophage mice exhibited a remarkably Faecalibaculum genus-enhanced microenvironment, which can be horizontally transmitted to co-housed wild-type mice, leading to an attenuation of DSS-induced colitis; however, when administered to antibiotics, the transmission effect was lost. By analyzing the UC patient cohort, we demonstrated significant positive correlation between PFKFB3 and microbiota-associated gene expression. Our study first elucidates the relationship of PFKFB3 in macrophages with intestinal inflammation and gut microbiota in UC, which may provide a new strategy for the treatment.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
The science of obesity.
South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde, 115(9b):e3600.
KEY MESSAGES • Obesity arises from a complex interplay of genetic, biological, behavioural, psychosocial and environmental factors. • Obesity has a strong genetic component, with twin studies indicating a 50 - 80% concordance in body mass index (BMI) and regional fat distribution. A Swedish study on identical twins raised apart found no correlation between BMI and their adoptive families but a strong correlation with their biological twin, despite being raised in separate households. • The regulation of appetite, body weight and energy balance is highly complex, governed by a network of hormonal signals from the gut, adipose tissue and other organs, as well as neural signals that shape eating behaviours. Many of these signalling pathways are disrupted in people living with obesity. • Since body weight is homeostatically regulated, weight loss triggers physiological adaptations that promote weight regain. These include a decrease in energy expenditure, and hormonal changes that enhance appetite while reducing satiety. • Adipose tissue influences the central regulation of energy homeostasis, and excess adiposity can become dysfunctional, with production of proinflammatory cytokines and associated metabolic health complications. • Individual variations in body composition, fat distribution and function result in a highly variable threshold at which excess adiposity begins to negatively affect health. • Emerging research in obesity science has widened to include brown fat, the gut microbiome, immune system regulation, and the intricate mechanisms that regulate body weight. • Obesity can be classified as primary, secondary and genetic obesity. • In the current management of primary obesity, prevention (the path in) and treatment (the path out) need to be distinctly separated. • Effective primary obesity treatment requires an integrated approach that addresses the non-modifiable cause (increased appetite) together with modifiable contributors (poor diet quality, increased stress, poor sleep, reduced physical activity and increased sedentary behaviour). Behavioural modification and psychological support provide additional benefit. • Effective treatment in genetic and secondary obesity requires treatment of the underlying causes along with modification of the contributors.
Additional Links: PMID-41378649
Publisher:
PubMed:
Citation:
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@article {pmid41378649,
year = {2025},
author = {May, W and Goedecke, JH and Conradie-Smit, M},
title = {The science of obesity.},
journal = {South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde},
volume = {115},
number = {9b},
pages = {e3600},
doi = {10.7196/SAMJ.2025.v115i9b.3600},
pmid = {41378649},
issn = {2078-5135},
mesh = {Humans ; *Obesity/genetics/physiopathology/etiology/therapy ; Energy Metabolism ; Body Mass Index ; Appetite ; },
abstract = {KEY MESSAGES • Obesity arises from a complex interplay of genetic, biological, behavioural, psychosocial and environmental factors. • Obesity has a strong genetic component, with twin studies indicating a 50 - 80% concordance in body mass index (BMI) and regional fat distribution. A Swedish study on identical twins raised apart found no correlation between BMI and their adoptive families but a strong correlation with their biological twin, despite being raised in separate households. • The regulation of appetite, body weight and energy balance is highly complex, governed by a network of hormonal signals from the gut, adipose tissue and other organs, as well as neural signals that shape eating behaviours. Many of these signalling pathways are disrupted in people living with obesity. • Since body weight is homeostatically regulated, weight loss triggers physiological adaptations that promote weight regain. These include a decrease in energy expenditure, and hormonal changes that enhance appetite while reducing satiety. • Adipose tissue influences the central regulation of energy homeostasis, and excess adiposity can become dysfunctional, with production of proinflammatory cytokines and associated metabolic health complications. • Individual variations in body composition, fat distribution and function result in a highly variable threshold at which excess adiposity begins to negatively affect health. • Emerging research in obesity science has widened to include brown fat, the gut microbiome, immune system regulation, and the intricate mechanisms that regulate body weight. • Obesity can be classified as primary, secondary and genetic obesity. • In the current management of primary obesity, prevention (the path in) and treatment (the path out) need to be distinctly separated. • Effective primary obesity treatment requires an integrated approach that addresses the non-modifiable cause (increased appetite) together with modifiable contributors (poor diet quality, increased stress, poor sleep, reduced physical activity and increased sedentary behaviour). Behavioural modification and psychological support provide additional benefit. • Effective treatment in genetic and secondary obesity requires treatment of the underlying causes along with modification of the contributors.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Obesity/genetics/physiopathology/etiology/therapy
Energy Metabolism
Body Mass Index
Appetite
RevDate: 2025-12-11
Association of Subgingival Microbiota Composition With Risk, Severity, and Outcome of Cryptogenic Ischemic Stroke in Young Adults.
Journal of the American Heart Association [Epub ahead of print].
BACKGROUND: Oral and gut dysbiosis has been linked to stroke pathogenesis and its prognosis. However, the relationship between the subgingival microbiota and cryptogenic ischemic stroke (CIS) remains unclear. We compared the subgingival microbiota of patients with CIS and their age-and sex-matched stroke-free controls to identify the specific microbiota associated with CIS, stroke symptom severity, and clinical outcome.
METHODS: This multicenter, case-control study was conducted between 2013 and 2019 as part of a screening protocol for the SECRETO (Searching for Explanations for Cryptogenic Stroke in the Young: Revealing the Etiology, Triggers, and Outcome) study (NCT01934725). Stroke severity was assessed using the National Institutes of Health Stroke Scale score. After thorough clinical and radiographic oral examinations, subgingival samples were collected and analyzed using 16S rRNA gene sequencing.
RESULTS: A total of 272 participants (134 patients and 138 controls) were included. There were no differences in the following clinical characteristics between patients and controls: diabetes, hypertension, smoking, alcohol use, abdominal obesity, physical activity, and chronic multiorgan disease. Beta diversity differed significantly between patients and controls (P<0.05). The abundance of Spirochaetota and Treponema was higher and Pseudomonadota, Veillonella, and Capnocytophaga were lower in patients than in controls (P<0.05). The abundance of T. denticola was associated with an increased risk of CIS (odds ratio [OR], 1.002 [95% CI, 1.000-1.003], P=0.023), and this association persisted after adjusting for relevant comorbidities and medications (OR, 1.002 [95% CI, 1.000-1.003], P=0.021).
CONCLUSIONS: The subgingival microbiota is associated with CIS, suggesting a possible link between oral health and stroke pathophysiology. Although causality cannot be proven, oral microbiota may be a modifiable treatment target for the prevention of CIS and improving its outcome.
Additional Links: PMID-41378491
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PubMed:
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@article {pmid41378491,
year = {2025},
author = {Manzoor, M and Zaric, S and Dong, A and Leskelä, J and Pietiäinen, M and Könönen, E and Ylikotila, P and Enzinger, C and Ropele, S and Gattringer, T and Eppinger, S and Sinisalo, J and Putaala, J and Pussinen, PJ and Paju, S},
title = {Association of Subgingival Microbiota Composition With Risk, Severity, and Outcome of Cryptogenic Ischemic Stroke in Young Adults.},
journal = {Journal of the American Heart Association},
volume = {},
number = {},
pages = {e043495},
doi = {10.1161/JAHA.125.043495},
pmid = {41378491},
issn = {2047-9980},
abstract = {BACKGROUND: Oral and gut dysbiosis has been linked to stroke pathogenesis and its prognosis. However, the relationship between the subgingival microbiota and cryptogenic ischemic stroke (CIS) remains unclear. We compared the subgingival microbiota of patients with CIS and their age-and sex-matched stroke-free controls to identify the specific microbiota associated with CIS, stroke symptom severity, and clinical outcome.
METHODS: This multicenter, case-control study was conducted between 2013 and 2019 as part of a screening protocol for the SECRETO (Searching for Explanations for Cryptogenic Stroke in the Young: Revealing the Etiology, Triggers, and Outcome) study (NCT01934725). Stroke severity was assessed using the National Institutes of Health Stroke Scale score. After thorough clinical and radiographic oral examinations, subgingival samples were collected and analyzed using 16S rRNA gene sequencing.
RESULTS: A total of 272 participants (134 patients and 138 controls) were included. There were no differences in the following clinical characteristics between patients and controls: diabetes, hypertension, smoking, alcohol use, abdominal obesity, physical activity, and chronic multiorgan disease. Beta diversity differed significantly between patients and controls (P<0.05). The abundance of Spirochaetota and Treponema was higher and Pseudomonadota, Veillonella, and Capnocytophaga were lower in patients than in controls (P<0.05). The abundance of T. denticola was associated with an increased risk of CIS (odds ratio [OR], 1.002 [95% CI, 1.000-1.003], P=0.023), and this association persisted after adjusting for relevant comorbidities and medications (OR, 1.002 [95% CI, 1.000-1.003], P=0.021).
CONCLUSIONS: The subgingival microbiota is associated with CIS, suggesting a possible link between oral health and stroke pathophysiology. Although causality cannot be proven, oral microbiota may be a modifiable treatment target for the prevention of CIS and improving its outcome.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Cohort-specific determinants of donor strain engraftment following multi-donor faecal microbiota transplantation in two randomised clinical trials.
Gut microbes, 17(1):2597628.
Disrupted human gut microbiota have been associated with the development of certain disease states, including obesity and ulcerative colitis (UC). Faecal microbiota transplantation (FMT) from healthy donors is a promising avenue to shift the microbiome profile of the recipient towards that of the donor, potentially ameliorating related symptoms. Several recent meta-analyses have investigated the clinical and microbial determinants that influence the retention of transplanted donor microbial strains within the recipient gut microbiome following FMT (i.e. engraftment). However, the specific factors that affect donor strain engraftment in different disease states require further exploration. Here, we perform a strain engraftment analysis on data from two multi-donor FMT clinical trials: the Gut Bugs Trial for obesity and the FOCUS Trial for UC. Using donor strain matching, the donor-recipient pairings of the FOCUS Trial were first predicted in a blinded manner. The subsequent, unblinded, strain engraftment analysis of both datasets highlighted a differential effect of donor-recipient microbiome complementarity on engraftment across the two disease cohorts; greater engraftment efficiency was associated with increased donor-recipient microbial similarity in the FOCUS Trial, and decreased similarity in the Gut Bugs Trial, suggesting that the factors influencing engraftment may differ across disease cohorts.
Additional Links: PMID-41378445
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PubMed:
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@article {pmid41378445,
year = {2025},
author = {Behling, AH and Portlock, T and Ho, D and Wilson, BC and Paramsothy, S and Kamm, MA and Cutfield, WS and Kaakoush, NO and O'Sullivan, JM and Vatanen, T},
title = {Cohort-specific determinants of donor strain engraftment following multi-donor faecal microbiota transplantation in two randomised clinical trials.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2597628},
doi = {10.1080/19490976.2025.2597628},
pmid = {41378445},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; *Colitis, Ulcerative/therapy/microbiology ; Tissue Donors ; Feces/microbiology ; *Obesity/therapy/microbiology ; Bacteria/classification/isolation & purification/genetics ; Randomized Controlled Trials as Topic ; Male ; Female ; Adult ; Middle Aged ; Cohort Studies ; },
abstract = {Disrupted human gut microbiota have been associated with the development of certain disease states, including obesity and ulcerative colitis (UC). Faecal microbiota transplantation (FMT) from healthy donors is a promising avenue to shift the microbiome profile of the recipient towards that of the donor, potentially ameliorating related symptoms. Several recent meta-analyses have investigated the clinical and microbial determinants that influence the retention of transplanted donor microbial strains within the recipient gut microbiome following FMT (i.e. engraftment). However, the specific factors that affect donor strain engraftment in different disease states require further exploration. Here, we perform a strain engraftment analysis on data from two multi-donor FMT clinical trials: the Gut Bugs Trial for obesity and the FOCUS Trial for UC. Using donor strain matching, the donor-recipient pairings of the FOCUS Trial were first predicted in a blinded manner. The subsequent, unblinded, strain engraftment analysis of both datasets highlighted a differential effect of donor-recipient microbiome complementarity on engraftment across the two disease cohorts; greater engraftment efficiency was associated with increased donor-recipient microbial similarity in the FOCUS Trial, and decreased similarity in the Gut Bugs Trial, suggesting that the factors influencing engraftment may differ across disease cohorts.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
*Colitis, Ulcerative/therapy/microbiology
Tissue Donors
Feces/microbiology
*Obesity/therapy/microbiology
Bacteria/classification/isolation & purification/genetics
Randomized Controlled Trials as Topic
Male
Female
Adult
Middle Aged
Cohort Studies
RevDate: 2025-12-11
CmpDate: 2025-12-11
Deciphering Conserved Rhizosphere Metabolite-Microbiome Interactions for Crop Drought Resistance.
Global change biology, 31(12):e70652.
Drought stress is a major threat to global food security. It remains uncertain whether conserved drought-responsive microbes can be recruited by different crop species to help their adaptation to drought and how this recruitment occurs. Herein, we identified drought-responsive rhizosphere microbial genera conserved across multiple crop species under drought stress and elucidated their in situ regulatory mechanisms. Integrated amplicon sequencing of rhizosphere microbiomes from 26 crop species indicated 6 core genera (Streptomyces, Glycomyces, Inquilinus, Amycolatopsis, Acinetobacter, and Promicromonospora) consistently enriched under drought. Soil conditioning with 46 shared rhizosphere metabolites among multiple crops demonstrated that trehalose, myo-inositol, and phenylalanine synergistically enrich the six genera. The soil microbiome conditioned with three compounds significantly increased root length and leaf water content when evaluated in greenhouse trials (tomato, cucumber, and watermelon) and sorghum field studies. Furthermore, the conditioned soil microbiome exhibited enrichment in pathways related to energy supply, protective compound synthesis, and plant interaction signaling, driven by six core genera. Pure culture experiments revealed a potential cross-phylum interaction; that is, Streptomyces could synthesize phenylalanine to recruit Acinetobacter. Our findings reveal a potential conserved rhizosphere metabolite-microbiome interactions across multiple crops, offering a talent pathway to steer soil microbiome for drought resistance.
Additional Links: PMID-41378387
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PubMed:
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@article {pmid41378387,
year = {2025},
author = {Niu, G and Liu, W and Zhang, T and Ma, J and Yuan, X and Xie, P and Yang, S and Ding, Z and Fang, J and Zeng, J and Wen, T and Shen, Q and Yuan, J},
title = {Deciphering Conserved Rhizosphere Metabolite-Microbiome Interactions for Crop Drought Resistance.},
journal = {Global change biology},
volume = {31},
number = {12},
pages = {e70652},
doi = {10.1111/gcb.70652},
pmid = {41378387},
issn = {1365-2486},
support = {2025FRF05007//Central Guidance on Local Science and Technology Development Fund of Ningxia/ ; 42322708//Natural Science Foundation of China/ ; CARS-23//China Agriculture Research System/ ; 202302140601007//Key Research and Development Program of Shanxi Province/ ; KJJQ2025017//Fundamental Research Funds for the Central Universities/ ; },
mesh = {*Rhizosphere ; *Droughts ; *Crops, Agricultural/microbiology/physiology ; *Microbiota ; *Soil Microbiology ; Drought Resistance ; },
abstract = {Drought stress is a major threat to global food security. It remains uncertain whether conserved drought-responsive microbes can be recruited by different crop species to help their adaptation to drought and how this recruitment occurs. Herein, we identified drought-responsive rhizosphere microbial genera conserved across multiple crop species under drought stress and elucidated their in situ regulatory mechanisms. Integrated amplicon sequencing of rhizosphere microbiomes from 26 crop species indicated 6 core genera (Streptomyces, Glycomyces, Inquilinus, Amycolatopsis, Acinetobacter, and Promicromonospora) consistently enriched under drought. Soil conditioning with 46 shared rhizosphere metabolites among multiple crops demonstrated that trehalose, myo-inositol, and phenylalanine synergistically enrich the six genera. The soil microbiome conditioned with three compounds significantly increased root length and leaf water content when evaluated in greenhouse trials (tomato, cucumber, and watermelon) and sorghum field studies. Furthermore, the conditioned soil microbiome exhibited enrichment in pathways related to energy supply, protective compound synthesis, and plant interaction signaling, driven by six core genera. Pure culture experiments revealed a potential cross-phylum interaction; that is, Streptomyces could synthesize phenylalanine to recruit Acinetobacter. Our findings reveal a potential conserved rhizosphere metabolite-microbiome interactions across multiple crops, offering a talent pathway to steer soil microbiome for drought resistance.},
}
MeSH Terms:
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*Rhizosphere
*Droughts
*Crops, Agricultural/microbiology/physiology
*Microbiota
*Soil Microbiology
Drought Resistance
RevDate: 2025-12-11
Dietary and Physical Activity Interventions in Gynecologic Oncology: Mechanisms, Guidelines, and Clinical Evidence.
American journal of lifestyle medicine [Epub ahead of print].
Background: Obesity and modifiable lifestyle factors contribute significantly to the rising global burden of cancer, particularly gynecologic malignancies such as endometrial and ovarian cancer. Despite strong biological plausibility, the role of lifestyle interventions in improving outcomes for women with gynecologic cancers remains underexplored. Objective: This review synthesizes current evidence on the impact of dietary and physical activity interventions on gynecologic cancer outcomes, highlighting links and existing clinical guidelines. Methods: Literature exploring the influence of obesity, inflammation hormonal dysregulation, insulin resistance, and gut microbiome alterations on cancer progression were assessed, and studies assessing the effects of lifestyle interventions in gynecologic cancers were explored. Results: Obesity-induced inflammation and hormonal imbalances are key drivers of tumorigenesis. Structured exercise and adherence to anti-inflammatory diets, such as the Mediterranean diet, can reduce pro-inflammatory cytokines, improve insulin sensitivity, regulate estrogen metabolism, and enhance immune function. These interventions also modulate angiogenesis and promote a favorable gut microbiome, offering a biologically plausible approach to slowing cancer progression. Conclusion: Diet and exercise represent promising, low-risk strategies to improve quality of life and potentially enhance survival in women with gynecologic cancers. Greater integration of lifestyle interventions into gynecologic oncology care is warranted, guided by evidence and recommendations from national cancer organizations.
Additional Links: PMID-41378343
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Citation:
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@article {pmid41378343,
year = {2025},
author = {Shah, SS and Jackovic, A and Alhilli, M},
title = {Dietary and Physical Activity Interventions in Gynecologic Oncology: Mechanisms, Guidelines, and Clinical Evidence.},
journal = {American journal of lifestyle medicine},
volume = {},
number = {},
pages = {15598276251405209},
pmid = {41378343},
issn = {1559-8284},
abstract = {Background: Obesity and modifiable lifestyle factors contribute significantly to the rising global burden of cancer, particularly gynecologic malignancies such as endometrial and ovarian cancer. Despite strong biological plausibility, the role of lifestyle interventions in improving outcomes for women with gynecologic cancers remains underexplored. Objective: This review synthesizes current evidence on the impact of dietary and physical activity interventions on gynecologic cancer outcomes, highlighting links and existing clinical guidelines. Methods: Literature exploring the influence of obesity, inflammation hormonal dysregulation, insulin resistance, and gut microbiome alterations on cancer progression were assessed, and studies assessing the effects of lifestyle interventions in gynecologic cancers were explored. Results: Obesity-induced inflammation and hormonal imbalances are key drivers of tumorigenesis. Structured exercise and adherence to anti-inflammatory diets, such as the Mediterranean diet, can reduce pro-inflammatory cytokines, improve insulin sensitivity, regulate estrogen metabolism, and enhance immune function. These interventions also modulate angiogenesis and promote a favorable gut microbiome, offering a biologically plausible approach to slowing cancer progression. Conclusion: Diet and exercise represent promising, low-risk strategies to improve quality of life and potentially enhance survival in women with gynecologic cancers. Greater integration of lifestyle interventions into gynecologic oncology care is warranted, guided by evidence and recommendations from national cancer organizations.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Herbal formulas and gastrointestinal motility: Bridging traditional medicine and mechanistic insights.
World journal of gastroenterology, 31(45):113332.
Wang et al provide preclinical evidence that specific traditional herbal formulas, like Pyeongwi-san, can improve gastrointestinal (GI) motility under stress. Pyeongwi-san enhances GI transit, boosts serotonin levels, restores short-chain fatty acid balance, and reduces inflammation. The clinical significance of this research is its potential for standardized herbal remedies for GI disorders, such as dyspepsia and irritable bowel syndrome. At the same time, using only male mice, a single dose regimen, and relatively small cohorts highlights the need for further validation, including sex-specific responses, dose-effect relationships, and translational clinical studies. In summary, readers will find value in this article because it provides mechanistic details, bridges tradition with modern science, deals transparently with its limitations, and paves the way for clinically relevant innovation in GI health. Future investigations should focus on clinical validation and personalized therapeutic strategies that harness both microbiome-gut-brain interactions and the long history of herbal medicine.
Additional Links: PMID-41378331
PubMed:
Citation:
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@article {pmid41378331,
year = {2025},
author = {Zalzman, M and Banerjee, A},
title = {Herbal formulas and gastrointestinal motility: Bridging traditional medicine and mechanistic insights.},
journal = {World journal of gastroenterology},
volume = {31},
number = {45},
pages = {113332},
pmid = {41378331},
issn = {2219-2840},
mesh = {Humans ; *Gastrointestinal Motility/drug effects ; Animals ; *Drugs, Chinese Herbal/pharmacology/therapeutic use ; Gastrointestinal Microbiome/drug effects ; Gastrointestinal Transit/drug effects ; *Gastrointestinal Diseases/drug therapy ; Mice ; Phytotherapy/methods ; },
abstract = {Wang et al provide preclinical evidence that specific traditional herbal formulas, like Pyeongwi-san, can improve gastrointestinal (GI) motility under stress. Pyeongwi-san enhances GI transit, boosts serotonin levels, restores short-chain fatty acid balance, and reduces inflammation. The clinical significance of this research is its potential for standardized herbal remedies for GI disorders, such as dyspepsia and irritable bowel syndrome. At the same time, using only male mice, a single dose regimen, and relatively small cohorts highlights the need for further validation, including sex-specific responses, dose-effect relationships, and translational clinical studies. In summary, readers will find value in this article because it provides mechanistic details, bridges tradition with modern science, deals transparently with its limitations, and paves the way for clinically relevant innovation in GI health. Future investigations should focus on clinical validation and personalized therapeutic strategies that harness both microbiome-gut-brain interactions and the long history of herbal medicine.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Motility/drug effects
Animals
*Drugs, Chinese Herbal/pharmacology/therapeutic use
Gastrointestinal Microbiome/drug effects
Gastrointestinal Transit/drug effects
*Gastrointestinal Diseases/drug therapy
Mice
Phytotherapy/methods
RevDate: 2025-12-11
CmpDate: 2025-12-11
Gut microbiome and chemotherapy-induced cardiotoxicity: A systematic review of evidence and emerging therapies.
World journal of biological chemistry, 16(4):112221.
BACKGROUND: Chemotherapy-induced cardiotoxicity is a significant complication in cancer therapy, limiting treatment efficacy and worsening patient outcomes. Recent studies have implicated the gut microbiome and its key metabolites, such as short-chain fatty acids (SCFAs) and trimethylamine-N-oxide (TMAO), in mediating inflammation, oxidative stress, and cardiac damage. The gut-heart axis is increasingly recognized as a pivotal pathway linking microbiota dysregulation to chemotherapy-related cardiac dysfunction.
AIM: To systematically review existing evidence on the role of gut microbiome alterations in chemotherapy-induced cardiotoxicity and evaluate emerging microbiome-based therapeutic strategies aimed at mitigating cardiovascular risk in cancer patients.
METHODS: A systematic literature search was conducted in PubMed, Scopus, and Web of Science for studies published between January 2013 and December 2024. Studies were included if they examined chemotherapy-induced cardiotoxicity in relation to gut microbiota composition, microbial metabolites (e.g., SCFAs, TMAO), or microbiome-targeted interventions. Selection followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Data extraction focused on microbiota alterations, mechanistic pathways, cardiac outcomes, and quality assessments using standardized risk-of-bias tools.
RESULTS: Eighteen studies met the inclusion criteria. Chemotherapy was consistently associated with gut dysbiosis characterized by reduced SCFA-producing bacteria and increased TMAO-producing strains. This imbalance contributed to gut barrier disruption, systemic inflammation, and oxidative stress, all of which promote myocardial damage. SCFA depletion weakened anti-inflammatory responses, while elevated TMAO levels exacerbated cardiac fibrosis and dysfunction. Preclinical studies showed promising cardioprotective effects from probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation, though human data remain limited.
CONCLUSION: Gut microbiome dysregulation plays a crucial role in the development of chemotherapy-induced cardiotoxicity. Altered microbial composition and metabolite production trigger systemic inflammation and cardiac injury. Microbiome-targeted therapies represent a promising preventive and therapeutic approach in cardio-oncology, warranting further clinical validation through well-designed trials.
Additional Links: PMID-41378248
PubMed:
Citation:
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@article {pmid41378248,
year = {2025},
author = {Abdulaal, R and Afara, I and Harajli, A and Al Mashtoub, E and Tarchichi, A and Hassan, K and Afara, A and Abou Fakher, J and Salhab, S and Fassih, I and Tlais, M},
title = {Gut microbiome and chemotherapy-induced cardiotoxicity: A systematic review of evidence and emerging therapies.},
journal = {World journal of biological chemistry},
volume = {16},
number = {4},
pages = {112221},
pmid = {41378248},
issn = {1949-8454},
abstract = {BACKGROUND: Chemotherapy-induced cardiotoxicity is a significant complication in cancer therapy, limiting treatment efficacy and worsening patient outcomes. Recent studies have implicated the gut microbiome and its key metabolites, such as short-chain fatty acids (SCFAs) and trimethylamine-N-oxide (TMAO), in mediating inflammation, oxidative stress, and cardiac damage. The gut-heart axis is increasingly recognized as a pivotal pathway linking microbiota dysregulation to chemotherapy-related cardiac dysfunction.
AIM: To systematically review existing evidence on the role of gut microbiome alterations in chemotherapy-induced cardiotoxicity and evaluate emerging microbiome-based therapeutic strategies aimed at mitigating cardiovascular risk in cancer patients.
METHODS: A systematic literature search was conducted in PubMed, Scopus, and Web of Science for studies published between January 2013 and December 2024. Studies were included if they examined chemotherapy-induced cardiotoxicity in relation to gut microbiota composition, microbial metabolites (e.g., SCFAs, TMAO), or microbiome-targeted interventions. Selection followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Data extraction focused on microbiota alterations, mechanistic pathways, cardiac outcomes, and quality assessments using standardized risk-of-bias tools.
RESULTS: Eighteen studies met the inclusion criteria. Chemotherapy was consistently associated with gut dysbiosis characterized by reduced SCFA-producing bacteria and increased TMAO-producing strains. This imbalance contributed to gut barrier disruption, systemic inflammation, and oxidative stress, all of which promote myocardial damage. SCFA depletion weakened anti-inflammatory responses, while elevated TMAO levels exacerbated cardiac fibrosis and dysfunction. Preclinical studies showed promising cardioprotective effects from probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation, though human data remain limited.
CONCLUSION: Gut microbiome dysregulation plays a crucial role in the development of chemotherapy-induced cardiotoxicity. Altered microbial composition and metabolite production trigger systemic inflammation and cardiac injury. Microbiome-targeted therapies represent a promising preventive and therapeutic approach in cardio-oncology, warranting further clinical validation through well-designed trials.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
TMOD2 and DOCK4 as Novel Gut Microbiota-Associated Biomarkers for Colorectal Adenoma: Integrated Transcriptomic Analysis and Therapeutic Target Identification.
Mediators of inflammation, 2025:6267309.
Colorectal adenomas (CRA) represent critical precursors to colorectal cancer (CRC), yet reliable transcriptomic biomarkers for early detection and therapeutic targeting remain limited. Integration of gut microbiota (GM) genetics with transcriptomics offers a novel approach to identify disease-associated molecular signatures. We sought to identify GM-associated molecular signatures that could serve as early intervention targets. We integrated transcriptomic data with Mendelian randomization (MR) analysis to establish causal relationships between GM and CRA development. Machine learning algorithms identified robust biomarkers, which we validated through expression analysis and receiver operating characteristic (ROC) analysis to construct predictive nomogram models. Comprehensive molecular characterization included Gene Set Enrichment Analysis (GSEA), immune profiling, and regulatory network analysis. Single-cell RNA sequencing (scRNA-seq) analysis further validated biomarker expression patterns across distinct cell populations in the tumor microenvironment. We discovered 12 GM species with significant causal relationships to CRA risk. Two biomarkers, TMOD2 and DOCK4, emerged as powerful predictive indicators with strong correlation (r = 0.66, p < 0.001). These biomarkers demonstrated excellent diagnostic performance in ROC analysis and revealed previously unrecognized connections to cell adhesion pathways critical for adenoma progression. Single-cell analysis revealed TMOD2 expression across multiple cell clusters with notable exclusion in mast cells, while DOCK4 expression was predominantly restricted to fibroblasts, myeloid, and epithelial cells. Notably, we identified distinct immune cell infiltration patterns, including altered naive B cells and macrophage populations, suggesting immune dysregulation as a key mechanism. GSEA revealed enrichment in cell adhesion molecule (CAM) pathways. Regulatory network analysis uncovered complex control by 18 microRNAs (miRNAs), 40 long noncoding RNAs (lncRNAs), and 10 transcription factors (TFs), with EIF3A emerging as a key m6A reader protein. Drug screening identified 22 potential therapeutic compounds, with trichostatin A showing optimal binding affinity. These findings establish TMOD2 and DOCK4 as novel biomarkers linking GM dysbiosis to CRA development, opening new avenues for microbiome-targeted early intervention strategies.
Additional Links: PMID-41378121
PubMed:
Citation:
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@article {pmid41378121,
year = {2025},
author = {Liu, C and Wang, L and Huai, J and He, S and Su, Q and Min, Q and An, Z},
title = {TMOD2 and DOCK4 as Novel Gut Microbiota-Associated Biomarkers for Colorectal Adenoma: Integrated Transcriptomic Analysis and Therapeutic Target Identification.},
journal = {Mediators of inflammation},
volume = {2025},
number = {},
pages = {6267309},
pmid = {41378121},
issn = {1466-1861},
mesh = {Humans ; *Colorectal Neoplasms/metabolism/genetics/microbiology ; *Gastrointestinal Microbiome/genetics/physiology ; *Adenoma/metabolism/genetics/microbiology ; Gene Expression Profiling ; Biomarkers, Tumor/metabolism/genetics ; Transcriptome/genetics ; ROC Curve ; },
abstract = {Colorectal adenomas (CRA) represent critical precursors to colorectal cancer (CRC), yet reliable transcriptomic biomarkers for early detection and therapeutic targeting remain limited. Integration of gut microbiota (GM) genetics with transcriptomics offers a novel approach to identify disease-associated molecular signatures. We sought to identify GM-associated molecular signatures that could serve as early intervention targets. We integrated transcriptomic data with Mendelian randomization (MR) analysis to establish causal relationships between GM and CRA development. Machine learning algorithms identified robust biomarkers, which we validated through expression analysis and receiver operating characteristic (ROC) analysis to construct predictive nomogram models. Comprehensive molecular characterization included Gene Set Enrichment Analysis (GSEA), immune profiling, and regulatory network analysis. Single-cell RNA sequencing (scRNA-seq) analysis further validated biomarker expression patterns across distinct cell populations in the tumor microenvironment. We discovered 12 GM species with significant causal relationships to CRA risk. Two biomarkers, TMOD2 and DOCK4, emerged as powerful predictive indicators with strong correlation (r = 0.66, p < 0.001). These biomarkers demonstrated excellent diagnostic performance in ROC analysis and revealed previously unrecognized connections to cell adhesion pathways critical for adenoma progression. Single-cell analysis revealed TMOD2 expression across multiple cell clusters with notable exclusion in mast cells, while DOCK4 expression was predominantly restricted to fibroblasts, myeloid, and epithelial cells. Notably, we identified distinct immune cell infiltration patterns, including altered naive B cells and macrophage populations, suggesting immune dysregulation as a key mechanism. GSEA revealed enrichment in cell adhesion molecule (CAM) pathways. Regulatory network analysis uncovered complex control by 18 microRNAs (miRNAs), 40 long noncoding RNAs (lncRNAs), and 10 transcription factors (TFs), with EIF3A emerging as a key m6A reader protein. Drug screening identified 22 potential therapeutic compounds, with trichostatin A showing optimal binding affinity. These findings establish TMOD2 and DOCK4 as novel biomarkers linking GM dysbiosis to CRA development, opening new avenues for microbiome-targeted early intervention strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Colorectal Neoplasms/metabolism/genetics/microbiology
*Gastrointestinal Microbiome/genetics/physiology
*Adenoma/metabolism/genetics/microbiology
Gene Expression Profiling
Biomarkers, Tumor/metabolism/genetics
Transcriptome/genetics
ROC Curve
RevDate: 2025-12-11
CmpDate: 2025-12-11
Harnessing postbiotics for liver health: Emerging perspectives.
World journal of gastrointestinal pharmacology and therapeutics, 16(4):109177.
With emerging scientific breakthroughs, it has been established that gut microbiome dysbiosis has an undeniable correlation with hepatic diseases through complex interlinked metabolic pathways. There's always been a need for new therapeutic options to deal with the rising prevalence of metabolic dysfunction-associated steatotic liver disease, liver cirrhosis, alcoholic liver disease, hepatocellular carcinoma etc. Several researchers have studied the role of probiotics and prebiotics in altering gut microbiome to tackle microbial dysbiosis which has been proven to be the cause of several metabolic disorders. However, postbiotics remain an untapped potential due to the limited literature on their intake and associated benefits. These bioactive compounds include short chain fatty acids such as butyrate, propionate and acetate, exopolysaccharides, inactivated strains such as Akkermansia muciniphila and Bacillus coagulans etc., have hepatoprotective effects which are highlighted in this article. This review aims to discuss the findings of postbiotics research, their classification and their diverse role in serving as a therapeutic option for liver diseases.
Additional Links: PMID-41378079
PubMed:
Citation:
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@article {pmid41378079,
year = {2025},
author = {Jeyaraman, N and Jeyaraman, M and Mariappan, T and Nallakumarasamy, A and Subramanian, P and T, P and Vetrivel, VN},
title = {Harnessing postbiotics for liver health: Emerging perspectives.},
journal = {World journal of gastrointestinal pharmacology and therapeutics},
volume = {16},
number = {4},
pages = {109177},
pmid = {41378079},
issn = {2150-5349},
abstract = {With emerging scientific breakthroughs, it has been established that gut microbiome dysbiosis has an undeniable correlation with hepatic diseases through complex interlinked metabolic pathways. There's always been a need for new therapeutic options to deal with the rising prevalence of metabolic dysfunction-associated steatotic liver disease, liver cirrhosis, alcoholic liver disease, hepatocellular carcinoma etc. Several researchers have studied the role of probiotics and prebiotics in altering gut microbiome to tackle microbial dysbiosis which has been proven to be the cause of several metabolic disorders. However, postbiotics remain an untapped potential due to the limited literature on their intake and associated benefits. These bioactive compounds include short chain fatty acids such as butyrate, propionate and acetate, exopolysaccharides, inactivated strains such as Akkermansia muciniphila and Bacillus coagulans etc., have hepatoprotective effects which are highlighted in this article. This review aims to discuss the findings of postbiotics research, their classification and their diverse role in serving as a therapeutic option for liver diseases.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Targeting gut microbiota in liver disease: A pharmacological approach for hepatic encephalopathy and beyond.
World journal of gastrointestinal pharmacology and therapeutics, 16(4):110271.
The gut microbiota plays a pivotal role in the pathogenesis of liver diseases, particularly hepatic encephalopathy (HE), in which dysbiosis contributes to ammonia production, systemic inflammation, and neurocognitive dysfunction. Emerging evidence suggests that targeting the gut-liver axis through pharmacological and microbiota-based interventions can mitigate liver disease progression and HE severity. This review explored the latest therapeutic strategies aimed at modulating gut microbiota in liver disease, focusing on traditional approaches such as non-absorbable disaccharides (lactulose, lactitol), antibiotics (rifaximin), and probiotics as well as novel interventions, including postbiotics, synbiotics, and fecal microbiota transplantation. Additionally, bile acid modulators, short-chain fatty acid derivatives, and microbiome-targeted small molecules are being investigated for their potential to restore gut-liver homeostasis. We also discussed the implications of gut microbiota modulation in conditions beyond HE, such as metabolic dysfunction-associated steatotic liver disease and cirrhosis. By integrating gut microbiota-targeted therapies into liver disease management, we may develop more effective, personalized approaches to improve patient outcomes and reduce complications.
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@article {pmid41378067,
year = {2025},
author = {Vargas-Beltran, AM and Mialma-Omana, SJ and Vivanco-Tellez, DO},
title = {Targeting gut microbiota in liver disease: A pharmacological approach for hepatic encephalopathy and beyond.},
journal = {World journal of gastrointestinal pharmacology and therapeutics},
volume = {16},
number = {4},
pages = {110271},
pmid = {41378067},
issn = {2150-5349},
abstract = {The gut microbiota plays a pivotal role in the pathogenesis of liver diseases, particularly hepatic encephalopathy (HE), in which dysbiosis contributes to ammonia production, systemic inflammation, and neurocognitive dysfunction. Emerging evidence suggests that targeting the gut-liver axis through pharmacological and microbiota-based interventions can mitigate liver disease progression and HE severity. This review explored the latest therapeutic strategies aimed at modulating gut microbiota in liver disease, focusing on traditional approaches such as non-absorbable disaccharides (lactulose, lactitol), antibiotics (rifaximin), and probiotics as well as novel interventions, including postbiotics, synbiotics, and fecal microbiota transplantation. Additionally, bile acid modulators, short-chain fatty acid derivatives, and microbiome-targeted small molecules are being investigated for their potential to restore gut-liver homeostasis. We also discussed the implications of gut microbiota modulation in conditions beyond HE, such as metabolic dysfunction-associated steatotic liver disease and cirrhosis. By integrating gut microbiota-targeted therapies into liver disease management, we may develop more effective, personalized approaches to improve patient outcomes and reduce complications.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Gut microbiota phospholipids regulate intestinal gene expression and can counteract the effects of antibiotic treatment.
