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ESP: PubMed Auto Bibliography 29 Apr 2026 at 01:55 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2026-04-27
CmpDate: 2026-04-27
Consumer knowledge and motivations for consumption of fermented foods.
Frontiers in microbiology, 17:1789825.
Non-alcoholic fermented foods (FFs) are a popular food group with consumers; however limited studies exist evaluating the motivations for consuming FFs and the frequency of consumption. To begin to address this gap in knowledge, we developed an online survey to assess participant familiarity with different types of fermented products, determine consumption frequency, and gain insight into the motivation for consumption. A total of 751 participants completed the survey. Yogurt was the most frequently identified fermented food (n = 658; 87.62% of respondents). Participants reported consuming fermented cereal grains (n = 307; 46.17%), fruits and vegetables (n = 281; 42.26%), dairy products (n = 204; 39.70%), soy/rice products (n = 250; 37.60%) and fermented meats (n = 204; 30.68%). Reported daily consumption was highest for categories of fermented cereal and dairy products, compared to the other categories which typically were consumed on a weekly or monthly basis. The primary motivator for consumption was taste (n = 337; 50.68%) compared to health benefits (n = 235; 35.34%) and cultural reasons (n = 80; 12.03%). The most highly selected health benefits associated with FF consumption were "improved gut microbiome" (n = 513; 77.14%), "digestive benefits" (n = 508; 76.39%), and "probiotic" (n = 458; 68.87%). Participants associated health benefits with all fermented products listed in the survey. Therefore, consumers may assume that all fermented foods confer the same health benefits. The motivations for consumption (sensory attributes, health benefits, cultural reasons) did not vary when individuals were asked to respond for FFs as a broad category versus specifically for non-alcoholic, fermented fruits and vegetables. This suggests that consumers view FFs similarly regardless of the starting ingredients and fermentative process involved.
Additional Links: PMID-42039801
PubMed:
Citation:
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@article {pmid42039801,
year = {2026},
author = {Hanlon, M and Van Beeck, W and Wei, L and Tosta, I and Liao, R and Marco, ML and DiCaprio, E},
title = {Consumer knowledge and motivations for consumption of fermented foods.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1789825},
pmid = {42039801},
issn = {1664-302X},
abstract = {Non-alcoholic fermented foods (FFs) are a popular food group with consumers; however limited studies exist evaluating the motivations for consuming FFs and the frequency of consumption. To begin to address this gap in knowledge, we developed an online survey to assess participant familiarity with different types of fermented products, determine consumption frequency, and gain insight into the motivation for consumption. A total of 751 participants completed the survey. Yogurt was the most frequently identified fermented food (n = 658; 87.62% of respondents). Participants reported consuming fermented cereal grains (n = 307; 46.17%), fruits and vegetables (n = 281; 42.26%), dairy products (n = 204; 39.70%), soy/rice products (n = 250; 37.60%) and fermented meats (n = 204; 30.68%). Reported daily consumption was highest for categories of fermented cereal and dairy products, compared to the other categories which typically were consumed on a weekly or monthly basis. The primary motivator for consumption was taste (n = 337; 50.68%) compared to health benefits (n = 235; 35.34%) and cultural reasons (n = 80; 12.03%). The most highly selected health benefits associated with FF consumption were "improved gut microbiome" (n = 513; 77.14%), "digestive benefits" (n = 508; 76.39%), and "probiotic" (n = 458; 68.87%). Participants associated health benefits with all fermented products listed in the survey. Therefore, consumers may assume that all fermented foods confer the same health benefits. The motivations for consumption (sensory attributes, health benefits, cultural reasons) did not vary when individuals were asked to respond for FFs as a broad category versus specifically for non-alcoholic, fermented fruits and vegetables. This suggests that consumers view FFs similarly regardless of the starting ingredients and fermentative process involved.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Vaginal microbiota in assisted reproduction: determinants, dynamics, and impact on clinical outcomes.
Frontiers in microbiology, 17:1770446.
The vaginal microbiota (VMB), predominantly composed of Lactobacillus genus, plays a crucial role in maintaining female reproductive health through acid production, immune modulation, and protection against pathogens. However, substantial inter-individual variability exists in its composition and stability. In assisted reproduction, the vaginal microenvironment is increasingly recognized as an important factor influencing embryo implantation and pregnancy outcomes. Emerging evidence suggests that the composition and dynamics of the vaginal microbiome are not only predictive biomarkers but also potential regulatory targets influencing assisted reproduction outcomes. This review outlines vaginal microbial community types, key behavioral and host-related determinants, and their links to ART outcomes. We also discuss current limitations, including methodological heterogeneity, unclear causal mechanisms, and the lack of standardized intervention strategies. Finally, we highlight the need for longitudinal and multi-omics studies to support the clinical translation of vaginal microbiome research in reproductive medicine.
Additional Links: PMID-42039807
PubMed:
Citation:
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@article {pmid42039807,
year = {2026},
author = {Liu, X and Tang, W and Li, C and Jiao, Y and Bai, Y and Xiang, L and Wu, Z},
title = {Vaginal microbiota in assisted reproduction: determinants, dynamics, and impact on clinical outcomes.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1770446},
pmid = {42039807},
issn = {1664-302X},
abstract = {The vaginal microbiota (VMB), predominantly composed of Lactobacillus genus, plays a crucial role in maintaining female reproductive health through acid production, immune modulation, and protection against pathogens. However, substantial inter-individual variability exists in its composition and stability. In assisted reproduction, the vaginal microenvironment is increasingly recognized as an important factor influencing embryo implantation and pregnancy outcomes. Emerging evidence suggests that the composition and dynamics of the vaginal microbiome are not only predictive biomarkers but also potential regulatory targets influencing assisted reproduction outcomes. This review outlines vaginal microbial community types, key behavioral and host-related determinants, and their links to ART outcomes. We also discuss current limitations, including methodological heterogeneity, unclear causal mechanisms, and the lack of standardized intervention strategies. Finally, we highlight the need for longitudinal and multi-omics studies to support the clinical translation of vaginal microbiome research in reproductive medicine.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Data-driven enterosignatures link gut microbiome reorganization to heat stress responses in lactating sows.
Frontiers in microbiology, 17:1797687.
BACKGROUND: Heat stress (HS) can disrupt the gut microbiome, yet most livestock studies rely on taxonomic summaries that overlook the ecological structure of microbial communities. Enterosignatures (ES) as latent, co-occurring microbial assemblages learned from metagenomic data, offer a framework to capture these dynamics but have scarcely been applied in livestock HS research.
METHODS: Shotgun metagenomes were obtained from 25 lactating sows, belonging to two genetic lines (TOL, n = 13; SEN, n = 12), which were divergently selected based on genomic breeding values (GEBVs) for heat tolerance, and exposed to HS conditions. Results were decomposed using non-negative matrix factorization (NMF), yielding 8 taxonomic (T-ES) and 5 functional (F-ES) subcommunities. Functional profiles (based on KEGG Orthology, KOs) were mapped to metagenome-assembled genomes (MAGs) to integrate metabolic attributes within each ES.
RESULTS: Temporal shifts dominated T-ES variation, with limited genetic-line effects. T-ES 1 (p = 5.42 × 10[-4], Cohen's d = 0.723) and T-ES 7 (p = 0.007, Cohen's d = 0.303) showed increases from day 4 to day 14. Despite modest overall genetic line effects, TOL animals progressively transitioned toward phylogenetically diverse and balanced communities, whereas SEN animals shifted toward imbalanced states characterized by enrichment of taxa with pathobiont potential or single-taxon dominance. Other T-ES displayed small to moderate effects, and T-ES 8 showed a potentially noteworthy genetic line-specific effect size at late lactation (Cohen's d = 0.960; 95% CI: -1.80 to -0.10), though omnibus tests were non-significant (p = 0.757), and the wide confidence interval underscores substantial uncertainty at this sample size. No F-ES reached statistical significance (p > 0.05); moderate effect sizes (up to d = 0.638) suggest possible functional restructuring warranting investigation in larger cohorts.
CONCLUSION: This work presents the first use of ES to track microbiome responses to HS in lactating sows. ES revealed latent taxonomic and functional subcommunities with clear temporal reorganization, offering insights not detectable with standard clustering or diversity metrics. Although genetic-line effects were modest, several ES showed biologically relevant shifts, supporting ES as a hypothesis-generating exploratory framework for linking microbial ecology to physiological adaptation under HS conditions, while warranting validation in larger, controlled trials.
Additional Links: PMID-42039826
PubMed:
Citation:
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@article {pmid42039826,
year = {2026},
author = {Gini, C and Tiezzi, F and Jiang, J and Byrd, MH and Wen, H and Johnson, JS and Brito, LF and van Vliet, S and Maltecca, C},
title = {Data-driven enterosignatures link gut microbiome reorganization to heat stress responses in lactating sows.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1797687},
pmid = {42039826},
issn = {1664-302X},
abstract = {BACKGROUND: Heat stress (HS) can disrupt the gut microbiome, yet most livestock studies rely on taxonomic summaries that overlook the ecological structure of microbial communities. Enterosignatures (ES) as latent, co-occurring microbial assemblages learned from metagenomic data, offer a framework to capture these dynamics but have scarcely been applied in livestock HS research.
METHODS: Shotgun metagenomes were obtained from 25 lactating sows, belonging to two genetic lines (TOL, n = 13; SEN, n = 12), which were divergently selected based on genomic breeding values (GEBVs) for heat tolerance, and exposed to HS conditions. Results were decomposed using non-negative matrix factorization (NMF), yielding 8 taxonomic (T-ES) and 5 functional (F-ES) subcommunities. Functional profiles (based on KEGG Orthology, KOs) were mapped to metagenome-assembled genomes (MAGs) to integrate metabolic attributes within each ES.
RESULTS: Temporal shifts dominated T-ES variation, with limited genetic-line effects. T-ES 1 (p = 5.42 × 10[-4], Cohen's d = 0.723) and T-ES 7 (p = 0.007, Cohen's d = 0.303) showed increases from day 4 to day 14. Despite modest overall genetic line effects, TOL animals progressively transitioned toward phylogenetically diverse and balanced communities, whereas SEN animals shifted toward imbalanced states characterized by enrichment of taxa with pathobiont potential or single-taxon dominance. Other T-ES displayed small to moderate effects, and T-ES 8 showed a potentially noteworthy genetic line-specific effect size at late lactation (Cohen's d = 0.960; 95% CI: -1.80 to -0.10), though omnibus tests were non-significant (p = 0.757), and the wide confidence interval underscores substantial uncertainty at this sample size. No F-ES reached statistical significance (p > 0.05); moderate effect sizes (up to d = 0.638) suggest possible functional restructuring warranting investigation in larger cohorts.
CONCLUSION: This work presents the first use of ES to track microbiome responses to HS in lactating sows. ES revealed latent taxonomic and functional subcommunities with clear temporal reorganization, offering insights not detectable with standard clustering or diversity metrics. Although genetic-line effects were modest, several ES showed biologically relevant shifts, supporting ES as a hypothesis-generating exploratory framework for linking microbial ecology to physiological adaptation under HS conditions, while warranting validation in larger, controlled trials.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
A genomic atlas of gut clostridia: phylogeny, butyrate, and propionate production.
Frontiers in microbiology, 17:1761627.
INTRODUCTION: Clostridia is a major microbial class in the human gut, crucial for fermenting undigested carbohydrates and proteins, which produce short-chain fatty acids essential for gut health and immune balance. This study revised the taxonomic classification and phylogeny of all the species of intestinal Clostridia catalogued in the Unified Human Gastrointestinal Genome database using a whole-genome approach and assessed butyrate and propionate producing species.
METHODS: A total of 1,897 Clostridia species, including those with recognised binomial nomenclature and those lacking formal taxonomic classification, were retrieved and reclassified using GTDB-Tk. Their phylogeny was determined by identifying, concatenating, and aligning the 120 ubiquitous single-copy proteins defined in the GTDB. Average amino acid identity (AAI), percentage of conserved proteins (POCP), and phylogenetic relationships were used to organize the species into genera and families. The presence of enzymes belonging to the biosynthetic pathways for butyrate and propionate production was investigated in all genomes with the tool GapSeq.
RESULTS: Reclassification of the genomes resulted in 404 recognised species and 1,493 species lacking formal taxonomic classification. Oscillospirales and Lachnospirales encompassed most of the species. The pathways leading to butyrate and propionate production were analyzed in their entirety, revealing 519 species as potential butyrate producers, 257 as potential propionate producers and 77 capable of producing both. To assess the abundance of each species, 151 faecal metagenomes of healthy subjects were profiled, indicating that butyrate producing Clostridia accounted on average for 28.0% of each microbiome.
CONCLUSIONS: This study offers a comprehensive overview of intestinal Clostridia diversity, emphasising their role in gut ecosystems and their potential for butyrate and propionate production.
Additional Links: PMID-42039832
PubMed:
Citation:
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@article {pmid42039832,
year = {2026},
author = {Sola, L and Candeliere, F and Busi, E and Raimondi, S and Amaretti, A and Rossi, M},
title = {A genomic atlas of gut clostridia: phylogeny, butyrate, and propionate production.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1761627},
pmid = {42039832},
issn = {1664-302X},
abstract = {INTRODUCTION: Clostridia is a major microbial class in the human gut, crucial for fermenting undigested carbohydrates and proteins, which produce short-chain fatty acids essential for gut health and immune balance. This study revised the taxonomic classification and phylogeny of all the species of intestinal Clostridia catalogued in the Unified Human Gastrointestinal Genome database using a whole-genome approach and assessed butyrate and propionate producing species.
METHODS: A total of 1,897 Clostridia species, including those with recognised binomial nomenclature and those lacking formal taxonomic classification, were retrieved and reclassified using GTDB-Tk. Their phylogeny was determined by identifying, concatenating, and aligning the 120 ubiquitous single-copy proteins defined in the GTDB. Average amino acid identity (AAI), percentage of conserved proteins (POCP), and phylogenetic relationships were used to organize the species into genera and families. The presence of enzymes belonging to the biosynthetic pathways for butyrate and propionate production was investigated in all genomes with the tool GapSeq.
RESULTS: Reclassification of the genomes resulted in 404 recognised species and 1,493 species lacking formal taxonomic classification. Oscillospirales and Lachnospirales encompassed most of the species. The pathways leading to butyrate and propionate production were analyzed in their entirety, revealing 519 species as potential butyrate producers, 257 as potential propionate producers and 77 capable of producing both. To assess the abundance of each species, 151 faecal metagenomes of healthy subjects were profiled, indicating that butyrate producing Clostridia accounted on average for 28.0% of each microbiome.
CONCLUSIONS: This study offers a comprehensive overview of intestinal Clostridia diversity, emphasising their role in gut ecosystems and their potential for butyrate and propionate production.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Unmelted, melted, and deconstructed Cheddar cheese: effects on the gut microbiome from a human dietary intervention study.
Frontiers in microbiology, 17:1702111.
INTRODUCTION: Cheddar cheese is a nutritionally dense food matrix containing nutrients and bioactives with the potential to influence gut microbial characteristics. Food matrices influence nutrient absorption and digestibility, therefore the dairy matrix may affect gut microbial responses to dairy food intake. This research aims to identify gut microbial responses to Cheddar cheese consumption, considering aspects of the dairy matrix.
METHODS: Secondary analysis was conducted on a subset (n = 69) of participants' data collected during a 6-week parallel 3-armed intervention study. Interventions involved daily consumption of one of the following: (A) 120 g unmelted Cheddar cheese; (B) 120 g melted Cheddar cheese; (C) butter (49 g), calcium caseinate powder (30 g), and Ca supplement (500 mg). Demographics, anthropometry, dietary intake and fecal samples were collected at baseline (V1) and post-intervention (V2). Fecal samples underwent 16S rRNA gene sequencing, followed by bioinformatic processing and statistical analysis.
RESULTS: At V1, 52% were female, mean age was 58.2 ± 5.4 years, with no significant differences between groups or timepoints. Following sequencing, 12,098 unique bacterial taxa in total were identified. Under a False Discovery Rate (FDR) cutoff of 0.1, Dorea (W = 0.568, FDR = 0.079) and Erysipelotrichaceae UCG-003 (W = 0.887, FDR = 0.097) were significantly increased from V1 to V2 in the unmelted cheese group. At V2, Bacteroides was differentially more abundant in the unmelted cheese group, relative to the melted group (W = 0.587, FDR = 0.034). Bacterial alpha diversity (Shannon, Simpson) significantly increased in the unmelted cheese group only from V1 to V2 (p < 0.05). Beta diversity analysis showed a significant group effect considering both timepoints (F = 1.505, p < 0.01). Considering V2 only, Principal Coordinate Analysis showed the unmelted group clustered more closely relative to the other groups, although the effect was not significant.
DISCUSSION: Unmelted Cheddar cheese modulated the gut microbiome by increasing alpha diversity and abundance of several fermenting bacteria. Overall community structure also became more similar following consumption of unmelted cheese, relative to the other groups. Heating cheese and altering its physical structure disrupts the dairy matrix, potentially influencing downstream gut-nutrient interactions and subsequent gut microbial response.
Additional Links: PMID-42039839
PubMed:
Citation:
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@article {pmid42039839,
year = {2026},
author = {Chonnacháin, CN and Gibney, ER and Feeney, EL and Rooney, M and O'Connor, A and Noronha, N and Crispie, F and Cotter, PD and FitzGerald, JA},
title = {Unmelted, melted, and deconstructed Cheddar cheese: effects on the gut microbiome from a human dietary intervention study.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1702111},
pmid = {42039839},
issn = {1664-302X},
abstract = {INTRODUCTION: Cheddar cheese is a nutritionally dense food matrix containing nutrients and bioactives with the potential to influence gut microbial characteristics. Food matrices influence nutrient absorption and digestibility, therefore the dairy matrix may affect gut microbial responses to dairy food intake. This research aims to identify gut microbial responses to Cheddar cheese consumption, considering aspects of the dairy matrix.
METHODS: Secondary analysis was conducted on a subset (n = 69) of participants' data collected during a 6-week parallel 3-armed intervention study. Interventions involved daily consumption of one of the following: (A) 120 g unmelted Cheddar cheese; (B) 120 g melted Cheddar cheese; (C) butter (49 g), calcium caseinate powder (30 g), and Ca supplement (500 mg). Demographics, anthropometry, dietary intake and fecal samples were collected at baseline (V1) and post-intervention (V2). Fecal samples underwent 16S rRNA gene sequencing, followed by bioinformatic processing and statistical analysis.
RESULTS: At V1, 52% were female, mean age was 58.2 ± 5.4 years, with no significant differences between groups or timepoints. Following sequencing, 12,098 unique bacterial taxa in total were identified. Under a False Discovery Rate (FDR) cutoff of 0.1, Dorea (W = 0.568, FDR = 0.079) and Erysipelotrichaceae UCG-003 (W = 0.887, FDR = 0.097) were significantly increased from V1 to V2 in the unmelted cheese group. At V2, Bacteroides was differentially more abundant in the unmelted cheese group, relative to the melted group (W = 0.587, FDR = 0.034). Bacterial alpha diversity (Shannon, Simpson) significantly increased in the unmelted cheese group only from V1 to V2 (p < 0.05). Beta diversity analysis showed a significant group effect considering both timepoints (F = 1.505, p < 0.01). Considering V2 only, Principal Coordinate Analysis showed the unmelted group clustered more closely relative to the other groups, although the effect was not significant.