Research square pii:rs.3.rs-7924457.
Early-life antibiotic exposure perturbs the developing gut microbiome and increases risk for immune disorders such as type 1 diabetes (T1D) in non-obese diabetic (NOD) mice. Comparing germ-free and conventional mice, we identified 747 intestinal lipid compounds and defined a subset of gut microbially-produced lipids (GMPLs). Antibiotic treatment disrupted GMPL profiles in mice and in human volunteers, with partial restoration in mice after cecal microbiota transplantation. Among affected compounds, four phospholipids: LPG(13:0), LPG(16:0), LPG(18:0), and PG(15:0_15:0), were structurally defined and tested functionally. These lipids suppressed LPS-induced NFκB activation, modulated innate immune gene expression in intestinal epithelial cells, and enhanced epithelial cell mitochondrial respiration. Oral administration of LPG(16:0) or LPG(18:0) to antibiotic-treated NOD mice partially restored microbiome composition, normalized ileal gene expression, and improved epithelial transport and metabolic pathways. These findings identify bacterial phospholipids as regulators of intestinal immunity and metabolism, with potential therapeutic applications for inflammatory diseases.
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@article {pmid41377991,
year = {2025},
author = {Blaser, M and Zhang, XS and Zhang, M and Wang, Y and Sun, H and Scarnati, M and Gao, Z and Yin, Y and Zerbe, C and Falcone, E and Lally, M and Joshi, J and Bhattacharya, S and Diaz-Rubio, M and Bharj, D and Patel, D and Pan, S and Ro, G and Grenard, J and Armstrong, A and Valvezan, A and Holland, S and Mulle, J and Dominguez-Bello, M and Su, X},
title = {Gut microbiota phospholipids regulate intestinal gene expression and can counteract the effects of antibiotic treatment.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-7924457/v1},
pmid = {41377991},
issn = {2693-5015},
abstract = {Early-life antibiotic exposure perturbs the developing gut microbiome and increases risk for immune disorders such as type 1 diabetes (T1D) in non-obese diabetic (NOD) mice. Comparing germ-free and conventional mice, we identified 747 intestinal lipid compounds and defined a subset of gut microbially-produced lipids (GMPLs). Antibiotic treatment disrupted GMPL profiles in mice and in human volunteers, with partial restoration in mice after cecal microbiota transplantation. Among affected compounds, four phospholipids: LPG(13:0), LPG(16:0), LPG(18:0), and PG(15:0_15:0), were structurally defined and tested functionally. These lipids suppressed LPS-induced NFκB activation, modulated innate immune gene expression in intestinal epithelial cells, and enhanced epithelial cell mitochondrial respiration. Oral administration of LPG(16:0) or LPG(18:0) to antibiotic-treated NOD mice partially restored microbiome composition, normalized ileal gene expression, and improved epithelial transport and metabolic pathways. These findings identify bacterial phospholipids as regulators of intestinal immunity and metabolism, with potential therapeutic applications for inflammatory diseases.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Tracing NAD[+] metabolism uncovers adaptive coordination between host and microbiome during colitis.
Research square pii:rs.3.rs-8195970.
Host-microbiota metabolic interactions critically regulate nicotinamide adenine dinucleotide (NAD+) homeostasis, and their disruption is increasingly linked to chronic diseases including inflammatory bowel disease (IBD). However, it remains unclear whether NAD+ dysregulation in IBD arises from impaired production, enhanced consumption, or both. Using multi-omics approaches and stable isotope-labeled NAD+ precursors administered via intravenous infusion in a murine model of dextran sulfate sodium (DSS)-induced colitis, we mapped tissue- and lumen-specific NAD+ metabolism under inflammatory stress. Our results reveal tissue-specific rewiring of NAD+ metabolism, with increased flux through the salvage pathway compensating for reduced de novo NAD+ synthesis from tryptophan. In parallel, microbial de novo NAD+ production was elevated, highlighting a cooperative host-microbiota response to inflammatory stress. These findings demonstrate differential regulation of NAD+ biosynthesis during acute colitis and underscore the dynamic interplay between host and microbial metabolism in maintaining NAD+ homeostasis under inflammatory conditions.
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@article {pmid41377969,
year = {2025},
author = {McReynolds, M and Alsaadi, A and Welz, L and Pothakamury, A and Gilloteau, C and Prasad, P and Yahia, M and Sadler, J and Smith, J and Jenkins, B and Diven, G and Bornhäuser, J and Mekdoud, T and Tian, S and Rosenstiel, P and Schreiber, S and Bisanz, J and Aden, K},
title = {Tracing NAD[+] metabolism uncovers adaptive coordination between host and microbiome during colitis.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-8195970/v1},
pmid = {41377969},
issn = {2693-5015},
abstract = {Host-microbiota metabolic interactions critically regulate nicotinamide adenine dinucleotide (NAD+) homeostasis, and their disruption is increasingly linked to chronic diseases including inflammatory bowel disease (IBD). However, it remains unclear whether NAD+ dysregulation in IBD arises from impaired production, enhanced consumption, or both. Using multi-omics approaches and stable isotope-labeled NAD+ precursors administered via intravenous infusion in a murine model of dextran sulfate sodium (DSS)-induced colitis, we mapped tissue- and lumen-specific NAD+ metabolism under inflammatory stress. Our results reveal tissue-specific rewiring of NAD+ metabolism, with increased flux through the salvage pathway compensating for reduced de novo NAD+ synthesis from tryptophan. In parallel, microbial de novo NAD+ production was elevated, highlighting a cooperative host-microbiota response to inflammatory stress. These findings demonstrate differential regulation of NAD+ biosynthesis during acute colitis and underscore the dynamic interplay between host and microbial metabolism in maintaining NAD+ homeostasis under inflammatory conditions.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Increased gut Saccharomyces and decreased pathogenic fungi associated with food protein-induced enterocolitis syndrome resolution.
The journal of allergy and clinical immunology. Global, 5(1):100598.
BACKGROUND: Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated allergy, primarily affecting infants and children, with potentially severe gastrointestinal impacts. As with other allergic diseases, the cause of FPIES is unknown. Preliminary research suggests that the gut microbiome may play a role in FPIES, as well as other allergy, yet data on the mycobiome are limited.
OBJECTIVE: We sought to examine the role of the gut mycobiome in FPIES by comparing the stool mycobiome of children with FPIES to that of children who have outgrown FPIES.
METHODS: Caregivers of children with FPIES and children who had outgrown FPIES completed a demographic and lifestyle survey. DNA was extracted and sequenced from stool samples of 23 children with FPIES and 17 children with resolved FPIES. Fungal diversity and composition between the 2 groups were compared using QIIME2 (Quantitative Insights Into Microbial Ecology 2).
RESULTS: Children with resolved FPIES had significantly more Saccharomyces than children with current FPIES. Children with current FPIES had significantly more diverse samples and included opportunistic pathogens, such as Candida spp. Children with resolved FPIES reported significantly less infant antibiotic usage and proton pump inhibitor usage.
DISCUSSION: This study identified distinct mycobiome profiles in children with current versus resolved FPIES. Resolved FPIES was associated with Saccharomyces enrichment, whereas children with current FPIES had more diverse, opportunistic pathogen-associated communities and greater infant antibiotic and proton pump inhibitor usage. Although these associations do not establish causality, they underscore the need for larger, longitudinal studies to determine whether the mycobiome and early-life exposures influence FPIES outcomes, because it could have implications for treatment and prevention.
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@article {pmid41377758,
year = {2026},
author = {Benjamin, K and Yuan, Q and Boyer, J},
title = {Increased gut Saccharomyces and decreased pathogenic fungi associated with food protein-induced enterocolitis syndrome resolution.},
journal = {The journal of allergy and clinical immunology. Global},
volume = {5},
number = {1},
pages = {100598},
pmid = {41377758},
issn = {2772-8293},
abstract = {BACKGROUND: Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated allergy, primarily affecting infants and children, with potentially severe gastrointestinal impacts. As with other allergic diseases, the cause of FPIES is unknown. Preliminary research suggests that the gut microbiome may play a role in FPIES, as well as other allergy, yet data on the mycobiome are limited.
OBJECTIVE: We sought to examine the role of the gut mycobiome in FPIES by comparing the stool mycobiome of children with FPIES to that of children who have outgrown FPIES.
METHODS: Caregivers of children with FPIES and children who had outgrown FPIES completed a demographic and lifestyle survey. DNA was extracted and sequenced from stool samples of 23 children with FPIES and 17 children with resolved FPIES. Fungal diversity and composition between the 2 groups were compared using QIIME2 (Quantitative Insights Into Microbial Ecology 2).
RESULTS: Children with resolved FPIES had significantly more Saccharomyces than children with current FPIES. Children with current FPIES had significantly more diverse samples and included opportunistic pathogens, such as Candida spp. Children with resolved FPIES reported significantly less infant antibiotic usage and proton pump inhibitor usage.
DISCUSSION: This study identified distinct mycobiome profiles in children with current versus resolved FPIES. Resolved FPIES was associated with Saccharomyces enrichment, whereas children with current FPIES had more diverse, opportunistic pathogen-associated communities and greater infant antibiotic and proton pump inhibitor usage. Although these associations do not establish causality, they underscore the need for larger, longitudinal studies to determine whether the mycobiome and early-life exposures influence FPIES outcomes, because it could have implications for treatment and prevention.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Integrative analysis of the gut microbiota, bile acid pathways, and immune dysregulation in dyslipidemia models.
iScience, 28(12):114001.
Emerging evidence suggests a link between gut microbiota, bile acid metabolism, and immune dysregulation in dyslipidemia. Through a case-control study involving 140 participants and an animal experiment, we identified significantly elevated counts of peripheral blood CD3[+] T cells, CD4[+] T cells, CD8[+] T cells, and CD19[+] B cells in patients with dyslipidemia, alongside increased specific bile acids in fecal samples and distinct alterations in gut microbiota composition. The animal model confirmed changes in gut microbiota, bile acid metabolism, and percentage of specific lymphocyte subsets. Also, we identified downregulated hepatic expressions of bile acid metabolism-related proteins in hyperlipidemic rats. Integrated analysis suggested potential associations among gut microbiota, bile acid pathways, and immune dysregulation. Overall, these data highlight the critical role of the potential gut microbiota-bile acid metabolism-immune axis in dyslipidemia, providing potential therapeutic targets for diseases associated with lipid metabolism disorders.
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@article {pmid41377665,
year = {2025},
author = {Xia, J and Shao, Y and Li, B and Wu, T and He, Z and Feng, Z and Zhang, Z and Yin, S and Wang, Y and Yu, J and Wang, J and Sun, G},
title = {Integrative analysis of the gut microbiota, bile acid pathways, and immune dysregulation in dyslipidemia models.},
journal = {iScience},
volume = {28},
number = {12},
pages = {114001},
pmid = {41377665},
issn = {2589-0042},
abstract = {Emerging evidence suggests a link between gut microbiota, bile acid metabolism, and immune dysregulation in dyslipidemia. Through a case-control study involving 140 participants and an animal experiment, we identified significantly elevated counts of peripheral blood CD3[+] T cells, CD4[+] T cells, CD8[+] T cells, and CD19[+] B cells in patients with dyslipidemia, alongside increased specific bile acids in fecal samples and distinct alterations in gut microbiota composition. The animal model confirmed changes in gut microbiota, bile acid metabolism, and percentage of specific lymphocyte subsets. Also, we identified downregulated hepatic expressions of bile acid metabolism-related proteins in hyperlipidemic rats. Integrated analysis suggested potential associations among gut microbiota, bile acid pathways, and immune dysregulation. Overall, these data highlight the critical role of the potential gut microbiota-bile acid metabolism-immune axis in dyslipidemia, providing potential therapeutic targets for diseases associated with lipid metabolism disorders.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Gut Microbiome and Cardiovascular Health: Mechanisms, Therapeutic Potential and Future Directions.
Heart international, 19(2):12-20.
BACKGROUND: The gut microbiome has a crucial role in host metabolism and immune regulation, and there is growing evidence that dysbiosis may be associated with the pathogenesis of cardiovascular disease (CVD). This narrative review provides an overview of the recent literature on mechanistic connections between the gut and heart, as well as on the therapeutic strategies and research gaps in the gut-heart axis.
METHODS: We conducted a systematic literature search on PubMed and Embase databases with MeSH and keyword terms: 'gut microbiome', 'cardiovascular disease', 'TMAO', 'short-chain fatty acids', 'probiotics' and 'faecal microbiota transplantation'. We considered human and relevant animal studies focusing on mechanistic pathways or microbiome treatments and excluded editorials, small (less than 10 subjects) case series and articles not published in the English language.
RESULTS: Key microbiota-derived metabolites, trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs), contribute to atherogenesis, blood pressure and myocardial inflammation. Dysbiosis-induced barrier dysfunction and disturbed bile acid signalling also serve as the mediators of cardiac remodelling. Dietary fibre, probiotics/prebiotics, postbiotics and faecal microbiota transplantation are emerging interventions for the modulation of CVD risk. Nevertheless, most result from observational studies, whilst such are heterogeneous in sequencing platforms and too small to draw any definitive conclusions.
CONCLUSION: The modulation of gut microbiome might be a new target for CVD prevention and treatment. Large-scale, standardized randomized trials with hard cardiovascular endpoints, as well as integrated multi-omics profiling, will be required to validate microbial biomarkers and to optimize microbiome-based interventions.
Additional Links: PMID-41377642
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@article {pmid41377642,
year = {2025},
author = {Edpuganti, S and Subhash, S and Subrahmaniyan, SL and Latheef, S and Albarari, SS},
title = {Gut Microbiome and Cardiovascular Health: Mechanisms, Therapeutic Potential and Future Directions.},
journal = {Heart international},
volume = {19},
number = {2},
pages = {12-20},
pmid = {41377642},
issn = {2036-2579},
abstract = {BACKGROUND: The gut microbiome has a crucial role in host metabolism and immune regulation, and there is growing evidence that dysbiosis may be associated with the pathogenesis of cardiovascular disease (CVD). This narrative review provides an overview of the recent literature on mechanistic connections between the gut and heart, as well as on the therapeutic strategies and research gaps in the gut-heart axis.
METHODS: We conducted a systematic literature search on PubMed and Embase databases with MeSH and keyword terms: 'gut microbiome', 'cardiovascular disease', 'TMAO', 'short-chain fatty acids', 'probiotics' and 'faecal microbiota transplantation'. We considered human and relevant animal studies focusing on mechanistic pathways or microbiome treatments and excluded editorials, small (less than 10 subjects) case series and articles not published in the English language.
RESULTS: Key microbiota-derived metabolites, trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs), contribute to atherogenesis, blood pressure and myocardial inflammation. Dysbiosis-induced barrier dysfunction and disturbed bile acid signalling also serve as the mediators of cardiac remodelling. Dietary fibre, probiotics/prebiotics, postbiotics and faecal microbiota transplantation are emerging interventions for the modulation of CVD risk. Nevertheless, most result from observational studies, whilst such are heterogeneous in sequencing platforms and too small to draw any definitive conclusions.
CONCLUSION: The modulation of gut microbiome might be a new target for CVD prevention and treatment. Large-scale, standardized randomized trials with hard cardiovascular endpoints, as well as integrated multi-omics profiling, will be required to validate microbial biomarkers and to optimize microbiome-based interventions.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Natural strategies to optimize estrogen levels in aging women: mini review.
Frontiers in aging, 6:1706117.
INTRODUCTION: Menopause triggers declining estradiol, causing vasomotor symptoms, bone loss, and urogenital changes. Despite hormone therapy's effectiveness, safety concerns drive 40%-50% of Western women toward natural alternatives.
AIM: To evaluate evidence supporting non-pharmacological interventions that modulate endogenous estrogen activity in postmenopausal women.
METHODS: 48 high-quality publications (2015-2025) examining dietary interventions, micronutrient supplementation, gut microbiome modulation, lifestyle modifications, and botanical remedies for menopausal symptoms were analyzed and included in this review. Selection criteria included randomized controlled trials, systematic reviews, meta-analyses, and cohort studies specifically addressing natural interventions in perimenopausal and postmenopausal women.
RESULTS: Multiple natural approaches demonstrated clinically meaningful effects. Dietary phytoestrogens (50-80 mg/day isoflavones) reduced severe hot flashes by up to 92%, improved metabolic parameters, and were confirmed safe for reproductive tissues. Flaxseed lignans reduced perimenopausal symptoms. Combined vitamin E and omega-3 lowered hot flush intensity, while vitamin E alone showed estrogenic receptor activation. Curcumin (500 mg/day) reduced hot flashes after 4 weeks and improved metabolic profiles. Probiotics containing L. brevis KABP052 increased circulating estrogens by up to 26% over 12 weeks. Stress reduction interventions improved quality of life, and cognitive behavioral therapy reduced insomnia severity. Botanicals including black cohosh, red clover, and rhapontic rhubarb reduced vasomotor symptoms, while resveratrol (75 mg twice daily) significantly improved bone mineral density over 12 months. Research gaps remain regarding dosing and genetic variability.
CONCLUSION: A multi-domain approach incorporating phytoestrogen-rich foods, targeted micronutrients, gut microbiome optimization, and regular exercise provides evidence-based options for managing estrogen decline. While these approaches cannot fully replace hormone therapy, they provide valuable alternatives for women with contraindications or preferences against pharmaceutical intervention. Future research should focus on personalized approaches incorporating genetic profiling.
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@article {pmid41377590,
year = {2025},
author = {Bolgova, O and Shypilova, I and Mavrych, V},
title = {Natural strategies to optimize estrogen levels in aging women: mini review.},
journal = {Frontiers in aging},
volume = {6},
number = {},
pages = {1706117},
pmid = {41377590},
issn = {2673-6217},
abstract = {INTRODUCTION: Menopause triggers declining estradiol, causing vasomotor symptoms, bone loss, and urogenital changes. Despite hormone therapy's effectiveness, safety concerns drive 40%-50% of Western women toward natural alternatives.
AIM: To evaluate evidence supporting non-pharmacological interventions that modulate endogenous estrogen activity in postmenopausal women.
METHODS: 48 high-quality publications (2015-2025) examining dietary interventions, micronutrient supplementation, gut microbiome modulation, lifestyle modifications, and botanical remedies for menopausal symptoms were analyzed and included in this review. Selection criteria included randomized controlled trials, systematic reviews, meta-analyses, and cohort studies specifically addressing natural interventions in perimenopausal and postmenopausal women.
RESULTS: Multiple natural approaches demonstrated clinically meaningful effects. Dietary phytoestrogens (50-80 mg/day isoflavones) reduced severe hot flashes by up to 92%, improved metabolic parameters, and were confirmed safe for reproductive tissues. Flaxseed lignans reduced perimenopausal symptoms. Combined vitamin E and omega-3 lowered hot flush intensity, while vitamin E alone showed estrogenic receptor activation. Curcumin (500 mg/day) reduced hot flashes after 4 weeks and improved metabolic profiles. Probiotics containing L. brevis KABP052 increased circulating estrogens by up to 26% over 12 weeks. Stress reduction interventions improved quality of life, and cognitive behavioral therapy reduced insomnia severity. Botanicals including black cohosh, red clover, and rhapontic rhubarb reduced vasomotor symptoms, while resveratrol (75 mg twice daily) significantly improved bone mineral density over 12 months. Research gaps remain regarding dosing and genetic variability.
CONCLUSION: A multi-domain approach incorporating phytoestrogen-rich foods, targeted micronutrients, gut microbiome optimization, and regular exercise provides evidence-based options for managing estrogen decline. While these approaches cannot fully replace hormone therapy, they provide valuable alternatives for women with contraindications or preferences against pharmaceutical intervention. Future research should focus on personalized approaches incorporating genetic profiling.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Sarcopenia and lower urinary tract diseases: links, mechanisms, and clinical implications.
Frontiers in nutrition, 12:1704456.
Lower urinary tract diseases (LUTDs), including lower urinary tract symptoms (LUTS), overactive bladder (OAB), urinary incontinence (UI), bladder cancer (BC), prostate cancer (PCa), and benign prostatic hyperplasia (BPH), severely impair the quality of life of the elderly. Emerging evidence highlights a strong association between sarcopenia (progressive loss of muscle mass, strength, and function) and the prevalence, severity, and progression of LUTDs, as well as poorer treatment responses in affected patients-though most supporting studies are cross-sectional or retrospective, with prospective trials needed to confirm causality. Potential mechanisms linking sarcopenia to LUTDs include pelvic floor muscle weakening, neuromuscular dysfunction, metabolic/endocrine disturbances, genetic factors, and gut microbiome dysregulation. Clinically, interventions such as resistance exercise, nutritional support, gut microbiome-targeted strategies, pelvic floor training, and pharmacological therapies show promise in mitigating LUTDs symptoms by targeting sarcopenia. Integrating sarcopenia assessment into LUTDs management could improve patient care; future research should prioritize large-scale prospective trials to validate causal relationships, clarify key mediating mechanisms (e.g., specific gut microbial taxa, neuromuscular signaling pathways), and develop personalized intervention protocols tailored to distinct LUTD subtypes and patient characteristics.
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@article {pmid41377560,
year = {2025},
author = {Liu, S and Cao, H and Wang, L and Li, S and Liang, Y and Feng, Y and Gao, Z and Wang, S and Lian, X},
title = {Sarcopenia and lower urinary tract diseases: links, mechanisms, and clinical implications.},
journal = {Frontiers in nutrition},
volume = {12},
number = {},
pages = {1704456},
pmid = {41377560},
issn = {2296-861X},
abstract = {Lower urinary tract diseases (LUTDs), including lower urinary tract symptoms (LUTS), overactive bladder (OAB), urinary incontinence (UI), bladder cancer (BC), prostate cancer (PCa), and benign prostatic hyperplasia (BPH), severely impair the quality of life of the elderly. Emerging evidence highlights a strong association between sarcopenia (progressive loss of muscle mass, strength, and function) and the prevalence, severity, and progression of LUTDs, as well as poorer treatment responses in affected patients-though most supporting studies are cross-sectional or retrospective, with prospective trials needed to confirm causality. Potential mechanisms linking sarcopenia to LUTDs include pelvic floor muscle weakening, neuromuscular dysfunction, metabolic/endocrine disturbances, genetic factors, and gut microbiome dysregulation. Clinically, interventions such as resistance exercise, nutritional support, gut microbiome-targeted strategies, pelvic floor training, and pharmacological therapies show promise in mitigating LUTDs symptoms by targeting sarcopenia. Integrating sarcopenia assessment into LUTDs management could improve patient care; future research should prioritize large-scale prospective trials to validate causal relationships, clarify key mediating mechanisms (e.g., specific gut microbial taxa, neuromuscular signaling pathways), and develop personalized intervention protocols tailored to distinct LUTD subtypes and patient characteristics.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Sedation and analgesia strategies in the neuro intensive care unit.
World journal of critical care medicine, 14(4):111787.
Intensivists are often plagued with the challenges of managing critically ill patients in the neurocritical intensive care unit (neuro ICU); one such challenge is the level of illness and the need for sedation, inhibiting the provider's ability to adequately assess the patient. Most sedatives alter neurological and physical exam findings, only compounding potential barriers to providing the best care for each patient. It is important to emphasize that even in the altered mentation of these patients, physical and neurological exams reign supreme as diagnostic tools and should be used in conjunction with multimodal neuromonitoring methods, rather than labs or imaging alone. Additionally, selecting the appropriate analgesic(s) and sedative(s) based on these findings are highly important when determining the best course of individualized management. Thus, providers in the neuro ICU should be highly familiar with the appropriate analgesic and sedative options available in order to determine not only which may be best for each patient, but to also better understand how each drug may impact assessment findings. This comprehensive review aims to provide a structured overview of the pertinent sedatives commonly used in neuro ICUs, their risks and benefits, and how providers can best utilize each in practice to further improve patient outcomes. The novel contribution of this work provides comparative drug tables, dosing guidance for pediatric and very elderly (> 85-years-old) populations, and an exploration into the future possibilities of utilizing artificial intelligence and the human gut microbiome to further enhance the prospects of precision medicine.
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@article {pmid41377537,
year = {2025},
author = {Merhavy, ZI and Raeburn, T and Torres-Ayala, GM and McCulloch, MA and Varkey, TC},
title = {Sedation and analgesia strategies in the neuro intensive care unit.},
journal = {World journal of critical care medicine},
volume = {14},
number = {4},
pages = {111787},
pmid = {41377537},
issn = {2220-3141},
abstract = {Intensivists are often plagued with the challenges of managing critically ill patients in the neurocritical intensive care unit (neuro ICU); one such challenge is the level of illness and the need for sedation, inhibiting the provider's ability to adequately assess the patient. Most sedatives alter neurological and physical exam findings, only compounding potential barriers to providing the best care for each patient. It is important to emphasize that even in the altered mentation of these patients, physical and neurological exams reign supreme as diagnostic tools and should be used in conjunction with multimodal neuromonitoring methods, rather than labs or imaging alone. Additionally, selecting the appropriate analgesic(s) and sedative(s) based on these findings are highly important when determining the best course of individualized management. Thus, providers in the neuro ICU should be highly familiar with the appropriate analgesic and sedative options available in order to determine not only which may be best for each patient, but to also better understand how each drug may impact assessment findings. This comprehensive review aims to provide a structured overview of the pertinent sedatives commonly used in neuro ICUs, their risks and benefits, and how providers can best utilize each in practice to further improve patient outcomes. The novel contribution of this work provides comparative drug tables, dosing guidance for pediatric and very elderly (> 85-years-old) populations, and an exploration into the future possibilities of utilizing artificial intelligence and the human gut microbiome to further enhance the prospects of precision medicine.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Disrupted tRNA modification leads to intestinal mitochondrial dysfunction and microbial dysbiosis.
bioRxiv : the preprint server for biology pii:2025.11.27.690007.
BACKGROUND AND AIMS: Transfer RNA (tRNA) modifications determine translation fidelity and efficiency. It occurs through the action of specific enzymes that modify the nucleotides within the tRNA molecule. Our previous study demonstrated tRNA modopathies and altered queuine-related metabolites in inflammatory bowel diseases. Queuine tRNA-ribosyltransferase catalytic subunit 1 (QTRT1) and QTRT 2 co-localize in mitochondria and form a heterodimeric TGT participating in tRNA Queuosine (tRNA-Q) modification. Human body acquires Queuine/Vitamin Q from intestinal microbiota or from diet. However, the roles of tRNA-Q modifications in the maintenance of intestinal mitochondrial homeostasis and microbiome are still unclear.
METHODS: We used publicly available human IBD datasets, QTRT1 knockout (KO) mice, QTRT1 intestinal epithelial conditional KO (QTRT1 [ΔIEC]) mice, cultured cell lines with QTRT1-specific siRNA, and organoids from patients with IBD to investigate the mechanism of tRNA-Q modifications in intestinal mitochondrial homeostasis and therapeutic potential in anti-inflammation.
RESULTS: In single cell RNA sequencing datasets of human IBD, we identified significant reduced intestinal epithelial QTRT1 expression in the patients with Crohn's Disease. Using publicly available datasets, we identified significantly changes of Vitamin Q-associated bacteria in human IBD, compared to the healthy control. Qtrt1 [-/-] mice had significant reduction of Q-associated bacteria, e.g., Bacteroides . Alcian Blue and Mucin-2 staining revealed mucosal barrier damage and disrupted homeostasis, with reduced colonic cell proliferation. Intestinal tight junction integrity was impaired in QTRT1-KO mice, as evidenced by reduced ZO-1 and increased Claudin-10 expression. QTRT1 [ΔIEC] mice also showed dysbiosis and disrupted TJs. ATP synthesis was significantly decreased in the colon of QTRT1-KO mice, accompanied by severe mitochondrial dysfunction: reduced mitochondrial quality, Cytochrome-C release, and mitochondrial DNA (mtDNA) leakage. Mitochondrial dysfunction contributed to colonic cell death, as shown by elevated expressions of Cleaved Caspase-3 and Cleaved Caspase-1, increased BAX/Bcl-2 ratio, and positive TUNEL signals. Elevated CDC42, CD14, and CD4 levels in QTRT1-KO colon suggested mucosal immune activation and tissue repair responses. QTRT1-deficient CaCO2-BBE cells showed mitochondrial dysfunction. Cytochrome-C and mito-DNA release leading to cell death characterized by elevated expressions of Cleaved Caspase-3 and Caspase-1, increased BAX/Bcl-2 ratio, and higher apoptosis rate. Organoids isolated from patients with IBD showed reduced levels of QTRT1 and dysfunctional mitochondria. Restoring mitochondrial function leads to enhanced QTRT1.
CONCLUSIONS: These findings underscore the critical role of QTRT1/Q-tRNA modification in maintaining intestinal and microbial homeostasis. Mechanistically, QTRT1 loss impacts mitochondrial integrity and mucosal homeostasis. Our study highlights the novel roles of tRNA-Q modification in maintaining mucosal barriers and innate immunity in intestinal health.
Eukaryotes acquire queuine (q), also known as Vitamin Q, as a micronutrient factor from intestinal microbiota or from diet.Vitamin Q is needed for queuosine (Q) modification of tRNAs for the protein translation rate and fidelity.Queuine tRNA-ribosyltransferase catalytic subunit 1 (QTRT1) is reduced in human IBD.However, health consequences of disturbed availability of queuine and altered Q-tRNA modification in digestive diseases remain to be investigated.
WHAT ARE THE NEW FINDINGS?: QTRT1 deficiency leads to altered microbiome and reduced Vitamin Q-associated bacteria in human IBD and a QTRT1 KO animal model.QTRT1 protects the host against losing intestinal integrity during inflammation.QTRT1 localizes in mitochondria and plays novel functions by maintaining intestinal mitochondrial function. QTRT1 loss impacts tRNA modification in the intestine, linking to mitochondrial integrity and mucosal homeostasis.Human IBD showed reduced levels of QTRT1 and dysfunctional mitochondria. Restoring mitochondrial function leads to enhanced QTRT1.
Targeting tRNA-Q modification in enhancing mitochondrial function will be a novel method to maintain intestinal health.
Additional Links: PMID-41377497
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@article {pmid41377497,
year = {2025},
author = {Ran, D and Zhang, Y and An, Y and Hu, Y and Xia, Y and Sun, J},
title = {Disrupted tRNA modification leads to intestinal mitochondrial dysfunction and microbial dysbiosis.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.11.27.690007},
pmid = {41377497},
issn = {2692-8205},
abstract = {BACKGROUND AND AIMS: Transfer RNA (tRNA) modifications determine translation fidelity and efficiency. It occurs through the action of specific enzymes that modify the nucleotides within the tRNA molecule. Our previous study demonstrated tRNA modopathies and altered queuine-related metabolites in inflammatory bowel diseases. Queuine tRNA-ribosyltransferase catalytic subunit 1 (QTRT1) and QTRT 2 co-localize in mitochondria and form a heterodimeric TGT participating in tRNA Queuosine (tRNA-Q) modification. Human body acquires Queuine/Vitamin Q from intestinal microbiota or from diet. However, the roles of tRNA-Q modifications in the maintenance of intestinal mitochondrial homeostasis and microbiome are still unclear.
METHODS: We used publicly available human IBD datasets, QTRT1 knockout (KO) mice, QTRT1 intestinal epithelial conditional KO (QTRT1 [ΔIEC]) mice, cultured cell lines with QTRT1-specific siRNA, and organoids from patients with IBD to investigate the mechanism of tRNA-Q modifications in intestinal mitochondrial homeostasis and therapeutic potential in anti-inflammation.
RESULTS: In single cell RNA sequencing datasets of human IBD, we identified significant reduced intestinal epithelial QTRT1 expression in the patients with Crohn's Disease. Using publicly available datasets, we identified significantly changes of Vitamin Q-associated bacteria in human IBD, compared to the healthy control. Qtrt1 [-/-] mice had significant reduction of Q-associated bacteria, e.g., Bacteroides . Alcian Blue and Mucin-2 staining revealed mucosal barrier damage and disrupted homeostasis, with reduced colonic cell proliferation. Intestinal tight junction integrity was impaired in QTRT1-KO mice, as evidenced by reduced ZO-1 and increased Claudin-10 expression. QTRT1 [ΔIEC] mice also showed dysbiosis and disrupted TJs. ATP synthesis was significantly decreased in the colon of QTRT1-KO mice, accompanied by severe mitochondrial dysfunction: reduced mitochondrial quality, Cytochrome-C release, and mitochondrial DNA (mtDNA) leakage. Mitochondrial dysfunction contributed to colonic cell death, as shown by elevated expressions of Cleaved Caspase-3 and Cleaved Caspase-1, increased BAX/Bcl-2 ratio, and positive TUNEL signals. Elevated CDC42, CD14, and CD4 levels in QTRT1-KO colon suggested mucosal immune activation and tissue repair responses. QTRT1-deficient CaCO2-BBE cells showed mitochondrial dysfunction. Cytochrome-C and mito-DNA release leading to cell death characterized by elevated expressions of Cleaved Caspase-3 and Caspase-1, increased BAX/Bcl-2 ratio, and higher apoptosis rate. Organoids isolated from patients with IBD showed reduced levels of QTRT1 and dysfunctional mitochondria. Restoring mitochondrial function leads to enhanced QTRT1.
CONCLUSIONS: These findings underscore the critical role of QTRT1/Q-tRNA modification in maintaining intestinal and microbial homeostasis. Mechanistically, QTRT1 loss impacts mitochondrial integrity and mucosal homeostasis. Our study highlights the novel roles of tRNA-Q modification in maintaining mucosal barriers and innate immunity in intestinal health.
Eukaryotes acquire queuine (q), also known as Vitamin Q, as a micronutrient factor from intestinal microbiota or from diet.Vitamin Q is needed for queuosine (Q) modification of tRNAs for the protein translation rate and fidelity.Queuine tRNA-ribosyltransferase catalytic subunit 1 (QTRT1) is reduced in human IBD.However, health consequences of disturbed availability of queuine and altered Q-tRNA modification in digestive diseases remain to be investigated.
WHAT ARE THE NEW FINDINGS?: QTRT1 deficiency leads to altered microbiome and reduced Vitamin Q-associated bacteria in human IBD and a QTRT1 KO animal model.QTRT1 protects the host against losing intestinal integrity during inflammation.QTRT1 localizes in mitochondria and plays novel functions by maintaining intestinal mitochondrial function. QTRT1 loss impacts tRNA modification in the intestine, linking to mitochondrial integrity and mucosal homeostasis.Human IBD showed reduced levels of QTRT1 and dysfunctional mitochondria. Restoring mitochondrial function leads to enhanced QTRT1.
Targeting tRNA-Q modification in enhancing mitochondrial function will be a novel method to maintain intestinal health.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Engineered microbes over immunosuppression: MAGIC as a transformative strategy for vasculitides.
Annals of medicine and surgery (2012), 87(12):9131-9132.
Additional Links: PMID-41377425
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@article {pmid41377425,
year = {2025},
author = {Nawaz, S and Nadeem, IA and Talha, M and Irshad, NUN and Imran, SB},
title = {Engineered microbes over immunosuppression: MAGIC as a transformative strategy for vasculitides.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9131-9132},
pmid = {41377425},
issn = {2049-0801},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Reassessment of microbial DNA in cancer genomes: addressing contamination controversies.
Annals of medicine and surgery (2012), 87(12):9085-9086.
The proposed existence of a widespread "tumor microbiome" has sparked considerable interest, yet recent evidence suggests many microbial DNA signals in cancer genomes arise from contamination rather than true colonization. A September 2025 Science Translational Medicine analysis of over 5700 cancer genomes demonstrated that most detected sequences reflected artifacts, underscoring earlier concerns about low-biomass sequencing studies. While enthusiasm for a universal tumor microbiome must be tempered, robust associations remain in specific cancers, including Helicobacter pylori in gastric carcinoma, Fusobacterium nucleatum in colorectal cancer, and human papillomavirus in cervical malignancies. This reassessment highlights the urgent need for rigorous methodological standards, such as robust negative controls, contamination-aware pipelines, and transparent reporting, to ensure reproducibility. Rather than discouragement, this represents an opportunity to refocus research on biologically plausible, clinically relevant cancer-microbe interactions.
Additional Links: PMID-41377407
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@article {pmid41377407,
year = {2025},
author = {Mehmood, MS and Hajj, F},
title = {Reassessment of microbial DNA in cancer genomes: addressing contamination controversies.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9085-9086},
pmid = {41377407},
issn = {2049-0801},
abstract = {The proposed existence of a widespread "tumor microbiome" has sparked considerable interest, yet recent evidence suggests many microbial DNA signals in cancer genomes arise from contamination rather than true colonization. A September 2025 Science Translational Medicine analysis of over 5700 cancer genomes demonstrated that most detected sequences reflected artifacts, underscoring earlier concerns about low-biomass sequencing studies. While enthusiasm for a universal tumor microbiome must be tempered, robust associations remain in specific cancers, including Helicobacter pylori in gastric carcinoma, Fusobacterium nucleatum in colorectal cancer, and human papillomavirus in cervical malignancies. This reassessment highlights the urgent need for rigorous methodological standards, such as robust negative controls, contamination-aware pipelines, and transparent reporting, to ensure reproducibility. Rather than discouragement, this represents an opportunity to refocus research on biologically plausible, clinically relevant cancer-microbe interactions.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Intratumoral microbiota as prognostic biomarkers in gastrointestinal cancers.
Annals of medicine and surgery (2012), 87(12):9137-9138.
Recent evidence highlights that the tumor microenvironment in gastrointestinal (GI) cancers harbors distinct microbial communities with potential prognostic value. GI malignancies account for nearly 25% of all cancer-related deaths worldwide, yet patients with comparable histopathological features often display markedly different clinical outcomes. Emerging multi-omics studies involving over 3000 tumor specimens have revealed that specific microbial taxa, including Granulicella, Fusobacterium nucleatum, and Parvimonas micra, are linked to advanced disease stages, lymphatic spread, and poorer overall survival. F. nucleatum, in particular, has been implicated in promoting chemoresistance via Toll-like receptor 4 activation and modulation of the immune microenvironment. Reduced microbial alpha diversity within tumors has also been correlated with disease aggressiveness, suggesting a dysbiosis-mediated influence on tumor immunity. Integration of microbial profiles with transcriptomic and immunologic datasets has produced hybrid models that outperform conventional TNM staging in predicting recurrence and therapy response. Standardizing sampling, sequencing, and analytical methodologies remains a critical challenge. The incorporation of microbiome profiling into diagnostic and registry systems could enable routine use of intratumoral microbial signatures as prognostic biomarkers, paving the way toward microbiome-informed precision oncology.