DISCUSSION: Unmelted Cheddar cheese modulated the gut microbiome by increasing alpha diversity and abundance of several fermenting bacteria. Overall community structure also became more similar following consumption of unmelted cheese, relative to the other groups. Heating cheese and altering its physical structure disrupts the dairy matrix, potentially influencing downstream gut-nutrient interactions and subsequent gut microbial response.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Abnormal intestinal microbial colonization in prenatally stressed offspring is related to lung and intestinal cytokine expression.
Frontiers in microbiology, 17:1813467.
INTRODUCTION: Prenatal stress (PNS) is associated with deleterious effects on childhood health and wellbeing. Among these consequential health repercussions, PNS-exposed children are at increased risk for acquiring early-life infections, with respiratory infections frequently reported. Stress-induced perturbations in the maternal microbiome during pregnancy represent a key link between stress in utero and aberrant offspring development and can drive abnormal pioneer colonization of offspring microbiomes.
METHODS: Using a mouse model of PNS, we aimed to understand the extent to which these early-life intestinal microbial perturbations are related to intestinal and lung cytokine gene expression. The intestinal microbiome alongside intestinal and lung tissue gene expression were assessed over the first five weeks of life in PNS-exposed offspring to characterize basal cytokine differences in relation to intestinal microbial composition.
RESULTS: In addition to significant changes in microbiome diversity and differential abundance, PNS offspring exhibited significant differences in ileal and lung cytokines characterized by overall increased interferon and proinflammatory gene signatures. PNS-associated microbiome changes also correlated to gene expression in both the ileum and lung. Finally, PNS-associated cytokine differences were not observed in MyD88[-/-] offspring which lack the ability to initiate inflammatory responses through microbially-stimulated toll-like receptor signaling.
CONCLUSION: These findings suggest that PNS-mediated changes in the early-life microbiome are linked to respiratory and ileal immune development and the microbe-immune interactions are MyD88 pathway-dependent.
Additional Links: PMID-42039844
PubMed:
Citation:
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@article {pmid42039844,
year = {2026},
author = {Duff, AF and Bailey, MT},
title = {Abnormal intestinal microbial colonization in prenatally stressed offspring is related to lung and intestinal cytokine expression.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1813467},
pmid = {42039844},
issn = {1664-302X},
abstract = {INTRODUCTION: Prenatal stress (PNS) is associated with deleterious effects on childhood health and wellbeing. Among these consequential health repercussions, PNS-exposed children are at increased risk for acquiring early-life infections, with respiratory infections frequently reported. Stress-induced perturbations in the maternal microbiome during pregnancy represent a key link between stress in utero and aberrant offspring development and can drive abnormal pioneer colonization of offspring microbiomes.
METHODS: Using a mouse model of PNS, we aimed to understand the extent to which these early-life intestinal microbial perturbations are related to intestinal and lung cytokine gene expression. The intestinal microbiome alongside intestinal and lung tissue gene expression were assessed over the first five weeks of life in PNS-exposed offspring to characterize basal cytokine differences in relation to intestinal microbial composition.
RESULTS: In addition to significant changes in microbiome diversity and differential abundance, PNS offspring exhibited significant differences in ileal and lung cytokines characterized by overall increased interferon and proinflammatory gene signatures. PNS-associated microbiome changes also correlated to gene expression in both the ileum and lung. Finally, PNS-associated cytokine differences were not observed in MyD88[-/-] offspring which lack the ability to initiate inflammatory responses through microbially-stimulated toll-like receptor signaling.
CONCLUSION: These findings suggest that PNS-mediated changes in the early-life microbiome are linked to respiratory and ileal immune development and the microbe-immune interactions are MyD88 pathway-dependent.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Exploring the molecular crosstalk between the sex steroids drospirenone and ethinylestradiol with vaginal lactobacilli.
Frontiers in microbiology, 17:1725887.
INTRODUCTION: The vaginal microbiota, dominated by the genus Lactobacillus spp., plays a crucial role in maintaining vaginal homeostasis and protecting against infection through lactic acid production, antimicrobial compound secretion and competitive exclusion of pathogens. Although hormonal fluctuations are known to influence microbial composition, the molecular mechanisms underlying these interactions remain largely unexplored. The aim of this study was to investigate the direct effects of the synthetic sex hormones drospirenone and ethinylestradiol, key components of hormonal contraceptives, on representative vaginal Lactobacillus species.
METHODS: Representative Lactobacillus species associated with different vaginal Community State Types (CSTs) were exposed to drospirenone and ethinylestradiol under simulated vaginal conditions. Lactobacilli responses were assessed using growth assays and RNA-seq transcriptome profiling to evaluate species-specific transcriptional changes following hormonal exposure.
RESULTS: Among the tested strains, Lactobacillus crispatus PRL2021 showed the most pronounced transcriptomic modulation. In this strain, hormone treatment led to the upregulation of genes involved in cell wall biosynthesis, amino acid and carbohydrate metabolism, and stress adaptation. Specifically, expression of the histidine kinase gene sasA_1, part of a two-component regulatory system potentially involved in environmental sensing, was induced. Additionally, the ribBA and ribE genes, predicted to be involved in riboflavin biosynthesis and associated with antioxidant defense and mucosal protection, were upregulated.
CONCLUSION: These findings demonstrate that drospirenone and ethinylestradiol can directly modulate bacterial gene expression, revealing a previously underinvestigated molecular crosstalk between host endocrine signals and the vaginal microbiota. This interaction may contribute to the maintenance of vaginal eubiosis and has potential implications for the development of microbiome-targeted strategies to support women's health. Further studies are needed to elucidate the broader functional consequences of hormone-microbiota interactions and their clinical relevance.
Additional Links: PMID-42039845
PubMed:
Citation:
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@article {pmid42039845,
year = {2026},
author = {Muscò, A and Tarracchini, C and Rizzo, SM and Viappiani, A and Ventura, M and Turroni, F},
title = {Exploring the molecular crosstalk between the sex steroids drospirenone and ethinylestradiol with vaginal lactobacilli.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1725887},
pmid = {42039845},
issn = {1664-302X},
abstract = {INTRODUCTION: The vaginal microbiota, dominated by the genus Lactobacillus spp., plays a crucial role in maintaining vaginal homeostasis and protecting against infection through lactic acid production, antimicrobial compound secretion and competitive exclusion of pathogens. Although hormonal fluctuations are known to influence microbial composition, the molecular mechanisms underlying these interactions remain largely unexplored. The aim of this study was to investigate the direct effects of the synthetic sex hormones drospirenone and ethinylestradiol, key components of hormonal contraceptives, on representative vaginal Lactobacillus species.
METHODS: Representative Lactobacillus species associated with different vaginal Community State Types (CSTs) were exposed to drospirenone and ethinylestradiol under simulated vaginal conditions. Lactobacilli responses were assessed using growth assays and RNA-seq transcriptome profiling to evaluate species-specific transcriptional changes following hormonal exposure.
RESULTS: Among the tested strains, Lactobacillus crispatus PRL2021 showed the most pronounced transcriptomic modulation. In this strain, hormone treatment led to the upregulation of genes involved in cell wall biosynthesis, amino acid and carbohydrate metabolism, and stress adaptation. Specifically, expression of the histidine kinase gene sasA_1, part of a two-component regulatory system potentially involved in environmental sensing, was induced. Additionally, the ribBA and ribE genes, predicted to be involved in riboflavin biosynthesis and associated with antioxidant defense and mucosal protection, were upregulated.
CONCLUSION: These findings demonstrate that drospirenone and ethinylestradiol can directly modulate bacterial gene expression, revealing a previously underinvestigated molecular crosstalk between host endocrine signals and the vaginal microbiota. This interaction may contribute to the maintenance of vaginal eubiosis and has potential implications for the development of microbiome-targeted strategies to support women's health. Further studies are needed to elucidate the broader functional consequences of hormone-microbiota interactions and their clinical relevance.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Interplay of iron and sulfur with syntrophic propionate oxidation.
Frontiers in microbiology, 17:1798413.
In anaerobic environments, different chemical forms of iron and sulfur influence microbial community composition and functions. This study employs mesophilic and thermophilic ammonia-tolerant syntrophic propionate-oxidizing (SPO) cultures to investigate how different iron and sulfur species influence propionate oxidation, as well as downstream syntrophic acetate oxidation and methanogenesis. Elevated concentrations of both Fe[3+] and Fe[2+] species strongly inhibited SPO activity and suppressed propionate oxidation by the mesophilic culture. In contrast, FeSO4 addition to the thermophilic SPO culture markedly enhanced propionate oxidation and methane formation. Notably, neither Na2SO4 nor FeCl2 alone produced comparable stimulation, suggesting that the observed response was driven by a synergistic effect of Fe[2+] and SO4 [2-] on the SPO microbial network. Following Fe[2+] amendment of thermophilic cultures, a bacterium associated with the glycine cleavage pathway became enriched. Subsequently, with the onset of syntrophic propionate and acetate oxidation, the SPO candidate "Candidatus Thermosyntrophopropionicum ammoniitolerans," a syntrophic acetate-oxidizing bacterium affiliated with the family Thermacetogeniaceae, and a hydrogenotrophic methanogen affiliated with the genus Methanothermobacter increased in relative abundance. Overall, the study demonstrates that predicting the outcomes of iron amendments to the anaerobic microbiome demands careful consideration of the prevailing iron and sulfur chemical speciation and their relative molar concentrations, as these factors drive divergent microbial responses under mesophilic and thermophilic conditions. The outcomes support developing targeted strategies to optimize anaerobic digestion and enhance renewable methane yields in high-ammonia biogas systems.
Additional Links: PMID-42039849
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@article {pmid42039849,
year = {2026},
author = {Weng, N and Pinela, E and Shakeri Yekta, S and Moestedt, J and Westerholm, M},
title = {Interplay of iron and sulfur with syntrophic propionate oxidation.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1798413},
pmid = {42039849},
issn = {1664-302X},
abstract = {In anaerobic environments, different chemical forms of iron and sulfur influence microbial community composition and functions. This study employs mesophilic and thermophilic ammonia-tolerant syntrophic propionate-oxidizing (SPO) cultures to investigate how different iron and sulfur species influence propionate oxidation, as well as downstream syntrophic acetate oxidation and methanogenesis. Elevated concentrations of both Fe[3+] and Fe[2+] species strongly inhibited SPO activity and suppressed propionate oxidation by the mesophilic culture. In contrast, FeSO4 addition to the thermophilic SPO culture markedly enhanced propionate oxidation and methane formation. Notably, neither Na2SO4 nor FeCl2 alone produced comparable stimulation, suggesting that the observed response was driven by a synergistic effect of Fe[2+] and SO4 [2-] on the SPO microbial network. Following Fe[2+] amendment of thermophilic cultures, a bacterium associated with the glycine cleavage pathway became enriched. Subsequently, with the onset of syntrophic propionate and acetate oxidation, the SPO candidate "Candidatus Thermosyntrophopropionicum ammoniitolerans," a syntrophic acetate-oxidizing bacterium affiliated with the family Thermacetogeniaceae, and a hydrogenotrophic methanogen affiliated with the genus Methanothermobacter increased in relative abundance. Overall, the study demonstrates that predicting the outcomes of iron amendments to the anaerobic microbiome demands careful consideration of the prevailing iron and sulfur chemical speciation and their relative molar concentrations, as these factors drive divergent microbial responses under mesophilic and thermophilic conditions. The outcomes support developing targeted strategies to optimize anaerobic digestion and enhance renewable methane yields in high-ammonia biogas systems.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Marine-derived extracts of Peyssonnelia caulifera Okamura and Meristotheca papulosa demonstrate differential efficacy in modulating obesity-related metabolic skewing revealed by integrative analysis of extract metabolomics and microbiome profiles.
Frontiers in nutrition, 13:1749413.
This study investigated the anti-obesity efficacy of Peyssonnelia caulifera Okamura extract (PCE) and Meristotheca papulosa extract (MPE) in a high-fat diet (HFD)-induced obese mouse model. Both extracts improved hyperinsulinemia, adipocyte hypertrophy, and adipose/hepatic inflammation. PCE significantly reduced fasting glucose and hepatic triglyceride levels, while MPE effectively normalized colonic histopathology. Both extracts restored tight junction protein expression and mitigated gut barrier disruption. At the phylum level, both supplementations decreased Bacteroidota and increased Verrucomicrobiota; At the genus level, MPE significantly enriched Lachnospiraceae NK4A136, Dubosiella, Faecalibaculum, and Ruminococcaceae NK4A214, while PCE showed modest, non-significant increase. PCE more potently suppressed LPS-induced cytokines expression and adipogenesis than MPE in vitro. UPLC-QTOF-MS revealed distinct metabolite fingerprints for each extract, and correlation analysis linked key metabolites (e.g., carnitine, valyl isoleucine) to inflammatory and metabolic indices. These findings identify PCE and MPE confer metabolic benefits in HFD-induced obesity through coordinated effects on gut, hepatic, and adipose tissue responses, with PCE showing superior efficacy.
Additional Links: PMID-42039890
PubMed:
Citation:
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@article {pmid42039890,
year = {2026},
author = {Feng, F and Choi, J and Ahn, D and Truong, TMT and Yim, KJ and Kim, HJ and Jung, MY and Lee, HW and Kim, DS and Kang, I},
title = {Marine-derived extracts of Peyssonnelia caulifera Okamura and Meristotheca papulosa demonstrate differential efficacy in modulating obesity-related metabolic skewing revealed by integrative analysis of extract metabolomics and microbiome profiles.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1749413},
pmid = {42039890},
issn = {2296-861X},
abstract = {This study investigated the anti-obesity efficacy of Peyssonnelia caulifera Okamura extract (PCE) and Meristotheca papulosa extract (MPE) in a high-fat diet (HFD)-induced obese mouse model. Both extracts improved hyperinsulinemia, adipocyte hypertrophy, and adipose/hepatic inflammation. PCE significantly reduced fasting glucose and hepatic triglyceride levels, while MPE effectively normalized colonic histopathology. Both extracts restored tight junction protein expression and mitigated gut barrier disruption. At the phylum level, both supplementations decreased Bacteroidota and increased Verrucomicrobiota; At the genus level, MPE significantly enriched Lachnospiraceae NK4A136, Dubosiella, Faecalibaculum, and Ruminococcaceae NK4A214, while PCE showed modest, non-significant increase. PCE more potently suppressed LPS-induced cytokines expression and adipogenesis than MPE in vitro. UPLC-QTOF-MS revealed distinct metabolite fingerprints for each extract, and correlation analysis linked key metabolites (e.g., carnitine, valyl isoleucine) to inflammatory and metabolic indices. These findings identify PCE and MPE confer metabolic benefits in HFD-induced obesity through coordinated effects on gut, hepatic, and adipose tissue responses, with PCE showing superior efficacy.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Plant health in the era of global changes, holobiont biology, and microbiome-based solutions.
Horticulture research, 13(4):uhaf364.
Agriculture faces unprecedented challenges due to climate change, increasing food demand, and resource scarcity, which needs sustainable and innovative solutions. This review explores the emerging paradigm of holobiont biology (host and its microbiome as biological unit) in the context of emerging plant health challenges driven by global changes. We highlight three critical challenges: the rise of complex plant syndromes, the emergence and re-emergence of plant diseases, and the consequences of dysbiotic plant microbiomes. We discuss how microbiome-based strategies can enhance plant resilience, reduce reliance on agrochemicals, and foster sustainable agriculture. Integrating these strategies with advanced frameworks, such as holo-omics and machine learning, opens avenues for microbiome-based solutions to address agricultural challenges in the era of global changes, ensuring resilient crop systems and planetary health.
Additional Links: PMID-42040226
PubMed:
Citation:
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@article {pmid42040226,
year = {2026},
author = {Francomano, E and Aci, MM and Mosca, S and Mohamed, NZ and Agosteo, GE and Li Destri Nicosia, MG and Malacrinò, A and Schena, L},
title = {Plant health in the era of global changes, holobiont biology, and microbiome-based solutions.},
journal = {Horticulture research},
volume = {13},
number = {4},
pages = {uhaf364},
pmid = {42040226},
issn = {2662-6810},
abstract = {Agriculture faces unprecedented challenges due to climate change, increasing food demand, and resource scarcity, which needs sustainable and innovative solutions. This review explores the emerging paradigm of holobiont biology (host and its microbiome as biological unit) in the context of emerging plant health challenges driven by global changes. We highlight three critical challenges: the rise of complex plant syndromes, the emergence and re-emergence of plant diseases, and the consequences of dysbiotic plant microbiomes. We discuss how microbiome-based strategies can enhance plant resilience, reduce reliance on agrochemicals, and foster sustainable agriculture. Integrating these strategies with advanced frameworks, such as holo-omics and machine learning, opens avenues for microbiome-based solutions to address agricultural challenges in the era of global changes, ensuring resilient crop systems and planetary health.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Organic amendments boost maize yield (Zea mays L.) in karst soils via a hierarchical process driven by soil phosphorus enhancement and microbial-mediated nutrient cycling.
Frontiers in plant science, 17:1782544.
INTRODUCTION: Sustainable food production in fragile karst landscapes requires moving beyond input-intensive agriculture.
METHODS: This study investigated how long-term organic amendments affected maize yield, using a 15-year field trial on karst yellow soil. Integrating soil analysis, metagenomics, and causal modeling, revealed that adding farmyard manure or bio-organic fertilizer to mineral NPK increased yield by 12.08% and 11.48%, respectively, and improved key soil properties, most notably available phosphorus.
RESULTS: Organic inputs shifted the soil microbiome toward copiotrophic taxa and enriched genes for organic matter decomposition and phosphorus mobilization. However, statistical modeling revealed that these biological changes did not directly drive yield. Instead, the primary pathway was hierarchical: amendments first enhanced the soil's chemical habitat, which then directly boosted crop growth while simultaneously shaping the microbial community and its functional potential. The interaction of soil, microbes, and genes together explained 81% of the yield variation.
DISCUSSION: Our findings demonstrate that in phosphorus-limited karst soils, organic amendments act foremost as soil conditioners. Microbial processes, though crucial, are secondary mediators that translate improved soil conditions into efficient nutrient cycling. Therefore, sustainable intensification in these vulnerable agroecosystems should prioritize managing soil health over directly targeting microbial processes.
Additional Links: PMID-42040306
PubMed:
Citation:
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@article {pmid42040306,
year = {2026},
author = {Yang, R and Zhu, J and Zhang, Y and Liu, Y and Li, Z and Zhang, H and Li, Q and Wang, X and Chen, X and Chen, D and Liu, Q},
title = {Organic amendments boost maize yield (Zea mays L.) in karst soils via a hierarchical process driven by soil phosphorus enhancement and microbial-mediated nutrient cycling.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1782544},
pmid = {42040306},
issn = {1664-462X},
abstract = {INTRODUCTION: Sustainable food production in fragile karst landscapes requires moving beyond input-intensive agriculture.
METHODS: This study investigated how long-term organic amendments affected maize yield, using a 15-year field trial on karst yellow soil. Integrating soil analysis, metagenomics, and causal modeling, revealed that adding farmyard manure or bio-organic fertilizer to mineral NPK increased yield by 12.08% and 11.48%, respectively, and improved key soil properties, most notably available phosphorus.
RESULTS: Organic inputs shifted the soil microbiome toward copiotrophic taxa and enriched genes for organic matter decomposition and phosphorus mobilization. However, statistical modeling revealed that these biological changes did not directly drive yield. Instead, the primary pathway was hierarchical: amendments first enhanced the soil's chemical habitat, which then directly boosted crop growth while simultaneously shaping the microbial community and its functional potential. The interaction of soil, microbes, and genes together explained 81% of the yield variation.
DISCUSSION: Our findings demonstrate that in phosphorus-limited karst soils, organic amendments act foremost as soil conditioners. Microbial processes, though crucial, are secondary mediators that translate improved soil conditions into efficient nutrient cycling. Therefore, sustainable intensification in these vulnerable agroecosystems should prioritize managing soil health over directly targeting microbial processes.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Genotype-matched mapping reveals consistent regional flavour signatures and rhizosphere microbial correlates in spring-flush Yunnan large-leaf tea.
Food chemistry: X, 35:103869.
Microbial correlates of tea terroir are often confounded by cultivar. Using eight SNP-confirmed genotype-matched pairs large-leaf tea cultivar pairs across Menghai and Pu'er, we tested whether rhizosphere communities covary with flavour chemistry during the spring flush. Under genotype control, the volatile Signature Index (VSI) was consistently higher in Menghai in all pairs, with a β-caryophyllene detection/non-detect contrast (7/8 detected in Pu'er vs 0/8 in Menghai). Non-volatiles chemistry showed a two-tier response: EGCG increased in Menghai, whereas nitrogen-associated taste allocation varied by pair. Bulk soil nitrogen and enzyme activities did not directly explain leaf patterns, while bacterial and fungal communities showed significant regional separation and cross-kingdom concordance. Within this strict genotype-matched framework, the results identify spring-flush regional flavour signatures and their microbial correlates as association-level patterns, providing candidate targets for subsequent mechanistic study.
Additional Links: PMID-42040322
PubMed:
Citation:
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@article {pmid42040322,
year = {2026},
author = {Tong, J and Li, Y and Zhang, Y and Zhang, P and Wang, K and Zou, Q and Shen, S},
title = {Genotype-matched mapping reveals consistent regional flavour signatures and rhizosphere microbial correlates in spring-flush Yunnan large-leaf tea.},
journal = {Food chemistry: X},
volume = {35},
number = {},
pages = {103869},
pmid = {42040322},
issn = {2590-1575},
abstract = {Microbial correlates of tea terroir are often confounded by cultivar. Using eight SNP-confirmed genotype-matched pairs large-leaf tea cultivar pairs across Menghai and Pu'er, we tested whether rhizosphere communities covary with flavour chemistry during the spring flush. Under genotype control, the volatile Signature Index (VSI) was consistently higher in Menghai in all pairs, with a β-caryophyllene detection/non-detect contrast (7/8 detected in Pu'er vs 0/8 in Menghai). Non-volatiles chemistry showed a two-tier response: EGCG increased in Menghai, whereas nitrogen-associated taste allocation varied by pair. Bulk soil nitrogen and enzyme activities did not directly explain leaf patterns, while bacterial and fungal communities showed significant regional separation and cross-kingdom concordance. Within this strict genotype-matched framework, the results identify spring-flush regional flavour signatures and their microbial correlates as association-level patterns, providing candidate targets for subsequent mechanistic study.},
}
RevDate: 2026-04-27
Characterization of the intrahepatic microbiome in patients with HBV-Related end-stage liver disease.
Virulence [Epub ahead of print].
BACKGROUND: Dysregulated microbiota is a hallmark of end-stage liver disease (ESLD). This study aimed to elucidate the intrahepatic microbiome in hepatitis B virus (HBV)-related ESLD.
METHODS: We collected liver tissue samples from patients undergoing liver transplantation due to decompensated cirrhosis (DC) (n = 20) or acute-on-chronic liver failure (ACLF) (n = 24), as well as 18 samples from donors. Metatranscriptomic sequencing was performed to profile liver microbiome and transcriptome.
RESULTS: 2208 bacterial species were detected across 13 phyla and 165 genera. Metatranscriptomic profiling revealed that Proteobacteria and Actinobacteria dominated the intrahepatic microbiome, with Escherichia coli and Pseudomonas most prevalent across groups. Principal coordinate analysis showed distinct microbial community structures among donors, DC, and ACLF patients. Compared with donors, both groups exhibited increased abundance of Bacteroides heparinolyticus, Moraxella osloensis, and Gardnerella vaginalis, while ACLF patients were further enriched with Alcaligenes faecalis and Burkholderia insecticola, and DC patients had higher B. heparinolyticus. Most taxa originated from the gut, with additional oral- and respiratory-derived species. Despite similar abundance between groups, E. coli in ESLD displayed marked functional activation, including nutrient acquisition systems and virulence factors linked to adhesion, invasion, and toxin production. Integrated host - microbiome analysis revealed taxa-specific associations with impaired hepatic metabolic, immune, and structural integrity.
CONCLUSION: This study delineates the compositional and functional reprogramming of the intrahepatic microbiome in patients with ESLD and its coupling with liver metabolic, immune, and structural pathways. These findings suggest the intrahepatic microbiome as a promising therapeutic target for ESLD.
Additional Links: PMID-42041114
Publisher:
PubMed:
Citation:
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@article {pmid42041114,
year = {2026},
author = {Chen, J and Liang, T and Xu, X and Yu, X and Li, Z and Zheng, X and Liu, Y and Yang, S and Meng, Z and Zhou, Y and Ye, C and Tu, H and Cao, G and Chen, H and Chen, L and Li, B and Nie, Y and Sun, S and Zhang, Y and Lu, Y and Zhang, X and Yu, G and Lv, Y and Jia, H and Deng, Z and Pei, N and Shi, Y and Yang, Y},
title = {Characterization of the intrahepatic microbiome in patients with HBV-Related end-stage liver disease.},
journal = {Virulence},
volume = {},
number = {},
pages = {2665492},
doi = {10.1080/21505594.2026.2665492},
pmid = {42041114},
issn = {2150-5608},
abstract = {BACKGROUND: Dysregulated microbiota is a hallmark of end-stage liver disease (ESLD). This study aimed to elucidate the intrahepatic microbiome in hepatitis B virus (HBV)-related ESLD.
METHODS: We collected liver tissue samples from patients undergoing liver transplantation due to decompensated cirrhosis (DC) (n = 20) or acute-on-chronic liver failure (ACLF) (n = 24), as well as 18 samples from donors. Metatranscriptomic sequencing was performed to profile liver microbiome and transcriptome.
RESULTS: 2208 bacterial species were detected across 13 phyla and 165 genera. Metatranscriptomic profiling revealed that Proteobacteria and Actinobacteria dominated the intrahepatic microbiome, with Escherichia coli and Pseudomonas most prevalent across groups. Principal coordinate analysis showed distinct microbial community structures among donors, DC, and ACLF patients. Compared with donors, both groups exhibited increased abundance of Bacteroides heparinolyticus, Moraxella osloensis, and Gardnerella vaginalis, while ACLF patients were further enriched with Alcaligenes faecalis and Burkholderia insecticola, and DC patients had higher B. heparinolyticus. Most taxa originated from the gut, with additional oral- and respiratory-derived species. Despite similar abundance between groups, E. coli in ESLD displayed marked functional activation, including nutrient acquisition systems and virulence factors linked to adhesion, invasion, and toxin production. Integrated host - microbiome analysis revealed taxa-specific associations with impaired hepatic metabolic, immune, and structural integrity.
CONCLUSION: This study delineates the compositional and functional reprogramming of the intrahepatic microbiome in patients with ESLD and its coupling with liver metabolic, immune, and structural pathways. These findings suggest the intrahepatic microbiome as a promising therapeutic target for ESLD.},
}
RevDate: 2026-04-28
Akkermansia muciniphila impacts group B Streptococcus vaginal colonization.
mBio [Epub ahead of print].
Streptococcus agalactiae, or group B Streptococcus (GBS), is an opportunistic pathogen that asymptomatically colonizes the vaginal tract of up to 30% of healthy individuals. However, during pregnancy, it is associated with adverse pregnancy outcomes, and GBS can be transmitted to the fetus in utero or the newborn during vaginal birth, resulting in invasive neonatal disease. Previously, we identified that Akkermansia muciniphila increases GBS vaginal persistence in a cohort of human vaginal microbiome samples collected throughout pregnancy and promotes GBS vaginal colonization in a murine model. However, the mechanisms responsible for these observations are unknown. Here, we analyze additional vaginal shotgun metagenomic data sets and show that across independent studies with diverse populations, A. muciniphila-positive samples had higher GBS abundance. We determined that A. muciniphila aggregates with human vaginal isolates of GBS across all serotypes and promotes GBS attachment to human vaginal epithelial cells (hVECs). RNA-sequencing analysis reveals that A. muciniphila changed the expression of 281 unique GBS genes during hVEC co-colonization, many of which are involved in cell wall/membrane/envelope biogenesis. We demonstrate the importance of the GBS capsule and pili for direct interaction with A. muciniphila and increased attachment to hVECs, respectively. Lastly, we found that A. muciniphila promoted GBS aggregation in the murine vaginal lumen and that continual treatment with A. muciniphila reduced GBS vaginal persistence. Our results provide mechanistic insights and further evidence of the impact of A. muciniphila on GBS vaginal colonization and also demonstrate a beneficial potential of A. muciniphila treatment in the vaginal environment.IMPORTANCEGroup B Streptococcus (GBS) is a frequent colonizer of the vaginal tract of healthy people; however, during pregnancy, maternal colonization is associated with adverse pregnancy outcomes. GBS is a leading cause of neonatal sepsis and meningitis, with transmission to neonates occurring either during vaginal delivery or through ascension into the uterus during pregnancy. The influence of the vaginal microbiota on GBS pathogenesis remains greatly underappreciated. We have found that GBS is associated with the mucin-degrading intestinal commensal Akkermansia muciniphila, a newly identified colonizer of the vaginal tract. Our research identifies the mechanistic impact of this commensal organism on GBS aggregation, cell adherence, and gene expression, as well as its therapeutic potential during GBS vaginal colonization. Unraveling relationships between GBS and the vaginal microbiota will improve maternal-fetal health and may facilitate the development of alternative methods to reduce GBS in utero complications and neonatal disease.
Additional Links: PMID-42041249
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@article {pmid42041249,
year = {2026},
author = {Marroquin, SM and Cohen, S and Neely, MN and Doran, KS},
title = {Akkermansia muciniphila impacts group B Streptococcus vaginal colonization.},
journal = {mBio},
volume = {},
number = {},
pages = {e0286825},
doi = {10.1128/mbio.02868-25},
pmid = {42041249},
issn = {2150-7511},
support = {F32 AI186285/AI/NIAID NIH HHS/United States ; L40 HD116358/HD/NICHD NIH HHS/United States ; R01 AI153332/AI/NIAID NIH HHS/United States ; R21 AI186346/AI/NIAID NIH HHS/United States ; },
abstract = {Streptococcus agalactiae, or group B Streptococcus (GBS), is an opportunistic pathogen that asymptomatically colonizes the vaginal tract of up to 30% of healthy individuals. However, during pregnancy, it is associated with adverse pregnancy outcomes, and GBS can be transmitted to the fetus in utero or the newborn during vaginal birth, resulting in invasive neonatal disease. Previously, we identified that Akkermansia muciniphila increases GBS vaginal persistence in a cohort of human vaginal microbiome samples collected throughout pregnancy and promotes GBS vaginal colonization in a murine model. However, the mechanisms responsible for these observations are unknown. Here, we analyze additional vaginal shotgun metagenomic data sets and show that across independent studies with diverse populations, A. muciniphila-positive samples had higher GBS abundance. We determined that A. muciniphila aggregates with human vaginal isolates of GBS across all serotypes and promotes GBS attachment to human vaginal epithelial cells (hVECs). RNA-sequencing analysis reveals that A. muciniphila changed the expression of 281 unique GBS genes during hVEC co-colonization, many of which are involved in cell wall/membrane/envelope biogenesis. We demonstrate the importance of the GBS capsule and pili for direct interaction with A. muciniphila and increased attachment to hVECs, respectively. Lastly, we found that A. muciniphila promoted GBS aggregation in the murine vaginal lumen and that continual treatment with A. muciniphila reduced GBS vaginal persistence. Our results provide mechanistic insights and further evidence of the impact of A. muciniphila on GBS vaginal colonization and also demonstrate a beneficial potential of A. muciniphila treatment in the vaginal environment.IMPORTANCEGroup B Streptococcus (GBS) is a frequent colonizer of the vaginal tract of healthy people; however, during pregnancy, maternal colonization is associated with adverse pregnancy outcomes. GBS is a leading cause of neonatal sepsis and meningitis, with transmission to neonates occurring either during vaginal delivery or through ascension into the uterus during pregnancy. The influence of the vaginal microbiota on GBS pathogenesis remains greatly underappreciated. We have found that GBS is associated with the mucin-degrading intestinal commensal Akkermansia muciniphila, a newly identified colonizer of the vaginal tract. Our research identifies the mechanistic impact of this commensal organism on GBS aggregation, cell adherence, and gene expression, as well as its therapeutic potential during GBS vaginal colonization. Unraveling relationships between GBS and the vaginal microbiota will improve maternal-fetal health and may facilitate the development of alternative methods to reduce GBS in utero complications and neonatal disease.},
}
RevDate: 2026-04-27
Insects shape the cadaver decomposition microbiome and postmortem interval estimation accuracy.
mSystems [Epub ahead of print].
The breakdown and recycling of carrion is a crucial ecological process that largely relies on a community of necrophagous insects and microbes. Recent work has shown that a specialized microbial network, likely dispersed throughout the environment by insects, assembles during cadaver decomposition to break down flesh regardless of climate and geography. Because of their broad distribution and successional nature, decomposer microbes have been used in machine learning models to predict the postmortem interval (PMI) of human remains, an important contribution to the field of forensics. How factors such as an indoor environment, which alters insect activity, impact the composition of microbial communities decomposing human remains is unclear. Here, we investigate the effects of enclosed shelter on microbial community assembly and successional patterns during human decomposition and provide important considerations for PMI modeling. Compared to outdoor cadavers, we show that indoor cadavers experienced delayed colonization of key decomposer microbes over the course of decomposition due to restricted insect access. Consequently, machine learning models trained on outdoor cadavers frequently underestimated the PMI of cadavers decomposing indoors. Delayed colonization by blow fly maggots (Diptera: Calliphoridae) was correlated with higher PMI prediction errors, suggesting that insects are an important source of microbial decomposers that drive PMI model predictions. Incorporating microbial data from indoor cadavers and insect activity into PMI models significantly improved prediction capabilities for both indoor and outdoor decomposition environments. Ultimately, we demonstrate the important role insects play in the maintenance and distribution of microbes that help to recycle vertebrate remains.IMPORTANCEMicrobes are critical for the decomposition and recycling of organic matter. Recently, microbiome-based models have shown promising performance in estimating the postmortem interval (PMI). However, many deaths occur indoors, yet no studies have investigated the impact of enclosed shelter on the cadaver microbiome in a controlled setting. Here, cadavers were decomposed indoors, and we found that blow fly maggots serve as an important source of decomposer taxa that significantly alter the cadaver microbiome following infestation. Notably, PMI estimation models trained on outdoor data sets failed to accurately predict the PMI when insect colonization was delayed. We show that incorporating 16S rRNA amplicon data from cadavers decomposing indoors, along with environmental variables, significantly improves PMI estimates, suggesting a microbiome-based forensic tool may be feasible across decomposition environments. Importantly, this research demonstrates the critical ecological role insects play in the dispersal of specialized microbes that are involved in the breakdown and recycling of vertebrate remains.
Additional Links: PMID-42041258
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PubMed:
Citation:
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@article {pmid42041258,
year = {2026},
author = {Nieciecki, V and Seitz, VA and Burcham, ZM and Otto, K and Cantrell, K and Kirkland, J and Ackermann, G and Knight, R and Lynne, A and Metcalf, JL and Bucheli, S},
title = {Insects shape the cadaver decomposition microbiome and postmortem interval estimation accuracy.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0068125},
doi = {10.1128/msystems.00681-25},
pmid = {42041258},
issn = {2379-5077},
abstract = {The breakdown and recycling of carrion is a crucial ecological process that largely relies on a community of necrophagous insects and microbes. Recent work has shown that a specialized microbial network, likely dispersed throughout the environment by insects, assembles during cadaver decomposition to break down flesh regardless of climate and geography. Because of their broad distribution and successional nature, decomposer microbes have been used in machine learning models to predict the postmortem interval (PMI) of human remains, an important contribution to the field of forensics. How factors such as an indoor environment, which alters insect activity, impact the composition of microbial communities decomposing human remains is unclear. Here, we investigate the effects of enclosed shelter on microbial community assembly and successional patterns during human decomposition and provide important considerations for PMI modeling. Compared to outdoor cadavers, we show that indoor cadavers experienced delayed colonization of key decomposer microbes over the course of decomposition due to restricted insect access. Consequently, machine learning models trained on outdoor cadavers frequently underestimated the PMI of cadavers decomposing indoors. Delayed colonization by blow fly maggots (Diptera: Calliphoridae) was correlated with higher PMI prediction errors, suggesting that insects are an important source of microbial decomposers that drive PMI model predictions. Incorporating microbial data from indoor cadavers and insect activity into PMI models significantly improved prediction capabilities for both indoor and outdoor decomposition environments. Ultimately, we demonstrate the important role insects play in the maintenance and distribution of microbes that help to recycle vertebrate remains.IMPORTANCEMicrobes are critical for the decomposition and recycling of organic matter. Recently, microbiome-based models have shown promising performance in estimating the postmortem interval (PMI). However, many deaths occur indoors, yet no studies have investigated the impact of enclosed shelter on the cadaver microbiome in a controlled setting. Here, cadavers were decomposed indoors, and we found that blow fly maggots serve as an important source of decomposer taxa that significantly alter the cadaver microbiome following infestation. Notably, PMI estimation models trained on outdoor data sets failed to accurately predict the PMI when insect colonization was delayed. We show that incorporating 16S rRNA amplicon data from cadavers decomposing indoors, along with environmental variables, significantly improves PMI estimates, suggesting a microbiome-based forensic tool may be feasible across decomposition environments. Importantly, this research demonstrates the critical ecological role insects play in the dispersal of specialized microbes that are involved in the breakdown and recycling of vertebrate remains.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Antibiotic Mechanisms and Resistance: Molecular Insights and Therapeutic Strategies.
Antibiotics (Basel, Switzerland), 15(4):.
Antibiotic resistance is a critical global health threat, already causing over 1.27 million deaths annually and projected to exceed 10 million by 2050. This crisis is compounded by stagnation in novel antibiotic discovery, highlighting the need for mechanism-based innovation. Here, we provide an integrative framework linking antibiotic mechanisms of action, bacterial resistance pathways, and emerging therapeutic strategies. Antibiotics are systematically categorized by their molecular targets, cell wall synthesis, membrane integrity, nucleic acid replication, protein synthesis, and metabolic pathways, while resistance mechanisms are outlined in parallel, including enzymatic degradation, target modification, efflux, and permeability barriers. We further highlight novel approaches such as structure-guided drug design, synergistic combinations, nanoparticle delivery, and artificial intelligence-driven discovery. Precision medicine and microbiome modulation are also emphasized as next-generation interventions. By bridging molecular mechanisms with translational strategies, this review outlines opportunities to guide antibiotic innovation and advance precision therapies against the escalating threat of antimicrobial resistance.