Additional Links: PMID-41377390
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@article {pmid41377390,
year = {2025},
author = {Mehmood, MS and Iqbal, I and Hajj, F},
title = {Intratumoral microbiota as prognostic biomarkers in gastrointestinal cancers.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9137-9138},
pmid = {41377390},
issn = {2049-0801},
abstract = {Recent evidence highlights that the tumor microenvironment in gastrointestinal (GI) cancers harbors distinct microbial communities with potential prognostic value. GI malignancies account for nearly 25% of all cancer-related deaths worldwide, yet patients with comparable histopathological features often display markedly different clinical outcomes. Emerging multi-omics studies involving over 3000 tumor specimens have revealed that specific microbial taxa, including Granulicella, Fusobacterium nucleatum, and Parvimonas micra, are linked to advanced disease stages, lymphatic spread, and poorer overall survival. F. nucleatum, in particular, has been implicated in promoting chemoresistance via Toll-like receptor 4 activation and modulation of the immune microenvironment. Reduced microbial alpha diversity within tumors has also been correlated with disease aggressiveness, suggesting a dysbiosis-mediated influence on tumor immunity. Integration of microbial profiles with transcriptomic and immunologic datasets has produced hybrid models that outperform conventional TNM staging in predicting recurrence and therapy response. Standardizing sampling, sequencing, and analytical methodologies remains a critical challenge. The incorporation of microbiome profiling into diagnostic and registry systems could enable routine use of intratumoral microbial signatures as prognostic biomarkers, paving the way toward microbiome-informed precision oncology.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Zero-gravity microbiome vortices: decoding orbital sepsis mimics and probiotic dysregulation in space health systems.
Annals of medicine and surgery (2012), 87(12):9208-9210.
Additional Links: PMID-41377381
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@article {pmid41377381,
year = {2025},
author = {Memon, U and Memon, D and Talha, M and Fatima, M},
title = {Zero-gravity microbiome vortices: decoding orbital sepsis mimics and probiotic dysregulation in space health systems.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9208-9210},
pmid = {41377381},
issn = {2049-0801},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Microbiome-gut-heart axis in cardiac complications of Gaucher disease type 3.
Annals of medicine and surgery (2012), 87(12):9091-9092.
Additional Links: PMID-41377324
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@article {pmid41377324,
year = {2025},
author = {Abedin, ZU and Iqbal, MU and Shahriar, Z},
title = {Microbiome-gut-heart axis in cardiac complications of Gaucher disease type 3.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9091-9092},
pmid = {41377324},
issn = {2049-0801},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
From microbiome dysbiosis to virtual reality and nanomedicine: a multidisciplinary roadmap for pediatric glaucoma care.
Annals of medicine and surgery (2012), 87(12):9115-9116.
Additional Links: PMID-41377295
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@article {pmid41377295,
year = {2025},
author = {Talha, M and Bilal, M and Fatima, M and Hassan, M and Gill, OA},
title = {From microbiome dysbiosis to virtual reality and nanomedicine: a multidisciplinary roadmap for pediatric glaucoma care.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9115-9116},
pmid = {41377295},
issn = {2049-0801},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
The interplay of the microbiome and breast cancer: beyond the gut: a narrative review.
Annals of medicine and surgery (2012), 87(12):8496-8507.
Breast cancer remains a leading cause of morbidity and mortality among women worldwide, with emerging evidence underscoring the microbiota's pivotal role in its etiology, progression, and therapeutic response. This narrative review synthesizes the intricate interplay between the breast tissue, skin, and lung microbiomes in breast cancer pathogenesis, with particular emphasis on inflammatory breast cancer (IBC) and metastatic dissemination. The healthy breast microbiome, dominated by Firmicutes, Proteobacteria, Actinobacteria, and Bacteroidetes, maintains tissue homeostasis through pH regulation, metabolite production, and immune modulation. Dysbiosis disrupts this equilibrium, fostering carcinogenesis via chronic inflammation, estrogen deconjugation, and DNA damage-induced genomic instability, with subtype-specific microbial signatures influencing tumor growth and therapy resistance. In IBC, skin microbiome alterations characterized by overgrowth of pathogens like Pseudomonas aeruginosa and Staphylococcus aureus exacerbate inflammation, epithelial-mesenchymal transition (EMT), and lymphatic invasion, while promoting a pro-tumorigenic microenvironment enriched in regulatory T cells and M2 macrophages. Concurrently, lung microbiota dysbiosis impairs immune surveillance, remodels the extracellular matrix, and facilitates metastatic seeding through neutrophil extracellular traps and cytokine storms. Cross-talk among these microbiomes amplifies systemic effects, highlighting their synergistic contributions to disease aggressiveness. Advanced analytical techniques, including 16S rRNA sequencing, metagenomics, and metabolomics, offer promising microbial biomarkers for early detection and risk stratification. By elucidating these host-microbe dynamics, this review advocates for microbiome-centric interventionssuch as probiotics, fecal microbiota transplantation, and targeted antimicrobials to enhance precision diagnostics and therapies, ultimately improving outcomes in breast cancer management.
Additional Links: PMID-41377246
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@article {pmid41377246,
year = {2025},
author = {Singh, PK and Rathi, D and Shweliya, MA and Farooq, A and Anfaal, Z and Saleem, NUA and Hamza, M and Qadri, M and Rath, S and Hemida, MF and Rani, H and Mahgoub, AMA and Wazir, HU},
title = {The interplay of the microbiome and breast cancer: beyond the gut: a narrative review.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {8496-8507},
pmid = {41377246},
issn = {2049-0801},
abstract = {Breast cancer remains a leading cause of morbidity and mortality among women worldwide, with emerging evidence underscoring the microbiota's pivotal role in its etiology, progression, and therapeutic response. This narrative review synthesizes the intricate interplay between the breast tissue, skin, and lung microbiomes in breast cancer pathogenesis, with particular emphasis on inflammatory breast cancer (IBC) and metastatic dissemination. The healthy breast microbiome, dominated by Firmicutes, Proteobacteria, Actinobacteria, and Bacteroidetes, maintains tissue homeostasis through pH regulation, metabolite production, and immune modulation. Dysbiosis disrupts this equilibrium, fostering carcinogenesis via chronic inflammation, estrogen deconjugation, and DNA damage-induced genomic instability, with subtype-specific microbial signatures influencing tumor growth and therapy resistance. In IBC, skin microbiome alterations characterized by overgrowth of pathogens like Pseudomonas aeruginosa and Staphylococcus aureus exacerbate inflammation, epithelial-mesenchymal transition (EMT), and lymphatic invasion, while promoting a pro-tumorigenic microenvironment enriched in regulatory T cells and M2 macrophages. Concurrently, lung microbiota dysbiosis impairs immune surveillance, remodels the extracellular matrix, and facilitates metastatic seeding through neutrophil extracellular traps and cytokine storms. Cross-talk among these microbiomes amplifies systemic effects, highlighting their synergistic contributions to disease aggressiveness. Advanced analytical techniques, including 16S rRNA sequencing, metagenomics, and metabolomics, offer promising microbial biomarkers for early detection and risk stratification. By elucidating these host-microbe dynamics, this review advocates for microbiome-centric interventionssuch as probiotics, fecal microbiota transplantation, and targeted antimicrobials to enhance precision diagnostics and therapies, ultimately improving outcomes in breast cancer management.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Microbiome modulation strategies to enhance chemotherapy response and minimize toxicity.
Annals of medicine and surgery (2012), 87(12):9087-9088.
Additional Links: PMID-41377223
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@article {pmid41377223,
year = {2025},
author = {Mehmood, MS and Hajj, F},
title = {Microbiome modulation strategies to enhance chemotherapy response and minimize toxicity.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {12},
pages = {9087-9088},
pmid = {41377223},
issn = {2049-0801},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Metagenomic sequencing dataset of microbial communities in onion and cabbage microgreens across substrates, Salmonella inoculation, and bacteriophage application.
Data in brief, 63:112297.
This dataset comprises shotgun metagenomic sequencing results from edible portion of onion (Allium cepa) and cabbage (Brassica oleracea) microgreens cultivated on soil, biostrate, and jute fiber substrates, with and without Salmonella inoculation and bacteriophage application. Table 1 contains detailed sequencing quality metrics and National Center for Biotechnology Information Sequence Read Archive accession numbers (BioProject: PRJNA1327464) for all 24 samples. Figure 1 provides a species-level (≥5% relative abundance) heatmap highlighting microbial community clustering by seed type. These data can be reused for comparative microbiome analyses, evaluation of pathogen-phage-substrate interactions, and benchmarking of metagenomic workflows.
Additional Links: PMID-41377184
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@article {pmid41377184,
year = {2025},
author = {Ayilaran, E and McHugh, O and Jung, Y},
title = {Metagenomic sequencing dataset of microbial communities in onion and cabbage microgreens across substrates, Salmonella inoculation, and bacteriophage application.},
journal = {Data in brief},
volume = {63},
number = {},
pages = {112297},
pmid = {41377184},
issn = {2352-3409},
abstract = {This dataset comprises shotgun metagenomic sequencing results from edible portion of onion (Allium cepa) and cabbage (Brassica oleracea) microgreens cultivated on soil, biostrate, and jute fiber substrates, with and without Salmonella inoculation and bacteriophage application. Table 1 contains detailed sequencing quality metrics and National Center for Biotechnology Information Sequence Read Archive accession numbers (BioProject: PRJNA1327464) for all 24 samples. Figure 1 provides a species-level (≥5% relative abundance) heatmap highlighting microbial community clustering by seed type. These data can be reused for comparative microbiome analyses, evaluation of pathogen-phage-substrate interactions, and benchmarking of metagenomic workflows.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Low-calorie diet intervention ameliorates gut microbiota dysbiosis and metabolic changes in obese patients with type 2 diabetes under standard care.
Computational and structural biotechnology journal, 27:5307-5317.
BACKGROUND: Dietary interventions can modulate the gut bacteria community (microbiota) and offer a complementary strategy for improving metabolic control in type 2 diabetes (T2D). This pilot study evaluated clinical clinical outcomes and gut microbiota changes following a structured low-calorie diet (LCD) intervention in obese T2D individuals under standard care.
METHODS: Twenty obese T2D patients were randomized into an intervention group (n = 15) (6-week 1000-1200 kcal/day of glycemic and metabolic control LCD), or a matched control group (n = 5). Clinical parameters and fecal microbiota profiles were assessed at baseline, week 6, and week 12.
RESULTS: The intervention group showed clinical trends toward improved glycemic and metabolic parameters, including reductions in fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), and lipid levels (i.e., cholesterol) (P > 0.05), accompanied by significant loss of body weight, body mass index (BMI), and body fat (P < 0.05). Four intervention participants (26.7 %) achieved normoglycemia without glucose-lowering medication. Gut microbiota analyses revealed significant alterations in alpha and beta diversity over time in the intervention group (AMOVA: P(control baseline, intervention 12-week) = 0.025 and P(intervention baseline, intervention 12-week) = 0.002), with increased abundance of beneficial genera i.e. Streptococcus, Bifidobacterium and Lactobacillus, and enrichment of Actinobacteria, Candidatus Saccharibacteria (TM7), and Firmicutes at week 12. Linear discriminant analysis effect size (LEfSe) analysis identified distinct microbial biomarkers differentiating groups. Microbial functional predictions revealed significantly decreased inferred activity in pathways related to adipocytokine signaling, D-glutamine and D-glutamate metabolism, and type I diabetes mellitus (P < 0.05); however, these predictions were computational inferences and not experimentally validated.
CONCLUSION: A structured LCD combined with standard care led to metabolic improvement and remodeling of gut microbiota trend in obese Thai individuals with T2D. The findings support the dietary interventions to beneficially modulate the gut microbiome and metabolic health, while highlighting the need for larger studies and functional validation.
Additional Links: PMID-41377121
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@article {pmid41377121,
year = {2025},
author = {Umphonsathien, M and Prutanopajai, P and Cheibchalard, T and Somboonna, N},
title = {Low-calorie diet intervention ameliorates gut microbiota dysbiosis and metabolic changes in obese patients with type 2 diabetes under standard care.},
journal = {Computational and structural biotechnology journal},
volume = {27},
number = {},
pages = {5307-5317},
pmid = {41377121},
issn = {2001-0370},
abstract = {BACKGROUND: Dietary interventions can modulate the gut bacteria community (microbiota) and offer a complementary strategy for improving metabolic control in type 2 diabetes (T2D). This pilot study evaluated clinical clinical outcomes and gut microbiota changes following a structured low-calorie diet (LCD) intervention in obese T2D individuals under standard care.
METHODS: Twenty obese T2D patients were randomized into an intervention group (n = 15) (6-week 1000-1200 kcal/day of glycemic and metabolic control LCD), or a matched control group (n = 5). Clinical parameters and fecal microbiota profiles were assessed at baseline, week 6, and week 12.
RESULTS: The intervention group showed clinical trends toward improved glycemic and metabolic parameters, including reductions in fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), and lipid levels (i.e., cholesterol) (P > 0.05), accompanied by significant loss of body weight, body mass index (BMI), and body fat (P < 0.05). Four intervention participants (26.7 %) achieved normoglycemia without glucose-lowering medication. Gut microbiota analyses revealed significant alterations in alpha and beta diversity over time in the intervention group (AMOVA: P(control baseline, intervention 12-week) = 0.025 and P(intervention baseline, intervention 12-week) = 0.002), with increased abundance of beneficial genera i.e. Streptococcus, Bifidobacterium and Lactobacillus, and enrichment of Actinobacteria, Candidatus Saccharibacteria (TM7), and Firmicutes at week 12. Linear discriminant analysis effect size (LEfSe) analysis identified distinct microbial biomarkers differentiating groups. Microbial functional predictions revealed significantly decreased inferred activity in pathways related to adipocytokine signaling, D-glutamine and D-glutamate metabolism, and type I diabetes mellitus (P < 0.05); however, these predictions were computational inferences and not experimentally validated.
CONCLUSION: A structured LCD combined with standard care led to metabolic improvement and remodeling of gut microbiota trend in obese Thai individuals with T2D. The findings support the dietary interventions to beneficially modulate the gut microbiome and metabolic health, while highlighting the need for larger studies and functional validation.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Integrative network pharmacology, transcriptomics, and microbiomics elucidate the therapeutic mechanism of Polygala tenuifolia Willd water extract in chronic obstructive pulmonary disease.
Frontiers in microbiology, 16:1703853.
BACKGROUND: Polygala tenuifolia Willd (PT) is a plant with both medicinal and edible values. Traditionally, it has been used for sedation, enhancing cognition, resolving phlegm, and relieving cough. However, its protective effects and mechanisms against chronic obstructive pulmonary disease (COPD) remain unclear.
AIM OF THE STUDY: This study aims to observe the protective effects of the water extract of Polygala tenuifolia Willd (WEPT) on COPD, and to preliminarily elucidate its potential therapeutic mechanisms by integrating network pharmacology, molecular docking, multi-omics analysis, and molecular experiments.
METHODS AND MATERIALS: HPLC quantified WEPT constituents. COPD mice models established via chronic smoke exposure underwent WEPT treatment, and the therapeutic effect was evaluated by lung function test, histopathology and cytokine profiling. Integrated multi-omics analyses (network pharmacology, transcriptomics, microbiomics) identified bioactive compounds, therapeutic targets, pathway regulations, and microbiota dynamics. Molecular docking validated compound-target interactions, while immunohistochemical/fluorescence assays confirmed key protein expression in lung tissues.
RESULTS: WEPT administration effectively reduced inflammatory cytokine levels in COPD mice, improved lung function, and alleviated histopathological damage like alveolar structural injury and airway inflammation. Network pharmacology and transcriptomic analyses identified Norhyoscyamine and Onjixanthone I as key active components, targeting PIK3CA and AKT1 via PI3K-AKT pathway regulation. Microbiome analysis showed WEPT restored gut microbiota balance. Molecular docking confirmed strong binding of bioactive compounds to core targets, while immunostaining assays demonstrated WEPT suppressed p-PI3K and p-AKT protein expression.
CONCLUSION: WEPT may exert its intervention effects on COPD through a multi-target and multi-level comprehensive regulatory mechanism.
Additional Links: PMID-41377050
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@article {pmid41377050,
year = {2025},
author = {An, Y and Yu, X and Wang, C and Yu, X and Zheng, J and Lin, H},
title = {Integrative network pharmacology, transcriptomics, and microbiomics elucidate the therapeutic mechanism of Polygala tenuifolia Willd water extract in chronic obstructive pulmonary disease.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1703853},
pmid = {41377050},
issn = {1664-302X},
abstract = {BACKGROUND: Polygala tenuifolia Willd (PT) is a plant with both medicinal and edible values. Traditionally, it has been used for sedation, enhancing cognition, resolving phlegm, and relieving cough. However, its protective effects and mechanisms against chronic obstructive pulmonary disease (COPD) remain unclear.
AIM OF THE STUDY: This study aims to observe the protective effects of the water extract of Polygala tenuifolia Willd (WEPT) on COPD, and to preliminarily elucidate its potential therapeutic mechanisms by integrating network pharmacology, molecular docking, multi-omics analysis, and molecular experiments.
METHODS AND MATERIALS: HPLC quantified WEPT constituents. COPD mice models established via chronic smoke exposure underwent WEPT treatment, and the therapeutic effect was evaluated by lung function test, histopathology and cytokine profiling. Integrated multi-omics analyses (network pharmacology, transcriptomics, microbiomics) identified bioactive compounds, therapeutic targets, pathway regulations, and microbiota dynamics. Molecular docking validated compound-target interactions, while immunohistochemical/fluorescence assays confirmed key protein expression in lung tissues.
RESULTS: WEPT administration effectively reduced inflammatory cytokine levels in COPD mice, improved lung function, and alleviated histopathological damage like alveolar structural injury and airway inflammation. Network pharmacology and transcriptomic analyses identified Norhyoscyamine and Onjixanthone I as key active components, targeting PIK3CA and AKT1 via PI3K-AKT pathway regulation. Microbiome analysis showed WEPT restored gut microbiota balance. Molecular docking confirmed strong binding of bioactive compounds to core targets, while immunostaining assays demonstrated WEPT suppressed p-PI3K and p-AKT protein expression.
CONCLUSION: WEPT may exert its intervention effects on COPD through a multi-target and multi-level comprehensive regulatory mechanism.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Characterization of gut microbiome dysbiosis in calcium oxalate stone patients with comorbid metabolic syndrome.
Frontiers in microbiology, 16:1644416.
OBJECTIVE: Metabolic syndrome is an important risk factor for calcium oxalate stone, yet the underlying mechanism remain unclear. Gut microbiota is involved in human metabolic processes and is associated with both metabolic syndrome and calcium oxalate stone formation.
METHODS: In this study, 100 subjects were divided into four groups: calcium oxalate stone with metabolic syndrome (Group A), metabolic syndrome only (Group B), calcium oxalate stone only (Group C), and healthy controls (Group D), with 25 cases in each group. Gut microbiota composition and function were analyzed using 16S rRNA gene sequencing. Microbiota diversity, species differences, and metabolic function changes were assessed by combining clinical parameters and metabolic pathway (KEGG) annotation.
RESULTS: The α diversity in Group A was significantly lower than in the other three groups (Shannon index, P < 0.05), and β diversity analysis revealed significant differences in bacterial community structure among all four groups (ANOSIM, P < 0.05). In Group A, short-chain fatty acid (SCFA)-producing probiotics (e.g., Faecalibacterium, Faecalibacillus, Prevotella) were reduced, while pro-inflammatory bacteria (e.g., Eggerthella and Anaerobacteriaceae) were enriched. RDA correlation analysis indicated that Faecalibacterium is negatively correlated with blood glucose levels, Faecalibacterium and Roseburia are positively correlated with urinary pH. KEGG analysis showed that the bisphenol degradation pathway was reduced (logFC = -1.45, P = 0.027) and the retinol metabolism pathway was enriched (logFC = 0.928, P = 0.006) in Group A compared to Group B.
CONCLUSION: Patients with calcium oxalate stone and metabolic syndrome exhibit a "double imbalance" in gut microbiota: on the one hand, the reduced diversity of the microbiota and the decrease of SCFAs-producing microbiota weakened the metabolic protective effect of the gut microbiota; on the other hand, the enrichment of pro-inflammatory and pathogenic bacteria exacerbated metabolic disorders and inflammatory reactions. The present study reveals that gut microbiota play a role in the mechanism of metabolic syndrome promoting calcium oxalate stone formation, and these findings provide a theoretical basis for the use of probiotics to prevent calcium oxalate stone.
Additional Links: PMID-41377043
PubMed:
Citation:
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@article {pmid41377043,
year = {2025},
author = {Batur, M and Li, X and Liu, B and Wang, S and Dong, Q and Abudurexiti, N and Liu, Z},
title = {Characterization of gut microbiome dysbiosis in calcium oxalate stone patients with comorbid metabolic syndrome.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1644416},
pmid = {41377043},
issn = {1664-302X},
abstract = {OBJECTIVE: Metabolic syndrome is an important risk factor for calcium oxalate stone, yet the underlying mechanism remain unclear. Gut microbiota is involved in human metabolic processes and is associated with both metabolic syndrome and calcium oxalate stone formation.
METHODS: In this study, 100 subjects were divided into four groups: calcium oxalate stone with metabolic syndrome (Group A), metabolic syndrome only (Group B), calcium oxalate stone only (Group C), and healthy controls (Group D), with 25 cases in each group. Gut microbiota composition and function were analyzed using 16S rRNA gene sequencing. Microbiota diversity, species differences, and metabolic function changes were assessed by combining clinical parameters and metabolic pathway (KEGG) annotation.
RESULTS: The α diversity in Group A was significantly lower than in the other three groups (Shannon index, P < 0.05), and β diversity analysis revealed significant differences in bacterial community structure among all four groups (ANOSIM, P < 0.05). In Group A, short-chain fatty acid (SCFA)-producing probiotics (e.g., Faecalibacterium, Faecalibacillus, Prevotella) were reduced, while pro-inflammatory bacteria (e.g., Eggerthella and Anaerobacteriaceae) were enriched. RDA correlation analysis indicated that Faecalibacterium is negatively correlated with blood glucose levels, Faecalibacterium and Roseburia are positively correlated with urinary pH. KEGG analysis showed that the bisphenol degradation pathway was reduced (logFC = -1.45, P = 0.027) and the retinol metabolism pathway was enriched (logFC = 0.928, P = 0.006) in Group A compared to Group B.
CONCLUSION: Patients with calcium oxalate stone and metabolic syndrome exhibit a "double imbalance" in gut microbiota: on the one hand, the reduced diversity of the microbiota and the decrease of SCFAs-producing microbiota weakened the metabolic protective effect of the gut microbiota; on the other hand, the enrichment of pro-inflammatory and pathogenic bacteria exacerbated metabolic disorders and inflammatory reactions. The present study reveals that gut microbiota play a role in the mechanism of metabolic syndrome promoting calcium oxalate stone formation, and these findings provide a theoretical basis for the use of probiotics to prevent calcium oxalate stone.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Evaluation of four DNA extraction kits for implementation of nanopore sequencing in routine surveillance of antimicrobial resistance in low-resource settings.
Frontiers in microbiology, 16:1715467.
INTRODUCTION: Whole genome sequencing (WGS) is a valuable tool in surveillance of antimicrobial resistance (AMR). However, the technology faces several implementation challenges in low-resource settings. While advances in Oxford Nanopore Technologies (ONT) field sequencing have enabled sequencing in low-resource settings, DNA extraction remains a critical barrier to implementation.
METHODS: We evaluated four commercially available DNA extraction kits: QIAGEN DNeasy Blood & Tissue, NEB Monarch® HMW, Thermo Fisher MagMAX™ Microbiome, and Thermo Fisher MagMax™ Viral/Pathogen, for their suitability in ONT-based AMR surveillance across Gram-positive and Gram-negative bacterial strains. Kits were evaluated for DNA purity, yield, and fragment length, as well as sequencing metrics including mean read quality, read N50, sequencing depth, multilocus sequence typing concordance, and AMR gene detection. Practical parameters such as cost, hand-on time, and equipment requirements were also assessed.
RESULTS: The DNeasy Blood & Tissue kit consistently produced DNA of sufficient quality and quantity to enable high-sequencing depth ONT sequencing, enabling robust multi-locus sequence typing and AMR gene recovery, while remaining cost-effective and requiring minimal technical expertise.
DISCUSSION: These findings support the integration of optimized DNA extraction workflows into public health surveillance systems. The DNeasy Blood & Tissue kit offers a reliable and scalable solution for real-time genomic monitoring of antimicrobial resistance in resource-limited settings.
Additional Links: PMID-41377037
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Citation:
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@article {pmid41377037,
year = {2025},
author = {Thornval, NR and Lacy-Roberts, N and Nilsson, P and Espinosa-Gongora, C and Hasman, H and Mourão, J and Rasmussen, A and Rebelo, AR and Gibson, C and Hendriksen, RS},
title = {Evaluation of four DNA extraction kits for implementation of nanopore sequencing in routine surveillance of antimicrobial resistance in low-resource settings.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1715467},
pmid = {41377037},
issn = {1664-302X},
abstract = {INTRODUCTION: Whole genome sequencing (WGS) is a valuable tool in surveillance of antimicrobial resistance (AMR). However, the technology faces several implementation challenges in low-resource settings. While advances in Oxford Nanopore Technologies (ONT) field sequencing have enabled sequencing in low-resource settings, DNA extraction remains a critical barrier to implementation.
METHODS: We evaluated four commercially available DNA extraction kits: QIAGEN DNeasy Blood & Tissue, NEB Monarch® HMW, Thermo Fisher MagMAX™ Microbiome, and Thermo Fisher MagMax™ Viral/Pathogen, for their suitability in ONT-based AMR surveillance across Gram-positive and Gram-negative bacterial strains. Kits were evaluated for DNA purity, yield, and fragment length, as well as sequencing metrics including mean read quality, read N50, sequencing depth, multilocus sequence typing concordance, and AMR gene detection. Practical parameters such as cost, hand-on time, and equipment requirements were also assessed.
RESULTS: The DNeasy Blood & Tissue kit consistently produced DNA of sufficient quality and quantity to enable high-sequencing depth ONT sequencing, enabling robust multi-locus sequence typing and AMR gene recovery, while remaining cost-effective and requiring minimal technical expertise.
DISCUSSION: These findings support the integration of optimized DNA extraction workflows into public health surveillance systems. The DNeasy Blood & Tissue kit offers a reliable and scalable solution for real-time genomic monitoring of antimicrobial resistance in resource-limited settings.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Rooted intelligence: Integrating AI, Omics, and Synthetic biology to engineer the plant microbiome.
3 Biotech, 16(1):10.
This review synthesizes recent advances in the integration of omics, synthetic biology, and artificial intelligence (AI) to deepen understanding of plant-microbe interactions and support sustainable agriculture. Omics approaches have provided molecular-level insights into microbial diversity, functional genes, and regulatory pathways shaping rhizosphere dynamics. Synthetic biology has enabled the design of microbial strains and synthetic communities (SynComs) with enhanced traits such as nutrient solubilization, stress tolerance, and pathogen suppression, offering targeted solutions for crop improvement. AI-driven tools have accelerated these advances by enabling predictive modelling, multi-omics data integration, and real-time phenotyping, while also enhancing disease forecasting and microbiome-informed crop management. The combined application of these technologies demonstrates potential for the rational design of next-generation plant growth-promoting rhizobacteria and synthetic microbial consortia optimized for diverse agroecosystems. Key challenges remain in translating laboratory findings to field conditions, ensuring biosafety of engineered microbes, and addressing ethical and regulatory issues. Addressing these barriers through interdisciplinary frameworks and responsible innovation will pave the way for climate specific high-yielding, and sustainable cropping systems.
Additional Links: PMID-41376894
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Citation:
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@article {pmid41376894,
year = {2026},
author = {Kamath, A and Patel, D and Saraf, M and Patel, S},
title = {Rooted intelligence: Integrating AI, Omics, and Synthetic biology to engineer the plant microbiome.},
journal = {3 Biotech},
volume = {16},
number = {1},
pages = {10},
pmid = {41376894},
issn = {2190-572X},
abstract = {This review synthesizes recent advances in the integration of omics, synthetic biology, and artificial intelligence (AI) to deepen understanding of plant-microbe interactions and support sustainable agriculture. Omics approaches have provided molecular-level insights into microbial diversity, functional genes, and regulatory pathways shaping rhizosphere dynamics. Synthetic biology has enabled the design of microbial strains and synthetic communities (SynComs) with enhanced traits such as nutrient solubilization, stress tolerance, and pathogen suppression, offering targeted solutions for crop improvement. AI-driven tools have accelerated these advances by enabling predictive modelling, multi-omics data integration, and real-time phenotyping, while also enhancing disease forecasting and microbiome-informed crop management. The combined application of these technologies demonstrates potential for the rational design of next-generation plant growth-promoting rhizobacteria and synthetic microbial consortia optimized for diverse agroecosystems. Key challenges remain in translating laboratory findings to field conditions, ensuring biosafety of engineered microbes, and addressing ethical and regulatory issues. Addressing these barriers through interdisciplinary frameworks and responsible innovation will pave the way for climate specific high-yielding, and sustainable cropping systems.},
}
RevDate: 2025-12-11
Sonication findings do not support routine removal of paediatric orthopaedic implants.
Journal of children's orthopaedics [Epub ahead of print].
PURPOSE: The risk of implant-associated infection (IAI) is occasionally cited as an indication for routine removal of orthopaedic implants in children, but evidence is lacking. This study aimed at exploring the frequency of microbial colonization of paediatric orthopaedic implants by sonication, a gold standard for diagnosing IAI.
METHODS: Data of all patients aged <18 years at index implantation who underwent implant removal over a 34-month period at a single institution were retrospectively reviewed. Sonication culture results were classified according to microbial growth as negative (no/non-significant growth) or positive (significant growth/colonization). Descriptive statistics were performed, correlations were analysed via crosstabs and univariate ANOVA (p < 0.05).
RESULTS: One hundred and twenty-nine sonicated devices from 63 patients were included. Mean patient age at implantation was 9.8 years (standard deviation (SD) 3.4; range 3.0-15.6), mean implant in situ time was 2.2 years (SD 1.5; range 0.6-8.8). In all, 63 tension band plates, 35 locking screw plates, 26 cannulated screws, 3 intramedullary nails and 2 K-wires were evaluated. In total, 128/129 (99%) of implant sites were asymptomatic. Sonication fluid cultures of 24/128 (19%) implants from 21 asymptomatic patients showed non-significant growth of pathogens mainly related to the human skin microbiome, suggesting contamination.
CONCLUSIONS: Sonication of implants removed from asymptomatic implant sites showed no significant microbial growth. Thus, the risk of IAI should be irrelevant for scheduling implant removal in children without signs and symptoms of infection.
SIGNIFICANCE OF STUDY: This study investigates for the first time the role of sonication in non-spinal paediatric orthopaedics and provides important insights into the question of routine implant removal in children, providing a foundation for future research.
Additional Links: PMID-41376863
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Citation:
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@article {pmid41376863,
year = {2025},
author = {Rakow, A and Lebek, S and Renz, N and Funk, J},
title = {Sonication findings do not support routine removal of paediatric orthopaedic implants.},
journal = {Journal of children's orthopaedics},
volume = {},
number = {},
pages = {18632521251400162},
pmid = {41376863},
issn = {1863-2521},
abstract = {PURPOSE: The risk of implant-associated infection (IAI) is occasionally cited as an indication for routine removal of orthopaedic implants in children, but evidence is lacking. This study aimed at exploring the frequency of microbial colonization of paediatric orthopaedic implants by sonication, a gold standard for diagnosing IAI.
METHODS: Data of all patients aged <18 years at index implantation who underwent implant removal over a 34-month period at a single institution were retrospectively reviewed. Sonication culture results were classified according to microbial growth as negative (no/non-significant growth) or positive (significant growth/colonization). Descriptive statistics were performed, correlations were analysed via crosstabs and univariate ANOVA (p < 0.05).
RESULTS: One hundred and twenty-nine sonicated devices from 63 patients were included. Mean patient age at implantation was 9.8 years (standard deviation (SD) 3.4; range 3.0-15.6), mean implant in situ time was 2.2 years (SD 1.5; range 0.6-8.8). In all, 63 tension band plates, 35 locking screw plates, 26 cannulated screws, 3 intramedullary nails and 2 K-wires were evaluated. In total, 128/129 (99%) of implant sites were asymptomatic. Sonication fluid cultures of 24/128 (19%) implants from 21 asymptomatic patients showed non-significant growth of pathogens mainly related to the human skin microbiome, suggesting contamination.
CONCLUSIONS: Sonication of implants removed from asymptomatic implant sites showed no significant microbial growth. Thus, the risk of IAI should be irrelevant for scheduling implant removal in children without signs and symptoms of infection.
SIGNIFICANCE OF STUDY: This study investigates for the first time the role of sonication in non-spinal paediatric orthopaedics and provides important insights into the question of routine implant removal in children, providing a foundation for future research.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Capitalizing on the GLP-1 RA revolution for behavioral health through digital companions.
Digital health, 11:20552076251406308.
Additional Links: PMID-41376848
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Citation:
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@article {pmid41376848,
year = {2025},
author = {Naegele, C and Jones, G},
title = {Capitalizing on the GLP-1 RA revolution for behavioral health through digital companions.},
journal = {Digital health},
volume = {11},
number = {},
pages = {20552076251406308},
pmid = {41376848},
issn = {2055-2076},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Fetal development and the air pollution exposome: an integrative perspective of health pathways.
Frontiers in cellular neuroscience, 19:1688437.
We offer an integrative perspective on how the air-pollution exposome shapes fetal development during the first 1,000 days and reverberates across mental health and behavior. Pregnant individuals and young children are disproportionately exposed to particulate matter (PM2.5), nitrogen dioxide (NO2), ozone (O3), and volatile organic compounds (VOCs) with social disadvantage amplifying risk. We bridge exposure to biology through three conduits. First, the placenta acts as a sensor and recorder, transducing signals that alter growth, immune tone, and neuroendocrine programming. Second, fetal autonomic control-captured by beat-to-beat fetal heart rate variability (fHRV) offers a relevant biomarker of neurodevelopmental integrity; the absence of direct ambient-pollution-fHRV studies is a pressing gap. Third, maternal immune activation, oxidative and endoplasmic reticulum (ER) stress, and disrupted morphogenesis reshape developing circuits, changes now traceable in utero by advanced fetal MRI. These pathways fit a developmental-programming frame: epigenetic remodeling, gene-environment interplay, endocrine-disrupting co-exposures, and gut-microbiome shifts create durable susceptibility. Clinically, the result is structural and functional brain alterations and child phenotypes spanning attention, executive control, affecting regulation, and learning, with clear pediatric and educational implications. We propose an exposome-based research agenda coupling high-resolution exposure assessment with placental molecular profiling, fetal/neonatal autonomic biomarkers (including fHRV), fetal/child neuroimaging, and longitudinal microbiome readouts in harmonized cohorts. In parallel, multisectoral actions-clean air urban design, targeted protection of pregnancy and early childhood, chemical regulation, and risk communication-should narrow exposure inequities while trials test biomarker-guided prevention. Aligning placental biology, autonomic metrics, and exposome science may transform risk stratification and safeguard the developing brain.
Additional Links: PMID-41376716
PubMed:
Citation:
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@article {pmid41376716,
year = {2025},
author = {Abarca-Castro, EA and Reyes-Lagos, JJ and Guzmán Ramos, K and Montiel-Castro, AJ and Arano-Varela, H and Mayer-Villa, PA and Aguilar-Toalá, JE and Montesillo-Cedillo, JL and Talavera-Peña, AK},
title = {Fetal development and the air pollution exposome: an integrative perspective of health pathways.},
journal = {Frontiers in cellular neuroscience},
volume = {19},
number = {},
pages = {1688437},
pmid = {41376716},
issn = {1662-5102},
abstract = {We offer an integrative perspective on how the air-pollution exposome shapes fetal development during the first 1,000 days and reverberates across mental health and behavior. Pregnant individuals and young children are disproportionately exposed to particulate matter (PM2.5), nitrogen dioxide (NO2), ozone (O3), and volatile organic compounds (VOCs) with social disadvantage amplifying risk. We bridge exposure to biology through three conduits. First, the placenta acts as a sensor and recorder, transducing signals that alter growth, immune tone, and neuroendocrine programming. Second, fetal autonomic control-captured by beat-to-beat fetal heart rate variability (fHRV) offers a relevant biomarker of neurodevelopmental integrity; the absence of direct ambient-pollution-fHRV studies is a pressing gap. Third, maternal immune activation, oxidative and endoplasmic reticulum (ER) stress, and disrupted morphogenesis reshape developing circuits, changes now traceable in utero by advanced fetal MRI. These pathways fit a developmental-programming frame: epigenetic remodeling, gene-environment interplay, endocrine-disrupting co-exposures, and gut-microbiome shifts create durable susceptibility. Clinically, the result is structural and functional brain alterations and child phenotypes spanning attention, executive control, affecting regulation, and learning, with clear pediatric and educational implications. We propose an exposome-based research agenda coupling high-resolution exposure assessment with placental molecular profiling, fetal/neonatal autonomic biomarkers (including fHRV), fetal/child neuroimaging, and longitudinal microbiome readouts in harmonized cohorts. In parallel, multisectoral actions-clean air urban design, targeted protection of pregnancy and early childhood, chemical regulation, and risk communication-should narrow exposure inequities while trials test biomarker-guided prevention. Aligning placental biology, autonomic metrics, and exposome science may transform risk stratification and safeguard the developing brain.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Dual signaling cascade regulating gut-lung axis in Interleukin-6/Interleukin-17 for NSCLC immuno pathogenesis.
Frontiers in immunology, 16:1649517.