Additional Links: PMID-42041314
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@article {pmid42041314,
year = {2026},
author = {Ma, H and Zhang, L and Wang, L and Yang, Z and Liu, J and Sun, H and Ge, S and Quan, C},
title = {Antibiotic Mechanisms and Resistance: Molecular Insights and Therapeutic Strategies.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {4},
pages = {},
pmid = {42041314},
issn = {2079-6382},
support = {2022020332-JH2/1013//Applied Basic Research Project of Liaoning Provincial Science and Technology Department/ ; LJKMZ20220401//Basic scientific research projects of Liaoning Provincial Department of Education/ ; },
abstract = {Antibiotic resistance is a critical global health threat, already causing over 1.27 million deaths annually and projected to exceed 10 million by 2050. This crisis is compounded by stagnation in novel antibiotic discovery, highlighting the need for mechanism-based innovation. Here, we provide an integrative framework linking antibiotic mechanisms of action, bacterial resistance pathways, and emerging therapeutic strategies. Antibiotics are systematically categorized by their molecular targets, cell wall synthesis, membrane integrity, nucleic acid replication, protein synthesis, and metabolic pathways, while resistance mechanisms are outlined in parallel, including enzymatic degradation, target modification, efflux, and permeability barriers. We further highlight novel approaches such as structure-guided drug design, synergistic combinations, nanoparticle delivery, and artificial intelligence-driven discovery. Precision medicine and microbiome modulation are also emphasized as next-generation interventions. By bridging molecular mechanisms with translational strategies, this review outlines opportunities to guide antibiotic innovation and advance precision therapies against the escalating threat of antimicrobial resistance.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Targeting Bacterial Infections in Periodontal Disease: From Conventional Antibiotics to Next-Generation Therapeutics.
Antibiotics (Basel, Switzerland), 15(4):.
Periodontitis is a highly prevalent chronic inflammatory disease with significant oral and systemic consequences, including associations with cardiovascular disease, diabetes, and adverse pregnancy outcomes. Although mechanical debridement remains the cornerstone of therapy, adjunctive antibiotic use is increasingly limited by antimicrobial resistance, biofilm-associated tolerance, pharmacokinetic constraints, and disruption of the commensal microbiome, leading to inconsistent outcomes and disease recurrence. This review highlights the mechanistic limitations of conventional antibiotic therapies in periodontitis and critically examines emerging next-generation therapeutic strategies aimed at overcoming these challenges. Specifically, it explores antimicrobial peptides, quorum sensing inhibitors, nanotechnology-based drug delivery systems, host modulation approaches, and microbiome-targeted therapies, with emphasis on their molecular mechanisms, clinical relevance, and translational potential. By integrating microbial, host, and pharmacological perspectives, this review provides a comprehensive framework for advancing precision-guided periodontal therapy and supports the shift toward targeted, sustainable, and personalized treatment strategies.
Additional Links: PMID-42041360
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@article {pmid42041360,
year = {2026},
author = {Hashim, NT and Babiker, R and Rahman, MM and Mohammed, R and Padmanabhan, V and Islam, MS and Elsheikh, M and Abduljalil, SMA and Mahmoud, G and Chaitanya, NCSK and Siriwardena, BSMS and Ahmed, A and Gismalla, BG},
title = {Targeting Bacterial Infections in Periodontal Disease: From Conventional Antibiotics to Next-Generation Therapeutics.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {4},
pages = {},
pmid = {42041360},
issn = {2079-6382},
abstract = {Periodontitis is a highly prevalent chronic inflammatory disease with significant oral and systemic consequences, including associations with cardiovascular disease, diabetes, and adverse pregnancy outcomes. Although mechanical debridement remains the cornerstone of therapy, adjunctive antibiotic use is increasingly limited by antimicrobial resistance, biofilm-associated tolerance, pharmacokinetic constraints, and disruption of the commensal microbiome, leading to inconsistent outcomes and disease recurrence. This review highlights the mechanistic limitations of conventional antibiotic therapies in periodontitis and critically examines emerging next-generation therapeutic strategies aimed at overcoming these challenges. Specifically, it explores antimicrobial peptides, quorum sensing inhibitors, nanotechnology-based drug delivery systems, host modulation approaches, and microbiome-targeted therapies, with emphasis on their molecular mechanisms, clinical relevance, and translational potential. By integrating microbial, host, and pharmacological perspectives, this review provides a comprehensive framework for advancing precision-guided periodontal therapy and supports the shift toward targeted, sustainable, and personalized treatment strategies.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Gut Microbiota and Acute Myeloid Leukemia: State of the Art, Clinical Signals, and Translational Opportunities.
Antibiotics (Basel, Switzerland), 15(4):.
Acute myeloid leukemia (AML) remains a highly morbid malignancy in which outcomes are constrained not only by disease refractoriness and relapse, but also by therapy-related toxicity-particularly infections, mucosal injury, and delayed hematopoietic reconstitution. The gut microbiota has emerged as a potentially modifiable layer of host vulnerability and resilience during AML treatment. Microbiome disruption is detectable already at diagnosis, even in antibiotic-naïve patients, and is often characterized by reduced community diversity, depletion of anaerobic taxa linked to short-chain fatty acids (SCFAs) production, and enrichment of pathobiont-associated profiles. During induction, cytotoxic therapy and antimicrobials precipitates diversity loss, domination events, and persistent shifts beyond discharge. Clinically, the most consistent translational signal is the association between baseline or early-treatment microbiome features and infectious outcomes, while emerging data suggest that diagnosis-time microbiome structure may also relate to hematologic recovery kinetics. Mechanistic models converge on pathways linking barrier integrity, microbial metabolites (notably butyrate and other SCFAs), immune calibration, and inflammatory translocation of microbial products. These insights support hypotheses: antimicrobial stewardship may preserve microbiome function; ecosystem repair strategies such as autologous fecal microbiota transfer (A-FMT) are feasible and can restore community structure; and metabolite or nutritional interventions merit evaluation in immunocompromised hosts. Regimen-specific microbiome effects and microbiome-drug interactions suggest that treatment choice could have downstream microbiome-mediated consequences. We synthesize evidence, outline interventional concepts, and define methodological priorities for next-generation trials assessing causality and clinical benefit. Progress will require longitudinal sampling, multi-omic integration (metabolomics, resistomics, and barrier/inflammatory biomarkers), and interventional designs linking microbiome dynamics to clinically meaningful outcomes.
Additional Links: PMID-42041380
PubMed:
Citation:
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@article {pmid42041380,
year = {2026},
author = {Alvaro, ME and Caserta, S and Martino, EA and Skafi, M and Bruzzese, A and Amodio, N and Lucia, E and Olivito, V and Labanca, C and Mendicino, F and Vigna, E and Morabito, F and Gentile, M},
title = {Gut Microbiota and Acute Myeloid Leukemia: State of the Art, Clinical Signals, and Translational Opportunities.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {4},
pages = {},
pmid = {42041380},
issn = {2079-6382},
abstract = {Acute myeloid leukemia (AML) remains a highly morbid malignancy in which outcomes are constrained not only by disease refractoriness and relapse, but also by therapy-related toxicity-particularly infections, mucosal injury, and delayed hematopoietic reconstitution. The gut microbiota has emerged as a potentially modifiable layer of host vulnerability and resilience during AML treatment. Microbiome disruption is detectable already at diagnosis, even in antibiotic-naïve patients, and is often characterized by reduced community diversity, depletion of anaerobic taxa linked to short-chain fatty acids (SCFAs) production, and enrichment of pathobiont-associated profiles. During induction, cytotoxic therapy and antimicrobials precipitates diversity loss, domination events, and persistent shifts beyond discharge. Clinically, the most consistent translational signal is the association between baseline or early-treatment microbiome features and infectious outcomes, while emerging data suggest that diagnosis-time microbiome structure may also relate to hematologic recovery kinetics. Mechanistic models converge on pathways linking barrier integrity, microbial metabolites (notably butyrate and other SCFAs), immune calibration, and inflammatory translocation of microbial products. These insights support hypotheses: antimicrobial stewardship may preserve microbiome function; ecosystem repair strategies such as autologous fecal microbiota transfer (A-FMT) are feasible and can restore community structure; and metabolite or nutritional interventions merit evaluation in immunocompromised hosts. Regimen-specific microbiome effects and microbiome-drug interactions suggest that treatment choice could have downstream microbiome-mediated consequences. We synthesize evidence, outline interventional concepts, and define methodological priorities for next-generation trials assessing causality and clinical benefit. Progress will require longitudinal sampling, multi-omic integration (metabolomics, resistomics, and barrier/inflammatory biomarkers), and interventional designs linking microbiome dynamics to clinically meaningful outcomes.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
How Glyphosate and Its Derivatives Influence Antimicrobial Resistance Emergence and Transmission: A One Health Perspective.
Antibiotics (Basel, Switzerland), 15(4):.
Background/Objectives: Glyphosate-based formulations are globally pervasive pollutants increasingly recognized as potential contributors to antimicrobial resistance (AMR) in environmental microbiomes. Although glyphosate is designed to inhibit plant 5-enolpyruvylshikimate-3-phosphate synthase, it also affects microbial metabolism, stress response, and genetic exchange. This review synthesizes the pathways through which glyphosate, its metabolite aminomethylphosphonic acid (AMPA), and commercial mixtures influence resistance-associated phenotypes and the dissemination of antibiotic resistance (ABR). Methods: A critical synthesis of the literature was conducted to evaluate the mechanistic and ecological interactions between glyphosate exposure and bacterial resistance in soil, aquatic, and host-associated microbiomes. Results: Experimental evidence showed that sublethal glyphosate exposure induced oxidative stress, altered membrane permeability, activated multidrug efflux pumps, and promoted tolerance phenotypes that could modify antibiotic susceptibility. It also enhances mutation rates and horizontal gene transfer processes associated with the emergence of resistance under controlled conditions. At the community level, glyphosate exposure is associated with microbiome restructuring and enrichment of resistance determinants, often without major shifts in overall diversity of the microbiome. These effects have been reported at environmentally relevant concentrations, although the evidence remains largely derived from laboratory and mesocosm studies. Conclusions: Glyphosate acts as both a biochemical modulator of resistance-related phenotypes and an environmental selective pressure that shapes microbial communities. Its widespread use and environmental persistence position it as a context-dependent contributor to the emergence and dissemination of AMR through interacting mechanistic and ecological pathways. Integrating AMR endpoints into pesticide risk assessments and surveillance frameworks is warranted, in addition to expanded field-based validation.
Additional Links: PMID-42041382
PubMed:
Citation:
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@article {pmid42041382,
year = {2026},
author = {Malinoski, L and Silva, GG and Rodrigues, LKI and Carneiro, LF and Gomes, MP},
title = {How Glyphosate and Its Derivatives Influence Antimicrobial Resistance Emergence and Transmission: A One Health Perspective.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {4},
pages = {},
pmid = {42041382},
issn = {2079-6382},
support = {302226/2022-2//National Council for Scientific and Technological Development/ ; SUS2025831000005//Fundação Araucária/ ; },
abstract = {Background/Objectives: Glyphosate-based formulations are globally pervasive pollutants increasingly recognized as potential contributors to antimicrobial resistance (AMR) in environmental microbiomes. Although glyphosate is designed to inhibit plant 5-enolpyruvylshikimate-3-phosphate synthase, it also affects microbial metabolism, stress response, and genetic exchange. This review synthesizes the pathways through which glyphosate, its metabolite aminomethylphosphonic acid (AMPA), and commercial mixtures influence resistance-associated phenotypes and the dissemination of antibiotic resistance (ABR). Methods: A critical synthesis of the literature was conducted to evaluate the mechanistic and ecological interactions between glyphosate exposure and bacterial resistance in soil, aquatic, and host-associated microbiomes. Results: Experimental evidence showed that sublethal glyphosate exposure induced oxidative stress, altered membrane permeability, activated multidrug efflux pumps, and promoted tolerance phenotypes that could modify antibiotic susceptibility. It also enhances mutation rates and horizontal gene transfer processes associated with the emergence of resistance under controlled conditions. At the community level, glyphosate exposure is associated with microbiome restructuring and enrichment of resistance determinants, often without major shifts in overall diversity of the microbiome. These effects have been reported at environmentally relevant concentrations, although the evidence remains largely derived from laboratory and mesocosm studies. Conclusions: Glyphosate acts as both a biochemical modulator of resistance-related phenotypes and an environmental selective pressure that shapes microbial communities. Its widespread use and environmental persistence position it as a context-dependent contributor to the emergence and dissemination of AMR through interacting mechanistic and ecological pathways. Integrating AMR endpoints into pesticide risk assessments and surveillance frameworks is warranted, in addition to expanded field-based validation.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Evaluation of the Antifungal Activity of the Polyphenol Formulation Viroelixir Against Candida albicans.
Antibiotics (Basel, Switzerland), 15(4):.
UNLABELLED: Candida albicans (C. albicans) is an opportunistic fungal pathogen capable of causing a wide range of infections, including mucosal and systemic candidiasis. In the oral cavity, fungi represent a minor component of the microbiome but can significantly contribute to morbidity, particularly under conditions of dysbiosis or immunosuppression. Treatment remains challenging due to increasing multidrug resistance. This study investigates the in vitro antifungal potential of Viroelixir, a standardized polyphenol blend derived from green tea and pomegranate and enriched in catechins (including epigallocatechin gallate, EGCG), ellagitannins (notably punicalagin), ellagic acid, and flavonoids, with particular focus on its potential anti-virulence mechanisms.
METHODS: The effect of Viroelixir on C. albicans growth was assessed using MTT assay, optical density measurements, colony formation, carbohydrate quantification, and pH variation analysis. Biofilm formation, morphological transition, ROS production, necrosis, virulence gene expression, adhesion, and host immune responses were also evaluated.
RESULTS: Viroelixir significantly inhibited C. albicans growth and reduced colony formation compared with untreated controls. The formulation also inhibited biofilm formation and markedly reduced pseudohyphal development, reaching up to 94% reduction under specific treatment conditions. Flow cytometry analysis showed an increase in dead fungal cells, reaching approximately 88% following exposure to Viroelixir at the highest tested concentration. In addition, Viroelixir reduced the transcript levels of several virulence-associated genes, including SAP1-SAP9 and EAP1. In epithelial cell co-culture models, pre-treatment of C. albicans with Viroelixir reduced fungal adhesion and attenuated epithelial inflammatory responses, including IL-6, IL-8, and hBD-2 production, and was associated with reduced activation of the TLR4-NF-κB signaling pathway.
CONCLUSIONS: These findings suggest that the antifungal and anti-virulence effects observed may be associated with the polyphenolic compounds present in the Viroelixir formulation, highlighting its potential as a promising in vitro antifungal candidate against C. albicans.
Additional Links: PMID-42041383
PubMed:
Citation:
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@article {pmid42041383,
year = {2026},
author = {Dahdah, M and Ettouil, Y and Issa, H and Koussih, L and Almutairi, MH and Rouabhia, M and Semlali, A},
title = {Evaluation of the Antifungal Activity of the Polyphenol Formulation Viroelixir Against Candida albicans.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {4},
pages = {},
pmid = {42041383},
issn = {2079-6382},
abstract = {UNLABELLED: Candida albicans (C. albicans) is an opportunistic fungal pathogen capable of causing a wide range of infections, including mucosal and systemic candidiasis. In the oral cavity, fungi represent a minor component of the microbiome but can significantly contribute to morbidity, particularly under conditions of dysbiosis or immunosuppression. Treatment remains challenging due to increasing multidrug resistance. This study investigates the in vitro antifungal potential of Viroelixir, a standardized polyphenol blend derived from green tea and pomegranate and enriched in catechins (including epigallocatechin gallate, EGCG), ellagitannins (notably punicalagin), ellagic acid, and flavonoids, with particular focus on its potential anti-virulence mechanisms.
METHODS: The effect of Viroelixir on C. albicans growth was assessed using MTT assay, optical density measurements, colony formation, carbohydrate quantification, and pH variation analysis. Biofilm formation, morphological transition, ROS production, necrosis, virulence gene expression, adhesion, and host immune responses were also evaluated.
RESULTS: Viroelixir significantly inhibited C. albicans growth and reduced colony formation compared with untreated controls. The formulation also inhibited biofilm formation and markedly reduced pseudohyphal development, reaching up to 94% reduction under specific treatment conditions. Flow cytometry analysis showed an increase in dead fungal cells, reaching approximately 88% following exposure to Viroelixir at the highest tested concentration. In addition, Viroelixir reduced the transcript levels of several virulence-associated genes, including SAP1-SAP9 and EAP1. In epithelial cell co-culture models, pre-treatment of C. albicans with Viroelixir reduced fungal adhesion and attenuated epithelial inflammatory responses, including IL-6, IL-8, and hBD-2 production, and was associated with reduced activation of the TLR4-NF-κB signaling pathway.
CONCLUSIONS: These findings suggest that the antifungal and anti-virulence effects observed may be associated with the polyphenolic compounds present in the Viroelixir formulation, highlighting its potential as a promising in vitro antifungal candidate against C. albicans.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Rapid Electrochemical Profiling of Fecal Short-Chain Fatty Acids Using Esterification/Dissociation Fingerprints and Artificial Neural Networks.
Biosensors, 16(4):.
Short-chain fatty acids (SCFAs) are key biomarkers of gut microbiota activity; however, routine quantification in fecal samples relies largely on chromatography, which is instrument-intensive and throughput-limited chromatography techniques. Herein, we present a rapid machine-learning-assisted electroanalysis platform for SCFAs profiling that integrates a disposable three-electrode planar gold chip with voltammetric fingerprinting and artificial neural network (ANN)-based signal decoupling. To generate orthogonal chemical information and improve the discrimination of structurally similar species, a dual pretreatment strategy combining acid-catalyzed esterification and alkaline dissociation was employed prior to electrochemical analyses. Differential pulse voltammetry (DPV) and cyclic voltammetry (CV) were employed to acquire high-dimensional fingerprints, from which current-, potential-, and area-based descriptors were extracted using a cross-information feature strategy. A hierarchical modeling framework improved total SCFAs prediction by incorporating ANN-predicted propionate and butyrate concentrations as auxiliary inputs. While linear calibration was achievable in standard mixtures, direct linear models performed poorly in real fecal matrices due to strong sample-dependent matrix interference. In contrast, the ANN captured nonlinear relationships among multifeature inputs and suppressed matrix effects. Validation against gas chromatography-mass spectrometry in an independent fecal test cohort (n = 30) demonstrated excellent agreement and low prediction errors, with mean absolute error/root mean square error values of 0.063/0.072 mM (propionic acid), 0.029/0.034 mM (butyric acid), and 0.135/0.202 mM (total SCFAs). The DPV/CV acquisition requires only minutes per sample, whereas pretreatment takes 1~3 h depending on the target route but can be performed in parallel for batch processing; thus, overall throughput is determined mainly by batch pretreatment rather than per-sample instrument time. This electrochemical-ANN workflow provides a portable, high-throughput alternative to chromatography for fecal SCFAs profiling in clinical screening and microbiome research.