Non-small cell lung cancer is the leading cause of death globally, affecting both men and women. Emerging evidence has highlighted the apparent role of gut microbiota in reshaping the lung microbial community. Notably, imbalances in the gut microbiome disrupt lung physiology, which increases an individual's susceptibility to lung diseases. The homing of gut residents to pulmonary sites prompts tumorigenic processes by altering microbial synergism that metabolically reprograms immune effectors to complement tumor growth. Nevertheless, the additive effect of microbiomes induces immune-responsive mechanisms that excessively induce IL-6 and IL-17 at the inflamed site. Consequently, perturbations in cytokine pool boost inflammatory responses toward a pro-tumor effect, implying cytokine duality and the role of these interleukins in regulating gut-lung crosstalk. Inflammation is a natural host defense mechanism activated against foreign stimulants to mount an immune response. At later stages, the inductive effect of IL-6/17 triggers inflammasome assembly where their accelerated response induces lung epithelial damage, leading to cellular transformation. This implies that the unexplored interconnections between microbiomes and interleukin biology influence immune dynamics that regulate the processes of neoplastic transformation. Here, in this comprehensive review, we comment on the gut-lung crosstalk along with the role of resident microbes in generating immunological responses. Besides, we discuss the IL-6/17-mediated activation of the inflammasome in attuning tumoral immunity. These dictate the potential of microbiotal lifeforms in generating inflammatory responses, which can therefore serve as potential diagnostic markers in NSCLC.
Additional Links: PMID-41376623
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@article {pmid41376623,
year = {2025},
author = {Khilwani, R and Singh, S},
title = {Dual signaling cascade regulating gut-lung axis in Interleukin-6/Interleukin-17 for NSCLC immuno pathogenesis.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1649517},
pmid = {41376623},
issn = {1664-3224},
mesh = {Humans ; *Carcinoma, Non-Small-Cell Lung/immunology/metabolism/pathology/microbiology/etiology ; *Gastrointestinal Microbiome/immunology ; *Lung Neoplasms/immunology/metabolism/pathology/microbiology/etiology ; *Interleukin-17/metabolism/immunology ; *Interleukin-6/metabolism/immunology ; *Signal Transduction/immunology ; Animals ; *Lung/immunology/metabolism/microbiology ; },
abstract = {Non-small cell lung cancer is the leading cause of death globally, affecting both men and women. Emerging evidence has highlighted the apparent role of gut microbiota in reshaping the lung microbial community. Notably, imbalances in the gut microbiome disrupt lung physiology, which increases an individual's susceptibility to lung diseases. The homing of gut residents to pulmonary sites prompts tumorigenic processes by altering microbial synergism that metabolically reprograms immune effectors to complement tumor growth. Nevertheless, the additive effect of microbiomes induces immune-responsive mechanisms that excessively induce IL-6 and IL-17 at the inflamed site. Consequently, perturbations in cytokine pool boost inflammatory responses toward a pro-tumor effect, implying cytokine duality and the role of these interleukins in regulating gut-lung crosstalk. Inflammation is a natural host defense mechanism activated against foreign stimulants to mount an immune response. At later stages, the inductive effect of IL-6/17 triggers inflammasome assembly where their accelerated response induces lung epithelial damage, leading to cellular transformation. This implies that the unexplored interconnections between microbiomes and interleukin biology influence immune dynamics that regulate the processes of neoplastic transformation. Here, in this comprehensive review, we comment on the gut-lung crosstalk along with the role of resident microbes in generating immunological responses. Besides, we discuss the IL-6/17-mediated activation of the inflammasome in attuning tumoral immunity. These dictate the potential of microbiotal lifeforms in generating inflammatory responses, which can therefore serve as potential diagnostic markers in NSCLC.},
}
MeSH Terms:
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Humans
*Carcinoma, Non-Small-Cell Lung/immunology/metabolism/pathology/microbiology/etiology
*Gastrointestinal Microbiome/immunology
*Lung Neoplasms/immunology/metabolism/pathology/microbiology/etiology
*Interleukin-17/metabolism/immunology
*Interleukin-6/metabolism/immunology
*Signal Transduction/immunology
Animals
*Lung/immunology/metabolism/microbiology
RevDate: 2025-12-11
CmpDate: 2025-12-11
Microbial metabolite trimethylamine-N-oxide facilitates colorectal inflammation-cancer transformation by blocking lysosomal degradation of Wnt signaling.
Gut microbes, 17(1):2597626.
Chronic inflammation is closely related to the occurrence and development of many tumors, including colorectal cancer (CRC), a typical inflammation-dependent cancer. The gut bacteria and their metabolites, as signaling molecules or substrates of metabolic processes, have attracted increasing attention during the colorectal inflammation-cancer transformation process. However, how commensal microbiota-derived metabolites create a favorable internal environment for carcinogenesis through the chronic inflammatory response is not entirely understood. Here, we conducted multiomics analysis, including single-cell RNA-sequencing (scRNA-seq), microbiome and metabolome to explore the intricate cross-talk of host-microbe-metabolite. By employing colitis-associated CRC mice models, as well as patient-derived CRC organoids, we identified that trimethylamine n-oxide (TMAO), a metabolic product derived from the gut microbiota, was crucial for inflammation-mediated colorectal carcinogenesis by enhancing Wnt signaling. Further mechanistic studies revealed that TMAO interacted with heat shock protein family A member 8 (Hspa8, also known as Hsc70), a molecular chaperone that mediates autophagy, to block the lysosomal degradation of the β-catenin protein, leading to an increase in the downstream targets cyclin D1 and c-Myc, thus contributing to colorectal carcinogenesis. Our results indicated that TMAO serves as a bridge to establish the connection between microbiota and colorectal carcinogenesis, playing a critical pathogenic role during CRC progression and therefore provides novel mechanistic insights into the intestinal inflammation in colorectal neoplasia progression.
Additional Links: PMID-41376600
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@article {pmid41376600,
year = {2025},
author = {Yang, K and Liu, Z and Wang, H and Xiao, Z and Zhao, W and Gong, W},
title = {Microbial metabolite trimethylamine-N-oxide facilitates colorectal inflammation-cancer transformation by blocking lysosomal degradation of Wnt signaling.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2597626},
doi = {10.1080/19490976.2025.2597626},
pmid = {41376600},
issn = {1949-0984},
mesh = {Animals ; *Methylamines/metabolism ; Mice ; *Gastrointestinal Microbiome ; Humans ; *Wnt Signaling Pathway/drug effects ; *Colorectal Neoplasms/metabolism/pathology/microbiology ; *Lysosomes/metabolism ; Bacteria/metabolism/genetics/classification ; Mice, Inbred C57BL ; Disease Models, Animal ; *Cell Transformation, Neoplastic ; beta Catenin/metabolism ; Colitis/microbiology ; Inflammation ; },
abstract = {Chronic inflammation is closely related to the occurrence and development of many tumors, including colorectal cancer (CRC), a typical inflammation-dependent cancer. The gut bacteria and their metabolites, as signaling molecules or substrates of metabolic processes, have attracted increasing attention during the colorectal inflammation-cancer transformation process. However, how commensal microbiota-derived metabolites create a favorable internal environment for carcinogenesis through the chronic inflammatory response is not entirely understood. Here, we conducted multiomics analysis, including single-cell RNA-sequencing (scRNA-seq), microbiome and metabolome to explore the intricate cross-talk of host-microbe-metabolite. By employing colitis-associated CRC mice models, as well as patient-derived CRC organoids, we identified that trimethylamine n-oxide (TMAO), a metabolic product derived from the gut microbiota, was crucial for inflammation-mediated colorectal carcinogenesis by enhancing Wnt signaling. Further mechanistic studies revealed that TMAO interacted with heat shock protein family A member 8 (Hspa8, also known as Hsc70), a molecular chaperone that mediates autophagy, to block the lysosomal degradation of the β-catenin protein, leading to an increase in the downstream targets cyclin D1 and c-Myc, thus contributing to colorectal carcinogenesis. Our results indicated that TMAO serves as a bridge to establish the connection between microbiota and colorectal carcinogenesis, playing a critical pathogenic role during CRC progression and therefore provides novel mechanistic insights into the intestinal inflammation in colorectal neoplasia progression.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*Methylamines/metabolism
Mice
*Gastrointestinal Microbiome
Humans
*Wnt Signaling Pathway/drug effects
*Colorectal Neoplasms/metabolism/pathology/microbiology
*Lysosomes/metabolism
Bacteria/metabolism/genetics/classification
Mice, Inbred C57BL
Disease Models, Animal
*Cell Transformation, Neoplastic
beta Catenin/metabolism
Colitis/microbiology
Inflammation
RevDate: 2025-12-11
CmpDate: 2025-12-11
Akkermansia muciniphila Alleviates Olanzapine-Induced Hepatic Steatosis via the Gut Microbiota-IGFBP2/APOA1-Liver Axis.
Microbial biotechnology, 18(12):e70281.
Olanzapine is associated with a high risk of hepatic steatosis as a commonly used atypical antipsychotic. In this study, we observed differential susceptibility to olanzapine-induced fatty liver disease in both rats and patients. Notably, patients with olanzapine-induced liver damage exhibited an altered gut microbiota composition, with Akkermansia muciniphila showing the most pronounced alteration. To explore its therapeutic potential, we administered A. muciniphila to olanzapine-treated rats, which significantly reduced hepatic lipid accumulation and liver injury. Gut microbiome analysis revealed significant alterations in microbial diversity and composition following A. muciniphila treatment. Transcriptomic analysis further identified differentially expressed genes in the liver, highlighting the involvement of IGFBP2 and APOA1 in the protective effects of A. muciniphila . Functional validation demonstrated that overexpression of IGFBP2 and APOA1 alleviated olanzapine-induced hepatic steatosis in both cellular and animal models. These findings suggest that A. muciniphila exerts hepatoprotective effects via the gut microbiota-IGFBP2/APOA1-liver axis, offering a potential microbiota-targeted strategy to mitigate olanzapine-induced metabolic dysfunction.
Additional Links: PMID-41376147
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@article {pmid41376147,
year = {2025},
author = {Wang, J and Chen, P and Deng, Y and Yu, L and Tu, C and Xu, X and Fang, X and Li, W},
title = {Akkermansia muciniphila Alleviates Olanzapine-Induced Hepatic Steatosis via the Gut Microbiota-IGFBP2/APOA1-Liver Axis.},
journal = {Microbial biotechnology},
volume = {18},
number = {12},
pages = {e70281},
doi = {10.1111/1751-7915.70281},
pmid = {41376147},
issn = {1751-7915},
support = {82173903//National Natural Science Foundation of China/ ; 81903686//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Olanzapine/adverse effects ; Humans ; *Fatty Liver/chemically induced/metabolism ; Rats ; Male ; Liver/metabolism/pathology/drug effects ; *Apolipoprotein A-I/metabolism/genetics ; *Akkermansia ; Disease Models, Animal ; Rats, Sprague-Dawley ; Antipsychotic Agents/adverse effects ; },
abstract = {Olanzapine is associated with a high risk of hepatic steatosis as a commonly used atypical antipsychotic. In this study, we observed differential susceptibility to olanzapine-induced fatty liver disease in both rats and patients. Notably, patients with olanzapine-induced liver damage exhibited an altered gut microbiota composition, with Akkermansia muciniphila showing the most pronounced alteration. To explore its therapeutic potential, we administered A. muciniphila to olanzapine-treated rats, which significantly reduced hepatic lipid accumulation and liver injury. Gut microbiome analysis revealed significant alterations in microbial diversity and composition following A. muciniphila treatment. Transcriptomic analysis further identified differentially expressed genes in the liver, highlighting the involvement of IGFBP2 and APOA1 in the protective effects of A. muciniphila . Functional validation demonstrated that overexpression of IGFBP2 and APOA1 alleviated olanzapine-induced hepatic steatosis in both cellular and animal models. These findings suggest that A. muciniphila exerts hepatoprotective effects via the gut microbiota-IGFBP2/APOA1-liver axis, offering a potential microbiota-targeted strategy to mitigate olanzapine-induced metabolic dysfunction.},
}
MeSH Terms:
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Animals
*Gastrointestinal Microbiome/drug effects
*Olanzapine/adverse effects
Humans
*Fatty Liver/chemically induced/metabolism
Rats
Male
Liver/metabolism/pathology/drug effects
*Apolipoprotein A-I/metabolism/genetics
*Akkermansia
Disease Models, Animal
Rats, Sprague-Dawley
Antipsychotic Agents/adverse effects
RevDate: 2025-12-11
CmpDate: 2025-12-11
Host Dietary Nutrients Shape GH32-Mediated Microbial Responses to Prebiotic Fructans: A Randomized Trial.
Foods (Basel, Switzerland), 14(23): pii:foods14234090.
Prebiotics, such as short- and long-chain fructans, beneficially modulate the microbiota; however, individual variability in response remains unclear. In this randomized, double-blind, placebo-controlled trial, 40 healthy adults received either a combined fructan supplement-1-Kestose (Kes) and inulin (Inu)-or a placebo (maltose + cornstarch) for 4 weeks. We investigated the fecal microbiome, bacterial growth, and glycoside hydrolase family 32 (GH32) gene abundance, and further examined the association between dietary intake and GH32. Kes and Inu co-supplementation selectively increased Bifidobacterium adolescentis and B. longum, harboring the GH32 genes inuA and cscA, respectively. Growth assays revealed that B. longum, which expresses cscA, grew only on Kes, whereas B. adolescentis, which expresses inuA, showed growth on Kes and Inu. Only responders-participants showing increases in both species-exhibited consistent upregulation of GH32 genes and were associated with higher retinol and C16:3 (n-6) fatty acid intake, as well as greater green leafy vegetable and canned tuna consumption. This study provides insights into species level responses to prebiotics, supporting personalized dietary strategies for gut microbiota modulation.
Additional Links: PMID-41376027
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@article {pmid41376027,
year = {2025},
author = {Takahashi, H and Fujii, T and Yamada, C and Kondo, N and Kuramitsu, K and Funasaka, K and Ohno, E and Hirooka, Y and Tochio, T and Fujiki, K},
title = {Host Dietary Nutrients Shape GH32-Mediated Microbial Responses to Prebiotic Fructans: A Randomized Trial.},
journal = {Foods (Basel, Switzerland)},
volume = {14},
number = {23},
pages = {},
doi = {10.3390/foods14234090},
pmid = {41376027},
issn = {2304-8158},
support = {JP24K14784//JSPS KAKENHI/ ; No grant number//The Anzu no Mori Foundation 2024 Research Grant/ ; },
abstract = {Prebiotics, such as short- and long-chain fructans, beneficially modulate the microbiota; however, individual variability in response remains unclear. In this randomized, double-blind, placebo-controlled trial, 40 healthy adults received either a combined fructan supplement-1-Kestose (Kes) and inulin (Inu)-or a placebo (maltose + cornstarch) for 4 weeks. We investigated the fecal microbiome, bacterial growth, and glycoside hydrolase family 32 (GH32) gene abundance, and further examined the association between dietary intake and GH32. Kes and Inu co-supplementation selectively increased Bifidobacterium adolescentis and B. longum, harboring the GH32 genes inuA and cscA, respectively. Growth assays revealed that B. longum, which expresses cscA, grew only on Kes, whereas B. adolescentis, which expresses inuA, showed growth on Kes and Inu. Only responders-participants showing increases in both species-exhibited consistent upregulation of GH32 genes and were associated with higher retinol and C16:3 (n-6) fatty acid intake, as well as greater green leafy vegetable and canned tuna consumption. This study provides insights into species level responses to prebiotics, supporting personalized dietary strategies for gut microbiota modulation.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Dietary Intervention with Resistant Starch-Rich Unripe Plantain Flour Restores Gut Microbiome-Metabolome Axis and Ameliorates Type 2 Diabetes in Rats.
Foods (Basel, Switzerland), 14(23): pii:foods14233996.
Plantain (Musa spp., AAB group) possesses a complex triploid genetics originating from interspecific hybridization, which underlies its agronomic traits and nutritional composition, making it a vital global staple food crop. Unripe plantain flour (UPF), a rich source of resistant starch (RS), has demonstrated anti-diabetic properties in diabetic rats, yet its mechanisms of action remain unclear. This study investigated whether unripe plantain flour attenuates type 2 diabetic traits in rats made diabetic with a high-fat diet plus streptozotocin through regulation of the gut microbiome-metabolome axis, including short-chain fatty acids and bile acids. We found that UPF intervention significantly ameliorated gut microbiota dysbiosis. It enriched beneficial bacteria, particularly SCFA producers (Lachnoclostridium, Blautia, Butyricicoccus) and others (Bifidobacterium, Akkermansia), while inhibiting harmful genera (Romboutsia, Allobaculum). Consequently, UPF altered bile-acid composition by lowering hydrophobic species (e.g., cholic acid and deoxycholic acid) while elevating hydrophilic species (e.g., ursodeoxycholic acid and tauroursodeoxycholic acid). It also enhanced the excretion of secondary bile acids (lithocholic acid). These coordinated changes in the gut ecosystem are conducive to improved glycolipid metabolism. Spearman correlation analysis further reinforced the close relationships between the altered microbiota and metabolites. Our results elucidate that UPF exerts its anti-diabetic effects by remodeling the gut microbiota and modulating its associated metabolites, highlighting a novel dietary intervention strategy for diabetes management.
Additional Links: PMID-41375934
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PubMed:
Citation:
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@article {pmid41375934,
year = {2025},
author = {Fu, J and Liu, C and Tu, S and Liu, H and Liu, Z and He, W and Dong, L and Yi, G and Xia, Y and Wang, J and Sheng, O},
title = {Dietary Intervention with Resistant Starch-Rich Unripe Plantain Flour Restores Gut Microbiome-Metabolome Axis and Ameliorates Type 2 Diabetes in Rats.},
journal = {Foods (Basel, Switzerland)},
volume = {14},
number = {23},
pages = {},
doi = {10.3390/foods14233996},
pmid = {41375934},
issn = {2304-8158},
support = {2023YFD2300802-1//National Key Research and Development Program of China/ ; 2024CXTD09//Guangdong Provincial Modern Agricultural Industry Technology System Innovation Team Construction Program/ ; CARS-31-01//the earmarked fund for CARS/ ; },
abstract = {Plantain (Musa spp., AAB group) possesses a complex triploid genetics originating from interspecific hybridization, which underlies its agronomic traits and nutritional composition, making it a vital global staple food crop. Unripe plantain flour (UPF), a rich source of resistant starch (RS), has demonstrated anti-diabetic properties in diabetic rats, yet its mechanisms of action remain unclear. This study investigated whether unripe plantain flour attenuates type 2 diabetic traits in rats made diabetic with a high-fat diet plus streptozotocin through regulation of the gut microbiome-metabolome axis, including short-chain fatty acids and bile acids. We found that UPF intervention significantly ameliorated gut microbiota dysbiosis. It enriched beneficial bacteria, particularly SCFA producers (Lachnoclostridium, Blautia, Butyricicoccus) and others (Bifidobacterium, Akkermansia), while inhibiting harmful genera (Romboutsia, Allobaculum). Consequently, UPF altered bile-acid composition by lowering hydrophobic species (e.g., cholic acid and deoxycholic acid) while elevating hydrophilic species (e.g., ursodeoxycholic acid and tauroursodeoxycholic acid). It also enhanced the excretion of secondary bile acids (lithocholic acid). These coordinated changes in the gut ecosystem are conducive to improved glycolipid metabolism. Spearman correlation analysis further reinforced the close relationships between the altered microbiota and metabolites. Our results elucidate that UPF exerts its anti-diabetic effects by remodeling the gut microbiota and modulating its associated metabolites, highlighting a novel dietary intervention strategy for diabetes management.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Sputum Microbiome Based on the Etiology and Severity of Nontuberculous Mycobacterial Pulmonary Disease.
Journal of clinical medicine, 14(23): pii:jcm14238482.
Background: Nontuberculous mycobacterial pulmonary disease (NTM-PD) is a chronic respiratory infection primarily caused by Mycobacterium avium complex (MAC) and Mycobacterium abscessus. These species differ markedly in antibiotic susceptibility and treatment response, yet the contribution of the respiratory microbiome to this clinical variability remains unclear. To date, however, comparative analyses of microbiome differences between MAC-PD and M. abscessus-PD and their associations with disease severity are limited. Methods: We conducted microbiome analysis of sputum from 37 patients with NTM-PD. Patients were antibiotic-naïve and classified into MAC-PD (n = 29) and M. abscessus-PD (n = 8) groups. Disease severity was determined using radiologic extent on chest computed tomography. Bacterial communities were profiled by 16S rRNA gene sequencing, and differential taxa and predicted functional pathways were analyzed using LEfSe and KEGG orthology databases. Results: Distinct microbiome profiles were observed between MAC-PD and M. abscessus-PD. Three anaerobic species-Porphyromonas pasteri, Fusobacterium periodonticum, and Prevotella nanceiensis-were significantly enriched in M. abscessus-PD (LDA effect size > 3, p < 0.05). Functional biomarker analysis revealed significant enrichment of the cobalamin (vitamin B12) biosynthesis pathway in patients with severe disease, while the C19/C18 steroid hormone biosynthesis pathway was enriched in those with mild disease (p < 0.05). Conclusions: In conclusion, our study demonstrates distinct differences in the respiratory microbiome between MAC-PD and M. abscessus-PD and identifies specific functional pathways associated with disease severity in NTM-PD. These findings highlight the potential value of microbial metabolic signatures as biomarkers for disease assessment.
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PubMed:
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@article {pmid41375785,
year = {2025},
author = {Choe, J and Kim, SY and Kim, DH and Jhun, BW},
title = {Sputum Microbiome Based on the Etiology and Severity of Nontuberculous Mycobacterial Pulmonary Disease.},
journal = {Journal of clinical medicine},
volume = {14},
number = {23},
pages = {},
doi = {10.3390/jcm14238482},
pmid = {41375785},
issn = {2077-0383},
support = {RS-2024-00333691//National Research Foundation of Korea/ ; },
abstract = {Background: Nontuberculous mycobacterial pulmonary disease (NTM-PD) is a chronic respiratory infection primarily caused by Mycobacterium avium complex (MAC) and Mycobacterium abscessus. These species differ markedly in antibiotic susceptibility and treatment response, yet the contribution of the respiratory microbiome to this clinical variability remains unclear. To date, however, comparative analyses of microbiome differences between MAC-PD and M. abscessus-PD and their associations with disease severity are limited. Methods: We conducted microbiome analysis of sputum from 37 patients with NTM-PD. Patients were antibiotic-naïve and classified into MAC-PD (n = 29) and M. abscessus-PD (n = 8) groups. Disease severity was determined using radiologic extent on chest computed tomography. Bacterial communities were profiled by 16S rRNA gene sequencing, and differential taxa and predicted functional pathways were analyzed using LEfSe and KEGG orthology databases. Results: Distinct microbiome profiles were observed between MAC-PD and M. abscessus-PD. Three anaerobic species-Porphyromonas pasteri, Fusobacterium periodonticum, and Prevotella nanceiensis-were significantly enriched in M. abscessus-PD (LDA effect size > 3, p < 0.05). Functional biomarker analysis revealed significant enrichment of the cobalamin (vitamin B12) biosynthesis pathway in patients with severe disease, while the C19/C18 steroid hormone biosynthesis pathway was enriched in those with mild disease (p < 0.05). Conclusions: In conclusion, our study demonstrates distinct differences in the respiratory microbiome between MAC-PD and M. abscessus-PD and identifies specific functional pathways associated with disease severity in NTM-PD. These findings highlight the potential value of microbial metabolic signatures as biomarkers for disease assessment.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Patient with Inflammatory Bowel Disease in a Dental Office-Which Antibiotic to Choose?-Narrative Review.
Journal of clinical medicine, 14(23): pii:jcm14238392.
Background/Objectives: The rising global prevalence of inflammatory bowel disease (IBD), encompassing Crohn's disease and ulcerative colitis, has resulted in an increase in the number of affected patients requiring dental care. The heightened risk of Clostridioides difficile infection (CDI) in IBD patients, particularly when exposed to commonly used dental antibiotics, is attributable to their altered gut microbiota and frequent immunosuppressive therapy. The objective of this review is to evaluate current antibiotic strategies for dental management in IBD and to identify safe and effective alternatives that minimise CDI risk. Methods: A narrative review was conducted in accordance with the SANRA guidelines. A comprehensive analysis of literature sourced from PubMed, Embase, Scopus, and Google Scholar was conducted. Results: The available evidence suggests that first- and second-line dental antibiotics-amoxicillin, ampicillin, and clindamycin-carry the highest risk of CDI. In contrast, metronidazole, which exhibits a comparable antimicrobial spectrum, has been shown to possess significantly reduced CDI potential and minimal disruption of gut microbiota. The utilisation of emerging local delivery systems, such as platelet-rich fibrin (PRF), has the potential to further reduce systemic antibiotic exposure. The adjunctive use of probiotics, prebiotics and synbiotics has been demonstrated to have the capacity to maintain microbial balance during therapy. Conclusions: Tailored, microbiome-conscious antibiotic strategies are essential in dental management of IBD patients. Further clinical research is needed to develop evidence-based guidelines and validate promising adjunctive approaches.
Additional Links: PMID-41375698
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PubMed:
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@article {pmid41375698,
year = {2025},
author = {Niemczyk, S and Niemczyk, W and Bąk-Drabik, K and Latusek-Kotyczka, K and Zawilska, A and Wiench, R and Hadzik, J and Dominiak, M},
title = {Patient with Inflammatory Bowel Disease in a Dental Office-Which Antibiotic to Choose?-Narrative Review.},
journal = {Journal of clinical medicine},
volume = {14},
number = {23},
pages = {},
doi = {10.3390/jcm14238392},
pmid = {41375698},
issn = {2077-0383},
abstract = {Background/Objectives: The rising global prevalence of inflammatory bowel disease (IBD), encompassing Crohn's disease and ulcerative colitis, has resulted in an increase in the number of affected patients requiring dental care. The heightened risk of Clostridioides difficile infection (CDI) in IBD patients, particularly when exposed to commonly used dental antibiotics, is attributable to their altered gut microbiota and frequent immunosuppressive therapy. The objective of this review is to evaluate current antibiotic strategies for dental management in IBD and to identify safe and effective alternatives that minimise CDI risk. Methods: A narrative review was conducted in accordance with the SANRA guidelines. A comprehensive analysis of literature sourced from PubMed, Embase, Scopus, and Google Scholar was conducted. Results: The available evidence suggests that first- and second-line dental antibiotics-amoxicillin, ampicillin, and clindamycin-carry the highest risk of CDI. In contrast, metronidazole, which exhibits a comparable antimicrobial spectrum, has been shown to possess significantly reduced CDI potential and minimal disruption of gut microbiota. The utilisation of emerging local delivery systems, such as platelet-rich fibrin (PRF), has the potential to further reduce systemic antibiotic exposure. The adjunctive use of probiotics, prebiotics and synbiotics has been demonstrated to have the capacity to maintain microbial balance during therapy. Conclusions: Tailored, microbiome-conscious antibiotic strategies are essential in dental management of IBD patients. Further clinical research is needed to develop evidence-based guidelines and validate promising adjunctive approaches.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
A Distinct Intestinal Domination Fingerprint in Patients Undergoing Allo-HSCT: Dynamics, Predictors and Implications on Clinical Outcomes.
Journal of clinical medicine, 14(23): pii:jcm14238351.
Background: Although Enterococcus domination has been extensively evaluated in the context of allogeneic hematopoietic stem cell transplantation (allo-HSCT), the prevalence and clinical implications of other dominant genera remain poorly understood. Objective: In this study, we sought to determine the dynamics, predictors and clinical implications of intestinal domination in Brazilian patients undergoing allo-HSCT. Methods: In a prospective study of four Brazilian centers, fecal specimens were collected longitudinally prior to allo-HSCT until six months post-transplantation. To identify intestinal domination, we performed 16S rRNA gene sequencing using the Illumina platform. We then evaluated the impact of intestinal domination on overall survival and acute Graft-versus-Host-Disease (aGvHD) incidence. Finally, to identify predictors of intestinal domination, we performed a logistic regression model. Results: A total of 192 fecal specimens were collected from 69 patients. No significant changes in alpha or beta diversity were observed over the course of allo-HSCT. Among the 192 specimens, 131 (68%) presented intestinal domination. The top four dominant genera were Bacteroides, Akkermansia, Phascolarctobacterium, and Escherichia-Shigella. No significant associations were found between domination by these genera and either overall survival or aGvHD incidence. Furthermore, no patient-level characteristics, including age, sex, underlying disease, conditioning regimen, or stem cell source, reliably predicted intestinal domination. Conclusions: Our findings reveal a unique intestinal domination fingerprint in Brazilian patients and highlight the importance of geographic context in interpreting microbiota-outcome associations in allo-HSCT settings.
Additional Links: PMID-41375654
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PubMed:
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@article {pmid41375654,
year = {2025},
author = {Soares Ferreira Junior, A and Amanda Niz Alvarez, D and da Silva Souza, L and Linares Silva, N and Dias Machado, L and Yoshio Hirai, W and Mesquita Ciconelli, R and Piccolo Feliciano, JV and Colturato, I and Maurício Navarro Barros, G and Scheinberg, P and Chao, NJA and Lelis Vilela de Oliveira, G},
title = {A Distinct Intestinal Domination Fingerprint in Patients Undergoing Allo-HSCT: Dynamics, Predictors and Implications on Clinical Outcomes.},
journal = {Journal of clinical medicine},
volume = {14},
number = {23},
pages = {},
doi = {10.3390/jcm14238351},
pmid = {41375654},
issn = {2077-0383},
support = {#2022/12989-6//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; #2023/08142-0//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; #2024/02936-8//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; #2023/12271-0//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; #313190/2021-6//National Council for Scientific and Technological Development/ ; Finance Code 001//Coordenação de Aperfeicoamento de Pessoal de Nível Superior/ ; },
abstract = {Background: Although Enterococcus domination has been extensively evaluated in the context of allogeneic hematopoietic stem cell transplantation (allo-HSCT), the prevalence and clinical implications of other dominant genera remain poorly understood. Objective: In this study, we sought to determine the dynamics, predictors and clinical implications of intestinal domination in Brazilian patients undergoing allo-HSCT. Methods: In a prospective study of four Brazilian centers, fecal specimens were collected longitudinally prior to allo-HSCT until six months post-transplantation. To identify intestinal domination, we performed 16S rRNA gene sequencing using the Illumina platform. We then evaluated the impact of intestinal domination on overall survival and acute Graft-versus-Host-Disease (aGvHD) incidence. Finally, to identify predictors of intestinal domination, we performed a logistic regression model. Results: A total of 192 fecal specimens were collected from 69 patients. No significant changes in alpha or beta diversity were observed over the course of allo-HSCT. Among the 192 specimens, 131 (68%) presented intestinal domination. The top four dominant genera were Bacteroides, Akkermansia, Phascolarctobacterium, and Escherichia-Shigella. No significant associations were found between domination by these genera and either overall survival or aGvHD incidence. Furthermore, no patient-level characteristics, including age, sex, underlying disease, conditioning regimen, or stem cell source, reliably predicted intestinal domination. Conclusions: Our findings reveal a unique intestinal domination fingerprint in Brazilian patients and highlight the importance of geographic context in interpreting microbiota-outcome associations in allo-HSCT settings.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Age Versus Immunity: Dietary Influences on Immunosenescence.
Journal of clinical medicine, 14(23): pii:jcm14238313.
Background: Immunosenescence, or the age-related weakening of the immune system, leads to greater susceptibility to chronic diseases, infections, and metabolic disorders. This process involves changes in the number and function of lymphocytes, increased levels of inflammatory markers, and modifications to the gut microbiome. In recent years, increasing importance has been placed on diet-both functional, rich in bioactive ingredients, and conventional, often pesticide-laden-as a factor modulating immune system aging. Methods: This paper provides a literature review on the effects of dietary components on immunosenescence. Results from 2010 to 2025 and from clinical and experimental studies on substances such as curcumin, butyrate, vitamin D3, omega-3 fatty acids, and conventional products containing pesticides were analyzed. Their impact on the microbiome, intestinal barrier integrity, inflammatory biomarkers, and the overall immune response was considered. Results: Numerous beneficial effects of functional foods were identified. Curcumin increases microbiota diversity and lowers C-Reactive Protein (CRP) and Tumor Necrosis Factor α (TNF-α) levels. Butyrate supports remission in inflammatory bowel disease by reducing Interleukin (IL) 6 and TNF-α levels. Vitamin D3 lowers inflammatory markers and reduces calprotectin in inflammatory bowel disease. Omega-3 fatty acids modulate microbiome composition and improve lipid profiles. In contrast, conventional foods high in pesticides lead to dysbiosis, intestinal barrier damage, and increased pro-inflammatory cytokines. Conclusions: Diet is a key factor in modulating immunosenescence. Functional foods can support the microbiome and reduce chronic inflammation, while conventional foods may exacerbate the aging process of the immune system. Further clinical research is needed to develop dietary recommendations to support immunity in older adults.
Additional Links: PMID-41375615
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PubMed:
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@article {pmid41375615,
year = {2025},
author = {Daniłowska, K and Picheta, N and Piekarz, J and Żyła, D and Zych, K and Szklener, K and Mańdziuk, S},
title = {Age Versus Immunity: Dietary Influences on Immunosenescence.},
journal = {Journal of clinical medicine},
volume = {14},
number = {23},
pages = {},
doi = {10.3390/jcm14238313},
pmid = {41375615},
issn = {2077-0383},
abstract = {Background: Immunosenescence, or the age-related weakening of the immune system, leads to greater susceptibility to chronic diseases, infections, and metabolic disorders. This process involves changes in the number and function of lymphocytes, increased levels of inflammatory markers, and modifications to the gut microbiome. In recent years, increasing importance has been placed on diet-both functional, rich in bioactive ingredients, and conventional, often pesticide-laden-as a factor modulating immune system aging. Methods: This paper provides a literature review on the effects of dietary components on immunosenescence. Results from 2010 to 2025 and from clinical and experimental studies on substances such as curcumin, butyrate, vitamin D3, omega-3 fatty acids, and conventional products containing pesticides were analyzed. Their impact on the microbiome, intestinal barrier integrity, inflammatory biomarkers, and the overall immune response was considered. Results: Numerous beneficial effects of functional foods were identified. Curcumin increases microbiota diversity and lowers C-Reactive Protein (CRP) and Tumor Necrosis Factor α (TNF-α) levels. Butyrate supports remission in inflammatory bowel disease by reducing Interleukin (IL) 6 and TNF-α levels. Vitamin D3 lowers inflammatory markers and reduces calprotectin in inflammatory bowel disease. Omega-3 fatty acids modulate microbiome composition and improve lipid profiles. In contrast, conventional foods high in pesticides lead to dysbiosis, intestinal barrier damage, and increased pro-inflammatory cytokines. Conclusions: Diet is a key factor in modulating immunosenescence. Functional foods can support the microbiome and reduce chronic inflammation, while conventional foods may exacerbate the aging process of the immune system. Further clinical research is needed to develop dietary recommendations to support immunity in older adults.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
The Role of Short-Chain Fatty Acids (SCFAs) in Colic and Anti-Inflammatory Pathways in Horses.
Animals : an open access journal from MDPI, 15(23): pii:ani15233482.
Equine colic remains a prevalent and potentially life-threatening condition with multifactorial origins, including dietary imbalances, stress, and microbial dysbiosis. Central to equine gut health is the production of short-chain fatty acids (SCFAs), primarily acetate, propionate, and butyrate, generated through microbial fermentation of dietary fibers in the hindgut. These metabolites not only serve as vital energy sources but also play crucial roles in maintaining intestinal barrier integrity, modulating motility, and suppressing inflammation. This review explores the role of SCFAs in equine gastrointestinal health, with particular emphasis on their anti-inflammatory effects and potential to prevent or mitigate colic. We examine how SCFAs interact with immune pathways, via G-protein-coupled receptors and regulatory T-cell promotion, to reduce pro-inflammatory cytokines such as TNF-α and IL-6. Evidence suggests that dietary shifts toward high-starch or low-fiber intake can reduce SCFA production, contributing to microbial imbalance, increased gut permeability, and systemic inflammation, all hallmarks of colic pathophysiology. Strategies to enhance SCFA levels, including high-forage diets, targeted prebiotic and probiotic supplementation, and emerging approaches like fecal microbiota transplantation, are discussed. Despite promising findings, significant gaps remain in equine-specific research, highlighting the need for longitudinal and mechanistic studies. Understanding and harnessing the therapeutic potential of SCFAs could pave the way for novel, microbiome-based interventions in colic prevention and treatment.
Additional Links: PMID-41375540
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PubMed:
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@article {pmid41375540,
year = {2025},
author = {Schank, N and Cottone, A and Wulf, M and Seiter, K and Thomas, B and Miller, LMJ and Anderson, SL and Sahyoun, A and Abidi, AH and Kassan, M and Verma, A},
title = {The Role of Short-Chain Fatty Acids (SCFAs) in Colic and Anti-Inflammatory Pathways in Horses.},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {23},
pages = {},
doi = {10.3390/ani15233482},
pmid = {41375540},
issn = {2076-2615},
abstract = {Equine colic remains a prevalent and potentially life-threatening condition with multifactorial origins, including dietary imbalances, stress, and microbial dysbiosis. Central to equine gut health is the production of short-chain fatty acids (SCFAs), primarily acetate, propionate, and butyrate, generated through microbial fermentation of dietary fibers in the hindgut. These metabolites not only serve as vital energy sources but also play crucial roles in maintaining intestinal barrier integrity, modulating motility, and suppressing inflammation. This review explores the role of SCFAs in equine gastrointestinal health, with particular emphasis on their anti-inflammatory effects and potential to prevent or mitigate colic. We examine how SCFAs interact with immune pathways, via G-protein-coupled receptors and regulatory T-cell promotion, to reduce pro-inflammatory cytokines such as TNF-α and IL-6. Evidence suggests that dietary shifts toward high-starch or low-fiber intake can reduce SCFA production, contributing to microbial imbalance, increased gut permeability, and systemic inflammation, all hallmarks of colic pathophysiology. Strategies to enhance SCFA levels, including high-forage diets, targeted prebiotic and probiotic supplementation, and emerging approaches like fecal microbiota transplantation, are discussed. Despite promising findings, significant gaps remain in equine-specific research, highlighting the need for longitudinal and mechanistic studies. Understanding and harnessing the therapeutic potential of SCFAs could pave the way for novel, microbiome-based interventions in colic prevention and treatment.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Cobalt and Vitamin B12 in Dairy Cattle Nutrition: Requirements, Functions, and Interactions.
Animals : an open access journal from MDPI, 15(23): pii:ani15233477.