Additional Links: PMID-42041444
PubMed:
Citation:
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@article {pmid42041444,
year = {2026},
author = {Gu, BC and Jiang, GY and Tseng, CH and Chen, YJ and Wu, CY and Lin, ZX and Yeh, ZW and Wu, CC},
title = {Rapid Electrochemical Profiling of Fecal Short-Chain Fatty Acids Using Esterification/Dissociation Fingerprints and Artificial Neural Networks.},
journal = {Biosensors},
volume = {16},
number = {4},
pages = {},
pmid = {42041444},
issn = {2079-6374},
support = {112-2221-E-005-087//National Science and Technology Council/ ; 113-2622-E-005-005//National Science and Technology Council/ ; 113-2221-E-005-058//National Science and Technology Council/ ; 114-2221-E-005-047-MY2//National Science and Technology Council/ ; },
mesh = {*Neural Networks, Computer ; *Feces/chemistry ; *Fatty Acids, Volatile/analysis ; Humans ; Esterification ; *Electrochemical Techniques ; Gas Chromatography-Mass Spectrometry ; Gastrointestinal Microbiome ; *Biosensing Techniques ; },
abstract = {Short-chain fatty acids (SCFAs) are key biomarkers of gut microbiota activity; however, routine quantification in fecal samples relies largely on chromatography, which is instrument-intensive and throughput-limited chromatography techniques. Herein, we present a rapid machine-learning-assisted electroanalysis platform for SCFAs profiling that integrates a disposable three-electrode planar gold chip with voltammetric fingerprinting and artificial neural network (ANN)-based signal decoupling. To generate orthogonal chemical information and improve the discrimination of structurally similar species, a dual pretreatment strategy combining acid-catalyzed esterification and alkaline dissociation was employed prior to electrochemical analyses. Differential pulse voltammetry (DPV) and cyclic voltammetry (CV) were employed to acquire high-dimensional fingerprints, from which current-, potential-, and area-based descriptors were extracted using a cross-information feature strategy. A hierarchical modeling framework improved total SCFAs prediction by incorporating ANN-predicted propionate and butyrate concentrations as auxiliary inputs. While linear calibration was achievable in standard mixtures, direct linear models performed poorly in real fecal matrices due to strong sample-dependent matrix interference. In contrast, the ANN captured nonlinear relationships among multifeature inputs and suppressed matrix effects. Validation against gas chromatography-mass spectrometry in an independent fecal test cohort (n = 30) demonstrated excellent agreement and low prediction errors, with mean absolute error/root mean square error values of 0.063/0.072 mM (propionic acid), 0.029/0.034 mM (butyric acid), and 0.135/0.202 mM (total SCFAs). The DPV/CV acquisition requires only minutes per sample, whereas pretreatment takes 1~3 h depending on the target route but can be performed in parallel for batch processing; thus, overall throughput is determined mainly by batch pretreatment rather than per-sample instrument time. This electrochemical-ANN workflow provides a portable, high-throughput alternative to chromatography for fecal SCFAs profiling in clinical screening and microbiome research.},
}
MeSH Terms:
show MeSH Terms
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*Neural Networks, Computer
*Feces/chemistry
*Fatty Acids, Volatile/analysis
Humans
Esterification
*Electrochemical Techniques
Gas Chromatography-Mass Spectrometry
Gastrointestinal Microbiome
*Biosensing Techniques
RevDate: 2026-04-27
CmpDate: 2026-04-27
Immunosenescence and Inflammaging as Drivers of Neurodegeneration: Cellular Mechanisms, Neuroimmune Crosstalk, and Therapeutic Implications.
Cells, 15(8):.
Aging is accompanied by profound alterations in immune function, termed immunosenescence, and by a chronic, low-grade inflammatory state known as inflammaging. These processes are increasingly recognized as central drivers of age-related neurodegenerative diseases, including Alzheimer's Disease, Parkinson's Disease, Amyotrophic Lateral Sclerosis and Multiple Sclerosis. In the central nervous system, senescent microglia and astrocytes lose their homeostatic and neuroprotective functions, while systemic immune aging and blood-brain barrier dysfunction further amplify neuroinflammation and impair protein aggregate clearance. This sustained pro-inflammatory environment promotes synaptic dysfunction, neuronal loss and cognitive decline. Here, we synthesize current knowledge of the mechanistic links among immunosenescence, inflammaging, and neurodegeneration, highlighting innate and adaptive immune dysregulation, mitochondrial impairment, and failed resolution pathways. We further discuss emerging therapeutic strategies, including senolytics, immunoceuticals, microbiome-based interventions and advanced drug delivery systems, aimed at restoring immune homeostasis and enhancing brain resilience. By integrating mechanistic and translational insights, this review provides a framework for developing novel interventions to target immune aging in neurodegenerative diseases.
Additional Links: PMID-42041525
PubMed:
Citation:
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@article {pmid42041525,
year = {2026},
author = {Bertoni, G and Ristori, S and Monti, D},
title = {Immunosenescence and Inflammaging as Drivers of Neurodegeneration: Cellular Mechanisms, Neuroimmune Crosstalk, and Therapeutic Implications.},
journal = {Cells},
volume = {15},
number = {8},
pages = {},
pmid = {42041525},
issn = {2073-4409},
support = {DM 1557 11.10.2022//Next Generation EU/ ; },
mesh = {Humans ; *Immunosenescence/immunology ; *Neurodegenerative Diseases/immunology/pathology/therapy ; *Inflammation/immunology/pathology ; Animals ; *Aging/immunology ; *Neuroimmunomodulation ; },
abstract = {Aging is accompanied by profound alterations in immune function, termed immunosenescence, and by a chronic, low-grade inflammatory state known as inflammaging. These processes are increasingly recognized as central drivers of age-related neurodegenerative diseases, including Alzheimer's Disease, Parkinson's Disease, Amyotrophic Lateral Sclerosis and Multiple Sclerosis. In the central nervous system, senescent microglia and astrocytes lose their homeostatic and neuroprotective functions, while systemic immune aging and blood-brain barrier dysfunction further amplify neuroinflammation and impair protein aggregate clearance. This sustained pro-inflammatory environment promotes synaptic dysfunction, neuronal loss and cognitive decline. Here, we synthesize current knowledge of the mechanistic links among immunosenescence, inflammaging, and neurodegeneration, highlighting innate and adaptive immune dysregulation, mitochondrial impairment, and failed resolution pathways. We further discuss emerging therapeutic strategies, including senolytics, immunoceuticals, microbiome-based interventions and advanced drug delivery systems, aimed at restoring immune homeostasis and enhancing brain resilience. By integrating mechanistic and translational insights, this review provides a framework for developing novel interventions to target immune aging in neurodegenerative diseases.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Immunosenescence/immunology
*Neurodegenerative Diseases/immunology/pathology/therapy
*Inflammation/immunology/pathology
Animals
*Aging/immunology
*Neuroimmunomodulation
RevDate: 2026-04-27
CmpDate: 2026-04-27
Exosomal microRNAs from Alveolar Macrophages Reveal a Protective Role of the Lung Microbiome Against Oncogenic Signaling During PAH Exposure.
Cells, 15(8):.
Polycyclic aromatic hydrocarbons (PAHs), such as benzo[a]pyrene (B[a]P), are major risk factors for lung cancer and other diseases, acting through the aryl hydrocarbon receptor (AHR). Alveolar macrophages (AMs) help regulate the lung microenvironment by responding to inhaled toxicants and resident microbiota. Although small extracellular vesicles (sEVs, aka exosomes) released by AMs mediate intercellular communication and immune responses, the influence of lung microbiota on sEV biogenesis and the mechanisms underlying sEV dysregulation during PAH exposure remain unknown. Here, we investigated the interplay between AMs, B[a]P, and lung microbiota, focusing on sEV-associated miRNAs (exo-miRNAs). Murine AMs (MH-S) were exposed to varying B[a]P concentrations in the presence or absence of murine lung microbiota with or without an AHR antagonist. sEVs from each condition were characterized and profiled for miRNA. Distinct miRNA signatures emerged: high-dose B[a]P enriched miRNAs linked to cancer progression, whereas lung microbiota alone or with low-dose B[a]P induced tumor-suppressor miRNAs that limit proliferation and metastasis and promote apoptosis, an effect enhanced by AHR antagonism. Lung microbiota appeared to counteract high-dose B[a]P by modulating tumor-suppressive exo-miRNAs. This study demonstrates that lung microbiota-induced exo-miRNAs critically shape AM-derived sEV-miRNA signaling during PAH exposure. The identified exosomal miRNAs could serve as important exposure biomarkers and therapeutic targets for mitigating B[a]P-induced toxicity and cancer development.
Additional Links: PMID-42041582
PubMed:
Citation:
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@article {pmid42041582,
year = {2026},
author = {Chandra, H and Yadav, B and Kuhnell, D and Langevin, S and Biesiada, J and Medvedovic, M and Yadav, JS},
title = {Exosomal microRNAs from Alveolar Macrophages Reveal a Protective Role of the Lung Microbiome Against Oncogenic Signaling During PAH Exposure.},
journal = {Cells},
volume = {15},
number = {8},
pages = {},
pmid = {42041582},
issn = {2073-4409},
support = {P30ES006096//NIH /NIEHS/ ; },
mesh = {Animals ; *MicroRNAs/metabolism/genetics ; *Exosomes/metabolism/genetics/drug effects ; *Macrophages, Alveolar/metabolism/drug effects ; Mice ; *Lung/microbiology/drug effects ; Signal Transduction/drug effects ; *Microbiota/drug effects ; Benzo(a)pyrene/toxicity ; Receptors, Aryl Hydrocarbon/metabolism ; Mice, Inbred C57BL ; *Polycyclic Aromatic Hydrocarbons/toxicity ; *Carcinogenesis/drug effects/genetics ; Lung Neoplasms/genetics ; },
abstract = {Polycyclic aromatic hydrocarbons (PAHs), such as benzo[a]pyrene (B[a]P), are major risk factors for lung cancer and other diseases, acting through the aryl hydrocarbon receptor (AHR). Alveolar macrophages (AMs) help regulate the lung microenvironment by responding to inhaled toxicants and resident microbiota. Although small extracellular vesicles (sEVs, aka exosomes) released by AMs mediate intercellular communication and immune responses, the influence of lung microbiota on sEV biogenesis and the mechanisms underlying sEV dysregulation during PAH exposure remain unknown. Here, we investigated the interplay between AMs, B[a]P, and lung microbiota, focusing on sEV-associated miRNAs (exo-miRNAs). Murine AMs (MH-S) were exposed to varying B[a]P concentrations in the presence or absence of murine lung microbiota with or without an AHR antagonist. sEVs from each condition were characterized and profiled for miRNA. Distinct miRNA signatures emerged: high-dose B[a]P enriched miRNAs linked to cancer progression, whereas lung microbiota alone or with low-dose B[a]P induced tumor-suppressor miRNAs that limit proliferation and metastasis and promote apoptosis, an effect enhanced by AHR antagonism. Lung microbiota appeared to counteract high-dose B[a]P by modulating tumor-suppressive exo-miRNAs. This study demonstrates that lung microbiota-induced exo-miRNAs critically shape AM-derived sEV-miRNA signaling during PAH exposure. The identified exosomal miRNAs could serve as important exposure biomarkers and therapeutic targets for mitigating B[a]P-induced toxicity and cancer development.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*MicroRNAs/metabolism/genetics
*Exosomes/metabolism/genetics/drug effects
*Macrophages, Alveolar/metabolism/drug effects
Mice
*Lung/microbiology/drug effects
Signal Transduction/drug effects
*Microbiota/drug effects
Benzo(a)pyrene/toxicity
Receptors, Aryl Hydrocarbon/metabolism
Mice, Inbred C57BL
*Polycyclic Aromatic Hydrocarbons/toxicity
*Carcinogenesis/drug effects/genetics
Lung Neoplasms/genetics
RevDate: 2026-04-27
CmpDate: 2026-04-27
Addressing Research Gaps in Early Childhood Caries: A Comprehensive Review.
Dentistry journal, 14(4):.
Background: Early childhood caries (ECC) is one of the most common chronic diseases in children and remains unevenly distributed across populations. It is associated with pain, impaired function, and long-term health consequences. Although advances have been made in understanding its aetiology and prevention, important gaps in evidence limit progress in prevention, early detection, and equitable care. Objective: To examine current evidence on ECC and identify key research gaps across biological, behavioral, social, and health system domains. Methods: This narrative review draws on peer-reviewed literature addressing ECC epidemiology, pathogenesis, risk factors, diagnosis, management, and service delivery. The literature was examined to identify areas where evidence is limited, inconsistent, or insufficient to inform clinical practice and public health policy. Results: Research on ECC remains uneven across levels. Longitudinal evidence linking microbiome dynamics, host susceptibility, and lesion progression is limited, restricting causal understanding. Genetic and epigenetic contributions are incompletely defined, particularly in diverse populations. Although socioeconomic gradients are well established, integrative models connecting structural determinants with biological mechanisms are scarce. Emerging diagnostic tools, including biomarkers and artificial intelligence, lack robust evidence demonstrating improved clinical or behavioral outcomes. Implementation research addressing scalability, cost-effectiveness, and equity impact is underdeveloped, especially in low-resource settings. Long-term systemic and developmental consequences of ECC remain insufficiently characterized. Conclusions: Addressing ECC requires integrated and equity-oriented research frameworks that bridge biological, social, diagnostic, and implementation domains. Clarifying these gaps is essential to inform coherent prevention strategies and reduce persistent disparities in child oral health.
Additional Links: PMID-42041649
PubMed:
Citation:
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@article {pmid42041649,
year = {2026},
author = {Cheng, AY and Zheng, FM and Chen, J and Chu, CH},
title = {Addressing Research Gaps in Early Childhood Caries: A Comprehensive Review.},
journal = {Dentistry journal},
volume = {14},
number = {4},
pages = {},
pmid = {42041649},
issn = {2304-6767},
support = {17104123//Research Grant Council General Research Fund/ ; },
abstract = {Background: Early childhood caries (ECC) is one of the most common chronic diseases in children and remains unevenly distributed across populations. It is associated with pain, impaired function, and long-term health consequences. Although advances have been made in understanding its aetiology and prevention, important gaps in evidence limit progress in prevention, early detection, and equitable care. Objective: To examine current evidence on ECC and identify key research gaps across biological, behavioral, social, and health system domains. Methods: This narrative review draws on peer-reviewed literature addressing ECC epidemiology, pathogenesis, risk factors, diagnosis, management, and service delivery. The literature was examined to identify areas where evidence is limited, inconsistent, or insufficient to inform clinical practice and public health policy. Results: Research on ECC remains uneven across levels. Longitudinal evidence linking microbiome dynamics, host susceptibility, and lesion progression is limited, restricting causal understanding. Genetic and epigenetic contributions are incompletely defined, particularly in diverse populations. Although socioeconomic gradients are well established, integrative models connecting structural determinants with biological mechanisms are scarce. Emerging diagnostic tools, including biomarkers and artificial intelligence, lack robust evidence demonstrating improved clinical or behavioral outcomes. Implementation research addressing scalability, cost-effectiveness, and equity impact is underdeveloped, especially in low-resource settings. Long-term systemic and developmental consequences of ECC remain insufficiently characterized. Conclusions: Addressing ECC requires integrated and equity-oriented research frameworks that bridge biological, social, diagnostic, and implementation domains. Clarifying these gaps is essential to inform coherent prevention strategies and reduce persistent disparities in child oral health.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Probiotics and Ozonated Olive Oil to Maintain Oral Eubiosis in Stage I and II Periodontitis Patients: A Randomized Triple-Blind Clinical Trial.
Dentistry journal, 14(4):.
Background: Researchers are now focusing on new and less invasive therapies to improve the domiciliary maintenance phase of periodontitis. Ozonated olive oil as an alternative to common local antiseptics and the assumption of probiotics to maintain a eubiotic oral microbiome show promising results. However, the literature is still limited on this topic. This RCT aims to investigate the clinical benefits of combining ozonated olive oil products (mouthwash and toothpaste) with probiotics on oral health status in patients with stage I and II periodontitis following the active phase of therapy. Methods: The study followed a triple-blind RCT design. Patients with stage I and II periodontitis were enrolled and randomly assigned to three groups: group A (placebo), group B (effective ozonated olive oil mouthwash and toothpaste), and group C (combined protocol with effective ozonated olive oil and probiotics). Clinical assessment was performed at the first visit and after 30 days, considering Full-Mouth Plaque Score (FMPS), Full-Mouth Bleeding Score (FMBS), and Probing Pocket Depth (PPD). Results: The FMPS percentages showed a significative reduction (p = 0.0002) of 24%, 33%, and 62% observed in group A, group B, and group C, respectively. Also, the FMBS percentages were significantly decreased (p < 0.0001): -15%, -20%, and -49% observed in group A, group B, and group C, respectively. The mean PPD showed significant differences (p < 0.0001): -0.10 mm, -0.40 mm, and -1.10 mm observed in group A, group B, and group C, respectively. Overall, group C showed the best improvement among the considered clinical indexes. Conclusions: The findings of this clinical trial support the use of a combined regime of the antimicrobial and anti-inflammatory effects of ozonated olive oil and the modulation of the oral microbiome of probiotic supplements as an adjunctive domiciliary strategy for patients affected by stage I and II periodontitis.
Additional Links: PMID-42041656
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@article {pmid42041656,
year = {2026},
author = {Abbinante, A and Barile, G and Antonacci, A and Basso, M and Pascale, F and Bartolomeo, N and Agneta, MT and D'Albis, G and Corsalini, T and Capodiferro, S and Corsalini, M},
title = {Probiotics and Ozonated Olive Oil to Maintain Oral Eubiosis in Stage I and II Periodontitis Patients: A Randomized Triple-Blind Clinical Trial.},
journal = {Dentistry journal},
volume = {14},
number = {4},
pages = {},
pmid = {42041656},
issn = {2304-6767},
abstract = {Background: Researchers are now focusing on new and less invasive therapies to improve the domiciliary maintenance phase of periodontitis. Ozonated olive oil as an alternative to common local antiseptics and the assumption of probiotics to maintain a eubiotic oral microbiome show promising results. However, the literature is still limited on this topic. This RCT aims to investigate the clinical benefits of combining ozonated olive oil products (mouthwash and toothpaste) with probiotics on oral health status in patients with stage I and II periodontitis following the active phase of therapy. Methods: The study followed a triple-blind RCT design. Patients with stage I and II periodontitis were enrolled and randomly assigned to three groups: group A (placebo), group B (effective ozonated olive oil mouthwash and toothpaste), and group C (combined protocol with effective ozonated olive oil and probiotics). Clinical assessment was performed at the first visit and after 30 days, considering Full-Mouth Plaque Score (FMPS), Full-Mouth Bleeding Score (FMBS), and Probing Pocket Depth (PPD). Results: The FMPS percentages showed a significative reduction (p = 0.0002) of 24%, 33%, and 62% observed in group A, group B, and group C, respectively. Also, the FMBS percentages were significantly decreased (p < 0.0001): -15%, -20%, and -49% observed in group A, group B, and group C, respectively. The mean PPD showed significant differences (p < 0.0001): -0.10 mm, -0.40 mm, and -1.10 mm observed in group A, group B, and group C, respectively. Overall, group C showed the best improvement among the considered clinical indexes. Conclusions: The findings of this clinical trial support the use of a combined regime of the antimicrobial and anti-inflammatory effects of ozonated olive oil and the modulation of the oral microbiome of probiotic supplements as an adjunctive domiciliary strategy for patients affected by stage I and II periodontitis.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Distinct Gut Microbiome Characteristics Associated with Mental Health Symptoms of Healthy Adults.
Brain sciences, 16(4):.
Background/Objectives: Mental health conditions, including stress, anxiety, depression, and sleep problems, represent a significant health concern globally. Mounting evidence suggests a link between mental health and the gut microbiome via the gut-brain axis. However, discrepancies in human microbiome data exist due to the heterogeneity in study design and analytical approaches. Thus, this study aimed to explore the gut microbial characteristics associated with self-reported mental health symptoms using multiple analytical methods. Methods: A total of 44 healthy adults, defined as individuals without any major chronic medical conditions, were assessed for mental health symptoms using self-reported questionnaire data. To evaluate gut microbial characteristics, stool samples were collected at six time points over 28 days and underwent 16S rRNA gene sequencing. Differential abundance was assessed via ANCOM-BC, and a random forest classifier was implemented to rank features important for the classification of mental health symptoms. Participants who did not report anxiety, stress, depression, or sleep problems served as the reference group for microbiome comparisons. Results: The proportion of participants with self-reported mental health symptoms was 11.4% (stress), 27.3% (depression), 31.8% (anxiety), and 15.9% (sleep problems). Participants reporting mental health symptoms showed differences in gut microbiome composition compared to asymptomatic participants, including variation in alpha- and beta-diversity. Differential analysis identified specific taxa with higher or lower relative abundance in participants reporting specific mental health symptoms. Random forest feature ranking identified partially overlapping taxa across methods, suggesting candidate associations warranting further investigation. Conclusions: These exploratory findings suggest that self-reported mental health symptoms in otherwise healthy adults are associated with differences in the gut microbiome. The taxa identified in this study represent candidates for validation in larger, independent cohorts.
Additional Links: PMID-42041792
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@article {pmid42041792,
year = {2026},
author = {Lee, S and Welch, CB and Zinka, K and Evans, M and Park, HJ and Lozada-Fernandez, VV and West, FD},
title = {Distinct Gut Microbiome Characteristics Associated with Mental Health Symptoms of Healthy Adults.},
journal = {Brain sciences},
volume = {16},
number = {4},
pages = {},
pmid = {42041792},
issn = {2076-3425},
support = {HATCH #GEO001002//Georgia Experimental Agricultural Station/ ; },
abstract = {Background/Objectives: Mental health conditions, including stress, anxiety, depression, and sleep problems, represent a significant health concern globally. Mounting evidence suggests a link between mental health and the gut microbiome via the gut-brain axis. However, discrepancies in human microbiome data exist due to the heterogeneity in study design and analytical approaches. Thus, this study aimed to explore the gut microbial characteristics associated with self-reported mental health symptoms using multiple analytical methods. Methods: A total of 44 healthy adults, defined as individuals without any major chronic medical conditions, were assessed for mental health symptoms using self-reported questionnaire data. To evaluate gut microbial characteristics, stool samples were collected at six time points over 28 days and underwent 16S rRNA gene sequencing. Differential abundance was assessed via ANCOM-BC, and a random forest classifier was implemented to rank features important for the classification of mental health symptoms. Participants who did not report anxiety, stress, depression, or sleep problems served as the reference group for microbiome comparisons. Results: The proportion of participants with self-reported mental health symptoms was 11.4% (stress), 27.3% (depression), 31.8% (anxiety), and 15.9% (sleep problems). Participants reporting mental health symptoms showed differences in gut microbiome composition compared to asymptomatic participants, including variation in alpha- and beta-diversity. Differential analysis identified specific taxa with higher or lower relative abundance in participants reporting specific mental health symptoms. Random forest feature ranking identified partially overlapping taxa across methods, suggesting candidate associations warranting further investigation. Conclusions: These exploratory findings suggest that self-reported mental health symptoms in otherwise healthy adults are associated with differences in the gut microbiome. The taxa identified in this study represent candidates for validation in larger, independent cohorts.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
A Randomised, Double-Blind, Placebo-Controlled Trial of Probiotic and Postbiotic Strains in Healthy Adults with Self-Reported Anxiety: Effects on Mood, Vitality, Quality of Life and Perceived Stress.
Brain sciences, 16(4):.
Background: Subclinical psychological symptoms-such as low mood, perceived stress, and poor sleep-affect a large portion of the population and can impair quality of life despite remaining below clinical thresholds. The gut-brain axis has emerged as a promising target for interventions that support emotional and psychological resilience. Probiotics and postbiotics are gaining attention for their potential to modulate mood and stress via microbiome-related mechanisms, but human evidence remains limited, particularly in non-clinical populations. Objectives: We aimed to assess the effects of a two-strain combination of live microorganisms alongside a two-strain combination of heat-treated inactivated microorganisms on outcomes associated with anxiety, mood, perceived stress, and quality of life in healthy adults experiencing mild stress. Methods: This study was conducted in two parts. In Part I, a randomized, double-blind, placebo-controlled study, 100 participants were randomized to receive either a blend of live microorganisms (Bifidobacterium longum CECT 7347 and Lactobacillus rhamnosus CECT 8361) or an identical placebo once daily for 12 weeks. In Part II, a pilot feasibility study, a subset of eight placebo non-responders from Part I received the heat-inactivated preparation of the same bacterial strains in a 6-week trial extension phase. For Parts I and II, the primary outcome was the change in the Hamilton Anxiety Rating Scale (HAM-A). Secondary outcomes included measures of mood (Beck Depression Inventory (BDI); Patient Health Questionnaire-9 (PHQ-9)), stress (state and trait anxiety inventory (STAI); Perceived Stress Scale (PSS)), sleep (Pittsburgh Sleep Quality Index (PSQI)), quality of life (36-item Short Form Survey (SF-36)), gastrointestinal symptoms (Gastrointestinal Symptom Rating Scale (GSRS)), salivary cortisol and microbiome modulation. Results: In Part I, there were no significant effects of the live blend on the HAM-A, indicating that the primary endpoint was not met. In addition, no significant effects were seen on the STAI or PSS scores when compared to the placebo. However, participants consuming the live blend trended toward a reduction in total PHQ-9 scores compared to placebo (p = 0.089), whilst preliminary exploratory analyses suggested an improvement in anhedonia (p = 0.045). Furthermore, there was a significant improvement in the vitality domain of the SF-36 compared to placebo (p = 0.017). On microbiome analysis, it was noted that consumption of the live blend was linked to the preservation of butyrate-producing bacteria, particularly members of the Pseudoflavonifractor genus and the Clostridium SGB6179 species. Furthermore, the abundance of B. longum species was found to be inversely associated with the total PSS Scores. In Part II, supplementation with the inactivated preparation resulted in significant within-group improvements for the vitality (p = 0.006) and social functioning (p = 0.010) domains of the SF-36 and improvements in PSS scores compared to baseline (p = 0.050). Conclusions: Supplementation with either the dual-strain live or inactivated formulations was associated with significant improvements in the vitality domain of the SF-36, whilst participants receiving the inactivated formulation demonstrated lower perceived stress and improved social functioning compared to baseline. Overall, the findings from this pilot study suggest that these two biotic consortia are well-tolerated and may be associated with improvements in measures of vitality in individuals with subclinical psychological symptoms. The subtle observations detected for stress and anhedonia suggest that further well-powered trials are needed to better characterize these findings, potentially in populations with greater baseline symptomatology.
Additional Links: PMID-42041827
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@article {pmid42041827,
year = {2026},
author = {Day, R and Friedman, D and Cardoso, A and Naghibi, M and Pont, A and Martinez-Blanch, J and Lamelas, A and Chenoll, E and Kakilla, C and Rea, K and Vijayakumar, V},
title = {A Randomised, Double-Blind, Placebo-Controlled Trial of Probiotic and Postbiotic Strains in Healthy Adults with Self-Reported Anxiety: Effects on Mood, Vitality, Quality of Life and Perceived Stress.},
journal = {Brain sciences},
volume = {16},
number = {4},
pages = {},
pmid = {42041827},
issn = {2076-3425},
support = {N/A//Archer Daniels Midland (United States)/ ; },
abstract = {Background: Subclinical psychological symptoms-such as low mood, perceived stress, and poor sleep-affect a large portion of the population and can impair quality of life despite remaining below clinical thresholds. The gut-brain axis has emerged as a promising target for interventions that support emotional and psychological resilience. Probiotics and postbiotics are gaining attention for their potential to modulate mood and stress via microbiome-related mechanisms, but human evidence remains limited, particularly in non-clinical populations. Objectives: We aimed to assess the effects of a two-strain combination of live microorganisms alongside a two-strain combination of heat-treated inactivated microorganisms on outcomes associated with anxiety, mood, perceived stress, and quality of life in healthy adults experiencing mild stress. Methods: This study was conducted in two parts. In Part I, a randomized, double-blind, placebo-controlled study, 100 participants were randomized to receive either a blend of live microorganisms (Bifidobacterium longum CECT 7347 and Lactobacillus rhamnosus CECT 8361) or an identical placebo once daily for 12 weeks. In Part II, a pilot feasibility study, a subset of eight placebo non-responders from Part I received the heat-inactivated preparation of the same bacterial strains in a 6-week trial extension phase. For Parts I and II, the primary outcome was the change in the Hamilton Anxiety Rating Scale (HAM-A). Secondary outcomes included measures of mood (Beck Depression Inventory (BDI); Patient Health Questionnaire-9 (PHQ-9)), stress (state and trait anxiety inventory (STAI); Perceived Stress Scale (PSS)), sleep (Pittsburgh Sleep Quality Index (PSQI)), quality of life (36-item Short Form Survey (SF-36)), gastrointestinal symptoms (Gastrointestinal Symptom Rating Scale (GSRS)), salivary cortisol and microbiome modulation. Results: In Part I, there were no significant effects of the live blend on the HAM-A, indicating that the primary endpoint was not met. In addition, no significant effects were seen on the STAI or PSS scores when compared to the placebo. However, participants consuming the live blend trended toward a reduction in total PHQ-9 scores compared to placebo (p = 0.089), whilst preliminary exploratory analyses suggested an improvement in anhedonia (p = 0.045). Furthermore, there was a significant improvement in the vitality domain of the SF-36 compared to placebo (p = 0.017). On microbiome analysis, it was noted that consumption of the live blend was linked to the preservation of butyrate-producing bacteria, particularly members of the Pseudoflavonifractor genus and the Clostridium SGB6179 species. Furthermore, the abundance of B. longum species was found to be inversely associated with the total PSS Scores. In Part II, supplementation with the inactivated preparation resulted in significant within-group improvements for the vitality (p = 0.006) and social functioning (p = 0.010) domains of the SF-36 and improvements in PSS scores compared to baseline (p = 0.050). Conclusions: Supplementation with either the dual-strain live or inactivated formulations was associated with significant improvements in the vitality domain of the SF-36, whilst participants receiving the inactivated formulation demonstrated lower perceived stress and improved social functioning compared to baseline. Overall, the findings from this pilot study suggest that these two biotic consortia are well-tolerated and may be associated with improvements in measures of vitality in individuals with subclinical psychological symptoms. The subtle observations detected for stress and anhedonia suggest that further well-powered trials are needed to better characterize these findings, potentially in populations with greater baseline symptomatology.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Profiling the Athletes' Gut Microbiome: A Critical Methodological Perspective on 16S Metabarcoding and Shotgun Metagenomics.
Biology, 15(8):.
The growing interest in the role of the gut microbiome in athletic performance has led to the application of various sequencing technologies in this field. This review critically examines the sequencing methodologies used in microbiome studies on physical performance and sport, comparing their advantages, limitations, and applicability. In particular, the focus is on 16S metabarcoding and shotgun metagenomics, evaluating how these methodological approaches influence the interpretation of results in sports contexts. Close attention is directed toward technical challenges, methodological biases, and future perspectives, including emerging technologies and multi-omics approaches. This review aims to bridge the gap between methodological rigor and sports-specific applicability, providing evidence-based methodological guidance to support researchers in designing robust athlete microbiome studies and translating sequencing-derived findings into concrete applications for performance and sports health.
Additional Links: PMID-42041878
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@article {pmid42041878,
year = {2026},
author = {Carlone, J and Ribeiro, ÁCDS and Parisi, A and Giampaoli, S and Fasano, A},
title = {Profiling the Athletes' Gut Microbiome: A Critical Methodological Perspective on 16S Metabarcoding and Shotgun Metagenomics.},
journal = {Biology},
volume = {15},
number = {8},
pages = {},
pmid = {42041878},
issn = {2079-7737},
abstract = {The growing interest in the role of the gut microbiome in athletic performance has led to the application of various sequencing technologies in this field. This review critically examines the sequencing methodologies used in microbiome studies on physical performance and sport, comparing their advantages, limitations, and applicability. In particular, the focus is on 16S metabarcoding and shotgun metagenomics, evaluating how these methodological approaches influence the interpretation of results in sports contexts. Close attention is directed toward technical challenges, methodological biases, and future perspectives, including emerging technologies and multi-omics approaches. This review aims to bridge the gap between methodological rigor and sports-specific applicability, providing evidence-based methodological guidance to support researchers in designing robust athlete microbiome studies and translating sequencing-derived findings into concrete applications for performance and sports health.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Redox Reprogramming of the Diseased Liver by Dietary Flavonoids: From Molecular Signalling to Gut-Liver Crosstalk.
Biology, 15(8):.
Liver diseases, including fatty liver, hepatitis, and cirrhosis, remain major global health challenges due to their disruption of metabolic homeostasis and detoxification processes. Redox imbalance plays a central role in liver disease progression by promoting inflammation, hepatic stellate cell activation, mitochondrial dysfunction, and fibrogenesis. Although flavonoids have historically been considered direct reactive oxygen species (ROS) scavengers, emerging evidence indicates that their biological effect at physiological concentrations are primarily mediated through modulation of intracellular redox signalling rather than simple radical neutralisation. This review highlights flavonoids as redox-modulating agents capable of restoring hepatic redox homeostasis through coordinated regulation of molecular pathways. Mechanistically, flavonoids activate the Nrf2-Keap1 axis to enhance endogenous antioxidant defences, including heme oxygenase-1 and glutathione biosynthesis enzyme, while suppressing NF-κB-mediated pro-inflammatory signalling and modulating MAPK and PI3K/Akt pathways. They also regulate mitochondrial redox balance, supporting mitophagy, metabolic adaptation, and cellular resilience to oxidative stress. In addition, flavonoid biotransformation by the gut microbiome improves intestinal barrier integrity, reduces endotoxin-driven hepatic inflammation, and contributes to gut-liver crosstalk. Collectively, these mechanisms position dietary flavonoids as multi-target redox modulators with promising therapeutic potential in chronic liver disease, although further studies are needed to improve their bioavailability and clinical translation.
Additional Links: PMID-42041903
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Citation:
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@article {pmid42041903,
year = {2026},
author = {Dogra, S and Arukha, AP and Koul, B and Rabbee, MF},
title = {Redox Reprogramming of the Diseased Liver by Dietary Flavonoids: From Molecular Signalling to Gut-Liver Crosstalk.},
journal = {Biology},
volume = {15},
number = {8},
pages = {},
pmid = {42041903},
issn = {2079-7737},
abstract = {Liver diseases, including fatty liver, hepatitis, and cirrhosis, remain major global health challenges due to their disruption of metabolic homeostasis and detoxification processes. Redox imbalance plays a central role in liver disease progression by promoting inflammation, hepatic stellate cell activation, mitochondrial dysfunction, and fibrogenesis. Although flavonoids have historically been considered direct reactive oxygen species (ROS) scavengers, emerging evidence indicates that their biological effect at physiological concentrations are primarily mediated through modulation of intracellular redox signalling rather than simple radical neutralisation. This review highlights flavonoids as redox-modulating agents capable of restoring hepatic redox homeostasis through coordinated regulation of molecular pathways. Mechanistically, flavonoids activate the Nrf2-Keap1 axis to enhance endogenous antioxidant defences, including heme oxygenase-1 and glutathione biosynthesis enzyme, while suppressing NF-κB-mediated pro-inflammatory signalling and modulating MAPK and PI3K/Akt pathways. They also regulate mitochondrial redox balance, supporting mitophagy, metabolic adaptation, and cellular resilience to oxidative stress. In addition, flavonoid biotransformation by the gut microbiome improves intestinal barrier integrity, reduces endotoxin-driven hepatic inflammation, and contributes to gut-liver crosstalk. Collectively, these mechanisms position dietary flavonoids as multi-target redox modulators with promising therapeutic potential in chronic liver disease, although further studies are needed to improve their bioavailability and clinical translation.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
From Microbial Ecology to Functional Components in Microbe-Host Interactions.
Biology, 15(8):.
Microbiome research is shifting from a focus on "whole microorganisms" to an emphasis on microbial functional components. This review systematically describes how the effects of microbial communities on the host are mediated by bioactive functional components released by microbes. These components primarily exert their effects through interactions with host Pattern Recognition Receptors (PRRs) and metabolic sensing receptors, thereby regulating host immune, metabolic, and barrier function networks. The biological effects of these functional components are highly context-dependent. Under homeostasis, metabolites such as SCFAs and bile acids promote mucosal immune tolerance and maintain epithelial barrier integrity. However, the same signals can become deleterious under dysbiosis, driving inflammation and contributing to colorectal tumorigenesis. Mechanistic dissection of individual components, such as lipopolysaccharide (LPS), is now propelling a transition in clinical translation from whole-microbe-based interventions toward component-oriented diagnostics and therapeutics. Component-oriented diagnostics and therapeutics use defined microbial molecules rather than whole microorganisms. Microbial nucleic acids (e.g., HPV DNA), metabolites (e.g., SCFAs), and proteins can serve as biomarkers for disease risk, diagnosis, and prognosis. Therapeutic strategies include targeted modulation of beneficial components, neutralization of harmful molecules, and engineered microbial delivery.
Additional Links: PMID-42041913
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Citation:
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@article {pmid42041913,
year = {2026},
author = {Wang, T and Wang, Z and Yang, X and Zhang, L},
title = {From Microbial Ecology to Functional Components in Microbe-Host Interactions.},
journal = {Biology},
volume = {15},
number = {8},
pages = {},
pmid = {42041913},
issn = {2079-7737},
support = {82370785//National Natural Science Foundation of China/ ; tscy20190612//TaiShan Industrial Experts Program/ ; tshw20120206//TaiShan Scholars Program of Shandong Province/ ; },
abstract = {Microbiome research is shifting from a focus on "whole microorganisms" to an emphasis on microbial functional components. This review systematically describes how the effects of microbial communities on the host are mediated by bioactive functional components released by microbes. These components primarily exert their effects through interactions with host Pattern Recognition Receptors (PRRs) and metabolic sensing receptors, thereby regulating host immune, metabolic, and barrier function networks. The biological effects of these functional components are highly context-dependent. Under homeostasis, metabolites such as SCFAs and bile acids promote mucosal immune tolerance and maintain epithelial barrier integrity. However, the same signals can become deleterious under dysbiosis, driving inflammation and contributing to colorectal tumorigenesis. Mechanistic dissection of individual components, such as lipopolysaccharide (LPS), is now propelling a transition in clinical translation from whole-microbe-based interventions toward component-oriented diagnostics and therapeutics. Component-oriented diagnostics and therapeutics use defined microbial molecules rather than whole microorganisms. Microbial nucleic acids (e.g., HPV DNA), metabolites (e.g., SCFAs), and proteins can serve as biomarkers for disease risk, diagnosis, and prognosis. Therapeutic strategies include targeted modulation of beneficial components, neutralization of harmful molecules, and engineered microbial delivery.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
The Gut Microbiome and Metabolome of Domestic Cats Were Altered by the Oral Administration of Complex Probiotics.
Biology, 15(8):.
Probiotics are commonly applied to maintain the balance of gut microbiota and regulate the intestinal metabolic function of companion animals. In the present study, complex probiotics (Bacillus coagulans SNZ-1969, Bacillus subtilis, and Bacillus licheniformis) were added into the basal diet of domestic cats to investigate their influence on the intestinal microbiome and metabolic characteristics. Results revealed that the alpha diversity of the gut microbiota in the probiotic group was enhanced when compared to the control group. The beta diversity of the gut microbiota was also altered by the oral consumption of the complex probiotics. Compared to the control group, the relative abundance of beneficial microbes (such as Clostridium, Bacteroides, Phocaeicola, and Ruminococcus) in the probiotic group was enhanced, while the relative abundance of opportunistic pathogens (such as Escherichia, Gallibacter, Corynebacterium) was decreased. Additionally, the intestinal metabolic characteristics of domestic cats were also changed. The metabolomic analysis identified 408 differential metabolites between the two groups, and the KEGG function pathway analysis proved that the dominant pathway related to the differential metabolites were the amino acid metabolism, lipid metabolism, carbohydrate metabolism, energy metabolism, endocrine system, digestive system, immune system, and other metabolic pathways. Spearman's correlation analysis revealed that the beneficial microbes had positive correlations with the differential metabolites. In conclusion, the current study demonstrated that oral administration of complex probiotics could regulate overall health and well-being in domestic cats through modulating the gut microbiome and metabolic characteristics.