Minerals are essential for ruminant health, productivity, and metabolic function, with trace minerals playing critical roles at narrow dietary margins. Cobalt (Co) is essential as it supports ruminal microbial synthesis of vitamin B12 (cobalamin), which acts as a crucial cofactor in energy and protein metabolism. This review summarizes the role of cobalt in dairy cattle nutrition, emphasizing its contribution to vitamin B12 synthesis, propionate metabolism, and milk production. Only 3-15% of dietary cobalt is converted to vitamin B12, and efficiency depends on dietary composition, forage-to-concentrate ratio, and ruminal microbiome. Deficiency leads to reduced intake, poor growth, anemia, reproductive failure, and decreased milk yield. Cow's milk contains ~0.5 µg/L of vitamin B12, with greater concentrations in colostrum; diet composition, supplementation, and genetics contribute to variability. Current recommendations set the cobalt requirement at 0.2 mg/kg diet DM, yet multiple environmental and nutritional factors can restrict vitamin B12 synthesis. Limitations of this review include heterogeneity among the studies reviewed, such as differences in trial design, animal genetics, diet composition, and environmental conditions, which may introduce variability and affect the generalizability and consistency of the findings. Collectively, findings highlight cobalt's pivotal role in supporting microbial activity, energy metabolism, and production outcomes in dairy cows.
Additional Links: PMID-41375535
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@article {pmid41375535,
year = {2025},
author = {Siregar, M and Salas-Solis, G and Faciola, AP},
title = {Cobalt and Vitamin B12 in Dairy Cattle Nutrition: Requirements, Functions, and Interactions.},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {23},
pages = {},
doi = {10.3390/ani15233477},
pmid = {41375535},
issn = {2076-2615},
abstract = {Minerals are essential for ruminant health, productivity, and metabolic function, with trace minerals playing critical roles at narrow dietary margins. Cobalt (Co) is essential as it supports ruminal microbial synthesis of vitamin B12 (cobalamin), which acts as a crucial cofactor in energy and protein metabolism. This review summarizes the role of cobalt in dairy cattle nutrition, emphasizing its contribution to vitamin B12 synthesis, propionate metabolism, and milk production. Only 3-15% of dietary cobalt is converted to vitamin B12, and efficiency depends on dietary composition, forage-to-concentrate ratio, and ruminal microbiome. Deficiency leads to reduced intake, poor growth, anemia, reproductive failure, and decreased milk yield. Cow's milk contains ~0.5 µg/L of vitamin B12, with greater concentrations in colostrum; diet composition, supplementation, and genetics contribute to variability. Current recommendations set the cobalt requirement at 0.2 mg/kg diet DM, yet multiple environmental and nutritional factors can restrict vitamin B12 synthesis. Limitations of this review include heterogeneity among the studies reviewed, such as differences in trial design, animal genetics, diet composition, and environmental conditions, which may introduce variability and affect the generalizability and consistency of the findings. Collectively, findings highlight cobalt's pivotal role in supporting microbial activity, energy metabolism, and production outcomes in dairy cows.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Integrative High-Throughput Screening and Microscopic Evidence Implicates Microsporidia as a Potential Pathogen of "Pus Crab" in the Mud Crab (Scylla paramamosain).
Animals : an open access journal from MDPI, 15(23): pii:ani15233463.
The mud crab (Scylla paramamosain), an economically important crustacean aquaculture species in southern China, is susceptible to infections due to its immune system lacking acquired immunity. An emergent disease locally termed "pus crab" has caused severe muscle lesions in pond-farmed crabs, but its etiology remained unclear. Here, we applied an integrated approach, histopathology, electron microscopy, metagenomic sequencing, and experimental infection to identify the pathogen of "pus crab". Histological staining (H&E, Wright-Giemsa, and Masson) revealed muscle fiber dissolution, disordered fiber arrangement, and abundant interstitial spore-like bodies. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) confirmed intracellular spore morphology consistent with microsporidia. Metagenomic profiling showed a pronounced shift in the muscle microbiome, with a marked increase in microsporidian taxa at the genus level and a concurrent decline in bacterial relative abundance. Functional annotation indicated enrichment of pathways related to protein processing, ribosome biogenesis, glycosylation, and the ubiquitin-proteasome system. Isolation of spores from diseased muscle and subsequent injection into healthy crabs reproduced wild-like clinical signs and histopathology, confirming infectivity and implicating microsporidia as the likely etiological agents of "pus crab". These findings establish a multidisciplinary framework for pathogen identification in aquaculture and provide candidate molecular and biochemical markers for early diagnosis and management.
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@article {pmid41375521,
year = {2025},
author = {Xiao, L and Liang, Y and Hao, S and Wu, K},
title = {Integrative High-Throughput Screening and Microscopic Evidence Implicates Microsporidia as a Potential Pathogen of "Pus Crab" in the Mud Crab (Scylla paramamosain).},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {23},
pages = {},
doi = {10.3390/ani15233463},
pmid = {41375521},
issn = {2076-2615},
abstract = {The mud crab (Scylla paramamosain), an economically important crustacean aquaculture species in southern China, is susceptible to infections due to its immune system lacking acquired immunity. An emergent disease locally termed "pus crab" has caused severe muscle lesions in pond-farmed crabs, but its etiology remained unclear. Here, we applied an integrated approach, histopathology, electron microscopy, metagenomic sequencing, and experimental infection to identify the pathogen of "pus crab". Histological staining (H&E, Wright-Giemsa, and Masson) revealed muscle fiber dissolution, disordered fiber arrangement, and abundant interstitial spore-like bodies. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) confirmed intracellular spore morphology consistent with microsporidia. Metagenomic profiling showed a pronounced shift in the muscle microbiome, with a marked increase in microsporidian taxa at the genus level and a concurrent decline in bacterial relative abundance. Functional annotation indicated enrichment of pathways related to protein processing, ribosome biogenesis, glycosylation, and the ubiquitin-proteasome system. Isolation of spores from diseased muscle and subsequent injection into healthy crabs reproduced wild-like clinical signs and histopathology, confirming infectivity and implicating microsporidia as the likely etiological agents of "pus crab". These findings establish a multidisciplinary framework for pathogen identification in aquaculture and provide candidate molecular and biochemical markers for early diagnosis and management.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Supplementation of Bacillus coagulans and Tributyrin to Danzhou Chickens: Effects on Growth Performance, Antioxidant Status, Immune Response, Intestinal Health, and Cecal Microbiome.
Animals : an open access journal from MDPI, 15(23): pii:ani15233428.
To investigate the effects of Bacillus coagulans (BC) and tributyrin (TB) on Danzhou chickens, a 2 × 2 factorial design was adopted. A total of 480 chickens were randomly assigned to four dietary treatments, consisting of two BC levels (0 and 1.5 g/kg) and two TB levels (0 and 1.0 g/kg), for a 35-day trial. The results showed that supplementation with BC or TB alone significantly increased the average daily gain (ADG), serum immune parameters (immunoglobulin A, immunoglobulin G, and anti-inflammatory cytokines interleukin-4 and interleukin-10), total antioxidant capacity, and catalase activity, while reducing pro-inflammatory cytokine levels and the feed-to-gain ratio (p < 0.05). In addition, individual supplementation with BC or TB also enhanced digestive enzyme activities in the intestine, increased villus height in the small intestine, and optimized the structure of the cecal microbiota (p < 0.05). More importantly, significant synergistic interactions between BC and TB were observed across multiple parameters (p < 0.05). Combined supplementation further increased ADG, serum immunoglobulin M levels, superoxide dismutase activity, lipase activity in the ileum, and villus height in the jejunum (p < 0.05). Meanwhile, the combined supplementation also significantly elevated the abundance of beneficial bacteria such as Bacteroides, Eubacterium_brachy_group, and Negativibacillus. In conclusion, supplementation with BC or TB effectively improved the growth performance, antioxidant status, immune function, intestinal morphology, and cecal microbiota composition of Danzhou chickens, and the combined supplementation demonstrated superior effects compared to individual supplementation.
Additional Links: PMID-41375486
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PubMed:
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@article {pmid41375486,
year = {2025},
author = {Yu, X and Xu, F and Zhao, D and Chai, H and Yu, Y and Peng, W and Xu, L and Wu, H},
title = {Supplementation of Bacillus coagulans and Tributyrin to Danzhou Chickens: Effects on Growth Performance, Antioxidant Status, Immune Response, Intestinal Health, and Cecal Microbiome.},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {23},
pages = {},
doi = {10.3390/ani15233428},
pmid = {41375486},
issn = {2076-2615},
support = {HNARS-06-G02//HNARS/ ; 325QN452//Hainan Provincial Natural Science Foundation of China/ ; CATASCXTD202407//Chinese Academy of Tropical Agricultural Sciences for Science and Technology Innovation Team of National Tropical Agricultural Science Center/ ; 1630032025011//Central Public-interest Scientific Institution Basal Research Fund/ ; },
abstract = {To investigate the effects of Bacillus coagulans (BC) and tributyrin (TB) on Danzhou chickens, a 2 × 2 factorial design was adopted. A total of 480 chickens were randomly assigned to four dietary treatments, consisting of two BC levels (0 and 1.5 g/kg) and two TB levels (0 and 1.0 g/kg), for a 35-day trial. The results showed that supplementation with BC or TB alone significantly increased the average daily gain (ADG), serum immune parameters (immunoglobulin A, immunoglobulin G, and anti-inflammatory cytokines interleukin-4 and interleukin-10), total antioxidant capacity, and catalase activity, while reducing pro-inflammatory cytokine levels and the feed-to-gain ratio (p < 0.05). In addition, individual supplementation with BC or TB also enhanced digestive enzyme activities in the intestine, increased villus height in the small intestine, and optimized the structure of the cecal microbiota (p < 0.05). More importantly, significant synergistic interactions between BC and TB were observed across multiple parameters (p < 0.05). Combined supplementation further increased ADG, serum immunoglobulin M levels, superoxide dismutase activity, lipase activity in the ileum, and villus height in the jejunum (p < 0.05). Meanwhile, the combined supplementation also significantly elevated the abundance of beneficial bacteria such as Bacteroides, Eubacterium_brachy_group, and Negativibacillus. In conclusion, supplementation with BC or TB effectively improved the growth performance, antioxidant status, immune function, intestinal morphology, and cecal microbiota composition of Danzhou chickens, and the combined supplementation demonstrated superior effects compared to individual supplementation.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Microbial Biomarkers Differ for Various Feed Efficiency Metrics in Beef Cattle.
Animals : an open access journal from MDPI, 15(23): pii:ani15233416.
Cattle feed efficiency can influence operating costs and revenues, and it is a complex phenotype that can be measured by different metrices. The objective of this study was to determine which microbial taxa in the ruminal and fecal microbiomes of Angus bulls are associated with residual feed intake (RFI), residual average daily gain (RADG), feed conversion ratio (FCR), and adjusted feed conversion ratio (AFCR) by using a large sample size. The metrics RFI and RADG are calculated from the difference between an animal's actual feed intake and actual gain, to their predicted intake and gain, respectively, and AFCR is the FCR adjusted for the animal's size. Rumen (n = 1176) and fecal (n = 1179) samples were collected from Angus bulls from 10 contemporary groups located across the continental U.S. Animals were assigned to three classifications (High, Medium, or Low) for each feed efficiency metric within each contemporary group, according to their individual performance data. To compare the feed efficiency metrics, a cost analysis scenario was performed, and bulls classified by RADG had the greatest correlation with predicted profit (r[2] = 0.98). For alpha diversity, only classification by FCR resulted in differences within both rumen and fecal samples. In the rumen environment, only 'X112' was significant (p = 0.02) by RFI classification, and Succinivibrionaceae was significant (p = 0.01) by FCR classification. In the fecal environment, a total of 19 families significantly differed, with bulls classified by RFI having the greatest number of different families. Bull feed efficiency status had greater impacts in the fecal microbiome compared to the rumen, but results should be taken in context since the animals were classified within each contemporary group. Still, differences detected within the fecal microbiome may allow for more assessable microbiome applications; however, the metric used to classify cattle as feed efficient will determine which microbial families are relevant.
Additional Links: PMID-41375474
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PubMed:
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@article {pmid41375474,
year = {2025},
author = {Dycus, MM and Lamichhane, U and Feldmann, K and Welch, C and Osorio-Doblado, A and Pringle, TD and Callaway, T and Lourenco, J},
title = {Microbial Biomarkers Differ for Various Feed Efficiency Metrics in Beef Cattle.},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {23},
pages = {},
doi = {10.3390/ani15233416},
pmid = {41375474},
issn = {2076-2615},
support = {N/A.//Kelly Products, Inc./ ; },
abstract = {Cattle feed efficiency can influence operating costs and revenues, and it is a complex phenotype that can be measured by different metrices. The objective of this study was to determine which microbial taxa in the ruminal and fecal microbiomes of Angus bulls are associated with residual feed intake (RFI), residual average daily gain (RADG), feed conversion ratio (FCR), and adjusted feed conversion ratio (AFCR) by using a large sample size. The metrics RFI and RADG are calculated from the difference between an animal's actual feed intake and actual gain, to their predicted intake and gain, respectively, and AFCR is the FCR adjusted for the animal's size. Rumen (n = 1176) and fecal (n = 1179) samples were collected from Angus bulls from 10 contemporary groups located across the continental U.S. Animals were assigned to three classifications (High, Medium, or Low) for each feed efficiency metric within each contemporary group, according to their individual performance data. To compare the feed efficiency metrics, a cost analysis scenario was performed, and bulls classified by RADG had the greatest correlation with predicted profit (r[2] = 0.98). For alpha diversity, only classification by FCR resulted in differences within both rumen and fecal samples. In the rumen environment, only 'X112' was significant (p = 0.02) by RFI classification, and Succinivibrionaceae was significant (p = 0.01) by FCR classification. In the fecal environment, a total of 19 families significantly differed, with bulls classified by RFI having the greatest number of different families. Bull feed efficiency status had greater impacts in the fecal microbiome compared to the rumen, but results should be taken in context since the animals were classified within each contemporary group. Still, differences detected within the fecal microbiome may allow for more assessable microbiome applications; however, the metric used to classify cattle as feed efficient will determine which microbial families are relevant.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Salinity Effects on Aquatic and Host Intestinal Microbiota Dynamics in Rhinogobio ventralis.
Animals : an open access journal from MDPI, 15(23): pii:ani15233407.
The endangered Rhinogobio ventralis, endemic to the upper Yangtze River, is dependent on captive breeding for its conservation. However, this highly stress-sensitive species is exceptionally susceptible to Ichthyophthirius multifiliis, leading to severe pathology and high mortality in culture. Elevated salinity holds potential for managing key aquaculture pathogens, including Ichthyophthirius multifiliis and Saprolegnia spp. However, its potential unintended ecological consequences remain insufficiently understood. This study evaluated the systemic impacts of 5‱ salinity on the culture environment of the endangered species Rhinogobio ventralis, using integrated 16S/18S rRNA gene sequencing and water quality analysis. The results demonstrated that while salinity treatment effectively reduced the environmental molecular signal of harmful eukaryotes such as Ichthyophthirius and Saprolegnia, it also induced significant ecological shifts: (1) aquatic prokaryotic diversity increased, yet the self-purification capacity of the water was compromised, indicated by elevated dissolved oxygen, nitrate nitrogen, and total nitrogen; (2) in the fish intestinal microbiome, a decline in potentially beneficial taxa (e.g., Exiguobacterium) co-occurred with an enrichment of genera containing potentially pathogenic species (e.g., Staphylococcus and Pseudomonas), collectively suggesting a state of dysbiosis; (3) co-occurrence network analysis revealed that the aquatic microbial community developed greater complexity, while the intestinal network became structurally simplified and more antagonistic. These findings reveal that elevating salinity in freshwater aquaculture systems compromises both host microbiome health and aquatic ecosystem functioning. As such, future aquaculture management should integrate supportive measures like probiotic supplementation to maintain overall system stability.
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PubMed:
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@article {pmid41375465,
year = {2025},
author = {Liu, K and Zhao, Q and Jin, T and Li, X and Sun, H and Wu, X and Ge, H and Li, F},
title = {Salinity Effects on Aquatic and Host Intestinal Microbiota Dynamics in Rhinogobio ventralis.},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {23},
pages = {},
doi = {10.3390/ani15233407},
pmid = {41375465},
issn = {2076-2615},
support = {32202971//National Natural Science Foundation of China/ ; CQFTIU2024-08//Chongqing Fisheries Science and Technology Innovation Alliance/ ; CQFTIU202501-4//Chongqing Fisheries Science and Technology Innovation Alliance/ ; KJZD-M202401301//Major Science and Technology Research Project of Chongqing Municipal Education Commission/ ; },
abstract = {The endangered Rhinogobio ventralis, endemic to the upper Yangtze River, is dependent on captive breeding for its conservation. However, this highly stress-sensitive species is exceptionally susceptible to Ichthyophthirius multifiliis, leading to severe pathology and high mortality in culture. Elevated salinity holds potential for managing key aquaculture pathogens, including Ichthyophthirius multifiliis and Saprolegnia spp. However, its potential unintended ecological consequences remain insufficiently understood. This study evaluated the systemic impacts of 5‱ salinity on the culture environment of the endangered species Rhinogobio ventralis, using integrated 16S/18S rRNA gene sequencing and water quality analysis. The results demonstrated that while salinity treatment effectively reduced the environmental molecular signal of harmful eukaryotes such as Ichthyophthirius and Saprolegnia, it also induced significant ecological shifts: (1) aquatic prokaryotic diversity increased, yet the self-purification capacity of the water was compromised, indicated by elevated dissolved oxygen, nitrate nitrogen, and total nitrogen; (2) in the fish intestinal microbiome, a decline in potentially beneficial taxa (e.g., Exiguobacterium) co-occurred with an enrichment of genera containing potentially pathogenic species (e.g., Staphylococcus and Pseudomonas), collectively suggesting a state of dysbiosis; (3) co-occurrence network analysis revealed that the aquatic microbial community developed greater complexity, while the intestinal network became structurally simplified and more antagonistic. These findings reveal that elevating salinity in freshwater aquaculture systems compromises both host microbiome health and aquatic ecosystem functioning. As such, future aquaculture management should integrate supportive measures like probiotic supplementation to maintain overall system stability.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Rumen-Protected Methionine Supplementation in the Diet Improved the Production Performance of Dairy Goats by Optimizing the Amino Acid Profile and Lipid Metabolism and Modulating the Colonic Microbiome.
Animals : an open access journal from MDPI, 15(23): pii:ani15233386.
This study aimed to investigate the effects of rumen-protected methionine (RPM) on the production performance of lactating dairy goats. Thirty first-time lactating Guanzhong dairy goats with identical kidding dates and comparable body weights (41.17 ± 3.05 kg) were randomly assigned to two groups: (1) CON: basal diet and (2) RPM: basal diet + 7.5 g/day RPM. The duration of the experiment was 21 days. Compared with the CON group, the RPM group presented a significant increase in milk yield, 4% fat-corrected milk (FCM), and feed efficiency; however, no significant difference was observed in dry feed intake (DMI). Moreover, milk fat, protein, lactose, and SNF production was greater in the PRM group than in the CON group. Compared with the CON group, the RPM group presented higher nonesterified fatty acid (NEFA) and very-low-density lipoprotein (VLDL) levels, and no significant differences in the other metabolites were detected. The concentrations of acetate, propionate, and total volatile fatty acids (TVFAs) in the feces of the RPM group were significantly greater than those in the CON group; however, no significant differences were detected in the concentrations of isobutyrate, butyrate, and valerate. Furthermore, genera such as Muribaculaceae, Bifidobacterium, and Christensenellaceae were significantly enriched in the feces of the RPM group. Concurrently, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that the RPM group was significantly enriched in pathways associated with amino acid synthesis, the immune system, and energy metabolism. In summary, dietary supplementation with RPM improved the lipid metabolism function of the liver, increased the abundance of beneficial bacteria such as Muribaculaceae and Bifidobacterium in the colon, and enriched microbial functions related to energy and amino acid metabolism, thereby enhancing colon fermentation and host metabolic status, ultimately improving the production performance of lactating dairy goats. These findings elucidate the positive effects of RPM on the production performance and metabolic health of dairy goats, potentially offering new perspectives and strategies for optimizing dairy production.
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@article {pmid41375445,
year = {2025},
author = {Jiang, X and Wang, J and Zhang, Y and Li, J and Liu, H and Wu, S and Yao, J},
title = {Rumen-Protected Methionine Supplementation in the Diet Improved the Production Performance of Dairy Goats by Optimizing the Amino Acid Profile and Lipid Metabolism and Modulating the Colonic Microbiome.},
journal = {Animals : an open access journal from MDPI},
volume = {15},
number = {23},
pages = {},
doi = {10.3390/ani15233386},
pmid = {41375445},
issn = {2076-2615},
support = {2022GD-TSLD-46-0501//the Shaanxi Livestock and Poultry Breeding Double-chain Fusion Key Project/ ; },
abstract = {This study aimed to investigate the effects of rumen-protected methionine (RPM) on the production performance of lactating dairy goats. Thirty first-time lactating Guanzhong dairy goats with identical kidding dates and comparable body weights (41.17 ± 3.05 kg) were randomly assigned to two groups: (1) CON: basal diet and (2) RPM: basal diet + 7.5 g/day RPM. The duration of the experiment was 21 days. Compared with the CON group, the RPM group presented a significant increase in milk yield, 4% fat-corrected milk (FCM), and feed efficiency; however, no significant difference was observed in dry feed intake (DMI). Moreover, milk fat, protein, lactose, and SNF production was greater in the PRM group than in the CON group. Compared with the CON group, the RPM group presented higher nonesterified fatty acid (NEFA) and very-low-density lipoprotein (VLDL) levels, and no significant differences in the other metabolites were detected. The concentrations of acetate, propionate, and total volatile fatty acids (TVFAs) in the feces of the RPM group were significantly greater than those in the CON group; however, no significant differences were detected in the concentrations of isobutyrate, butyrate, and valerate. Furthermore, genera such as Muribaculaceae, Bifidobacterium, and Christensenellaceae were significantly enriched in the feces of the RPM group. Concurrently, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that the RPM group was significantly enriched in pathways associated with amino acid synthesis, the immune system, and energy metabolism. In summary, dietary supplementation with RPM improved the lipid metabolism function of the liver, increased the abundance of beneficial bacteria such as Muribaculaceae and Bifidobacterium in the colon, and enriched microbial functions related to energy and amino acid metabolism, thereby enhancing colon fermentation and host metabolic status, ultimately improving the production performance of lactating dairy goats. These findings elucidate the positive effects of RPM on the production performance and metabolic health of dairy goats, potentially offering new perspectives and strategies for optimizing dairy production.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Second Genome: Rhizosphere Microbiome as a Key External Driver of Nitrogen Use Efficiency in Maize.
Plants (Basel, Switzerland), 14(23): pii:plants14233680.
Improving nitrogen use efficiency (NUE) in maize is critical for reducing fertilizer inputs and mitigating environmental impacts. The rhizosphere microbiome-the plant's "second genome"-plays a key role in nitrogen acquisition, assimilation, and signaling. This review synthesizes recent advances from multi-omics studies, functional validation, and field experiments, highlighting how maize roots recruit and coordinate microbial taxa, including diazotrophs, nitrifiers, organic nitrogen mineralizers, and growth-promoting bacteria, to enhance NUE under variable nitrogen availability. We integrate mechanistic insights into transporter-mediated nitrogen uptake, microbial regulation of root development and exudation, and host genetic determinants, such as ZmC2, ZmSBT3, and ZmNLP8, that influence microbiome assembly. Evidence from synthetic communities, isotope tracing, and host-microbiome association studies demonstrates that microbial contributions to plant nitrogen can be substantial and genetically modulated. Finally, we discuss microbiome-based interventions, including functional strain discovery, microbial fertilizers, biostimulants, and microbiome-assisted breeding, assessing their potential and limitations. We conclude by highlighting key challenges and proposing an integrative framework to guide microbiome-informed strategies for sustainable improvement of maize NUE.
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@article {pmid41375390,
year = {2025},
author = {Luo, P and Yang, L and Zhu, Y and Liu, M and He, Y and Liu, C and He, W},
title = {Second Genome: Rhizosphere Microbiome as a Key External Driver of Nitrogen Use Efficiency in Maize.},
journal = {Plants (Basel, Switzerland)},
volume = {14},
number = {23},
pages = {},
doi = {10.3390/plants14233680},
pmid = {41375390},
issn = {2223-7747},
abstract = {Improving nitrogen use efficiency (NUE) in maize is critical for reducing fertilizer inputs and mitigating environmental impacts. The rhizosphere microbiome-the plant's "second genome"-plays a key role in nitrogen acquisition, assimilation, and signaling. This review synthesizes recent advances from multi-omics studies, functional validation, and field experiments, highlighting how maize roots recruit and coordinate microbial taxa, including diazotrophs, nitrifiers, organic nitrogen mineralizers, and growth-promoting bacteria, to enhance NUE under variable nitrogen availability. We integrate mechanistic insights into transporter-mediated nitrogen uptake, microbial regulation of root development and exudation, and host genetic determinants, such as ZmC2, ZmSBT3, and ZmNLP8, that influence microbiome assembly. Evidence from synthetic communities, isotope tracing, and host-microbiome association studies demonstrates that microbial contributions to plant nitrogen can be substantial and genetically modulated. Finally, we discuss microbiome-based interventions, including functional strain discovery, microbial fertilizers, biostimulants, and microbiome-assisted breeding, assessing their potential and limitations. We conclude by highlighting key challenges and proposing an integrative framework to guide microbiome-informed strategies for sustainable improvement of maize NUE.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Organic Amendments and Trichoderma Change the Rhizosphere Microbiome and Improve Cucumber Yield and Fusarium Suppression.
Plants (Basel, Switzerland), 14(23): pii:plants14233660.
Conventional chemical-based control methods for soil-borne diseases often degrade soil quality. The recycling of organic wastes offers a promising solution to simultaneously alleviate environmental pollution and restore soil health. As a beneficial fungus, Trichoderma plays a crucial role in enhancing plant performance. However, knowledge of the mechanisms through which organic wastes and Trichoderma interact to influence plant performance remains limited. We investigated how the combined application of organic wastes (chitin and straw) and a biocontrol fungus (Trichoderma) influenced the rhizosphere microbiome to improve plant performance. Compared with the control, organic waste alone, and Trichoderma alone treatments, the combined application of organic wastes and Trichoderma significantly (p < 0.05) increased cucumber yield and reduced pathogen density. Increased yield and reduced pathogen density were associated with changes in bacterial and fungal communities induced by this combined application treatment. Indeed, this combined application treatment enabled plants to recruit certain potentially beneficial core bacterial (e.g., Streptomyces and Flavisolibacter) and fungal taxa (e.g., Trichoderma), increasing their positive interactions in the rhizosphere. We demonstrate that the combined application of organic wastes and Trichoderma can shape distinct rhizosphere bacterial and fungal communities, promoting an increase in beneficial microorganisms and their positive interactions, which contribute to enhanced plant performance.
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@article {pmid41375370,
year = {2025},
author = {Wang, Y and Hang, X and Shao, C and Zhang, Z and Guo, S and Li, R and Shen, Q},
title = {Organic Amendments and Trichoderma Change the Rhizosphere Microbiome and Improve Cucumber Yield and Fusarium Suppression.},
journal = {Plants (Basel, Switzerland)},
volume = {14},
number = {23},
pages = {},
doi = {10.3390/plants14233660},
pmid = {41375370},
issn = {2223-7747},
support = {ZZFH2024-2026QNRC001//the Young Elite Scientists Sponsorship Program by CAST/ ; 42307171//the National Natural Science Foundation of China/ ; 2023M731724//the Postdoctoral Science Foundation of China/ ; },
abstract = {Conventional chemical-based control methods for soil-borne diseases often degrade soil quality. The recycling of organic wastes offers a promising solution to simultaneously alleviate environmental pollution and restore soil health. As a beneficial fungus, Trichoderma plays a crucial role in enhancing plant performance. However, knowledge of the mechanisms through which organic wastes and Trichoderma interact to influence plant performance remains limited. We investigated how the combined application of organic wastes (chitin and straw) and a biocontrol fungus (Trichoderma) influenced the rhizosphere microbiome to improve plant performance. Compared with the control, organic waste alone, and Trichoderma alone treatments, the combined application of organic wastes and Trichoderma significantly (p < 0.05) increased cucumber yield and reduced pathogen density. Increased yield and reduced pathogen density were associated with changes in bacterial and fungal communities induced by this combined application treatment. Indeed, this combined application treatment enabled plants to recruit certain potentially beneficial core bacterial (e.g., Streptomyces and Flavisolibacter) and fungal taxa (e.g., Trichoderma), increasing their positive interactions in the rhizosphere. We demonstrate that the combined application of organic wastes and Trichoderma can shape distinct rhizosphere bacterial and fungal communities, promoting an increase in beneficial microorganisms and their positive interactions, which contribute to enhanced plant performance.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Holobiome Structure and Microbial Core Assemblages of Deschampsia antarctica Across the South Shetland Islands.
Plants (Basel, Switzerland), 14(23): pii:plants14233657.
Antarctica harbors some of the most extreme ecosystems on earth, where only two vascular plants persist. The native grass Deschampsia antarctica provides a model for plant-microbe interactions under intense abiotic stress. We present the first multi-compartmental and multi-kingdom characterization of bacterial and fungal communities associated with D. antarctica across three South Shetland Islands. Metabarcoding revealed strong compartmentalization: the rhizosphere displayed the highest richness and complex bacterial-fungal networks; the root endosphere showed intermediate diversity with keystone taxa such as Rhizobiales and Streptomyces; and the leaf endosphere was simplified, dominated by stress-tolerant taxa including Pseudomonas and Helotiales. Despite marked soil heterogeneity, phosphorus enrichment at Admiralty Bay, base cations at Coppermine Cove, and iron at Byers Peninsula, a conserved core (20 bacterial and 5 fungal genera) persisted, mainly cold-adapted saprotrophs and plant-associated taxa. Fungal assemblages were more responsive to soil chemistry, with site-specific enrichments such as Zymoseptoria and Herpotrichia. Overall, D. antarctica holobionts exhibited a dual strategy: conserved microbial backbones confer stability, while localized assemblages shaped by soil chemistry and geography enhance adaptability. Together, these findings provide one of the most integrative characterizations of the D. antarctica holobiont to date, revealing how conserved and adaptive microbial components support plant resilience under extreme Antarctic conditions and offering valuable insights for predicting biological responses to ongoing climate change.
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@article {pmid41375367,
year = {2025},
author = {Rodriguez, R and Barra, PJ and Saldivar-Diaz, M and Larama, G and Alvarado, R and López, D and Delgado, M and Orlando, J and Oses, R and Merino, C and Tortella, G and Duran, P},
title = {Holobiome Structure and Microbial Core Assemblages of Deschampsia antarctica Across the South Shetland Islands.},
journal = {Plants (Basel, Switzerland)},
volume = {14},
number = {23},
pages = {},
doi = {10.3390/plants14233657},
pmid = {41375367},
issn = {2223-7747},
support = {3230478//Fondecyt Postdoctoral ANID/ ; 1241293//Fondecyt Regular ANID/ ; ATE220038//Concurso Anillos de Investigación en Áreas Temáticas Especı́ficas/ ; },
abstract = {Antarctica harbors some of the most extreme ecosystems on earth, where only two vascular plants persist. The native grass Deschampsia antarctica provides a model for plant-microbe interactions under intense abiotic stress. We present the first multi-compartmental and multi-kingdom characterization of bacterial and fungal communities associated with D. antarctica across three South Shetland Islands. Metabarcoding revealed strong compartmentalization: the rhizosphere displayed the highest richness and complex bacterial-fungal networks; the root endosphere showed intermediate diversity with keystone taxa such as Rhizobiales and Streptomyces; and the leaf endosphere was simplified, dominated by stress-tolerant taxa including Pseudomonas and Helotiales. Despite marked soil heterogeneity, phosphorus enrichment at Admiralty Bay, base cations at Coppermine Cove, and iron at Byers Peninsula, a conserved core (20 bacterial and 5 fungal genera) persisted, mainly cold-adapted saprotrophs and plant-associated taxa. Fungal assemblages were more responsive to soil chemistry, with site-specific enrichments such as Zymoseptoria and Herpotrichia. Overall, D. antarctica holobionts exhibited a dual strategy: conserved microbial backbones confer stability, while localized assemblages shaped by soil chemistry and geography enhance adaptability. Together, these findings provide one of the most integrative characterizations of the D. antarctica holobiont to date, revealing how conserved and adaptive microbial components support plant resilience under extreme Antarctic conditions and offering valuable insights for predicting biological responses to ongoing climate change.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Iohexol as an Emerging Contaminant Potentially Influencing Structural and Functional Changes in the Activated Sludge Microbiome.
Molecules (Basel, Switzerland), 30(23): pii:molecules30234641.
Iohexol (IOX) is one of the most commonly used iodinated contrast agents due to its relatively low toxicity. However, owing to its low biodegradability, it accumulates in wastewater and sewage sludge, ultimately reaching wastewater treatment plants. With increasing IOX loads, the activated sludge (AS) microbiome is exposed to its long-term effects. Therefore, this study aimed to determine the impact of IOX on the structure and functioning of AS. The results demonstrated that IOX at lower concentrations does not affect the functional parameters of AS, and only long-term exposure of the microbiome to a concentration of 20 mg/L results in functional changes. These changes themselves, among other effects, concerning amino acid and carbohydrate metabolism and the phosphorus cycle. Furthermore, the study demonstrated that despite the activated sludge microbiome's ability to transform 20 mg/L of IOX, long-term exposure to this concentration reduces the efficiency of this process. This indicates that although IOX is a relatively safe compound, prolonged exposure of the AS microbiome to high doses may lead to functional changes in AS and potentially impair wastewater treatment processes.
Additional Links: PMID-41375236
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PubMed:
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@article {pmid41375236,
year = {2025},
author = {Nowak, A and Pacwa-Płociniczak, M and Guzik, U and Wojcieszyńska, D},
title = {Iohexol as an Emerging Contaminant Potentially Influencing Structural and Functional Changes in the Activated Sludge Microbiome.},
journal = {Molecules (Basel, Switzerland)},
volume = {30},
number = {23},
pages = {},
doi = {10.3390/molecules30234641},
pmid = {41375236},
issn = {1420-3049},
support = {2021/05/X/NZ9/00457//National Science Centre/ ; },
mesh = {*Sewage/microbiology ; *Microbiota/drug effects ; *Iohexol ; Wastewater/microbiology ; *Water Pollutants, Chemical ; *Contrast Media ; Biodegradation, Environmental ; },
abstract = {Iohexol (IOX) is one of the most commonly used iodinated contrast agents due to its relatively low toxicity. However, owing to its low biodegradability, it accumulates in wastewater and sewage sludge, ultimately reaching wastewater treatment plants. With increasing IOX loads, the activated sludge (AS) microbiome is exposed to its long-term effects. Therefore, this study aimed to determine the impact of IOX on the structure and functioning of AS. The results demonstrated that IOX at lower concentrations does not affect the functional parameters of AS, and only long-term exposure of the microbiome to a concentration of 20 mg/L results in functional changes. These changes themselves, among other effects, concerning amino acid and carbohydrate metabolism and the phosphorus cycle. Furthermore, the study demonstrated that despite the activated sludge microbiome's ability to transform 20 mg/L of IOX, long-term exposure to this concentration reduces the efficiency of this process. This indicates that although IOX is a relatively safe compound, prolonged exposure of the AS microbiome to high doses may lead to functional changes in AS and potentially impair wastewater treatment processes.},
}
MeSH Terms:
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*Sewage/microbiology
*Microbiota/drug effects
*Iohexol
Wastewater/microbiology
*Water Pollutants, Chemical
*Contrast Media
Biodegradation, Environmental
RevDate: 2025-12-11
CmpDate: 2025-12-11
Genitourinary Microbiome and Volatilome: A Pilot Study in Patients with Prostatic Adenocarcinoma Submitted to Radical Prostatectomy.
Cancers, 17(23): pii:cancers17233841.
Background/Objectives: The genitourinary microbiome and metabolome may contribute to prostate cancer (PC) biology, but evidence remains limited. This pilot study characterizes the urinary microbiota and volatilome in men with PC and investigates microbial and viral DNA in prostate tissue, comparing findings with benign prostatic hyperplasia (BPH). Methods: We prospectively enrolled 21 non-metastatic PC patients undergoing radical prostatectomy and 17 BPH controls. Lesional and non-lesional prostate tissues and urine were collected from PC patients, as well as urine samples from BPH participants. DNA samples were tested for sexually transmitted pathogens by multiplex real-time PCR. Urine and prostate tissue were analyzed for human polyomaviruses (JCPyV, BKPyV, MCPyV) by qPCR, bacterial profiles via 16S rRNA gene sequencing, and urinary volatile organic metabolites (VOMs) using HS-SPME/GC-MS. Microbial and metabolic profiles were compared, and taxa-metabolites were assessed. Results: JCPyV and BKPyV were detected in urine and tissue from PC patients; MCPyV was detected only in tissue, at low frequency. In BPH, viral prevalence was lower and MCPyV was absent. JCPyV/BKPyV co-infection was common in cancer. No sexually transmitted pathogen emerged. PC patients showed greater urinary microbial diversity and five enriched genera, along with specific metabolic pathways. 36 urinary VOMs were identified, with 14 differing significantly, with positive correlations between PC-associated genera and metabolites. In contrast, prostate tissue was low-biomass, dominated by Pseudomonas, and showed no significant differences between lesional and non-lesional areas. Conclusions: This preliminary, hypothesis-generating study indicates that urinary, rather than tissue, microbial and volatilome signatures show clearer differences between PC and BPH. These findings suggest possible microbiota-metabolite interactions in PC but require validation in larger cohorts.