Additional Links: PMID-42041929
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Citation:
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@article {pmid42041929,
year = {2026},
author = {Ma, Y and Hu, Y and Zhang, J and Sun, Q and Wang, H and Liu, X and Tian, W and Wang, W and Ma, X and Shao, D and Liu, K and Li, B and Qiu, Y and Ma, Z and Li, Z and Wei, J},
title = {The Gut Microbiome and Metabolome of Domestic Cats Were Altered by the Oral Administration of Complex Probiotics.},
journal = {Biology},
volume = {15},
number = {8},
pages = {},
pmid = {42041929},
issn = {2079-7737},
abstract = {Probiotics are commonly applied to maintain the balance of gut microbiota and regulate the intestinal metabolic function of companion animals. In the present study, complex probiotics (Bacillus coagulans SNZ-1969, Bacillus subtilis, and Bacillus licheniformis) were added into the basal diet of domestic cats to investigate their influence on the intestinal microbiome and metabolic characteristics. Results revealed that the alpha diversity of the gut microbiota in the probiotic group was enhanced when compared to the control group. The beta diversity of the gut microbiota was also altered by the oral consumption of the complex probiotics. Compared to the control group, the relative abundance of beneficial microbes (such as Clostridium, Bacteroides, Phocaeicola, and Ruminococcus) in the probiotic group was enhanced, while the relative abundance of opportunistic pathogens (such as Escherichia, Gallibacter, Corynebacterium) was decreased. Additionally, the intestinal metabolic characteristics of domestic cats were also changed. The metabolomic analysis identified 408 differential metabolites between the two groups, and the KEGG function pathway analysis proved that the dominant pathway related to the differential metabolites were the amino acid metabolism, lipid metabolism, carbohydrate metabolism, energy metabolism, endocrine system, digestive system, immune system, and other metabolic pathways. Spearman's correlation analysis revealed that the beneficial microbes had positive correlations with the differential metabolites. In conclusion, the current study demonstrated that oral administration of complex probiotics could regulate overall health and well-being in domestic cats through modulating the gut microbiome and metabolic characteristics.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Human and Marine Host Defense Peptides for Healthy Skin.
Marine drugs, 24(4):.
The skin serves as the first line barrier of innate immunity, protecting the body from external influences and maintaining its homeostasis. Exogenous and endogenous stress factors alter the structure and functional properties of the skin. The search for compounds capable of counteracting these processes has allowed the identification of peptides as promising ingredients of products for medicinal and cosmetic applications. This review comprehensively examines the mechanisms of action and dermatological applications of two distinct classes of natural products-endogenous human peptides and those derived from marine organisms. Human peptides exhibit numerous biological functions, including antimicrobial and immunomodulatory ones, as well as promoting antioxidant protection and wound healing. Microbiome-associated peptides are an underestimated but powerful regulator of skin aging through immunomodulation, inflammation control, barrier function maintenance, and selection of the proper microbial community. Peptides from marine organisms exhibit significant structural diversity and a broad spectrum of biological activity, including regenerative effects and effects on antibiotic-resistant microorganisms. This review summarizes current data obtained from in vitro, ex vivo, and clinical studies demonstrating a broad potential of peptides for maintaining skin health. Both peptide classes represent powerful, targeted strategies for innovative dermatological interventions aimed at promoting skin rejuvenation, protection, and overall homeostasis.
Additional Links: PMID-42042209
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@article {pmid42042209,
year = {2026},
author = {Guryanova, SV and Belogurova-Ovchinnikova, OY and Ovchinnikova, TV},
title = {Human and Marine Host Defense Peptides for Healthy Skin.},
journal = {Marine drugs},
volume = {24},
number = {4},
pages = {},
pmid = {42042209},
issn = {1660-3397},
support = {22-14-00380-P//Russian Science Foundation/ ; },
mesh = {Humans ; *Aquatic Organisms/chemistry ; *Skin/drug effects/metabolism ; Animals ; Skin Aging/drug effects ; *Antimicrobial Peptides/pharmacology ; *Biological Products/pharmacology ; Wound Healing/drug effects ; *Antimicrobial Cationic Peptides/pharmacology ; Immunity, Innate ; *Peptides/pharmacology ; },
abstract = {The skin serves as the first line barrier of innate immunity, protecting the body from external influences and maintaining its homeostasis. Exogenous and endogenous stress factors alter the structure and functional properties of the skin. The search for compounds capable of counteracting these processes has allowed the identification of peptides as promising ingredients of products for medicinal and cosmetic applications. This review comprehensively examines the mechanisms of action and dermatological applications of two distinct classes of natural products-endogenous human peptides and those derived from marine organisms. Human peptides exhibit numerous biological functions, including antimicrobial and immunomodulatory ones, as well as promoting antioxidant protection and wound healing. Microbiome-associated peptides are an underestimated but powerful regulator of skin aging through immunomodulation, inflammation control, barrier function maintenance, and selection of the proper microbial community. Peptides from marine organisms exhibit significant structural diversity and a broad spectrum of biological activity, including regenerative effects and effects on antibiotic-resistant microorganisms. This review summarizes current data obtained from in vitro, ex vivo, and clinical studies demonstrating a broad potential of peptides for maintaining skin health. Both peptide classes represent powerful, targeted strategies for innovative dermatological interventions aimed at promoting skin rejuvenation, protection, and overall homeostasis.},
}
MeSH Terms:
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Humans
*Aquatic Organisms/chemistry
*Skin/drug effects/metabolism
Animals
Skin Aging/drug effects
*Antimicrobial Peptides/pharmacology
*Biological Products/pharmacology
Wound Healing/drug effects
*Antimicrobial Cationic Peptides/pharmacology
Immunity, Innate
*Peptides/pharmacology
RevDate: 2026-04-27
CmpDate: 2026-04-27
Newer Therapeutics to Selectively Kill Clostridioides difficile and Restore the Microbiome.
Infectious disease reports, 18(2):.
BACKGROUND: The antibiotic ibezapolstat and the live biotherapeutic product live-JSLM are promising future approaches for treating Clostridioides difficile infection. Ibezapostat is a highly specific antibiotic for Clostridioides difficile, with minimal impact on the intestinal flora. Live-JSLM is designed to restore healthy intestinal microbiota, thus preventing recurrence of Clostridioides difficile infection. In this narrative review, we reviewed available data on ibezapostat and live-JSLM, considering that they are prototypes of two distinct, unique mechanisms of action against Clostridioides difficile.
METHODS: Data sources: PubMed and SCOPUS databases were searched from 1 January 2012 to 15 November 2025. Original articles reporting data on ibezapolstat and live-JSLM were included.
RESULTS: 31 studies were included. When compared to conventional anti-Clostridioides difficile antibiotics, ibezapolstat had a similar level of effectiveness and minimal impact on the gut microbiota. The available data confirm live-JSLM safety and efficacy in restoring the gut microbiota following the conclusion of the standard anti-Clostridioides difficile antibiotic regimen.
CONCLUSIONS: The results on ibezapolstat efficacy are promising, but require confirmation in larger patient populations through double-blind, randomised phase III trials. In the near future, an integrated approach may enhance the management of Clostridioides difficile infection: starting with highly specific antibiotics, i.e., ibezapolstat, followed by microbiome-based therapies such as live-JSLM.
Additional Links: PMID-42042323
PubMed:
Citation:
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@article {pmid42042323,
year = {2026},
author = {Granata, G and Petrosillo, N},
title = {Newer Therapeutics to Selectively Kill Clostridioides difficile and Restore the Microbiome.},
journal = {Infectious disease reports},
volume = {18},
number = {2},
pages = {},
pmid = {42042323},
issn = {2036-7430},
abstract = {BACKGROUND: The antibiotic ibezapolstat and the live biotherapeutic product live-JSLM are promising future approaches for treating Clostridioides difficile infection. Ibezapostat is a highly specific antibiotic for Clostridioides difficile, with minimal impact on the intestinal flora. Live-JSLM is designed to restore healthy intestinal microbiota, thus preventing recurrence of Clostridioides difficile infection. In this narrative review, we reviewed available data on ibezapostat and live-JSLM, considering that they are prototypes of two distinct, unique mechanisms of action against Clostridioides difficile.
METHODS: Data sources: PubMed and SCOPUS databases were searched from 1 January 2012 to 15 November 2025. Original articles reporting data on ibezapolstat and live-JSLM were included.
RESULTS: 31 studies were included. When compared to conventional anti-Clostridioides difficile antibiotics, ibezapolstat had a similar level of effectiveness and minimal impact on the gut microbiota. The available data confirm live-JSLM safety and efficacy in restoring the gut microbiota following the conclusion of the standard anti-Clostridioides difficile antibiotic regimen.
CONCLUSIONS: The results on ibezapolstat efficacy are promising, but require confirmation in larger patient populations through double-blind, randomised phase III trials. In the near future, an integrated approach may enhance the management of Clostridioides difficile infection: starting with highly specific antibiotics, i.e., ibezapolstat, followed by microbiome-based therapies such as live-JSLM.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Field Root-Associated Microbiome Characteristics of Astragalus membranaceus and Its Transcriptomic Response to Purpureocillium lilacinum BP2-7 Treatment.
Journal of fungi (Basel, Switzerland), 12(4):.
Astragalus membranaceus suffers severe yield and quality losses due to root rot caused by Fusarium solani. To address this, we analyzed the root-associated microbial communities of healthy and diseased plants in northwest China using high-throughput sequencing. Combining community analysis with pot experiments and transcriptomic profiling, we elucidated the molecular mechanisms by which the biocontrol fungus Purpureocilliu lilacinum BP2-7 suppresses root rot. Root rot reshaped root-associated microbial structure, affecting fungal diversity more than bacterial diversity. The antagonistic effect of P. lilacinum BP2-7 against F. solani reached 71.43% in plate assays and 63.7% control efficacy in pot experiments, representing the first report of P. lilacinum application for managing root rot in A. membranaceus. Transcriptomic analysis revealed that P. lilacinum BP2-7 promotes the transition of plants from a damaged to a recovering state by modulating translation and metabolic processes, and enhancing protein homeostasis, while moderately downregulating defense-related responses to alleviate pathogen-induced excessive defense mechanisms. Additionally, twenty candidate genes involved in the direct inhibition of F. solani were identified, suggesting a role in enhancing host resistance. This study supports eco-friendly biocontrol strategies and advances understanding of plant-microbe interactions for managing soil-borne diseases in other important crops.
Additional Links: PMID-42042338
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@article {pmid42042338,
year = {2026},
author = {Jiang, H and Xu, H and Meng, Z and Hao, K and Yang, Y and Zhao, Y and Yao, Q and Li, M},
title = {Field Root-Associated Microbiome Characteristics of Astragalus membranaceus and Its Transcriptomic Response to Purpureocillium lilacinum BP2-7 Treatment.},
journal = {Journal of fungi (Basel, Switzerland)},
volume = {12},
number = {4},
pages = {},
pmid = {42042338},
issn = {2309-608X},
support = {[2022ZD01]//Inner Mongolia Natural Science Foundation/ ; },
abstract = {Astragalus membranaceus suffers severe yield and quality losses due to root rot caused by Fusarium solani. To address this, we analyzed the root-associated microbial communities of healthy and diseased plants in northwest China using high-throughput sequencing. Combining community analysis with pot experiments and transcriptomic profiling, we elucidated the molecular mechanisms by which the biocontrol fungus Purpureocilliu lilacinum BP2-7 suppresses root rot. Root rot reshaped root-associated microbial structure, affecting fungal diversity more than bacterial diversity. The antagonistic effect of P. lilacinum BP2-7 against F. solani reached 71.43% in plate assays and 63.7% control efficacy in pot experiments, representing the first report of P. lilacinum application for managing root rot in A. membranaceus. Transcriptomic analysis revealed that P. lilacinum BP2-7 promotes the transition of plants from a damaged to a recovering state by modulating translation and metabolic processes, and enhancing protein homeostasis, while moderately downregulating defense-related responses to alleviate pathogen-induced excessive defense mechanisms. Additionally, twenty candidate genes involved in the direct inhibition of F. solani were identified, suggesting a role in enhancing host resistance. This study supports eco-friendly biocontrol strategies and advances understanding of plant-microbe interactions for managing soil-borne diseases in other important crops.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Characterization of Penicillium halotolerans with Antagonistic Activity Against Fusarium Root Rot in Astragalus membranaceus.
Journal of fungi (Basel, Switzerland), 12(4):.
Astragalus membranaceus is an important perennial medicinal plant whose roots constitute its primary medicinal organ; however, its cultivation is severely constrained by root rot caused by Fusarium oxysporum. This study aimed to characterize differences in the rhizosphere microbiome between healthy and diseased plants, identify antagonistic microorganisms from healthy rhizosphere soils, and investigate their suppressive effects on F. oxysporum and the associated host metabolic responses. High-throughput sequencing was used to compare bacterial and fungal communities in the rhizospheres of healthy and diseased plants. Microorganisms were isolated from healthy rhizosphere soils and screened for antagonistic activity against F. oxysporum, followed by validation in pot experiments. Metabolomic analysis was further conducted to assess host metabolic responses to microbial treatment. Root rot disease significantly altered the dominant composition of rhizosphere microbial communities and was associated with reduced fungal diversity and lower bacterial richness in diseased soils. Co-occurrence network analysis revealed increased complexity in bacterial networks and strengthened positive correlations among fungal taxa under diseased conditions. A total of 81 microbial strains were isolated from healthy rhizosphere soils, among which Penicillium halotolerans exhibited the strongest inhibitory activity against the mycelial growth of F. oxysporum. Pot experiments further supported its suppressive effect on Astragalus root rot. Metabolomic analysis indicated that P. halotolerans treatment was associated with changes in host metabolic profiles related to energy metabolism, defense-associated protein synthesis, and nutrient uptake. Overall, this study identified P. halotolerans as a fungal strain with antagonistic activity against F. oxysporum and provided initial evidence for its association with the suppression of Astragalus root rot. These findings offer candidate microbial resources and mechanistic insights for understanding rhizosphere-associated disease suppression in Astragalus membranaceus.
Additional Links: PMID-42042377
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@article {pmid42042377,
year = {2026},
author = {Yang, Y and Jiang, H and Yang, X and Hao, K and Zhao, Y and Yao, Q and Li, M},
title = {Characterization of Penicillium halotolerans with Antagonistic Activity Against Fusarium Root Rot in Astragalus membranaceus.},
journal = {Journal of fungi (Basel, Switzerland)},
volume = {12},
number = {4},
pages = {},
pmid = {42042377},
issn = {2309-608X},
support = {2022ZD01//Inner Mongolia Natural Science Foundation Project/ ; KJJYZX2026080//2026 Special Project of Surplus Funds in Natural Sciences, Inner Mongolia Normal University/ ; },
abstract = {Astragalus membranaceus is an important perennial medicinal plant whose roots constitute its primary medicinal organ; however, its cultivation is severely constrained by root rot caused by Fusarium oxysporum. This study aimed to characterize differences in the rhizosphere microbiome between healthy and diseased plants, identify antagonistic microorganisms from healthy rhizosphere soils, and investigate their suppressive effects on F. oxysporum and the associated host metabolic responses. High-throughput sequencing was used to compare bacterial and fungal communities in the rhizospheres of healthy and diseased plants. Microorganisms were isolated from healthy rhizosphere soils and screened for antagonistic activity against F. oxysporum, followed by validation in pot experiments. Metabolomic analysis was further conducted to assess host metabolic responses to microbial treatment. Root rot disease significantly altered the dominant composition of rhizosphere microbial communities and was associated with reduced fungal diversity and lower bacterial richness in diseased soils. Co-occurrence network analysis revealed increased complexity in bacterial networks and strengthened positive correlations among fungal taxa under diseased conditions. A total of 81 microbial strains were isolated from healthy rhizosphere soils, among which Penicillium halotolerans exhibited the strongest inhibitory activity against the mycelial growth of F. oxysporum. Pot experiments further supported its suppressive effect on Astragalus root rot. Metabolomic analysis indicated that P. halotolerans treatment was associated with changes in host metabolic profiles related to energy metabolism, defense-associated protein synthesis, and nutrient uptake. Overall, this study identified P. halotolerans as a fungal strain with antagonistic activity against F. oxysporum and provided initial evidence for its association with the suppression of Astragalus root rot. These findings offer candidate microbial resources and mechanistic insights for understanding rhizosphere-associated disease suppression in Astragalus membranaceus.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Dietary p-Coumaric Acid Modulates Non-Core Gut Microbiota and Sucrose Solution Consumption in Apis cerana.
Insects, 17(4):.
As the predominant native pollinator across Asia, Apis cerana is essential for the maintenance of biodiversity and agricultural productivity. The gut microbiota of honeybees plays a central role in host nutrition, detoxification, and immune function. p-Coumaric acid, a widespread phenolic acid enriched in pollen and nectar, has been reported to promote honeybee health by prolonging lifespan and increasing the expression of detoxification-related genes, hence improving tolerance to pesticides. Its influence on gut microbial communities, however, remains insufficiently characterized in A. cerana. This study evaluated the effects of dietary p-coumaric acid on survival, sucrose solution consumption, and gut microbiome composition in A. cerana workers using absolute quantification sequencing. Bees were provided sucrose solutions containing p-coumaric acid at concentrations of 41.0, 82.0, and 164.0 mg/L for durations of 5 and 10 days. The results indicated no effect on survival but revealed time-dependent changes in sucrose solution consumption. p-Coumaric acid exposure altered the abundance of non-core bacterial taxa, including Bombella and Apilactobacillus, whereas the core gut microbiota (Lactobacillus, Gilliamella, Snodgrassella, Apibacter, and Bifidobacterium) remained stable. These results suggest that p-coumaric acid modulates sucrose solution consumption and selectively influences non-core gut bacteria without disrupting survival or core microbiota stability, underscoring its role in regulating host-microbe interactions in honeybees.
Additional Links: PMID-42042414
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@article {pmid42042414,
year = {2026},
author = {Wu, H and Ji, C and Dong, K and Wang, R and Gao, L and Luo, W and Liu, J},
title = {Dietary p-Coumaric Acid Modulates Non-Core Gut Microbiota and Sucrose Solution Consumption in Apis cerana.},
journal = {Insects},
volume = {17},
number = {4},
pages = {},
pmid = {42042414},
issn = {2075-4450},
support = {22539C//Chongqing Municipal Fiscal Fund Project/ ; cstc2021jscx-gksbX0009//Key Project of Special Focus on Technological Innovation and Application Development/ ; CARS-44-SYZ12//Modern Agroindustry Technology Research System/ ; 25403//Chongqing Academy of Animal Science/ ; },
abstract = {As the predominant native pollinator across Asia, Apis cerana is essential for the maintenance of biodiversity and agricultural productivity. The gut microbiota of honeybees plays a central role in host nutrition, detoxification, and immune function. p-Coumaric acid, a widespread phenolic acid enriched in pollen and nectar, has been reported to promote honeybee health by prolonging lifespan and increasing the expression of detoxification-related genes, hence improving tolerance to pesticides. Its influence on gut microbial communities, however, remains insufficiently characterized in A. cerana. This study evaluated the effects of dietary p-coumaric acid on survival, sucrose solution consumption, and gut microbiome composition in A. cerana workers using absolute quantification sequencing. Bees were provided sucrose solutions containing p-coumaric acid at concentrations of 41.0, 82.0, and 164.0 mg/L for durations of 5 and 10 days. The results indicated no effect on survival but revealed time-dependent changes in sucrose solution consumption. p-Coumaric acid exposure altered the abundance of non-core bacterial taxa, including Bombella and Apilactobacillus, whereas the core gut microbiota (Lactobacillus, Gilliamella, Snodgrassella, Apibacter, and Bifidobacterium) remained stable. These results suggest that p-coumaric acid modulates sucrose solution consumption and selectively influences non-core gut bacteria without disrupting survival or core microbiota stability, underscoring its role in regulating host-microbe interactions in honeybees.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
New Personalized Medicine Model for Medication Management.