Additional Links: PMID-41375043
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PubMed:
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@article {pmid41375043,
year = {2025},
author = {Musleh, L and Passerini, S and Brunetti, F and Maurizi, L and Bevilacqua, G and Santodirocco, L and Sciarra, B and Moriconi, M and Fraschetti, C and Filippi, A and Conte, MP and Pietropaolo, V and Di Pietro, M and Filardo, S and Sciarra, A and Longhi, C},
title = {Genitourinary Microbiome and Volatilome: A Pilot Study in Patients with Prostatic Adenocarcinoma Submitted to Radical Prostatectomy.},
journal = {Cancers},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/cancers17233841},
pmid = {41375043},
issn = {2072-6694},
support = {Ricerca Scientifica 2023 "Sapienza" University of Rome//Catia Longhi/ ; },
abstract = {Background/Objectives: The genitourinary microbiome and metabolome may contribute to prostate cancer (PC) biology, but evidence remains limited. This pilot study characterizes the urinary microbiota and volatilome in men with PC and investigates microbial and viral DNA in prostate tissue, comparing findings with benign prostatic hyperplasia (BPH). Methods: We prospectively enrolled 21 non-metastatic PC patients undergoing radical prostatectomy and 17 BPH controls. Lesional and non-lesional prostate tissues and urine were collected from PC patients, as well as urine samples from BPH participants. DNA samples were tested for sexually transmitted pathogens by multiplex real-time PCR. Urine and prostate tissue were analyzed for human polyomaviruses (JCPyV, BKPyV, MCPyV) by qPCR, bacterial profiles via 16S rRNA gene sequencing, and urinary volatile organic metabolites (VOMs) using HS-SPME/GC-MS. Microbial and metabolic profiles were compared, and taxa-metabolites were assessed. Results: JCPyV and BKPyV were detected in urine and tissue from PC patients; MCPyV was detected only in tissue, at low frequency. In BPH, viral prevalence was lower and MCPyV was absent. JCPyV/BKPyV co-infection was common in cancer. No sexually transmitted pathogen emerged. PC patients showed greater urinary microbial diversity and five enriched genera, along with specific metabolic pathways. 36 urinary VOMs were identified, with 14 differing significantly, with positive correlations between PC-associated genera and metabolites. In contrast, prostate tissue was low-biomass, dominated by Pseudomonas, and showed no significant differences between lesional and non-lesional areas. Conclusions: This preliminary, hypothesis-generating study indicates that urinary, rather than tissue, microbial and volatilome signatures show clearer differences between PC and BPH. These findings suggest possible microbiota-metabolite interactions in PC but require validation in larger cohorts.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Modulating Prostate Cancer Therapy Through the Gut Microbiome: A Comprehensive Review.
Cancers, 17(23): pii:cancers17233842.
Background/Objectives: There is growing interest in the gut microbiome's role in cancer, particularly its influence on prostate cancer therapy. This review explores how the gut microbiota modulates treatment outcomes and how prostate cancer therapies affect microbial composition. Methods: A semi-systematic PubMed search was performed for English-language articles published between 2010 and 2025 using relevant keywords related to prostate cancer therapy and the gut microbiome. Both original research and reviews were included, with additional studies identified through citation tracking. Results: The literature reveals a dynamic, bidirectional relationship between the gut microbiome and prostate cancer therapies. Gut microbes can modulate treatment efficacy and toxicity through immune regulation, metabolic activity, and the production of bioactive compounds such as short-chain fatty acids and tryptophan derivatives. These interactions influence responses to androgen deprivation therapy, chemotherapy, radiotherapy, and immunotherapy. In parallel, prostate cancer treatments induce notable shifts in gut microbial composition, reducing diversity, increasing intestinal permeability, and promoting dysbiosis. These changes may impair therapeutic outcomes. Specific microbial taxa, including Akkermansia muciniphila, Faecalibacterium, and Bacteroides, have been linked to both therapeutic response and microbiome alterations. Conclusions: The reciprocal influence between gut microbes and prostate cancer therapies presents a compelling avenue for therapeutic innovation. However, current knowledge is largely derived from preclinical or cross-cancer studies, highlighting a major evidence gap in prostate-specific research. Bridging this gap through well-designed translational studies could inform clinical strategies that harness microbiome modulation to enhance treatment efficacy, reduce toxicity, and personalize prostate cancer therapy.
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PubMed:
Citation:
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@article {pmid41375042,
year = {2025},
author = {Magashi Ali, MA and Abdulkadir, SA},
title = {Modulating Prostate Cancer Therapy Through the Gut Microbiome: A Comprehensive Review.},
journal = {Cancers},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/cancers17233842},
pmid = {41375042},
issn = {2072-6694},
support = {P50 CA180995 (S.A.A.)//National Institute of Health/ ; R01 CA257258 (S.A.A.)//National Institute of Health/ ; TACTICAL Award (S.A.A.)//Prostate Cancer Foundation (PCF)/ ; },
abstract = {Background/Objectives: There is growing interest in the gut microbiome's role in cancer, particularly its influence on prostate cancer therapy. This review explores how the gut microbiota modulates treatment outcomes and how prostate cancer therapies affect microbial composition. Methods: A semi-systematic PubMed search was performed for English-language articles published between 2010 and 2025 using relevant keywords related to prostate cancer therapy and the gut microbiome. Both original research and reviews were included, with additional studies identified through citation tracking. Results: The literature reveals a dynamic, bidirectional relationship between the gut microbiome and prostate cancer therapies. Gut microbes can modulate treatment efficacy and toxicity through immune regulation, metabolic activity, and the production of bioactive compounds such as short-chain fatty acids and tryptophan derivatives. These interactions influence responses to androgen deprivation therapy, chemotherapy, radiotherapy, and immunotherapy. In parallel, prostate cancer treatments induce notable shifts in gut microbial composition, reducing diversity, increasing intestinal permeability, and promoting dysbiosis. These changes may impair therapeutic outcomes. Specific microbial taxa, including Akkermansia muciniphila, Faecalibacterium, and Bacteroides, have been linked to both therapeutic response and microbiome alterations. Conclusions: The reciprocal influence between gut microbes and prostate cancer therapies presents a compelling avenue for therapeutic innovation. However, current knowledge is largely derived from preclinical or cross-cancer studies, highlighting a major evidence gap in prostate-specific research. Bridging this gap through well-designed translational studies could inform clinical strategies that harness microbiome modulation to enhance treatment efficacy, reduce toxicity, and personalize prostate cancer therapy.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
High-Throughput Molecular Characterization of the Microbiome in Breast Implant-Associated Anaplastic Large Cell Lymphoma and Peri-Implant Benign Seromas.
Cancers, 17(23): pii:cancers17233839.
Background: Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) is a mature T-cell lymphoma linked to textured breast implants. A leading hypothesis suggests that chronic inflammation, combined with immunological and genetic factors, drives its pathogenesis. Two previous studies investigating bacterial biofilms on breast implant capsules have produced conflicting results, particularly regarding the enrichment of Ralstonia spp. Methods: We analyzed the microbiota profiles in seroma samples from 10 BIA-ALCL patients and 12 patients with non-neoplastic effusion, subclassified into acute-, mixed-, and chronic-type based on cellular composition. We used two metagenomic approaches: 16S rRNA gene sequencing and Nanopore sequencing with the "What's in My Pot?" (WIMP) taxonomic classifier. Our analyses included alpha and beta diversity metrics, as well as comparisons of Gram status and oxygen requirements. Results: Both sequencing methods identified Staphylococcaceae, Propionibacteriaceae, and Bradyrhizobiaceae as the most prevalent bacterial families in both BIA-ALCL and benign seroma samples. Notably, the Burkholderiaceae family was more abundant in some of the benign seromas according to the 16S rRNA sequencing, but Ralstonia spp. were not detected. BIA-ALCL showed higher richness (based on Nanopore data) and higher evenness (based on 16S rRNA data) compared to acute-type seromas, indicating a more homogenous representation of the different taxa identified. BIA-ALCL seromas did not cluster together based on Nanopore data, but they did form a distinct cluster with 16S rRNA data. This cluster was differentiated from the other two clusters by a relatively balanced presence of multiple families without overt dominance. We observed no significant differences in Gram staining between BIA-ALCL and benign samples using either method. However, non-aerobic bacterial families were enriched in BIA-ALCL cases only when analyzed with the Nanopore pipeline. Conclusions: Overall, our findings did not identify a distinctive microbial signature specifically associated with BIA-ALCL.
Additional Links: PMID-41375040
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PubMed:
Citation:
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@article {pmid41375040,
year = {2025},
author = {Rogges, E and Bertolazzi, G and Vacca, D and Borro, M and Lopez, G and Simmaco, M and Scattone, A and Firmani, G and Sorotos, M and Santanelli di Pompeo, F and Noccioli, N and Savino, E and Vecchione, A and Di Napoli, A},
title = {High-Throughput Molecular Characterization of the Microbiome in Breast Implant-Associated Anaplastic Large Cell Lymphoma and Peri-Implant Benign Seromas.},
journal = {Cancers},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/cancers17233839},
pmid = {41375040},
issn = {2072-6694},
abstract = {Background: Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) is a mature T-cell lymphoma linked to textured breast implants. A leading hypothesis suggests that chronic inflammation, combined with immunological and genetic factors, drives its pathogenesis. Two previous studies investigating bacterial biofilms on breast implant capsules have produced conflicting results, particularly regarding the enrichment of Ralstonia spp. Methods: We analyzed the microbiota profiles in seroma samples from 10 BIA-ALCL patients and 12 patients with non-neoplastic effusion, subclassified into acute-, mixed-, and chronic-type based on cellular composition. We used two metagenomic approaches: 16S rRNA gene sequencing and Nanopore sequencing with the "What's in My Pot?" (WIMP) taxonomic classifier. Our analyses included alpha and beta diversity metrics, as well as comparisons of Gram status and oxygen requirements. Results: Both sequencing methods identified Staphylococcaceae, Propionibacteriaceae, and Bradyrhizobiaceae as the most prevalent bacterial families in both BIA-ALCL and benign seroma samples. Notably, the Burkholderiaceae family was more abundant in some of the benign seromas according to the 16S rRNA sequencing, but Ralstonia spp. were not detected. BIA-ALCL showed higher richness (based on Nanopore data) and higher evenness (based on 16S rRNA data) compared to acute-type seromas, indicating a more homogenous representation of the different taxa identified. BIA-ALCL seromas did not cluster together based on Nanopore data, but they did form a distinct cluster with 16S rRNA data. This cluster was differentiated from the other two clusters by a relatively balanced presence of multiple families without overt dominance. We observed no significant differences in Gram staining between BIA-ALCL and benign samples using either method. However, non-aerobic bacterial families were enriched in BIA-ALCL cases only when analyzed with the Nanopore pipeline. Conclusions: Overall, our findings did not identify a distinctive microbial signature specifically associated with BIA-ALCL.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Bacteroides fragilis Promotes Mesenchymal Subtype in Colorectal Cancer.
Cancers, 17(23): pii:cancers17233822.
Background/Objectives: Colorectal cancer (CRC) exhibits significant molecular heterogeneity, as reflected in Consensus Molecular Subtype (CMS) classification, and demonstrates extensive crosstalk with the microbiome. However, the role of the microbiome in determining subtypes of CRC, and CMS4 in particular, which represents an aggressive, stromal-rich variant associated with poor prognosis, remains poorly understood. Here, we reveal the role of the tumor microbiome in shaping the tumor microenvironment (TME) and its impact on CMS4 determination. Methods: A total of 25 CRC tissues were analyzed using RNA sequencing and classified with CMScaller to identify significantly enriched microbial species. Functional studies were performed using these CMS-specific microbial species and CMS2 organoids co-cultured with stromal (18Co) and immune (THP-1) cells. Results: 16S rRNA profiling of matched CRC tissues showed that Bacteroides fragilis was significantly enriched in CMS4 tumors (linear discriminant analysis score = 4.7). Functional studies revealed that exposure to enterotoxigenic Bacteroides fragilis (ETBF) induced CMS4-like features, including enhanced growth and gene expression patterns resembling those of primary CMS4 tumors. Conclusions: These findings suggest that ETBF contributes to the development of CMS4 and may facilitate the acquisition of aggressive phenotype associated with this CRC subtype.
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@article {pmid41375022,
year = {2025},
author = {Chang, SY and Park, J and Park, SJ and Park, JJ and Cheon, JH and Kim, DK and Kim, TI},
title = {Bacteroides fragilis Promotes Mesenchymal Subtype in Colorectal Cancer.},
journal = {Cancers},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/cancers17233822},
pmid = {41375022},
issn = {2072-6694},
support = {2021R1A2C2011641//National Research Foundation of Korea/ ; },
abstract = {Background/Objectives: Colorectal cancer (CRC) exhibits significant molecular heterogeneity, as reflected in Consensus Molecular Subtype (CMS) classification, and demonstrates extensive crosstalk with the microbiome. However, the role of the microbiome in determining subtypes of CRC, and CMS4 in particular, which represents an aggressive, stromal-rich variant associated with poor prognosis, remains poorly understood. Here, we reveal the role of the tumor microbiome in shaping the tumor microenvironment (TME) and its impact on CMS4 determination. Methods: A total of 25 CRC tissues were analyzed using RNA sequencing and classified with CMScaller to identify significantly enriched microbial species. Functional studies were performed using these CMS-specific microbial species and CMS2 organoids co-cultured with stromal (18Co) and immune (THP-1) cells. Results: 16S rRNA profiling of matched CRC tissues showed that Bacteroides fragilis was significantly enriched in CMS4 tumors (linear discriminant analysis score = 4.7). Functional studies revealed that exposure to enterotoxigenic Bacteroides fragilis (ETBF) induced CMS4-like features, including enhanced growth and gene expression patterns resembling those of primary CMS4 tumors. Conclusions: These findings suggest that ETBF contributes to the development of CMS4 and may facilitate the acquisition of aggressive phenotype associated with this CRC subtype.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Gut Microbiota Signatures Associate with Chemotherapy-Related Adverse Events in Breast Cancer Patients.
Cancers, 17(23): pii:cancers17233783.
Background/Objectives: Chemotherapy-induced adverse events significantly impact cancer treatment outcomes and patient quality of life. Emerging evidence suggests that gut microbiota composition may influence individual susceptibility to chemotherapy toxicity. This study investigated associations between gut microbiome alterations and specific chemotherapy-related adverse events in breast cancer patients undergoing cancer treatment. Methods: We conducted a prospective cohort study of 81 breast cancer patients receiving chemotherapy between May 2018 and October 2022. Gut microbiome composition was analyzed using 16S rRNA sequencing across multiple taxonomic levels. Alpha diversity (Chao1 estimator) and beta diversity (PERMANOVA) analyses were performed to assess microbial richness and community structure. Linear discriminant analysis effect size (LEfSe) identified differentially abundant taxa, with Cohen's d effect sizes calculated with 95% confidence intervals and false discovery rate correction applied for multiple comparisons. Results: Significant microbiome-toxicity associations were identified across 42 taxa (FDR q < 0.05, effect sizes d = -1.60 to +1.67). Severe anemia demonstrated the strongest associations, with large effect size enrichment of Eubacteriaceae (d = 1.38), Anaerofilum (d = 1.42), and Eubacterium (d = 1.38). Severe neutropenia was characterized by depletion of butyrate-producing bacteria, particularly Eubacterium_hallii_group (d = -1.08). Thrombocytopenia showed dramatic depletion of Eubacterium limosum (53-fold reduction, d = -1.60). Hepatotoxicity (ALT elevation) was associated with depletion of Eubacterium_hallii_group (d = -0.99) and Burkholderia-Caballeronia-Paraburkholderia (d = -1.19). Hand-foot syndrome exhibited significantly elevated microbial diversity with depletion of Lachnospiraceae taxa. Most adverse events showed enrichment rather than depletion patterns, with 54.8% of significant associations demonstrating medium to large effect sizes. Conclusions: Specific gut microbiota signatures associated with distinct chemotherapy-related adverse events, suggesting potential microbiome-based biomarkers for toxicity prediction and personalized cancer treatment strategies.
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@article {pmid41374985,
year = {2025},
author = {Hsu, JW and Su, YW and Tsai, CH and Lee, CC and Yang, HW and Lee, JJ and Hsu, HH and Lee, F and Yang, PS},
title = {Gut Microbiota Signatures Associate with Chemotherapy-Related Adverse Events in Breast Cancer Patients.},
journal = {Cancers},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/cancers17233783},
pmid = {41374985},
issn = {2072-6694},
support = {NSTC 112-2321-B-195-001 and NSTC 114-2321-B-195-001//National Science and Technology Council (NSTC), Taiwan/ ; MMH-114- 82//Mackay Memorial Hospital/ ; },
abstract = {Background/Objectives: Chemotherapy-induced adverse events significantly impact cancer treatment outcomes and patient quality of life. Emerging evidence suggests that gut microbiota composition may influence individual susceptibility to chemotherapy toxicity. This study investigated associations between gut microbiome alterations and specific chemotherapy-related adverse events in breast cancer patients undergoing cancer treatment. Methods: We conducted a prospective cohort study of 81 breast cancer patients receiving chemotherapy between May 2018 and October 2022. Gut microbiome composition was analyzed using 16S rRNA sequencing across multiple taxonomic levels. Alpha diversity (Chao1 estimator) and beta diversity (PERMANOVA) analyses were performed to assess microbial richness and community structure. Linear discriminant analysis effect size (LEfSe) identified differentially abundant taxa, with Cohen's d effect sizes calculated with 95% confidence intervals and false discovery rate correction applied for multiple comparisons. Results: Significant microbiome-toxicity associations were identified across 42 taxa (FDR q < 0.05, effect sizes d = -1.60 to +1.67). Severe anemia demonstrated the strongest associations, with large effect size enrichment of Eubacteriaceae (d = 1.38), Anaerofilum (d = 1.42), and Eubacterium (d = 1.38). Severe neutropenia was characterized by depletion of butyrate-producing bacteria, particularly Eubacterium_hallii_group (d = -1.08). Thrombocytopenia showed dramatic depletion of Eubacterium limosum (53-fold reduction, d = -1.60). Hepatotoxicity (ALT elevation) was associated with depletion of Eubacterium_hallii_group (d = -0.99) and Burkholderia-Caballeronia-Paraburkholderia (d = -1.19). Hand-foot syndrome exhibited significantly elevated microbial diversity with depletion of Lachnospiraceae taxa. Most adverse events showed enrichment rather than depletion patterns, with 54.8% of significant associations demonstrating medium to large effect sizes. Conclusions: Specific gut microbiota signatures associated with distinct chemotherapy-related adverse events, suggesting potential microbiome-based biomarkers for toxicity prediction and personalized cancer treatment strategies.},
}
RevDate: 2025-12-11
CmpDate: 2025-12-11
Low-Cost Temperature Sensing Reveals Thermal Signatures of Microbial Activity in Winogradsky Columns.
Sensors (Basel, Switzerland), 25(23): pii:s25237146.
Temperature is a key driver of microbial metabolism, yet non-invasive methods for quantifying microbially generated heat in complex environments remain limited. Here, we present a low-cost digital temperature sensing system integrated into an Arduino-controlled data acquisition setup to monitor microbial activity in stratified Winogradsky columns, which are self-contained sediment microcosms that reproduce natural oxygen and sulfide gradients. Localized temperature differences of up to 0.55 ± 0.04 °C were detected between aerobic and anaerobic layers, consistent with microbial heat generation in active sediment zones. Short-term insulation experiments further amplified these effects, demonstrating that microbial thermogenesis can serve as a reliable proxy for metabolic activity. Compared with infrared thermography or isothermal microcalorimetry, the proposed approach is simple, cost-effective, and compatible with aqueous and stratified systems. The method enables real-time, non-invasive observation of microbial metabolic dynamics and establishes a framework for continuous thermal monitoring in living environmental microcosms.
Additional Links: PMID-41374521
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@article {pmid41374521,
year = {2025},
author = {Itani, A and Mager, D and Rabe, KS and Niemeyer, CM},
title = {Low-Cost Temperature Sensing Reveals Thermal Signatures of Microbial Activity in Winogradsky Columns.},
journal = {Sensors (Basel, Switzerland)},
volume = {25},
number = {23},
pages = {},
doi = {10.3390/s25237146},
pmid = {41374521},
issn = {1424-8220},
support = {43.33.11//Helmholz Program/ ; },
mesh = {*Bacteria/metabolism ; Calorimetry ; Geologic Sediments/microbiology ; Temperature ; Thermography/methods ; },
abstract = {Temperature is a key driver of microbial metabolism, yet non-invasive methods for quantifying microbially generated heat in complex environments remain limited. Here, we present a low-cost digital temperature sensing system integrated into an Arduino-controlled data acquisition setup to monitor microbial activity in stratified Winogradsky columns, which are self-contained sediment microcosms that reproduce natural oxygen and sulfide gradients. Localized temperature differences of up to 0.55 ± 0.04 °C were detected between aerobic and anaerobic layers, consistent with microbial heat generation in active sediment zones. Short-term insulation experiments further amplified these effects, demonstrating that microbial thermogenesis can serve as a reliable proxy for metabolic activity. Compared with infrared thermography or isothermal microcalorimetry, the proposed approach is simple, cost-effective, and compatible with aqueous and stratified systems. The method enables real-time, non-invasive observation of microbial metabolic dynamics and establishes a framework for continuous thermal monitoring in living environmental microcosms.},
}
MeSH Terms:
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*Bacteria/metabolism
Calorimetry
Geologic Sediments/microbiology
Temperature
Thermography/methods
RevDate: 2025-12-11
CmpDate: 2025-12-11
Modulation of Gut Microbes and Hepatic Metabolites by PCP Ameliorates NASH and Fatigue-like Performance in Mice.
Nutrients, 17(23): pii:nu17233797.
Background/Objectives: Non-alcoholic steatohepatitis (NASH) is a progressive liver condition closely associated with gut microbial dysbiosis and hepatic metabolic abnormalities. Poria cocos polysaccharide (PCP), a bioactive component derived from the medicinal fungus Poria cocos, possesses hepatoprotective properties, yet the therapeutic mechanisms of PCP in NASH, particularly those involving microbial and metabolic regulation, remain incompletely elucidated. This study aimed to investigate the effects of PCP on improving NASH and explore its mechanisms related to prebiotic activity. Methods: Mice were induced to develop NASH using a Western diet, followed by PCP intervention for 12 weeks. Hepatic function, including liver enzymes and lipids, glucose metabolism, and liver histopathological changes, was assessed. Fatigue and neurobehavioral alterations were evaluated via rotarod, open field, and tail suspension tests. Hepatic pro-inflammatory cytokines were measured using RT-qPCR. Gut microbiota were analyzed through 16S RNA gene sequencing, and metabolites of liver tissue were analyzed through untargeted metabolomics. Results: PCP decreased blood glucose and hepatic lipid levels in NASH mice, alleviating liver inflammation, ballooning degeneration, and fibrosis. It also improved fatigue-like performance on rotarod test and reduced the hepatic expression of IL-6, IL-1β, TNF-α, and IL-18. Microbiota analysis revealed that PCP restored gut microbial diversity, promoted the growth of beneficial taxa such as Alistipes and Butyricoccaceae_UCG-009, and inhibited harmful bacteria, including Romboutsia ilealis. Liver metabolomics showed that PCP normalized key metabolites like taurocholate and regulated taurine and hypotaurine metabolism, which were correlated with reduced inflammation, fatigue-like performance, and fibrosis. Conclusions: PCP, as a promising edible agent, alleviates hepatic damage, metabolic disorders, and fatigue-like performance on rotarod test in NASH mice, probably by reshaping gut microbiota and modulating hepatic taurine and hypotaurine metabolism.
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@article {pmid41374088,
year = {2025},
author = {Hong, Y and Yang, J and Wang, Y and Chen, D and Wu, A and Li, M and Ou, W and Lin, G and Lin, C and Liang, Y},
title = {Modulation of Gut Microbes and Hepatic Metabolites by PCP Ameliorates NASH and Fatigue-like Performance in Mice.},
journal = {Nutrients},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/nu17233797},
pmid = {41374088},
issn = {2072-6643},
support = {No. 82174256//National Natural Science Foundation of China/ ; No. 202206785007//the Program of China Scholarships Council/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Non-alcoholic Fatty Liver Disease/drug therapy/metabolism/microbiology ; *Liver/metabolism/drug effects/pathology ; *Fatigue/drug therapy ; Mice ; Male ; Mice, Inbred C57BL ; Disease Models, Animal ; *Wolfiporia/chemistry ; *Fungal Polysaccharides/pharmacology ; Cytokines/metabolism ; Prebiotics ; Blood Glucose ; Lipid Metabolism/drug effects ; Dysbiosis ; },
abstract = {Background/Objectives: Non-alcoholic steatohepatitis (NASH) is a progressive liver condition closely associated with gut microbial dysbiosis and hepatic metabolic abnormalities. Poria cocos polysaccharide (PCP), a bioactive component derived from the medicinal fungus Poria cocos, possesses hepatoprotective properties, yet the therapeutic mechanisms of PCP in NASH, particularly those involving microbial and metabolic regulation, remain incompletely elucidated. This study aimed to investigate the effects of PCP on improving NASH and explore its mechanisms related to prebiotic activity. Methods: Mice were induced to develop NASH using a Western diet, followed by PCP intervention for 12 weeks. Hepatic function, including liver enzymes and lipids, glucose metabolism, and liver histopathological changes, was assessed. Fatigue and neurobehavioral alterations were evaluated via rotarod, open field, and tail suspension tests. Hepatic pro-inflammatory cytokines were measured using RT-qPCR. Gut microbiota were analyzed through 16S RNA gene sequencing, and metabolites of liver tissue were analyzed through untargeted metabolomics. Results: PCP decreased blood glucose and hepatic lipid levels in NASH mice, alleviating liver inflammation, ballooning degeneration, and fibrosis. It also improved fatigue-like performance on rotarod test and reduced the hepatic expression of IL-6, IL-1β, TNF-α, and IL-18. Microbiota analysis revealed that PCP restored gut microbial diversity, promoted the growth of beneficial taxa such as Alistipes and Butyricoccaceae_UCG-009, and inhibited harmful bacteria, including Romboutsia ilealis. Liver metabolomics showed that PCP normalized key metabolites like taurocholate and regulated taurine and hypotaurine metabolism, which were correlated with reduced inflammation, fatigue-like performance, and fibrosis. Conclusions: PCP, as a promising edible agent, alleviates hepatic damage, metabolic disorders, and fatigue-like performance on rotarod test in NASH mice, probably by reshaping gut microbiota and modulating hepatic taurine and hypotaurine metabolism.},
}
MeSH Terms:
show MeSH Terms
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Animals
*Gastrointestinal Microbiome/drug effects
*Non-alcoholic Fatty Liver Disease/drug therapy/metabolism/microbiology
*Liver/metabolism/drug effects/pathology
*Fatigue/drug therapy
Mice
Male
Mice, Inbred C57BL
Disease Models, Animal
*Wolfiporia/chemistry
*Fungal Polysaccharides/pharmacology
Cytokines/metabolism
Prebiotics
Blood Glucose
Lipid Metabolism/drug effects
Dysbiosis
RevDate: 2025-12-11
CmpDate: 2025-12-11
Can Beetroot (Beta vulgaris) Support Brain Health? A Perspective Review on Alzheimer's Disease.
Nutrients, 17(23): pii:nu17233790.
Alzheimer's disease (AD), the leading cause of dementia, has limited treatment options despite extensive pharmacological research. This has increased interest in dietary strategies that act across multiple pathological mechanisms. Beetroot (Beta vulgaris), known for its cardiovascular and metabolic benefits, contains a distinctive combination of bioactive compounds including inorganic nitrate, betalains, and polyphenols. Together these constituents influence vascular function, oxidative stress, mitochondrial efficiency, inflammation, and the microbiota. Previous reviews have typically focused on dietary nitrate in dementia prevention or have examined nitrate and betalains separately. In contrast, this review synthesises evidence on beetroot as a combined neuroprotective food. Preclinical data indicate that beetroot and its key constituents enhance antioxidant defences, support neuronal bioenergetics, and modulate cholinergic and inflammatory pathways. Human studies further suggest that nitrate-rich beetroot can improve cerebral blood flow and vascular responsiveness, and that higher intakes of plant-derived nitrate are associated with reduced cognitive decline. However, findings are inconsistent, most trials are small and short in duration, and research directly involving people with AD is scarce. By integrating vascular, antioxidant, and microbiome perspectives, this review identifies beetroot as a promising yet underexplored dietary candidate for AD management. Further mechanistic studies and multidomain approaches combining metagenomics, biomarkers, neuroimaging, and cognitive outcomes are needed.
Additional Links: PMID-41374080
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PubMed:
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@article {pmid41374080,
year = {2025},
author = {Kimble, R and Shannon, OM},
title = {Can Beetroot (Beta vulgaris) Support Brain Health? A Perspective Review on Alzheimer's Disease.},
journal = {Nutrients},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/nu17233790},
pmid = {41374080},
issn = {2072-6643},
mesh = {Humans ; *Alzheimer Disease/prevention & control ; *Beta vulgaris/chemistry ; *Brain/drug effects ; Antioxidants/pharmacology ; Nitrates/pharmacology ; Oxidative Stress/drug effects ; Neuroprotective Agents/pharmacology ; Animals ; Polyphenols/pharmacology ; Betalains/pharmacology ; },
abstract = {Alzheimer's disease (AD), the leading cause of dementia, has limited treatment options despite extensive pharmacological research. This has increased interest in dietary strategies that act across multiple pathological mechanisms. Beetroot (Beta vulgaris), known for its cardiovascular and metabolic benefits, contains a distinctive combination of bioactive compounds including inorganic nitrate, betalains, and polyphenols. Together these constituents influence vascular function, oxidative stress, mitochondrial efficiency, inflammation, and the microbiota. Previous reviews have typically focused on dietary nitrate in dementia prevention or have examined nitrate and betalains separately. In contrast, this review synthesises evidence on beetroot as a combined neuroprotective food. Preclinical data indicate that beetroot and its key constituents enhance antioxidant defences, support neuronal bioenergetics, and modulate cholinergic and inflammatory pathways. Human studies further suggest that nitrate-rich beetroot can improve cerebral blood flow and vascular responsiveness, and that higher intakes of plant-derived nitrate are associated with reduced cognitive decline. However, findings are inconsistent, most trials are small and short in duration, and research directly involving people with AD is scarce. By integrating vascular, antioxidant, and microbiome perspectives, this review identifies beetroot as a promising yet underexplored dietary candidate for AD management. Further mechanistic studies and multidomain approaches combining metagenomics, biomarkers, neuroimaging, and cognitive outcomes are needed.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Alzheimer Disease/prevention & control
*Beta vulgaris/chemistry
*Brain/drug effects
Antioxidants/pharmacology
Nitrates/pharmacology
Oxidative Stress/drug effects
Neuroprotective Agents/pharmacology
Animals
Polyphenols/pharmacology
Betalains/pharmacology
RevDate: 2025-12-11
CmpDate: 2025-12-11
The Gut-Muscle-Immune Axis in Motion: Mechanistic Synergies of SCFA Metabolism, Exercise, and Microbial Cross-Feeding.
Nutrients, 17(23): pii:nu17233786.
BACKGROUND: The gut microbiota plays a fundamental role in metabolic and immune homeostasis through the production of short-chain fatty acids (SCFAs). These metabolites influence mitochondrial biogenesis, muscle energetics, epithelial barrier stability, and inflammatory regulation via G-protein-coupled receptors, AMPK-PGC-1α signaling, and epigenetic remodeling.
OBJECTIVE: This review synthesizes current evidence on the gut-muscle-immune axis, emphasizing how dietary fermentable substrates, microbial cross-feeding interactions, and structured exercise modulate SCFA production and shape host physiological adaptation.
METHODS: We integrated findings from human and animal studies, multi-omic analyses, metabolomic and microbiome research, and exercise physiology to outline mechanistic links between microbial metabolism and systemic resilience.
RESULTS: Key mechanistic pathways connecting dietary fiber fermentation to mitochondrial function, redox regulation, immune homeostasis, and metabolic plasticity are summarized. We further present the Targeted Gut Protocol 2.0, a conceptual 12-week framework combining fiber-diversity targets, lactate-guided exercise periodization, biomarker monitoring, and adaptive feedback mechanisms to enhance endogenous SCFA availability.
CONCLUSIONS: SCFA-driven metabolic plasticity provides an integrative model through which lifestyle behaviors can modulate host physiology. Future research should prioritize standardized sampling approaches, causal inference methods, multi-omic integration, and AI-supported personalization to refine mechanistic understanding and strengthen translational potential.
Additional Links: PMID-41374076
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PubMed:
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@article {pmid41374076,
year = {2025},
author = {Réka, F and Zsófia, B and Ádám, B and Péter, F},
title = {The Gut-Muscle-Immune Axis in Motion: Mechanistic Synergies of SCFA Metabolism, Exercise, and Microbial Cross-Feeding.},
journal = {Nutrients},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/nu17233786},
pmid = {41374076},
issn = {2072-6643},
support = {8222//University of Szeged/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Fatty Acids, Volatile/metabolism ; *Exercise/physiology ; Animals ; *Muscle, Skeletal/metabolism/immunology ; Dietary Fiber/metabolism ; Fermentation ; Homeostasis ; },
abstract = {BACKGROUND: The gut microbiota plays a fundamental role in metabolic and immune homeostasis through the production of short-chain fatty acids (SCFAs). These metabolites influence mitochondrial biogenesis, muscle energetics, epithelial barrier stability, and inflammatory regulation via G-protein-coupled receptors, AMPK-PGC-1α signaling, and epigenetic remodeling.
OBJECTIVE: This review synthesizes current evidence on the gut-muscle-immune axis, emphasizing how dietary fermentable substrates, microbial cross-feeding interactions, and structured exercise modulate SCFA production and shape host physiological adaptation.
METHODS: We integrated findings from human and animal studies, multi-omic analyses, metabolomic and microbiome research, and exercise physiology to outline mechanistic links between microbial metabolism and systemic resilience.
RESULTS: Key mechanistic pathways connecting dietary fiber fermentation to mitochondrial function, redox regulation, immune homeostasis, and metabolic plasticity are summarized. We further present the Targeted Gut Protocol 2.0, a conceptual 12-week framework combining fiber-diversity targets, lactate-guided exercise periodization, biomarker monitoring, and adaptive feedback mechanisms to enhance endogenous SCFA availability.
CONCLUSIONS: SCFA-driven metabolic plasticity provides an integrative model through which lifestyle behaviors can modulate host physiology. Future research should prioritize standardized sampling approaches, causal inference methods, multi-omic integration, and AI-supported personalization to refine mechanistic understanding and strengthen translational potential.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology
*Fatty Acids, Volatile/metabolism
*Exercise/physiology
Animals
*Muscle, Skeletal/metabolism/immunology
Dietary Fiber/metabolism
Fermentation
Homeostasis
RevDate: 2025-12-11
CmpDate: 2025-12-11
Highly Processed Food and Functional Gastrointestinal Disorders in Children and Adolescents with Obesity: The Preventive Challenge-A Narrative Review.
Nutrients, 17(23): pii:nu17233744.
Objective: This narrative review summarizes current evidence on the associations between ultra-processed food (UPF) consumption, childhood and adolescent obesity, and functional gastrointestinal disorders (FGIDs), and examines the metabolic, inflammatory, microbial, and gut-brain mechanisms underlying these links. Methods: A comprehensive search of PubMed and Scopus identified articles published between January 2010 and September 2025. Eligible studies included human research in individuals aged 0-18 years; adult studies were considered when contributing relevant mechanistic insights. Of 335 records screened, 112 studies met the inclusion criteria and were synthesized narratively according to methodological appropriateness. Results: High UPF intake was consistently associated with increased adiposity, metabolic dysregulation, and greater cardiometabolic risk in youth. Children with overweight or obesity showed a higher prevalence of FGIDs compared with their normal-weight peers. Mechanistic evidence suggests that UPFs, rich in refined carbohydrates, unhealthy fats, and additives, may promote gut microbiota dysbiosis, impair intestinal barrier integrity, alter motility, and induce low-grade inflammation, thereby disrupting gut-brain signaling and contributing to FGID symptoms. Early-life and maternal UPF exposure may further increase susceptibility to metabolic and gastrointestinal disturbances through epigenetic and microbiome-mediated pathways. Conclusions: UPFs emerge as a shared etiological factor for obesity and FGIDs in childhood. This review contributes an integrated synthesis of epidemiological and mechanistic data while highlighting key research gaps, particularly the need for standardized methodologies and pediatric interventional studies to strengthen the evidence base.
Additional Links: PMID-41374033
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PubMed:
Citation:
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@article {pmid41374033,
year = {2025},
author = {Calcaterra, V and Cena, H and Ferrara, C and Magenes, VC and Boussetta, S and Zambon, I and Zuccotti, G},
title = {Highly Processed Food and Functional Gastrointestinal Disorders in Children and Adolescents with Obesity: The Preventive Challenge-A Narrative Review.},
journal = {Nutrients},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/nu17233744},
pmid = {41374033},
issn = {2072-6643},
support = {CUP D93C22000890001//Next Generation EU/ ; PODiaCar Project 101128946//European Union/ ; },
mesh = {Humans ; Child ; Adolescent ; *Gastrointestinal Diseases/etiology/epidemiology/prevention & control ; *Pediatric Obesity/etiology/epidemiology ; Gastrointestinal Microbiome ; Child, Preschool ; Infant ; Female ; Male ; *Food Handling ; Food, Processed ; },
abstract = {Objective: This narrative review summarizes current evidence on the associations between ultra-processed food (UPF) consumption, childhood and adolescent obesity, and functional gastrointestinal disorders (FGIDs), and examines the metabolic, inflammatory, microbial, and gut-brain mechanisms underlying these links. Methods: A comprehensive search of PubMed and Scopus identified articles published between January 2010 and September 2025. Eligible studies included human research in individuals aged 0-18 years; adult studies were considered when contributing relevant mechanistic insights. Of 335 records screened, 112 studies met the inclusion criteria and were synthesized narratively according to methodological appropriateness. Results: High UPF intake was consistently associated with increased adiposity, metabolic dysregulation, and greater cardiometabolic risk in youth. Children with overweight or obesity showed a higher prevalence of FGIDs compared with their normal-weight peers. Mechanistic evidence suggests that UPFs, rich in refined carbohydrates, unhealthy fats, and additives, may promote gut microbiota dysbiosis, impair intestinal barrier integrity, alter motility, and induce low-grade inflammation, thereby disrupting gut-brain signaling and contributing to FGID symptoms. Early-life and maternal UPF exposure may further increase susceptibility to metabolic and gastrointestinal disturbances through epigenetic and microbiome-mediated pathways. Conclusions: UPFs emerge as a shared etiological factor for obesity and FGIDs in childhood. This review contributes an integrated synthesis of epidemiological and mechanistic data while highlighting key research gaps, particularly the need for standardized methodologies and pediatric interventional studies to strengthen the evidence base.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Child
Adolescent
*Gastrointestinal Diseases/etiology/epidemiology/prevention & control
*Pediatric Obesity/etiology/epidemiology
Gastrointestinal Microbiome
Child, Preschool
Infant
Female
Male
*Food Handling
Food, Processed
RevDate: 2025-12-11
CmpDate: 2025-12-11
Can Early Nutrition Be Responsible for Future Gut Microbiota Changes and Different Health Outcomes?.
Nutrients, 17(23): pii:nu17233721.
Background/Objectives: Chronic inflammatory diseases (CIDs) often present a preclinical phase influenced by genetic and environmental factors, including nutrition. Early dietary habits may modulate long-term health trajectories by shaping the intestinal microbiota. Previous work showed that weaning with fresh foods from the Mediterranean diet (MD) improved dietary habits and microbiota composition at 3 years of age. This study aimed to assess whether such benefits persist at 9 years. Methods: This long-term follow-up included 191 children (96 MD, 95 controls) from the original randomized cohort (ClinicalTrials.gov NCT05297357). The primary endpoint was adherence to MD (KidMed score ≥ 8). Secondary endpoints included BMI, incidence of CID, maternal dietary adherence, and intestinal microbiota composition in a subset of 36 children. Results: At 9 years, no difference was found in overall MD adherence (27.4% controls vs. 27.1% MD; p > 0.99) or BMI (17.7 vs. 18.1 kg/m[2]; p = 0.384). However, children from the MD group reported higher daily vegetable intake (71.9% vs. 51.6%; p = 0.005). Microbiota analyses revealed persistent differences between groups, with higher alpha diversity in the MD group. Although not statistically significant, the MD group showed lower prevalence of atopic dermatitis, allergic rhinitis, autism spectrum disorder, and ADHD. Maternal adherence to MD did not differ between groups. Conclusions: Early introduction of Mediterranean-style foods during weaning exerts lasting effects on dietary patterns and gut microbiota, with a potential protective trend against CID. While overall MD adherence converged between groups by 9 years, these findings suggest that early-life nutritional interventions may induce durable microbiome-mediated benefits and contribute to preventive strategies for chronic disease, warranting confirmation in larger, extended cohorts. Moreover, this study highlights the value of the collaboration between the Italian primary care pediatric system and the integration of the pediatric residency program, demonstrating a feasible and cost-effective methodology to generate large-scale prospective data within routine clinical practice. Larger studies and a longer follow-up period are necessary to confirm these results.
Additional Links: PMID-41374011
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PubMed:
Citation:
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@article {pmid41374011,
year = {2025},
author = {de Franchis, R and Bozza, L and Cortese, P and D'Antonio, L and D'Avino, A and Gasparini, N and Ippolito, G and Spadaro, R and Tedesco, M and Antignani, A and De Filippis, F and Valentino, V and Auricchio, R and Auricchio, S and Bruzzese, D},
title = {Can Early Nutrition Be Responsible for Future Gut Microbiota Changes and Different Health Outcomes?.},
journal = {Nutrients},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/nu17233721},
pmid = {41374011},
issn = {2072-6643},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Diet, Mediterranean ; Female ; Male ; Child ; Child, Preschool ; Follow-Up Studies ; Weaning ; Feeding Behavior ; Body Mass Index ; },
abstract = {Background/Objectives: Chronic inflammatory diseases (CIDs) often present a preclinical phase influenced by genetic and environmental factors, including nutrition. Early dietary habits may modulate long-term health trajectories by shaping the intestinal microbiota. Previous work showed that weaning with fresh foods from the Mediterranean diet (MD) improved dietary habits and microbiota composition at 3 years of age. This study aimed to assess whether such benefits persist at 9 years. Methods: This long-term follow-up included 191 children (96 MD, 95 controls) from the original randomized cohort (ClinicalTrials.gov NCT05297357). The primary endpoint was adherence to MD (KidMed score ≥ 8). Secondary endpoints included BMI, incidence of CID, maternal dietary adherence, and intestinal microbiota composition in a subset of 36 children. Results: At 9 years, no difference was found in overall MD adherence (27.4% controls vs. 27.1% MD; p > 0.99) or BMI (17.7 vs. 18.1 kg/m[2]; p = 0.384). However, children from the MD group reported higher daily vegetable intake (71.9% vs. 51.6%; p = 0.005). Microbiota analyses revealed persistent differences between groups, with higher alpha diversity in the MD group. Although not statistically significant, the MD group showed lower prevalence of atopic dermatitis, allergic rhinitis, autism spectrum disorder, and ADHD. Maternal adherence to MD did not differ between groups. Conclusions: Early introduction of Mediterranean-style foods during weaning exerts lasting effects on dietary patterns and gut microbiota, with a potential protective trend against CID. While overall MD adherence converged between groups by 9 years, these findings suggest that early-life nutritional interventions may induce durable microbiome-mediated benefits and contribute to preventive strategies for chronic disease, warranting confirmation in larger, extended cohorts. Moreover, this study highlights the value of the collaboration between the Italian primary care pediatric system and the integration of the pediatric residency program, demonstrating a feasible and cost-effective methodology to generate large-scale prospective data within routine clinical practice. Larger studies and a longer follow-up period are necessary to confirm these results.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/physiology
*Diet, Mediterranean
Female
Male
Child
Child, Preschool
Follow-Up Studies
Weaning
Feeding Behavior
Body Mass Index
RevDate: 2025-12-11
CmpDate: 2025-12-11
Microbial Metabolite, Macro Impact: Urolithin A in the Nexus of Insulin Resistance and Colorectal Tumorigenesis.
Nutrients, 17(23): pii:nu17233712.
Urolithin A (UA), a metabolite of dietary ellagitannins produced by the gut microbiome, is a potential dual-purpose bioactive compound that may interfere with the shared pathogenic pathways linking colorectal cancer (CRC) and type 2 diabetes mellitus (T2DM). This review summarizes recent preclinical and clinical data on UA's mechanisms, therapeutic potential, and translational challenges. In CRC models, UA promotes G2/M cell cycle arrest, triggers both intrinsic and extrinsic caspase-mediated apoptosis, enhances CD8+ T-cell mitophagy and memory functions, suppresses Wnt/β-catenin signaling, and reduces chemoresistance, especially to 5-FU. For T2DM, UA enhances autophagic flux, mitophagy, insulin signaling, and GLUT4-mediated glucose uptake through the AMPK and PI3K/AKT pathways, reduces fasting glucose and insulin resistance in animal studies, and promotes adipose tissue browning and mitochondrial beta-oxidation. Human biomarker research is limited but indicates positive changes following interventions that increase UA. Future priorities include biomarker-driven, dose-finding trials stratified by metabotype, developing colon-targeted vs. systemic formulations, and testing combinations with chemotherapy and immunotherapy to determine safety and effectiveness.
Additional Links: PMID-41374004
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PubMed:
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@article {pmid41374004,
year = {2025},
author = {Joseph, V and Hornak, S and Kubatka, P and Büsselberg, D},
title = {Microbial Metabolite, Macro Impact: Urolithin A in the Nexus of Insulin Resistance and Colorectal Tumorigenesis.},
journal = {Nutrients},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/nu17233712},
pmid = {41374004},
issn = {2072-6643},
support = {NPRP 14S0311-210033//Qatar National Research Fund/ ; },
mesh = {Humans ; *Colorectal Neoplasms/metabolism/drug therapy ; *Insulin Resistance ; *Coumarins/pharmacology/metabolism ; *Gastrointestinal Microbiome/physiology ; Animals ; Diabetes Mellitus, Type 2/metabolism/drug therapy ; *Carcinogenesis/drug effects ; },
abstract = {Urolithin A (UA), a metabolite of dietary ellagitannins produced by the gut microbiome, is a potential dual-purpose bioactive compound that may interfere with the shared pathogenic pathways linking colorectal cancer (CRC) and type 2 diabetes mellitus (T2DM). This review summarizes recent preclinical and clinical data on UA's mechanisms, therapeutic potential, and translational challenges. In CRC models, UA promotes G2/M cell cycle arrest, triggers both intrinsic and extrinsic caspase-mediated apoptosis, enhances CD8+ T-cell mitophagy and memory functions, suppresses Wnt/β-catenin signaling, and reduces chemoresistance, especially to 5-FU. For T2DM, UA enhances autophagic flux, mitophagy, insulin signaling, and GLUT4-mediated glucose uptake through the AMPK and PI3K/AKT pathways, reduces fasting glucose and insulin resistance in animal studies, and promotes adipose tissue browning and mitochondrial beta-oxidation. Human biomarker research is limited but indicates positive changes following interventions that increase UA. Future priorities include biomarker-driven, dose-finding trials stratified by metabotype, developing colon-targeted vs. systemic formulations, and testing combinations with chemotherapy and immunotherapy to determine safety and effectiveness.},
}
MeSH Terms:
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Humans
*Colorectal Neoplasms/metabolism/drug therapy
*Insulin Resistance
*Coumarins/pharmacology/metabolism
*Gastrointestinal Microbiome/physiology
Animals
Diabetes Mellitus, Type 2/metabolism/drug therapy
*Carcinogenesis/drug effects
RevDate: 2025-12-11
CmpDate: 2025-12-11
Nutritional Modulation of the Gut Microbiome in Relation to Prenatal Lead-Induced Neurotoxicity: A Review.
Nutrients, 17(23): pii:nu17233700.
Prenatal exposure to lead (Pb) is a well-established risk factor for adverse neurodevelopmental outcomes. Despite its recognized risks, prenatal Pb exposure remains largely unregulated and poorly addressed in public health policy. Evidence suggests that the gut microbiome may mediate the neurotoxic effects of metals, offering a potential target for intervention. Here we discuss how nutritional factors, particularly those influencing the gut microbiome, may reduce the neurotoxicity of prenatal Pb exposure.
Additional Links: PMID-41373991
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PubMed:
Citation:
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@article {pmid41373991,
year = {2025},
author = {Eggers, S and Nagdeo, KP and Sachdev, K and Robinson, D and Deierlein, AL and Lane, JM and Gennings, C and Walker, RW and Snetselaar, L and Nidey, N and O'Neal, EE and Midya, V},
title = {Nutritional Modulation of the Gut Microbiome in Relation to Prenatal Lead-Induced Neurotoxicity: A Review.},
journal = {Nutrients},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/nu17233700},
pmid = {41373991},
issn = {2072-6643},
support = {R00ES032884/ES/NIEHS NIH HHS/United States ; R00HD102588//Eunice Kennedy Shriver National Institute of Child Health and Human Development/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects/physiology ; Pregnancy ; Female ; *Lead/toxicity ; *Prenatal Exposure Delayed Effects/prevention & control ; *Neurotoxicity Syndromes/prevention & control/microbiology ; *Maternal Nutritional Physiological Phenomena ; },
abstract = {Prenatal exposure to lead (Pb) is a well-established risk factor for adverse neurodevelopmental outcomes. Despite its recognized risks, prenatal Pb exposure remains largely unregulated and poorly addressed in public health policy. Evidence suggests that the gut microbiome may mediate the neurotoxic effects of metals, offering a potential target for intervention. Here we discuss how nutritional factors, particularly those influencing the gut microbiome, may reduce the neurotoxicity of prenatal Pb exposure.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/drug effects/physiology
Pregnancy
Female
*Lead/toxicity
*Prenatal Exposure Delayed Effects/prevention & control
*Neurotoxicity Syndromes/prevention & control/microbiology
*Maternal Nutritional Physiological Phenomena
RevDate: 2025-12-11
CmpDate: 2025-12-11
Pecans and Human Health: Distinctive Benefits of an American Nut.
Nutrients, 17(23): pii:nu17233686.
Pecans are a tree nut native to America with a rich content of unsaturated fatty acids, minerals, fiber, and a diverse array of bioactive components, including polyphenols, tocopherols, and phytosterols. This review summarizes variations in the phenolic composition of pecans from various parts of the world based on cultivar, maturity stage, postharvest storage, and processing. Additionally, the review delves into the bio-accessibility and bioavailability of bioactive components from pecans and their potential influence on diet quality, body weight, satiety, cardiometabolic, brain and gut health. Data from human clinical trials suggest that replacing foods/snacks with pecans improves overall diet quality and lipid profiles. However, inconsistent effects are observed on vascular function, glycemia, and inflammation. Body weight changes after pecan intake are reported as neutral, with promising results on satiety peptides and appetite regulation. Cognition and gut health are emerging areas of research with very limited data from both human and preclinical models, warranting further investigation. Overall, the current literature supports the cardiometabolic benefits of pecans within healthy dietary patterns. Future research should focus on well-controlled studies targeting at-risk populations to understand mechanistic endpoints such as metabolomics, microbiome, and vascular function assessments to substantiate the role of pecans in dietary guidance.
Additional Links: PMID-41373975
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@article {pmid41373975,
year = {2025},
author = {Sandhu, AK and Edirisinghe, I and Burton-Freeman, B},
title = {Pecans and Human Health: Distinctive Benefits of an American Nut.},
journal = {Nutrients},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/nu17233686},
pmid = {41373975},
issn = {2072-6643},
support = {NA//American Pecan Promotion Board/ ; },
mesh = {Humans ; *Nuts/chemistry ; United States ; Cognition/drug effects ; Diet ; },
abstract = {Pecans are a tree nut native to America with a rich content of unsaturated fatty acids, minerals, fiber, and a diverse array of bioactive components, including polyphenols, tocopherols, and phytosterols. This review summarizes variations in the phenolic composition of pecans from various parts of the world based on cultivar, maturity stage, postharvest storage, and processing. Additionally, the review delves into the bio-accessibility and bioavailability of bioactive components from pecans and their potential influence on diet quality, body weight, satiety, cardiometabolic, brain and gut health. Data from human clinical trials suggest that replacing foods/snacks with pecans improves overall diet quality and lipid profiles. However, inconsistent effects are observed on vascular function, glycemia, and inflammation. Body weight changes after pecan intake are reported as neutral, with promising results on satiety peptides and appetite regulation. Cognition and gut health are emerging areas of research with very limited data from both human and preclinical models, warranting further investigation. Overall, the current literature supports the cardiometabolic benefits of pecans within healthy dietary patterns. Future research should focus on well-controlled studies targeting at-risk populations to understand mechanistic endpoints such as metabolomics, microbiome, and vascular function assessments to substantiate the role of pecans in dietary guidance.},
}
MeSH Terms:
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Humans
*Nuts/chemistry
United States
Cognition/drug effects
Diet
RevDate: 2025-12-11
CmpDate: 2025-12-11
Obesity and Diabetes in Mexico: An Approach to the Intestinal Microbiota.
Nutrients, 17(23): pii:nu17233661.
Obesity and diabetes have reached alarming prevalence rates globally, with Mexico being one of the most affected countries. This review explores the epidemiology of these metabolic disorders and analyzes their prevalence and risk factors, as well as the crucial role of the intestinal microbiota in their development. Obesity and diabetes in Mexico have been linked to lifestyle factors, genetic predispositions, and alterations in the gut microbial composition. The intestinal microbiota plays a significant role in metabolic regulation, and its dysbiosis has been associated with insulin resistance, chronic inflammation, and increased fat accumulation. Studies in Mexico have highlighted specific microbial patterns in individuals with obesity and diabetes, suggesting a unique interplay between diet, microbiota composition, and metabolic health. Strategies to restore microbial balance, such as dietary modifications and probiotic interventions, have shown promising results in improving metabolic parameters and reducing disease progression. However, challenges remain in understanding the long-term effects of microbiota-targeted therapies and their individual variability. This review underscores the need for further research to develop personalized interventions aimed at modulating the gut microbiota for obesity and diabetes management. Future directions should focus on integrative approaches combining nutrition, prebiotics, and microbiome-based therapeutics to combat the increasing burden of metabolic diseases in Mexico.
Additional Links: PMID-41373952
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@article {pmid41373952,
year = {2025},
author = {Acosta-Meneses, RM and Ramírez-Moreno, E and Olvera-Rosales, LB and Cardelle-Cobas, A and Calderón-Ramos, ZG and Rodríguez-Serrano, GM and Franco-Abuín, CM and Cepeda-Saéz, A and González-Olivares, LG and Mondragón-Portocarrero, ADC},
title = {Obesity and Diabetes in Mexico: An Approach to the Intestinal Microbiota.},
journal = {Nutrients},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/nu17233661},
pmid = {41373952},
issn = {2072-6643},
mesh = {Humans ; Mexico/epidemiology ; *Gastrointestinal Microbiome/physiology ; *Obesity/epidemiology/microbiology ; *Diabetes Mellitus/epidemiology/microbiology ; Dysbiosis/epidemiology/microbiology ; Probiotics ; Risk Factors ; Prevalence ; Prebiotics ; Insulin Resistance ; },
abstract = {Obesity and diabetes have reached alarming prevalence rates globally, with Mexico being one of the most affected countries. This review explores the epidemiology of these metabolic disorders and analyzes their prevalence and risk factors, as well as the crucial role of the intestinal microbiota in their development. Obesity and diabetes in Mexico have been linked to lifestyle factors, genetic predispositions, and alterations in the gut microbial composition. The intestinal microbiota plays a significant role in metabolic regulation, and its dysbiosis has been associated with insulin resistance, chronic inflammation, and increased fat accumulation. Studies in Mexico have highlighted specific microbial patterns in individuals with obesity and diabetes, suggesting a unique interplay between diet, microbiota composition, and metabolic health. Strategies to restore microbial balance, such as dietary modifications and probiotic interventions, have shown promising results in improving metabolic parameters and reducing disease progression. However, challenges remain in understanding the long-term effects of microbiota-targeted therapies and their individual variability. This review underscores the need for further research to develop personalized interventions aimed at modulating the gut microbiota for obesity and diabetes management. Future directions should focus on integrative approaches combining nutrition, prebiotics, and microbiome-based therapeutics to combat the increasing burden of metabolic diseases in Mexico.},
}
MeSH Terms:
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Humans
Mexico/epidemiology
*Gastrointestinal Microbiome/physiology
*Obesity/epidemiology/microbiology
*Diabetes Mellitus/epidemiology/microbiology
Dysbiosis/epidemiology/microbiology
Probiotics
Risk Factors
Prevalence
Prebiotics
Insulin Resistance
RevDate: 2025-12-11
CmpDate: 2025-12-11
Personalized Nutritional Assessment and Intervention for Athletes: A Network Physiology Approach.
Nutrients, 17(23): pii:nu17233657.
Nutritional assessment and intervention in athletes, a central focus of sports medicine and healthcare, has increasingly shifted in recent years toward precision nutrition-an approach that individualizes dietary recommendations according to genetic profile, microbiome composition, lifestyle factors, and health status. Despite its promising potential, this approach faces significant limitations, including the challenge of integrating complex and dynamic interactions among multilevel indicators, and the relatively high costs associated with omics technologies. The aim of this paper is to propose a nutritional assessment and intervention model grounded in the Network Physiology of Exercise, an emerging scientific field that investigates the horizontal and vertical dynamic interactions among nested physiological levels and conceptualizes athletes as complex adaptive systems (CAS). The proposal integrates social, environmental, behavioral and psychobiological information, extracted particularly from semi-structured interviews based on CAS properties. Accordingly, the traditional dietary assessment tools are replaced by open and guided interviews that allow professionals and practitioners to co-construct meaningful insights and extract qualitative data through a reflexive thematic analysis. From a CAS perspective, the multidimensional and multi-timescale personal and environmental constrains affecting their eating behavior were integrated through a hierarchically nested organization. Eliciting the dynamics of emotional contexts, behavioral patterns, and psychophysiological states, the interviews become both a method of assessment and an intervention in itself.
Additional Links: PMID-41373948
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@article {pmid41373948,
year = {2025},
author = {Prieto, A and Lizarraga, MA and Balagué, N},
title = {Personalized Nutritional Assessment and Intervention for Athletes: A Network Physiology Approach.},
journal = {Nutrients},
volume = {17},
number = {23},
pages = {},
doi = {10.3390/nu17233657},
pmid = {41373948},
issn = {2072-6643},
mesh = {Humans ; *Athletes ; *Nutrition Assessment ; *Precision Medicine/methods ; Exercise/physiology ; *Sports Nutritional Physiological Phenomena ; Nutritional Status ; },
abstract = {Nutritional assessment and intervention in athletes, a central focus of sports medicine and healthcare, has increasingly shifted in recent years toward precision nutrition-an approach that individualizes dietary recommendations according to genetic profile, microbiome composition, lifestyle factors, and health status. Despite its promising potential, this approach faces significant limitations, including the challenge of integrating complex and dynamic interactions among multilevel indicators, and the relatively high costs associated with omics technologies. The aim of this paper is to propose a nutritional assessment and intervention model grounded in the Network Physiology of Exercise, an emerging scientific field that investigates the horizontal and vertical dynamic interactions among nested physiological levels and conceptualizes athletes as complex adaptive systems (CAS). The proposal integrates social, environmental, behavioral and psychobiological information, extracted particularly from semi-structured interviews based on CAS properties. Accordingly, the traditional dietary assessment tools are replaced by open and guided interviews that allow professionals and practitioners to co-construct meaningful insights and extract qualitative data through a reflexive thematic analysis. From a CAS perspective, the multidimensional and multi-timescale personal and environmental constrains affecting their eating behavior were integrated through a hierarchically nested organization. Eliciting the dynamics of emotional contexts, behavioral patterns, and psychophysiological states, the interviews become both a method of assessment and an intervention in itself.},
}
MeSH Terms:
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Humans
*Athletes
*Nutrition Assessment
*Precision Medicine/methods
Exercise/physiology
*Sports Nutritional Physiological Phenomena
Nutritional Status
RevDate: 2025-12-11
CmpDate: 2025-12-11
Resilience of the Skin Microbiome in Atopic Dermatitis During Short-Term Topical Treatment.
International journal of molecular sciences, 26(23): pii:ijms262311737.
Atopic dermatitis (AD) is associated with microbial dysbiosis and impaired skin barrier function. Topical therapies, such as moisturisers and antimicrobial fragrance compounds, may modulate the skin microbiome and support disease management. The objective was to evaluate how a moisturiser and a fragrance compound (farnesol) influence skin microbiome composition in individuals with AD and healthy controls. In a randomised, controlled, operator-blinded study, 15 AD patients and 15 healthy controls applied a moisturiser, farnesol, moisturiser + farnesol, or no treatment to defined skin areas over 7 days. Microbiome composition, alpha/beta diversity, and core taxa were analysed using shotgun metagenomics. At baseline, AD patients exhibited distinct microbial profiles, including elevated Staphylococcus aureus and Micrococcus luteus. Neither moisturiser nor farnesol significantly altered richness, beta diversity, or core taxa in either AD patients or controls. However, moisturiser use in healthy individuals modestly increased Shannon diversity, reflecting improved microbial evenness. Despite clear microbiome differences between AD and healthy skin, short-term topical treatment did not markedly shift microbial composition. The observed stability underscores the resilience of the skin microbiome and suggests that longer interventions or more targeted formulations may be necessary to influence microbial dysbiosis in AD.
Additional Links: PMID-41373884
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PubMed:
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@article {pmid41373884,
year = {2025},
author = {Ahlström, MG and Bjerre, RD and Hu, Y and Seifert, M and Boulund, F and Skov, L and Johansen, JD and Engstrand, L},
title = {Resilience of the Skin Microbiome in Atopic Dermatitis During Short-Term Topical Treatment.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311737},
pmid = {41373884},
issn = {1422-0067},
support = {LF-ST-21-500002//LEO Foundation/ ; },
mesh = {Humans ; *Dermatitis, Atopic/microbiology/drug therapy ; *Microbiota/drug effects ; *Skin/microbiology/drug effects ; Adult ; Female ; Male ; Middle Aged ; Administration, Topical ; Young Adult ; Dysbiosis/microbiology ; Skin Microbiome ; },
abstract = {Atopic dermatitis (AD) is associated with microbial dysbiosis and impaired skin barrier function. Topical therapies, such as moisturisers and antimicrobial fragrance compounds, may modulate the skin microbiome and support disease management. The objective was to evaluate how a moisturiser and a fragrance compound (farnesol) influence skin microbiome composition in individuals with AD and healthy controls. In a randomised, controlled, operator-blinded study, 15 AD patients and 15 healthy controls applied a moisturiser, farnesol, moisturiser + farnesol, or no treatment to defined skin areas over 7 days. Microbiome composition, alpha/beta diversity, and core taxa were analysed using shotgun metagenomics. At baseline, AD patients exhibited distinct microbial profiles, including elevated Staphylococcus aureus and Micrococcus luteus. Neither moisturiser nor farnesol significantly altered richness, beta diversity, or core taxa in either AD patients or controls. However, moisturiser use in healthy individuals modestly increased Shannon diversity, reflecting improved microbial evenness. Despite clear microbiome differences between AD and healthy skin, short-term topical treatment did not markedly shift microbial composition. The observed stability underscores the resilience of the skin microbiome and suggests that longer interventions or more targeted formulations may be necessary to influence microbial dysbiosis in AD.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Dermatitis, Atopic/microbiology/drug therapy
*Microbiota/drug effects
*Skin/microbiology/drug effects
Adult
Female
Male
Middle Aged
Administration, Topical
Young Adult
Dysbiosis/microbiology
Skin Microbiome
RevDate: 2025-12-11
CmpDate: 2025-12-11
Autoimmune Diseases of the Eyelid Skin: Molecular Pathways, Clinical Manifestations, and Therapeutic Insights.
International journal of molecular sciences, 26(23): pii:ijms262311730.
The eyelid skin represents a unique anatomical and immunological interface between the external environment and the ocular surface. Due to its structural delicacy, dense vascularization, and continuous exposure to microbial and environmental antigens, it is a primary target of inflammatory and autoimmune processes. This review aims to synthesize current molecular insights into eyelid skin inflammation, with particular emphasis on autoimmune mechanisms. We discuss autoimmune diseases such as ocular cicatricial pemphigoid, pemphigus, discoid and systemic lupus erythematosus, and thyroid-associated orbitopathy, focusing on the roles of T helper cell subsets, pro-inflammatory cytokines (IL-1β, IL-6, IL-17, TNF-α), and autoantibody-mediated complement activation. We further address the contribution of the periocular microbiome and meibomian gland dysfunction. Diagnostic advances, including confocal microscopy, in vivo molecular imaging, and tear proteomics, are highlighted alongside emerging targeted therapies such as biologics and small molecules directed at IL-17, TNF-α, and B-cell activity. Finally, we propose future perspectives for precision medicine approaches, integrating omics technologies and microbiome-based therapies to advance personalized management of eyelid skin inflammation.
Additional Links: PMID-41373875
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PubMed:
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@article {pmid41373875,
year = {2025},
author = {Luboń, W and Luboń, M and Sarnat-Kucharczyk, M and Dorecka, M and Wyględowska-Promieńska, D},
title = {Autoimmune Diseases of the Eyelid Skin: Molecular Pathways, Clinical Manifestations, and Therapeutic Insights.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311730},
pmid = {41373875},
issn = {1422-0067},
mesh = {Humans ; *Autoimmune Diseases/therapy/immunology/pathology/metabolism ; *Eyelids/immunology/pathology ; Animals ; *Skin/immunology/pathology ; Cytokines/metabolism ; *Eyelid Diseases/immunology/therapy ; },
abstract = {The eyelid skin represents a unique anatomical and immunological interface between the external environment and the ocular surface. Due to its structural delicacy, dense vascularization, and continuous exposure to microbial and environmental antigens, it is a primary target of inflammatory and autoimmune processes. This review aims to synthesize current molecular insights into eyelid skin inflammation, with particular emphasis on autoimmune mechanisms. We discuss autoimmune diseases such as ocular cicatricial pemphigoid, pemphigus, discoid and systemic lupus erythematosus, and thyroid-associated orbitopathy, focusing on the roles of T helper cell subsets, pro-inflammatory cytokines (IL-1β, IL-6, IL-17, TNF-α), and autoantibody-mediated complement activation. We further address the contribution of the periocular microbiome and meibomian gland dysfunction. Diagnostic advances, including confocal microscopy, in vivo molecular imaging, and tear proteomics, are highlighted alongside emerging targeted therapies such as biologics and small molecules directed at IL-17, TNF-α, and B-cell activity. Finally, we propose future perspectives for precision medicine approaches, integrating omics technologies and microbiome-based therapies to advance personalized management of eyelid skin inflammation.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Autoimmune Diseases/therapy/immunology/pathology/metabolism
*Eyelids/immunology/pathology
Animals
*Skin/immunology/pathology
Cytokines/metabolism
*Eyelid Diseases/immunology/therapy
RevDate: 2025-12-11
CmpDate: 2025-12-11
Physiological and Multi-Omics Insights into Trichoderma harzianum Alleviating Aged Microplastic Stress in Nicotiana benthamiana.
International journal of molecular sciences, 26(23): pii:ijms262311667.
Microplastics derived from biodegradable PBAT film, widely used in agriculture, pose ecological and biological hazards. This study explores how Trichoderma harzianum T4 mitigates this microplastic-induced stress in Nicotiana benthamiana. Using five experimental setup-control (CK), low/high-dose aged microplastics (MP80/MP320), and their co-treatments with T. harzianum T4 (MP80+T4/MP320+T4), multi-omics analyses reveal the microplastic stress-alleviating mechanisms of T. harzianum T4. Aged microplastics significantly inhibit plant growth, promote reactive oxygen species (ROS) and malondialdehyde (MDA) accumulation, and disrupt metabolic homeostasis. Conversely, T. harzianum T4 activates the plant antioxidant defense system, reducing ROS/MDA levels and upregulating superoxide dismutase (SOD)/peroxidase (POD) activities, and promotes biomass. Transcriptomic analysis shows T. harzianum T4 reverses gene expression patterns disrupted by microplastics, particularly in DNA replication and pentose-glucuronic acid pathways. Metagenomic sequencing indicates T. harzianum T4 restores soil microbial diversity, increases the abundance of Bacteroidota and Myxococcota, downregulates antibiotic resistance genes (e.g., tetA5, MDR), and upregulates carbohydrate-active enzymes (CAZys), thereby enhancing carbon metabolism. In conclusion, T. harzianum T4 alleviates microplastic stress through a tripartite mechanism: activating plant stress-response gene networks, reshaping soil microbial communities, and modulating functional gene expression, offering a promising bioremediation strategy.
Additional Links: PMID-41373816
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PubMed:
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@article {pmid41373816,
year = {2025},
author = {Wang, F and Sun, X and Wang, K and Long, B and Li, F and Xie, D},
title = {Physiological and Multi-Omics Insights into Trichoderma harzianum Alleviating Aged Microplastic Stress in Nicotiana benthamiana.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311667},
pmid = {41373816},
issn = {1422-0067},
support = {2022GDASZH-2022010110//'GDAS' Project of Science and Technology Development/ ; 0525149001//Innovation Capacity Building Project for Provincial Scientific Research Institutions/ ; 2024A1515030175//Guangdong Basic and Applied Basic Research/ ; },
mesh = {*Nicotiana/microbiology/drug effects/metabolism/genetics/growth & development ; *Stress, Physiological/drug effects ; *Microplastics/toxicity ; *Hypocreales/physiology ; Reactive Oxygen Species/metabolism ; Transcriptome ; Gene Expression Regulation, Plant/drug effects ; *Trichoderma ; Multiomics ; },
abstract = {Microplastics derived from biodegradable PBAT film, widely used in agriculture, pose ecological and biological hazards. This study explores how Trichoderma harzianum T4 mitigates this microplastic-induced stress in Nicotiana benthamiana. Using five experimental setup-control (CK), low/high-dose aged microplastics (MP80/MP320), and their co-treatments with T. harzianum T4 (MP80+T4/MP320+T4), multi-omics analyses reveal the microplastic stress-alleviating mechanisms of T. harzianum T4. Aged microplastics significantly inhibit plant growth, promote reactive oxygen species (ROS) and malondialdehyde (MDA) accumulation, and disrupt metabolic homeostasis. Conversely, T. harzianum T4 activates the plant antioxidant defense system, reducing ROS/MDA levels and upregulating superoxide dismutase (SOD)/peroxidase (POD) activities, and promotes biomass. Transcriptomic analysis shows T. harzianum T4 reverses gene expression patterns disrupted by microplastics, particularly in DNA replication and pentose-glucuronic acid pathways. Metagenomic sequencing indicates T. harzianum T4 restores soil microbial diversity, increases the abundance of Bacteroidota and Myxococcota, downregulates antibiotic resistance genes (e.g., tetA5, MDR), and upregulates carbohydrate-active enzymes (CAZys), thereby enhancing carbon metabolism. In conclusion, T. harzianum T4 alleviates microplastic stress through a tripartite mechanism: activating plant stress-response gene networks, reshaping soil microbial communities, and modulating functional gene expression, offering a promising bioremediation strategy.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Nicotiana/microbiology/drug effects/metabolism/genetics/growth & development
*Stress, Physiological/drug effects
*Microplastics/toxicity
*Hypocreales/physiology
Reactive Oxygen Species/metabolism
Transcriptome
Gene Expression Regulation, Plant/drug effects
*Trichoderma
Multiomics
RevDate: 2025-12-11
CmpDate: 2025-12-11
Modulation of α-Mannosidase 8 by Antarctic Endophytic Fungi in Strawberry Plants Under Heat Waves and Water Deficit Stress.
International journal of molecular sciences, 26(23): pii:ijms262311650.
Plant-microbe interactions exert a significant influence on host stress responses; however, the molecular mechanisms underlying these effects remain inadequately understood. In this study, we characterize FaMAN8, an α-mannosidase from Fragaria × ananassa, to explore its role in adaptation to heat waves and water deficit, as well as its modulation by fungal endophytes. Transcriptomic analysis identified FaMAN8 as the sole α-mannosidase isoform highly conserved across reported sequences, with root-specific induction under conditions of heat stress, deficient irrigation, and endophytic colonization. Structural modeling revealed that FaMAN8 exhibits the canonical domain organization of glycoside hydrolase family 38 (GH38) enzymes, featuring a conserved catalytic architecture and metal-binding site. Molecular docking and dynamics simulations with the Man3GlcNAc2 ligand indicated a stable binding pocket involving key catalytic residues and strong electrostatic complementarity. MM-GBSA and free energy landscape analyses further supported the thermodynamic stability of the protein-ligand complex. Cavity analysis revealed a larger active site in FaMAN8 compared to its homolog JbMAN, suggesting broader substrate accommodation. Collectively, these findings identify FaMAN8 as a stress-responsive glycosidase potentially involved in glycan remodeling during beneficial root-fungus interactions. This work provides molecular insights into plant-microbe symbiosis and lays the groundwork for microbiome-informed strategies to enhance crop stress resilience.
Additional Links: PMID-41373797
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@article {pmid41373797,
year = {2025},
author = {Bustos, D and Morales-Quintana, L and Urra, G and Arriaza-Rodríguez, F and Pollmann, S and Méndez-Yáñez, A and Ramos, P},
title = {Modulation of α-Mannosidase 8 by Antarctic Endophytic Fungi in Strawberry Plants Under Heat Waves and Water Deficit Stress.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311650},
pmid = {41373797},
issn = {1422-0067},
support = {Fondecyt 1250346; Fondecyt 1240771; ANILLO #ATE220014//Agencia Nacional de Investigación y Desarrollo/ ; },
mesh = {*alpha-Mannosidase/metabolism/genetics/chemistry ; *Fragaria/microbiology/enzymology/genetics ; *Endophytes/physiology ; Molecular Docking Simulation ; Plant Proteins/metabolism/genetics/chemistry ; Hot Temperature ; Molecular Dynamics Simulation ; *Stress, Physiological ; Plant Roots/microbiology ; },
abstract = {Plant-microbe interactions exert a significant influence on host stress responses; however, the molecular mechanisms underlying these effects remain inadequately understood. In this study, we characterize FaMAN8, an α-mannosidase from Fragaria × ananassa, to explore its role in adaptation to heat waves and water deficit, as well as its modulation by fungal endophytes. Transcriptomic analysis identified FaMAN8 as the sole α-mannosidase isoform highly conserved across reported sequences, with root-specific induction under conditions of heat stress, deficient irrigation, and endophytic colonization. Structural modeling revealed that FaMAN8 exhibits the canonical domain organization of glycoside hydrolase family 38 (GH38) enzymes, featuring a conserved catalytic architecture and metal-binding site. Molecular docking and dynamics simulations with the Man3GlcNAc2 ligand indicated a stable binding pocket involving key catalytic residues and strong electrostatic complementarity. MM-GBSA and free energy landscape analyses further supported the thermodynamic stability of the protein-ligand complex. Cavity analysis revealed a larger active site in FaMAN8 compared to its homolog JbMAN, suggesting broader substrate accommodation. Collectively, these findings identify FaMAN8 as a stress-responsive glycosidase potentially involved in glycan remodeling during beneficial root-fungus interactions. This work provides molecular insights into plant-microbe symbiosis and lays the groundwork for microbiome-informed strategies to enhance crop stress resilience.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*alpha-Mannosidase/metabolism/genetics/chemistry
*Fragaria/microbiology/enzymology/genetics
*Endophytes/physiology
Molecular Docking Simulation
Plant Proteins/metabolism/genetics/chemistry
Hot Temperature
Molecular Dynamics Simulation
*Stress, Physiological
Plant Roots/microbiology
RevDate: 2025-12-11
CmpDate: 2025-12-11
Benchmarking Cost-Effective DNA Extraction Kits for Diverse Metagenomic Samples.
International journal of molecular sciences, 26(23): pii:ijms262311616.
Extraction of high-quality microbial DNA remains a critical bottleneck in metagenomic research. Environmental samples often produce fragmented DNA and are prone to contaminations that interfere with downstream sequencing, while widely used commercial kits can be prohibitively expensive. Therefore, systematic evaluation of cost-effective alternatives is essential to support large-scale metagenomic studies. In this work, we benchmarked eight commercial DNA extraction kits from Magen, SkyGen, and Sileks against Qiagen reference kits. Four representative sample types were analyzed: freshwater, seafloor sediments, Pacific oyster (Magallana gigas) gut microbiome, and mammalian feces. DNA yield, integrity, purity, PCR inhibitor content, and eukaryotic DNA admixture were assessed. Microbial community composition, alpha diversity, reproducibility, and contamination ("kitome" and "splashome") were further evaluated using 16S rRNA amplicon sequencing. We revealed that several alternative kits performed comparably or better than the Qiagen reference standard. Magen Soil and Magen Bacterial provided high yields and reproducibility, though the latter produced more fragmented DNA. SkyGen Stool excelled with host-associated samples, while Sileks Soil and Metagenomic kits preserved higher diversity in sediments. Magen Microbiome consistently underperformed. This study identifies multiple cost-effective DNA extraction strategies and provides practical guidance for selecting balanced DNA purification methods for different sample types.
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@article {pmid41373768,
year = {2025},
author = {Sobolev, A and Sibiryakina, D and Chevokina, E and Slonova, D and Yurikova, D and Kozlova, S and Trofimova, A and Zubarev, V and Kiselev, A and Konovalova, O and Sutormin, D and Isaev, A},
title = {Benchmarking Cost-Effective DNA Extraction Kits for Diverse Metagenomic Samples.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311616},
pmid = {41373768},
issn = {1422-0067},
support = {075-10-2021-114//Ministry of Science and Higher Education/ ; 22-14-00004//Russian Science Foundation/ ; },
mesh = {*Metagenomics/methods/economics ; Animals ; RNA, Ribosomal, 16S/genetics ; Cost-Benefit Analysis ; Feces/microbiology ; Benchmarking ; *Metagenome ; *DNA, Bacterial/isolation & purification/genetics ; Reproducibility of Results ; Geologic Sediments/microbiology ; *DNA/isolation & purification ; Gastrointestinal Microbiome/genetics ; },
abstract = {Extraction of high-quality microbial DNA remains a critical bottleneck in metagenomic research. Environmental samples often produce fragmented DNA and are prone to contaminations that interfere with downstream sequencing, while widely used commercial kits can be prohibitively expensive. Therefore, systematic evaluation of cost-effective alternatives is essential to support large-scale metagenomic studies. In this work, we benchmarked eight commercial DNA extraction kits from Magen, SkyGen, and Sileks against Qiagen reference kits. Four representative sample types were analyzed: freshwater, seafloor sediments, Pacific oyster (Magallana gigas) gut microbiome, and mammalian feces. DNA yield, integrity, purity, PCR inhibitor content, and eukaryotic DNA admixture were assessed. Microbial community composition, alpha diversity, reproducibility, and contamination ("kitome" and "splashome") were further evaluated using 16S rRNA amplicon sequencing. We revealed that several alternative kits performed comparably or better than the Qiagen reference standard. Magen Soil and Magen Bacterial provided high yields and reproducibility, though the latter produced more fragmented DNA. SkyGen Stool excelled with host-associated samples, while Sileks Soil and Metagenomic kits preserved higher diversity in sediments. Magen Microbiome consistently underperformed. This study identifies multiple cost-effective DNA extraction strategies and provides practical guidance for selecting balanced DNA purification methods for different sample types.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Metagenomics/methods/economics
Animals
RNA, Ribosomal, 16S/genetics
Cost-Benefit Analysis
Feces/microbiology
Benchmarking
*Metagenome
*DNA, Bacterial/isolation & purification/genetics
Reproducibility of Results
Geologic Sediments/microbiology
*DNA/isolation & purification
Gastrointestinal Microbiome/genetics
RevDate: 2025-12-11
CmpDate: 2025-12-11
Environmental Mechanisms Influencing the Pathogenesis and Progression of Type 1 Diabetes.
International journal of molecular sciences, 26(23): pii:ijms262311613.
Type 1 diabetes (T1D) is a complex autoimmune disorder characterized by the selective destruction of insulin-producing pancreatic β-cells. While genetic predisposition establishes susceptibility, environmental factors play a pivotal role in triggering and modulating the autoimmune process. This narrative review synthesizes current evidence from epidemiological, clinical, and experimental studies to elucidate the mechanisms by which environmental exposures influence the pathogenesis and progression of T1D. We discuss how persistent organic pollutants, heavy metals, air pollutants, viral infections, and gut microbiome alterations contribute to β-cell dysfunction, loss of immune tolerance, and enhanced autoimmunity. Our analysis reveals that these environmental triggers act through multiple interconnected pathways, including oxidative stress, mitochondrial dysfunction, epigenetic modifications, innate immune activation, and gut barrier disruption. Understanding these mechanisms provides critical insights for developing preventive strategies and targeted interventions to mitigate environmental risks. These findings underscore the importance of addressing environmental exposures as modifiable risk factors, offering a potential framework for early interventions aimed at preventing or slowing T1D progression in at-risk populations.
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@article {pmid41373764,
year = {2025},
author = {Tang, Y and Wang, W and Huang, Z and Zhang, C and Zhang, J and Pang, Y and Li, S},
title = {Environmental Mechanisms Influencing the Pathogenesis and Progression of Type 1 Diabetes.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311613},
pmid = {41373764},
issn = {1422-0067},
support = {32270760//the National Natural Science Foundation of China/ ; 2022YFF0710700//the Fundamental Research Funds for the National Key R&D Projec/ ; },
mesh = {Humans ; *Diabetes Mellitus, Type 1/etiology/pathology/epidemiology/immunology ; *Environmental Exposure/adverse effects ; Disease Progression ; Animals ; Gastrointestinal Microbiome ; Oxidative Stress ; Insulin-Secreting Cells/immunology/pathology/metabolism ; Autoimmunity ; },
abstract = {Type 1 diabetes (T1D) is a complex autoimmune disorder characterized by the selective destruction of insulin-producing pancreatic β-cells. While genetic predisposition establishes susceptibility, environmental factors play a pivotal role in triggering and modulating the autoimmune process. This narrative review synthesizes current evidence from epidemiological, clinical, and experimental studies to elucidate the mechanisms by which environmental exposures influence the pathogenesis and progression of T1D. We discuss how persistent organic pollutants, heavy metals, air pollutants, viral infections, and gut microbiome alterations contribute to β-cell dysfunction, loss of immune tolerance, and enhanced autoimmunity. Our analysis reveals that these environmental triggers act through multiple interconnected pathways, including oxidative stress, mitochondrial dysfunction, epigenetic modifications, innate immune activation, and gut barrier disruption. Understanding these mechanisms provides critical insights for developing preventive strategies and targeted interventions to mitigate environmental risks. These findings underscore the importance of addressing environmental exposures as modifiable risk factors, offering a potential framework for early interventions aimed at preventing or slowing T1D progression in at-risk populations.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Diabetes Mellitus, Type 1/etiology/pathology/epidemiology/immunology
*Environmental Exposure/adverse effects
Disease Progression
Animals
Gastrointestinal Microbiome
Oxidative Stress
Insulin-Secreting Cells/immunology/pathology/metabolism
Autoimmunity
RevDate: 2025-12-11
CmpDate: 2025-12-11
Akkermansia muciniphila in Metabolic Disease: Far from Perfect.
International journal of molecular sciences, 26(23): pii:ijms262311602.
The root of metabolic disease lies in the gastrointestinal tract, where nutrient absorption occurs. Within this environment, a diverse community of microorganisms exerts effects that extend beyond the intestinal barrier. Akkermansia muciniphila (A. muciniphila), one such bacterium, has been associated with enhanced intestinal integrity, reduced intestinal inflammation, weight loss, and improved insulin sensitivity, mediated through mucus fermentation, production of short-chain fatty acids (SCFAs), bacterial proteins, and extracellular vesicles (EVs). Research in this field is promising, yet far from perfect. Its clinical applicability remains limited by factors such as strain variability, scarcity of human intervention studies, and the lack of established causality. While associations have been consistently observed in both rodent and human studies, causality has thus far been demonstrated only in animal models. This issue is of critical importance, as metabolic disease remains highly prevalent, carries systemic consequences, and imposes a substantial burden on healthcare systems, underscoring the urgent need for alternative therapeutic strategies. The aim of this narrative review is to synthesize current knowledge on A. muciniphila and to highlight the key limitations consistently reported in the literature. By addressing these factors, the review seeks to provide realistic perspectives on its therapeutic potential and to outline directions for future research.
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@article {pmid41373754,
year = {2025},
author = {Mierlan, OL and Busila, C and Amaritei, O and Elena, D and Raileanu, CR and Maftei, NM and Matei, MN and Gurau, G},
title = {Akkermansia muciniphila in Metabolic Disease: Far from Perfect.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311602},
pmid = {41373754},
issn = {1422-0067},
mesh = {Humans ; *Metabolic Diseases/microbiology/metabolism ; Animals ; *Gastrointestinal Microbiome ; Akkermansia ; Verrucomicrobia ; Probiotics ; },
abstract = {The root of metabolic disease lies in the gastrointestinal tract, where nutrient absorption occurs. Within this environment, a diverse community of microorganisms exerts effects that extend beyond the intestinal barrier. Akkermansia muciniphila (A. muciniphila), one such bacterium, has been associated with enhanced intestinal integrity, reduced intestinal inflammation, weight loss, and improved insulin sensitivity, mediated through mucus fermentation, production of short-chain fatty acids (SCFAs), bacterial proteins, and extracellular vesicles (EVs). Research in this field is promising, yet far from perfect. Its clinical applicability remains limited by factors such as strain variability, scarcity of human intervention studies, and the lack of established causality. While associations have been consistently observed in both rodent and human studies, causality has thus far been demonstrated only in animal models. This issue is of critical importance, as metabolic disease remains highly prevalent, carries systemic consequences, and imposes a substantial burden on healthcare systems, underscoring the urgent need for alternative therapeutic strategies. The aim of this narrative review is to synthesize current knowledge on A. muciniphila and to highlight the key limitations consistently reported in the literature. By addressing these factors, the review seeks to provide realistic perspectives on its therapeutic potential and to outline directions for future research.},
}
MeSH Terms:
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Humans
*Metabolic Diseases/microbiology/metabolism
Animals
*Gastrointestinal Microbiome
Akkermansia
Verrucomicrobia
Probiotics
RevDate: 2025-12-11
CmpDate: 2025-12-11
Roles of Small Noncoding Vault RNAs in Intestinal Epithelium Homeostasis and Diseases.
International journal of molecular sciences, 26(23): pii:ijms262311565.
The mammalian intestinal epithelium is a rapid self-renewing tissue that functions as a physical barrier against a wide array of noxious substances and the gut microbiome that inhabit the intestinal lumen. Homeostasis of the intestinal epithelium is tightly regulated via well-controlled mechanisms and depends on rapid gene expression pattern alterations to effectively regulate cell survival, adapt to stress, and keep epithelial integrity in stressful environments. Vault RNAs (vtRNAs) are small noncoding RNAs that are highly expressed in the intestinal epithelium and involved in many cellular processes essential for healthy and pathological states. In this review, we provide a broad discussion of vtRNA biogenesis, the roles of vtRNAs in intestinal mucosal renewal and gut barrier function regulation, and the interactions of vtRNAs with RNA-binding proteins in modulating mRNA stability and translation. We also highlight the implications of vtRNAs in human gut mucosal disorders and point out vtRNAs as potential biomarkers and/or novel targets for developing new diagnostic and/or therapeutic modalities for identifying and preserving the integrity of the intestinal epithelial lining in patients with critical disorders.
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@article {pmid41373720,
year = {2025},
author = {VanderStoep, A and Xiao, L and Wang, JY},
title = {Roles of Small Noncoding Vault RNAs in Intestinal Epithelium Homeostasis and Diseases.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311565},
pmid = {41373720},
issn = {1422-0067},
mesh = {Humans ; *Intestinal Mucosa/metabolism/pathology ; *Homeostasis/genetics ; Animals ; *RNA, Small Untranslated/genetics/metabolism ; },
abstract = {The mammalian intestinal epithelium is a rapid self-renewing tissue that functions as a physical barrier against a wide array of noxious substances and the gut microbiome that inhabit the intestinal lumen. Homeostasis of the intestinal epithelium is tightly regulated via well-controlled mechanisms and depends on rapid gene expression pattern alterations to effectively regulate cell survival, adapt to stress, and keep epithelial integrity in stressful environments. Vault RNAs (vtRNAs) are small noncoding RNAs that are highly expressed in the intestinal epithelium and involved in many cellular processes essential for healthy and pathological states. In this review, we provide a broad discussion of vtRNA biogenesis, the roles of vtRNAs in intestinal mucosal renewal and gut barrier function regulation, and the interactions of vtRNAs with RNA-binding proteins in modulating mRNA stability and translation. We also highlight the implications of vtRNAs in human gut mucosal disorders and point out vtRNAs as potential biomarkers and/or novel targets for developing new diagnostic and/or therapeutic modalities for identifying and preserving the integrity of the intestinal epithelial lining in patients with critical disorders.},
}
MeSH Terms:
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Humans
*Intestinal Mucosa/metabolism/pathology
*Homeostasis/genetics
Animals
*RNA, Small Untranslated/genetics/metabolism
RevDate: 2025-12-11
CmpDate: 2025-12-11
The Role of the Gut Microbiota in Vascular Physiology and Health.
International journal of molecular sciences, 26(23): pii:ijms262311553.
Cardiovascular diseases (CVD) are the leading cause of global morbidity and mortality. There are many well-known risk factors (dyslipidemia, atherosclerosis, diabetes mellitus, obesity) for these diseases, but there are also other factors with important implications in the pathogenesis of vascular diseases (VD). One of these is the gut microbiome, a metabolically active "organ" with many roles in physiological processes that are linked to VD. Moreover, in recent years, the microbiota has been studied as a "target" in the treatment of various diseases, from gastrointestinal diseases to cardiovascular or even neuropsychiatric diseases. Thus, nutraceuticals may have an important role in modulating the gut microbiota and preventing or treating VD. The aim of this review is to highlight the relationship between the intestinal microbiota and the development and progression of cardiovascular diseases, as well as the possible intervention by using nutraceuticals (vitamins, minerals, dietary supplements) to positively modulate the intestinal microbiota and thus to reduce the risk of VD.
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@article {pmid41373705,
year = {2025},
author = {Neag, MA and Moacă, LȘ and Deac, AL and Măgureanu, DC and Vulturar, DM and Todea, DA and Gherman, D and Buzoianu, AD and Gherman, CD and Militaru, FC},
title = {The Role of the Gut Microbiota in Vascular Physiology and Health.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311553},
pmid = {41373705},
issn = {1422-0067},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Dietary Supplements ; Animals ; *Cardiovascular Diseases/microbiology ; *Vascular Diseases/microbiology ; },
abstract = {Cardiovascular diseases (CVD) are the leading cause of global morbidity and mortality. There are many well-known risk factors (dyslipidemia, atherosclerosis, diabetes mellitus, obesity) for these diseases, but there are also other factors with important implications in the pathogenesis of vascular diseases (VD). One of these is the gut microbiome, a metabolically active "organ" with many roles in physiological processes that are linked to VD. Moreover, in recent years, the microbiota has been studied as a "target" in the treatment of various diseases, from gastrointestinal diseases to cardiovascular or even neuropsychiatric diseases. Thus, nutraceuticals may have an important role in modulating the gut microbiota and preventing or treating VD. The aim of this review is to highlight the relationship between the intestinal microbiota and the development and progression of cardiovascular diseases, as well as the possible intervention by using nutraceuticals (vitamins, minerals, dietary supplements) to positively modulate the intestinal microbiota and thus to reduce the risk of VD.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/physiology
Dietary Supplements
Animals
*Cardiovascular Diseases/microbiology
*Vascular Diseases/microbiology
RevDate: 2025-12-11
CmpDate: 2025-12-11
The Role of the Gut Microbiome in Type 2 Diabetes Mellitus.
International journal of molecular sciences, 26(23): pii:ijms262311412.
The gastrointestinal tract in humans hosts trillions of microorganisms, collectively termed the gut microbiota, which perform essential physiological processes and roles, including nutrient metabolism and immunomodulation. Influenced by genetics, age, diet, medication, and the environment, the disruption of this system leads to dysbiosis, which has been linked to a range of diseases, notably type 2 diabetes mellitus (T2DM). As the global prevalence of T2DM continues to trend upwards, research investigating and highlighting the influence the gut microbiome exerts on this disease is warranted. The literature was examined regarding microbial metabolites and metabolic signaling pathways, as well as interventions relating to diet, prebiotics, probiotics, pharmacological agents, and fecal microbiota transplantation (FMT). The gut microbiome, through its effects on insulin resistance, inflammation, bile acid signaling, and glucose-lipid metabolism, impacts the development and progression of T2DM. Furthermore, patients with T2DM have demonstrated reduced microbial diversity, depletion of butyrate-producing bacteria, and an increase in pathogenic species. Interventions including high-fiber diets, metformin, probiotics, and FMT were shown to enrich beneficial microbes and improve metabolic outcomes. Targeted modulation of the microbiome, such as through next-generation probiotics and CRISPR-based therapies, may enhance metabolic control in the context of the future of personalized medicine. This review investigates the intricate relationship between the gut microbiome and T2DM, emphasizing its role in disease pathogenesis, the factors that may impact the microbiome in these patients, as well as therapeutic approaches toward its management.
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@article {pmid41373570,
year = {2025},
author = {Mashal, R and Al-Muhanna, A and Khader, S and Khudair, A and Khudair, A and Butler, AE},
title = {The Role of the Gut Microbiome in Type 2 Diabetes Mellitus.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311412},
pmid = {41373570},
issn = {1422-0067},
mesh = {Humans ; *Diabetes Mellitus, Type 2/microbiology/metabolism/therapy ; *Gastrointestinal Microbiome ; Probiotics/therapeutic use ; Dysbiosis/microbiology ; Animals ; Fecal Microbiota Transplantation ; Prebiotics ; },
abstract = {The gastrointestinal tract in humans hosts trillions of microorganisms, collectively termed the gut microbiota, which perform essential physiological processes and roles, including nutrient metabolism and immunomodulation. Influenced by genetics, age, diet, medication, and the environment, the disruption of this system leads to dysbiosis, which has been linked to a range of diseases, notably type 2 diabetes mellitus (T2DM). As the global prevalence of T2DM continues to trend upwards, research investigating and highlighting the influence the gut microbiome exerts on this disease is warranted. The literature was examined regarding microbial metabolites and metabolic signaling pathways, as well as interventions relating to diet, prebiotics, probiotics, pharmacological agents, and fecal microbiota transplantation (FMT). The gut microbiome, through its effects on insulin resistance, inflammation, bile acid signaling, and glucose-lipid metabolism, impacts the development and progression of T2DM. Furthermore, patients with T2DM have demonstrated reduced microbial diversity, depletion of butyrate-producing bacteria, and an increase in pathogenic species. Interventions including high-fiber diets, metformin, probiotics, and FMT were shown to enrich beneficial microbes and improve metabolic outcomes. Targeted modulation of the microbiome, such as through next-generation probiotics and CRISPR-based therapies, may enhance metabolic control in the context of the future of personalized medicine. This review investigates the intricate relationship between the gut microbiome and T2DM, emphasizing its role in disease pathogenesis, the factors that may impact the microbiome in these patients, as well as therapeutic approaches toward its management.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Diabetes Mellitus, Type 2/microbiology/metabolism/therapy
*Gastrointestinal Microbiome
Probiotics/therapeutic use
Dysbiosis/microbiology
Animals
Fecal Microbiota Transplantation
Prebiotics
RevDate: 2025-12-11
CmpDate: 2025-12-11
Lacticaseibacillus rhamnosus MS27 Potentially Prevents Ulcerative Colitis Through Modulation of Gut Microbiota.
International journal of molecular sciences, 26(23): pii:ijms262311397.
(1) This study explored Lacticaseibacillus rhamnosus MS27, a newly isolated strain, as a potential probiotic candidate for alleviating the onset and severity of ulcerative colitis (UC). (2) L. rhamnosus MS27 was isolated and subjected to biochemical identification, antibiotic sensitivity testing, and antibacterial activity assessment. Dextran sulfate sodium (DSS) colitis model mice were used to evaluate its alleviating effects. In this study, 16S rRNA microbiome and eukaryotes reference transcriptome analyses were conducted to investigate its impact on intestinal microbial ecology and potential molecular mechanisms. (3) L. rhamnosus MS27 exhibits high acid tolerance at pH 3.23 and maintains a high viable bacterial count for 24 h. It can utilize sucrose, lactose, maltose, inulin, esculin, salicin, and mannitol but not raffinose, and it is sensitive to carbenicillin, erythromycin, tetracycline, chloramphenicol, clindamycin, and penicillin. It effectively increases the abundance of beneficial microbes, particularly Akkermansia, Muribaculaceae, and Limosilactobacillus reuteri (p < 0.05), while significantly reducing microorganisms linked to human pathogens causing diarrhea and gastroenteritis (p < 0.05). Transcriptomic analysis demonstrated that the expression levels of Igkv16-104 and C1qtnf3 were significantly downregulated in the presence of L. rhamnosus MS27 treatment compared to DSS treatment alone (p < 0.05). Further analysis revealed significant differences in genes related to immune functions, antigen presentation, and immune cell markers, indicating potential protein-protein interaction networks, particularly among genes of the major histocompatibility complex (MHC). (4) L. rhamnosus MS27, as a novel strain, demonstrates a significant capacity to alleviate inflammatory phenotypes. L. rhamnosus MS27 exhibits distinctive metabolic characteristics in lactic acid utilization, acetic acid and oleic acid production. Furthermore, it contributes to systemic homeostasis regulation by modulating Turicibacter to link intestinal microbiota composition with host immune function.
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@article {pmid41373555,
year = {2025},
author = {Zhang, J and Shen, J and Ji, L and Tan, P and Liu, C and Zhang, X and Ma, X},
title = {Lacticaseibacillus rhamnosus MS27 Potentially Prevents Ulcerative Colitis Through Modulation of Gut Microbiota.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311397},
pmid = {41373555},
issn = {1422-0067},
mesh = {Animals ; *Colitis, Ulcerative/prevention & control/microbiology/chemically induced ; *Gastrointestinal Microbiome/drug effects ; *Lacticaseibacillus rhamnosus/physiology/isolation & purification ; *Probiotics/pharmacology/therapeutic use ; Mice ; RNA, Ribosomal, 16S/genetics ; Disease Models, Animal ; Dextran Sulfate ; Male ; },
abstract = {(1) This study explored Lacticaseibacillus rhamnosus MS27, a newly isolated strain, as a potential probiotic candidate for alleviating the onset and severity of ulcerative colitis (UC). (2) L. rhamnosus MS27 was isolated and subjected to biochemical identification, antibiotic sensitivity testing, and antibacterial activity assessment. Dextran sulfate sodium (DSS) colitis model mice were used to evaluate its alleviating effects. In this study, 16S rRNA microbiome and eukaryotes reference transcriptome analyses were conducted to investigate its impact on intestinal microbial ecology and potential molecular mechanisms. (3) L. rhamnosus MS27 exhibits high acid tolerance at pH 3.23 and maintains a high viable bacterial count for 24 h. It can utilize sucrose, lactose, maltose, inulin, esculin, salicin, and mannitol but not raffinose, and it is sensitive to carbenicillin, erythromycin, tetracycline, chloramphenicol, clindamycin, and penicillin. It effectively increases the abundance of beneficial microbes, particularly Akkermansia, Muribaculaceae, and Limosilactobacillus reuteri (p < 0.05), while significantly reducing microorganisms linked to human pathogens causing diarrhea and gastroenteritis (p < 0.05). Transcriptomic analysis demonstrated that the expression levels of Igkv16-104 and C1qtnf3 were significantly downregulated in the presence of L. rhamnosus MS27 treatment compared to DSS treatment alone (p < 0.05). Further analysis revealed significant differences in genes related to immune functions, antigen presentation, and immune cell markers, indicating potential protein-protein interaction networks, particularly among genes of the major histocompatibility complex (MHC). (4) L. rhamnosus MS27, as a novel strain, demonstrates a significant capacity to alleviate inflammatory phenotypes. L. rhamnosus MS27 exhibits distinctive metabolic characteristics in lactic acid utilization, acetic acid and oleic acid production. Furthermore, it contributes to systemic homeostasis regulation by modulating Turicibacter to link intestinal microbiota composition with host immune function.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Colitis, Ulcerative/prevention & control/microbiology/chemically induced
*Gastrointestinal Microbiome/drug effects
*Lacticaseibacillus rhamnosus/physiology/isolation & purification
*Probiotics/pharmacology/therapeutic use
Mice
RNA, Ribosomal, 16S/genetics
Disease Models, Animal
Dextran Sulfate
Male
RevDate: 2025-12-11
CmpDate: 2025-12-11
Egg Hatching, Peptide Pheromones, and Endoproteinases in Barnacles.
International journal of molecular sciences, 26(23): pii:ijms262311393.
The striped barnacle, Amphibalanus amphitrite, is a simultaneous hermaphrodite crustacean that broods eggs. The eggs are physically and enzymatically cleaned in the mantle by the barnacle to manage biofouling during incubation. There is no physiological connection between the embryos and the adult. Instead, barnacles use enzyme products as pheromones to coordinate behavioral, physiological, and biochemical processes involved in egg hatching and larval release. Known larval release pheromones are peptides generated by exogenous trypsins that act on proteins. We characterized barnacle brooding endoproteinases using a proteomic analysis of peptides generated from the hydrolysis of pure proteins that were identified by high-resolution LC electrospray MS/MS. Utilizing pure proteins permitted us to completely identify sequences around proteolytic cleavage sites. Enzyme activity was 2.22 to 2.79 times greater in barnacle and barnacle microbiome samples compared to seawater samples. Distinct enzyme patterns emerged, with higher proline- and asparagine-cutting enzymes in barnacle samples and greater proportions of elastase in seawater. There are at least 13 endoproteinases based on the C-terminus amino acids of peptides, with major contributions from serine proteases. This approach has the potential to provide exceptionally detailed information on endoproteinases in any microbiome assemblage. With a little thought, this technique can be expanded to include exoproteinases as well.
Additional Links: PMID-41373551
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@article {pmid41373551,
year = {2025},
author = {Bolger, D and Osterberg, J and Orihuela, B and Moseley, A and Rittschof, D},
title = {Egg Hatching, Peptide Pheromones, and Endoproteinases in Barnacles.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311393},
pmid = {41373551},
issn = {1422-0067},
support = {P010234667//Leidos (United States)/ ; N00014-23-1-2205//Office of Naval Research/ ; NA//Oak Foundation/ ; },
mesh = {Animals ; *Thoracica/physiology/metabolism/enzymology ; *Pheromones/metabolism ; *Peptides/metabolism ; Proteomics/methods ; Tandem Mass Spectrometry ; Larva/metabolism ; *Peptide Hydrolases/metabolism ; },
abstract = {The striped barnacle, Amphibalanus amphitrite, is a simultaneous hermaphrodite crustacean that broods eggs. The eggs are physically and enzymatically cleaned in the mantle by the barnacle to manage biofouling during incubation. There is no physiological connection between the embryos and the adult. Instead, barnacles use enzyme products as pheromones to coordinate behavioral, physiological, and biochemical processes involved in egg hatching and larval release. Known larval release pheromones are peptides generated by exogenous trypsins that act on proteins. We characterized barnacle brooding endoproteinases using a proteomic analysis of peptides generated from the hydrolysis of pure proteins that were identified by high-resolution LC electrospray MS/MS. Utilizing pure proteins permitted us to completely identify sequences around proteolytic cleavage sites. Enzyme activity was 2.22 to 2.79 times greater in barnacle and barnacle microbiome samples compared to seawater samples. Distinct enzyme patterns emerged, with higher proline- and asparagine-cutting enzymes in barnacle samples and greater proportions of elastase in seawater. There are at least 13 endoproteinases based on the C-terminus amino acids of peptides, with major contributions from serine proteases. This approach has the potential to provide exceptionally detailed information on endoproteinases in any microbiome assemblage. With a little thought, this technique can be expanded to include exoproteinases as well.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Thoracica/physiology/metabolism/enzymology
*Pheromones/metabolism
*Peptides/metabolism
Proteomics/methods
Tandem Mass Spectrometry
Larva/metabolism
*Peptide Hydrolases/metabolism
RevDate: 2025-12-11
CmpDate: 2025-12-11
Special Issue: "Molecular Research in Human Microbiome 2.0".
International journal of molecular sciences, 26(23): pii:ijms262311379.
The human microbiome is crucial to the health and welfare of the global population; a healthy microbiome protects us against pathogens while preserving beneficial organisms, assists immune system development and generally maintains a good level of well-being [...].
Additional Links: PMID-41373536
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@article {pmid41373536,
year = {2025},
author = {Mascellino, MT},
title = {Special Issue: "Molecular Research in Human Microbiome 2.0".},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311379},
pmid = {41373536},
issn = {1422-0067},
mesh = {Humans ; *Microbiota ; Gastrointestinal Microbiome ; },
abstract = {The human microbiome is crucial to the health and welfare of the global population; a healthy microbiome protects us against pathogens while preserving beneficial organisms, assists immune system development and generally maintains a good level of well-being [...].},
}
MeSH Terms:
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Humans
*Microbiota
Gastrointestinal Microbiome
RevDate: 2025-12-11
CmpDate: 2025-12-11
Wounds and the Microbiota: The Healing Interplay Between Host and Microbial Communities.
International journal of molecular sciences, 26(23): pii:ijms262311365.
Chronic, non-healing wounds represent a major global health challenge, often aggravated by microbial dysbiosis and impaired host responses. Wound healing progresses through four overlapping phases-hemostasis, inflammation, proliferation, and remodeling-yet recent findings reveal that the skin microbiota actively participates in each step through immune, metabolic, and signaling mechanisms. Beneficial microorganisms such as Staphylococcus epidermidis and Lactobacillus plantarum promote tissue repair by inducing antimicrobial peptides and modulating cytokine production, whereas opportunistic pathogens (Staphylococcus aureus, Pseudomonas aeruginosa, Enterococcus faecalis) delay closure via biofilm formation and proteolytic activity. This review integrates current molecular insights and bibliometric trends to highlight advances and remaining challenges in understanding the wound-microbiome axis. A deeper grasp of these interactions can inform next-generation, microbiome-targeted therapies for chronic wounds.
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@article {pmid41373523,
year = {2025},
author = {Al-Taweel, R and Hammad, AS and Tajammul, A and Crovella, S and Al-Asmakh, M},
title = {Wounds and the Microbiota: The Healing Interplay Between Host and Microbial Communities.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311365},
pmid = {41373523},
issn = {1422-0067},
support = {(Grant No. QUPD-CHS-23-24-563), (Grant No. QUCP-CHS-2022-483)//Qatar University/ ; },
mesh = {Humans ; *Wound Healing ; *Microbiota ; Animals ; Skin/microbiology ; Biofilms ; },
abstract = {Chronic, non-healing wounds represent a major global health challenge, often aggravated by microbial dysbiosis and impaired host responses. Wound healing progresses through four overlapping phases-hemostasis, inflammation, proliferation, and remodeling-yet recent findings reveal that the skin microbiota actively participates in each step through immune, metabolic, and signaling mechanisms. Beneficial microorganisms such as Staphylococcus epidermidis and Lactobacillus plantarum promote tissue repair by inducing antimicrobial peptides and modulating cytokine production, whereas opportunistic pathogens (Staphylococcus aureus, Pseudomonas aeruginosa, Enterococcus faecalis) delay closure via biofilm formation and proteolytic activity. This review integrates current molecular insights and bibliometric trends to highlight advances and remaining challenges in understanding the wound-microbiome axis. A deeper grasp of these interactions can inform next-generation, microbiome-targeted therapies for chronic wounds.},
}
MeSH Terms:
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Humans
*Wound Healing
*Microbiota
Animals
Skin/microbiology
Biofilms
RevDate: 2025-12-11
CmpDate: 2025-12-11
Resveratrol as an Adjunct Antiviral Agent in Pediatric Viral Infections: A Review on Mechanistic Insights and Gut Microbiota Modulation.
International journal of molecular sciences, 26(23): pii:ijms262311341.
Pediatric viral infections impose a heavy burden on child health, often worsened by infection-induced gut dysbiosis. Resveratrol, a natural polyphenol with antiviral, anti-inflammatory, and microbiota-modulating properties, has been proposed to interrupt this pathogenic feedback. To our knowledge, this is the first narrative review focused on resveratrol's antiviral activity in pediatric viral infections, concurrently evaluating its impact on the gut microbiota and their interrelationship. We synthetized preclinical and the limited available pediatric clinical data regarding resveratrol's effect on SARS-CoV-2, respiratory syncytial virus, influenza, rotavirus, and norovirus, extracting information on the models, routes of administration, dosages, mechanisms, and outcomes. Resveratrol interferes with viral lifecycles via diverse mechanisms (modulation of host signaling cascades, capsid or structural protein interactions, and suppression of pro-viral chaperones) while concurrently reshaping the gut microbiota (reducing opportunistic taxa and enriching beneficial genera such as Bifidobacterium and Lactobacillus) leading to improved short-chain fatty acid profiles, barrier integrity, and dampened inflammation. Intranasal resveratrol in children shows clinical benefit, while oral use is underexplored and limited by poor bioavailability; adult data hint at supportive microbiome and anti-inflammatory effects if the delivery is optimized. These dual antiviral and microbiome-directed effects position resveratrol as a promising adjunct in pediatric viral disease management, though well-powered pediatric clinical trials are needed to define dosages, delivery strategies, and the contribution of microbiota-mediated synergy.
Additional Links: PMID-41373500
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@article {pmid41373500,
year = {2025},
author = {Leonardi, R and Lo Bianco, M and Spinello, S and Betta, P and Gagliano, C and Calabrese, V and Polizzi, A and Malaguarnera, G},
title = {Resveratrol as an Adjunct Antiviral Agent in Pediatric Viral Infections: A Review on Mechanistic Insights and Gut Microbiota Modulation.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311341},
pmid = {41373500},
issn = {1422-0067},
mesh = {Humans ; *Resveratrol/therapeutic use/pharmacology ; *Gastrointestinal Microbiome/drug effects ; *Antiviral Agents/therapeutic use/pharmacology ; Child ; *Virus Diseases/drug therapy/microbiology ; SARS-CoV-2/drug effects ; Dysbiosis/drug therapy ; COVID-19 ; Rotavirus/drug effects ; },
abstract = {Pediatric viral infections impose a heavy burden on child health, often worsened by infection-induced gut dysbiosis. Resveratrol, a natural polyphenol with antiviral, anti-inflammatory, and microbiota-modulating properties, has been proposed to interrupt this pathogenic feedback. To our knowledge, this is the first narrative review focused on resveratrol's antiviral activity in pediatric viral infections, concurrently evaluating its impact on the gut microbiota and their interrelationship. We synthetized preclinical and the limited available pediatric clinical data regarding resveratrol's effect on SARS-CoV-2, respiratory syncytial virus, influenza, rotavirus, and norovirus, extracting information on the models, routes of administration, dosages, mechanisms, and outcomes. Resveratrol interferes with viral lifecycles via diverse mechanisms (modulation of host signaling cascades, capsid or structural protein interactions, and suppression of pro-viral chaperones) while concurrently reshaping the gut microbiota (reducing opportunistic taxa and enriching beneficial genera such as Bifidobacterium and Lactobacillus) leading to improved short-chain fatty acid profiles, barrier integrity, and dampened inflammation. Intranasal resveratrol in children shows clinical benefit, while oral use is underexplored and limited by poor bioavailability; adult data hint at supportive microbiome and anti-inflammatory effects if the delivery is optimized. These dual antiviral and microbiome-directed effects position resveratrol as a promising adjunct in pediatric viral disease management, though well-powered pediatric clinical trials are needed to define dosages, delivery strategies, and the contribution of microbiota-mediated synergy.},
}
MeSH Terms:
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Humans
*Resveratrol/therapeutic use/pharmacology
*Gastrointestinal Microbiome/drug effects
*Antiviral Agents/therapeutic use/pharmacology
Child
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RevDate: 2025-12-11
CmpDate: 2025-12-11
Emerging Roles of Bile Acids in Neuroinflammation.
International journal of molecular sciences, 26(23): pii:ijms262311301.
Bile acids, once considered mere digestive detergents, have emerged as multifaceted signaling molecules with systemic influence extending far beyond the gastrointestinal tract. Recent discoveries reveal their capacity to modulate immune responses, cross the blood-brain barrier, and interact with central nervous system (CNS) cells through their receptors. Neuroinflammation, a key driver of neurodegenerative and neuroimmune disorders, is increasingly linked to bile acid signaling pathways that regulate glial activation, cytokine production, and neuronal survival. This review compiles the current evidence connecting bile acids to CNS inflammation, highlighting mechanistic insights, disease-specific alterations, and the gut-microbiome-bile acid-brain axis. It also explores the therapeutic potential of bile acid derivatives and receptor modulators, as well as their emerging role as biomarkers in conditions such as Alzheimer's disease, multiple sclerosis, and hepatic encephalopathy. Despite promising advances, critical gaps remain, including the need for bile receptor mapping in human CNS cells, standardized CNS bile acid profiling, and longitudinal metabolomic studies. Bridging these gaps may unlock new strategies for targeting neuroinflammation through bile acid-immune crosstalk.
Additional Links: PMID-41373461
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@article {pmid41373461,
year = {2025},
author = {Butcher, EL and Arthur, S},
title = {Emerging Roles of Bile Acids in Neuroinflammation.},
journal = {International journal of molecular sciences},
volume = {26},
number = {23},
pages = {},
doi = {10.3390/ijms262311301},
pmid = {41373461},
issn = {1422-0067},
mesh = {Humans ; *Bile Acids and Salts/metabolism ; *Neuroinflammatory Diseases/metabolism/pathology ; Animals ; Gastrointestinal Microbiome ; Signal Transduction ; Biomarkers/metabolism ; Blood-Brain Barrier/metabolism ; Inflammation/metabolism ; Central Nervous System/metabolism ; },
abstract = {Bile acids, once considered mere digestive detergents, have emerged as multifaceted signaling molecules with systemic influence extending far beyond the gastrointestinal tract. Recent discoveries reveal their capacity to modulate immune responses, cross the blood-brain barrier, and interact with central nervous system (CNS) cells through their receptors. Neuroinflammation, a key driver of neurodegenerative and neuroimmune disorders, is increasingly linked to bile acid signaling pathways that regulate glial activation, cytokine production, and neuronal survival. This review compiles the current evidence connecting bile acids to CNS inflammation, highlighting mechanistic insights, disease-specific alterations, and the gut-microbiome-bile acid-brain axis. It also explores the therapeutic potential of bile acid derivatives and receptor modulators, as well as their emerging role as biomarkers in conditions such as Alzheimer's disease, multiple sclerosis, and hepatic encephalopathy. Despite promising advances, critical gaps remain, including the need for bile receptor mapping in human CNS cells, standardized CNS bile acid profiling, and longitudinal metabolomic studies. Bridging these gaps may unlock new strategies for targeting neuroinflammation through bile acid-immune crosstalk.},
}
MeSH Terms:
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Humans
*Bile Acids and Salts/metabolism
*Neuroinflammatory Diseases/metabolism/pathology
Animals
Gastrointestinal Microbiome
Signal Transduction
Biomarkers/metabolism
Blood-Brain Barrier/metabolism
Inflammation/metabolism
Central Nervous System/metabolism
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