Journal of personalized medicine, 16(4):.
When using traditional approaches, such as pharmacokinetics and pharmacodynamics, the entire cellular or molecular response to drugs in the body cannot be fully ascertained or established. The oral medication process involves pharmacokinetics, followed by oral microbiomics and then gut microbiomics and pharmacodynamics. Recently, there has been increasing interest in the role of genetics (pharmacogenetics and pharmacogenomics) in both humans and microbiomes, as well as omics alterations (e.g., epigenetic, transcriptomic, proteomic, and metabolomic alterations as a consequence of drug exposure), which can help to ascertain the cellular responses to medications. Both the efficacy and toxicity of a drug are influenced by these factors. To assess these at an individual level, an integrative Personalized Medicine Model may be needed to help with medication management. Two example application cases for SSRIs and statins demonstrate the clinical usefulness of such a model, which can guide clinicians during drug selection and dosing to reduce reliance on trial-and-error, thus potentially improving patient outcomes and safety. Integrating this framework into practical clinical workflows requires the capture, analysis, and translation of multi-omics data in order to realize decision support protocols and actionable drug recommendations. This review also discusses IT requirements and different stakeholder roles. Although the proposed model can guide the treatment of diseases at the individual patient level, further research is still needed before it can be implemented as part of drug development research, clinical care, and healthcare delivery systems.
Additional Links: PMID-42042549
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@article {pmid42042549,
year = {2026},
author = {Alagiakrishnan, K and Halverson, T and Olivares, DVF and Sadowski, CA},
title = {New Personalized Medicine Model for Medication Management.},
journal = {Journal of personalized medicine},
volume = {16},
number = {4},
pages = {},
pmid = {42042549},
issn = {2075-4426},
abstract = {When using traditional approaches, such as pharmacokinetics and pharmacodynamics, the entire cellular or molecular response to drugs in the body cannot be fully ascertained or established. The oral medication process involves pharmacokinetics, followed by oral microbiomics and then gut microbiomics and pharmacodynamics. Recently, there has been increasing interest in the role of genetics (pharmacogenetics and pharmacogenomics) in both humans and microbiomes, as well as omics alterations (e.g., epigenetic, transcriptomic, proteomic, and metabolomic alterations as a consequence of drug exposure), which can help to ascertain the cellular responses to medications. Both the efficacy and toxicity of a drug are influenced by these factors. To assess these at an individual level, an integrative Personalized Medicine Model may be needed to help with medication management. Two example application cases for SSRIs and statins demonstrate the clinical usefulness of such a model, which can guide clinicians during drug selection and dosing to reduce reliance on trial-and-error, thus potentially improving patient outcomes and safety. Integrating this framework into practical clinical workflows requires the capture, analysis, and translation of multi-omics data in order to realize decision support protocols and actionable drug recommendations. This review also discusses IT requirements and different stakeholder roles. Although the proposed model can guide the treatment of diseases at the individual patient level, further research is still needed before it can be implemented as part of drug development research, clinical care, and healthcare delivery systems.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
From Gut to Shot: Microbiome-Guided Strategies to Improve Vaccine Responses in Food Animals.
Vaccines, 14(4):.
Vaccine performance in livestock and poultry often varies under field conditions. Conventional explanations, such as handling errors, cold-chain failures, or antigen mismatch do not fully account for inconsistent immunogenicity and durability. Increasing evidence suggests that the gut microbiome acts as an upstream regulator of vaccine responses through microbial structural signals and metabolites that shape antigen presentation, B-cell metabolism, and inflammatory tone. Early life microbiome disruption can impair antibody responses to multiple vaccines, highlighting a plausible causal role for dysbiosis in suboptimal vaccine efficacy. Microbiota-derived metabolites, particularly short-chain fatty acids (SCFAs), can influence B-cell differentiation and antibody production through metabolic and epigenetic pathways. However, these effects are dose- and context-dependent, highlighting the need for controlled translation rather than generalized assumptions that higher SCFA levels are beneficial. This review synthesizes microbiome-immunometabolism pathways relevant to vaccine responses in food animals and assesses practical nutritional and microbiome-targeted strategies, such as amino acids, trace minerals, organic acids, phytogenics, and postbiotics, that may modulate these pathways to improve outcomes. We also propose field-deployable biomarker panels that combine immune readouts with inflammation- and microbiome-linked metabolite proxies to stratify likely responders, monitor intervention effects, and improve trial comparability. Finally, we outline translational study designs that connect microbiome shifts to protective immune endpoints and performance outcomes, enabling evidence-based integration of microbiome-informed strategies into vaccination programs for poultry, with broader conceptual relevance to other food animals.
Additional Links: PMID-42042803
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Citation:
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@article {pmid42042803,
year = {2026},
author = {Akhtar, MS and Zaman, W},
title = {From Gut to Shot: Microbiome-Guided Strategies to Improve Vaccine Responses in Food Animals.},
journal = {Vaccines},
volume = {14},
number = {4},
pages = {},
pmid = {42042803},
issn = {2076-393X},
abstract = {Vaccine performance in livestock and poultry often varies under field conditions. Conventional explanations, such as handling errors, cold-chain failures, or antigen mismatch do not fully account for inconsistent immunogenicity and durability. Increasing evidence suggests that the gut microbiome acts as an upstream regulator of vaccine responses through microbial structural signals and metabolites that shape antigen presentation, B-cell metabolism, and inflammatory tone. Early life microbiome disruption can impair antibody responses to multiple vaccines, highlighting a plausible causal role for dysbiosis in suboptimal vaccine efficacy. Microbiota-derived metabolites, particularly short-chain fatty acids (SCFAs), can influence B-cell differentiation and antibody production through metabolic and epigenetic pathways. However, these effects are dose- and context-dependent, highlighting the need for controlled translation rather than generalized assumptions that higher SCFA levels are beneficial. This review synthesizes microbiome-immunometabolism pathways relevant to vaccine responses in food animals and assesses practical nutritional and microbiome-targeted strategies, such as amino acids, trace minerals, organic acids, phytogenics, and postbiotics, that may modulate these pathways to improve outcomes. We also propose field-deployable biomarker panels that combine immune readouts with inflammation- and microbiome-linked metabolite proxies to stratify likely responders, monitor intervention effects, and improve trial comparability. Finally, we outline translational study designs that connect microbiome shifts to protective immune endpoints and performance outcomes, enabling evidence-based integration of microbiome-informed strategies into vaccination programs for poultry, with broader conceptual relevance to other food animals.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
The Role of Lung Microbiota in Shaping Host Immunity and Mucosal Vaccine Responses.
Vaccines, 14(4):.
Respiratory infections remain a leading cause of morbidity and mortality worldwide, highlighting the urgent need to better understand host defense mechanisms in the respiratory tract. Recent advances in sequencing technologies have challenged the traditional view of the lungs as sterile organs and revealed the presence of a distinct, low-biomass microbial community known as the lung microbiota. These microbial populations interact closely with airway epithelial cells and immune cells to maintain respiratory homeostasis and regulate host immune responses. In healthy lungs, microbial communities dominated by Firmicutes, Bacteroidetes, and Proteobacteria contribute to immune regulation through interactions with innate and adaptive immune pathways. Microbiota-derived signals are detected by pattern recognition receptors, activating signaling pathways that regulate cytokine production, immune cell recruitment, and T-cell differentiation. In the respiratory mucosa, microbial stimulation can also induce epithelial and antigen-presenting cells to produce B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL), which promote immunoglobulin A (IgA) class-switch recombination and support mucosal antibody responses. During pulmonary infection, disruption of microbial communities can lead to dysbiosis that amplifies inflammatory responses, impairs epithelial barrier integrity, and increases susceptibility to secondary bacterial infections. In addition to local microbial interactions, the gut-lung axis represents a key communication pathway linking intestinal microbiota with respiratory immunity through microbial metabolites such as short-chain fatty acids (SCFAs) and immune signaling networks. This review summarizes current insights into microbiota-immune crosstalk in the lung during pulmonary infection and discusses how these interactions may inform mucosal vaccine development. A deeper understanding of host-microbiota interactions may enable microbiome-informed vaccines and therapeutic strategies to improve protection against respiratory diseases.
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@article {pmid42042831,
year = {2026},
author = {Alturaiki, W},
title = {The Role of Lung Microbiota in Shaping Host Immunity and Mucosal Vaccine Responses.},
journal = {Vaccines},
volume = {14},
number = {4},
pages = {},
pmid = {42042831},
issn = {2076-393X},
support = {R-2026-x2//Majmaah University/ ; },
abstract = {Respiratory infections remain a leading cause of morbidity and mortality worldwide, highlighting the urgent need to better understand host defense mechanisms in the respiratory tract. Recent advances in sequencing technologies have challenged the traditional view of the lungs as sterile organs and revealed the presence of a distinct, low-biomass microbial community known as the lung microbiota. These microbial populations interact closely with airway epithelial cells and immune cells to maintain respiratory homeostasis and regulate host immune responses. In healthy lungs, microbial communities dominated by Firmicutes, Bacteroidetes, and Proteobacteria contribute to immune regulation through interactions with innate and adaptive immune pathways. Microbiota-derived signals are detected by pattern recognition receptors, activating signaling pathways that regulate cytokine production, immune cell recruitment, and T-cell differentiation. In the respiratory mucosa, microbial stimulation can also induce epithelial and antigen-presenting cells to produce B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL), which promote immunoglobulin A (IgA) class-switch recombination and support mucosal antibody responses. During pulmonary infection, disruption of microbial communities can lead to dysbiosis that amplifies inflammatory responses, impairs epithelial barrier integrity, and increases susceptibility to secondary bacterial infections. In addition to local microbial interactions, the gut-lung axis represents a key communication pathway linking intestinal microbiota with respiratory immunity through microbial metabolites such as short-chain fatty acids (SCFAs) and immune signaling networks. This review summarizes current insights into microbiota-immune crosstalk in the lung during pulmonary infection and discusses how these interactions may inform mucosal vaccine development. A deeper understanding of host-microbiota interactions may enable microbiome-informed vaccines and therapeutic strategies to improve protection against respiratory diseases.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
The Role of the Gut Microbiota and Uraemic Toxins in Vaccine Responsiveness Among People Receiving Maintenance Haemodialysis.
Vaccines, 14(4):.
Background: Patients with kidney failure requiring dialysis experience a high burden of vaccine-preventable diseases, and vaccine hypo-responsiveness is a key contributor. Uraemic toxins and gut dysbiosis are potential causes of hypo-responsiveness. Aim: This study aimed to determine whether uraemic toxin concentrations or gut dysbiosis are associated with vaccine response in haemodialysis patients. Methods: This was a single centre, observational cohort study of maintenance dialysis patients receiving a conventional 2-dose primary COVID-19 vaccination course. Demographic, clinical and vaccination data were collected from the eMR. Vaccine response (Elecsys Anti-SARS-CoV-2 immunoassay), serum uraemic toxin concentrations (indoxyl sulphate, p-cresyl sulphate, and trimethylamine N-oxide by liquid chromatography), and stool microbiome (16S rRNA gene sequencing) were measured 8 weeks after the second dose of vaccine. Results: Forty participants (43% female, mean age 66 years; 59% Caucasian) were included, 70% of whom were classified as a vaccine responder. Antibiotic exposure, prednisolone use and lymphopenia were significantly associated with hypo-responsiveness. Microbiome profiling identified differences in beta diversity between responders and non-responders, positively correlated with short-chain fatty acid producers (Parabacteriodes) and negatively with pathobionts (Escherichia/Shigella). Differential abundance analysis identified lower levels of Tyzzerella, Gemmiger, and Hungatella and higher levels of Turicibacter in vaccine responders. Total uraemic toxin burden and individual toxin concentrations did not differ between responders and hypo-responders (all p > 0.05). Stratification by low versus high/very high toxin burden groupings was not associated with response (p > 0.99). Conclusions: Differences in gut microbial composition were observed between vaccine responder groups, while uraemic toxin concentrations were not associated with vaccine responsiveness. These findings suggest gut microbiota composition may contribute to vaccine hypo-responsiveness in individuals receiving dialysis and warrant further investigation in larger mechanistic studies.
Additional Links: PMID-42042833
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@article {pmid42042833,
year = {2026},
author = {Vaughan, E and Gilbert, A and Shi, B and Perkins, GB and Wu, H and Chadban, S},
title = {The Role of the Gut Microbiota and Uraemic Toxins in Vaccine Responsiveness Among People Receiving Maintenance Haemodialysis.},
journal = {Vaccines},
volume = {14},
number = {4},
pages = {},
pmid = {42042833},
issn = {2076-393X},
abstract = {Background: Patients with kidney failure requiring dialysis experience a high burden of vaccine-preventable diseases, and vaccine hypo-responsiveness is a key contributor. Uraemic toxins and gut dysbiosis are potential causes of hypo-responsiveness. Aim: This study aimed to determine whether uraemic toxin concentrations or gut dysbiosis are associated with vaccine response in haemodialysis patients. Methods: This was a single centre, observational cohort study of maintenance dialysis patients receiving a conventional 2-dose primary COVID-19 vaccination course. Demographic, clinical and vaccination data were collected from the eMR. Vaccine response (Elecsys Anti-SARS-CoV-2 immunoassay), serum uraemic toxin concentrations (indoxyl sulphate, p-cresyl sulphate, and trimethylamine N-oxide by liquid chromatography), and stool microbiome (16S rRNA gene sequencing) were measured 8 weeks after the second dose of vaccine. Results: Forty participants (43% female, mean age 66 years; 59% Caucasian) were included, 70% of whom were classified as a vaccine responder. Antibiotic exposure, prednisolone use and lymphopenia were significantly associated with hypo-responsiveness. Microbiome profiling identified differences in beta diversity between responders and non-responders, positively correlated with short-chain fatty acid producers (Parabacteriodes) and negatively with pathobionts (Escherichia/Shigella). Differential abundance analysis identified lower levels of Tyzzerella, Gemmiger, and Hungatella and higher levels of Turicibacter in vaccine responders. Total uraemic toxin burden and individual toxin concentrations did not differ between responders and hypo-responders (all p > 0.05). Stratification by low versus high/very high toxin burden groupings was not associated with response (p > 0.99). Conclusions: Differences in gut microbial composition were observed between vaccine responder groups, while uraemic toxin concentrations were not associated with vaccine responsiveness. These findings suggest gut microbiota composition may contribute to vaccine hypo-responsiveness in individuals receiving dialysis and warrant further investigation in larger mechanistic studies.},
}
RevDate: 2026-04-27
Burkholderia spp. from HLB-Escape Rhizosphere Suppress Candidatus Liberibacter asiaticus Titers and Induce Defense Responses in Citrus.
Journal of agricultural and food chemistry [Epub ahead of print].
Citrus Huanglongbing (HLB), caused by Candidatus Liberibacter asiaticus (CLas), is the most devastating citrus disease, with no effective control strategies currently available. This study investigated the contribution of the rhizosphere microbiome to HLB resistance by comparing bacterial communities associated with symptomatic and escape trees. Escape trees harbored distinct microbial communities, with notable enrichment of Paraburkholderia spp. Among over 300 isolates, four Burkholderia strains (G23, G24, G25, and G29) exhibited strong inhibitory activity against CLas-related bacteria and close phylogenetic affiliation with Burkholderia theae XITOU. Genomic analyses revealed genes associated with environmental adaptation and host interaction. All four strains suppressed CLas proliferation and induced defense-related gene expression in citrus. Notably, strain G24 significantly reduced CLas titers, alleviated disease symptoms, and promoted plant recovery under field conditions, highlighting its potential as a microbial strategy for HLB management.
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@article {pmid42042856,
year = {2026},
author = {Tian, Y and Wu, L and Xie, X and Gu, J and Zhang, S and Chen, H and Zhang, B and Deng, X and Wang, X and Jiang, Y and Zhong, Y and Chen, W},
title = {Burkholderia spp. from HLB-Escape Rhizosphere Suppress Candidatus Liberibacter asiaticus Titers and Induce Defense Responses in Citrus.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c18038},
pmid = {42042856},
issn = {1520-5118},
abstract = {Citrus Huanglongbing (HLB), caused by Candidatus Liberibacter asiaticus (CLas), is the most devastating citrus disease, with no effective control strategies currently available. This study investigated the contribution of the rhizosphere microbiome to HLB resistance by comparing bacterial communities associated with symptomatic and escape trees. Escape trees harbored distinct microbial communities, with notable enrichment of Paraburkholderia spp. Among over 300 isolates, four Burkholderia strains (G23, G24, G25, and G29) exhibited strong inhibitory activity against CLas-related bacteria and close phylogenetic affiliation with Burkholderia theae XITOU. Genomic analyses revealed genes associated with environmental adaptation and host interaction. All four strains suppressed CLas proliferation and induced defense-related gene expression in citrus. Notably, strain G24 significantly reduced CLas titers, alleviated disease symptoms, and promoted plant recovery under field conditions, highlighting its potential as a microbial strategy for HLB management.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Correlation Between Gut Microbiota and Plasma Metabolites in a Mouse Model for Post-Traumatic Stress Disorder.
Metabolites, 16(4):.
BACKGROUND: The gut microbiota and plasma metabolites have been shown to contribute to the etiology of post-traumatic stress disorder (PTSD). The relationship between the gut microbiome and plasma metabolome in PTSD is poorly understood. This study aims to integrate the gut microbiome data and plasma metabolome data to elucidate microbial-metabolite associations specific for PTSD in a mouse model.
METHODS: A PTSD mouse model was induced by single prolonged stress and electric foot shock (SPS&S). We sequenced the gut microbiota composition by 16S rRNA gene sequencing and used ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) for the plasma metabolomic profiling to explore the association between the gut microbiota and the plasma metabolites in mice with PTSD.
RESULTS: The PTSD mice exhibited robust anxiety-like behaviors, significantly elevated plasma IL-1β and TNF-α, and profound gut dysbiosis characterized by a marked depletion of Muribaculaceae and Akkermansia and expansion of the Lachnospiraceae_NK4A136_group. The plasma metabolomics identified 24 significantly dysregulated metabolites, including upregulated L-arginine, palmitic acid, and oleic acid, and downregulated uridine. The pathway enrichment analysis revealed coordinated perturbations in arginine biosynthesis, pyrimidine metabolism, unsaturated fatty acid biosynthesis, and glycerophospholipid metabolism. Critically, genus-level correlation analysis uncovered biologically coherent associations. The Muribaculaceae abundance showed strong negative correlations with L-arginine and palmitic acid and positive correlations with L-glutamine and thymidine.
CONCLUSIONS: This study provides an exploratory investigation into the association network between the gut microbiota and the plasma metabolites in a PTSD mouse model, offering preliminary insights into potential microbe-metabolite interactions in PTSD.
Additional Links: PMID-42042868
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Citation:
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@article {pmid42042868,
year = {2026},
author = {Zhou, D and Huang, Y and Li, F and Liu, Q and Wang, X and Wei, Q and Chen, J and Liu, Z and Huang, Y},
title = {Correlation Between Gut Microbiota and Plasma Metabolites in a Mouse Model for Post-Traumatic Stress Disorder.},
journal = {Metabolites},
volume = {16},
number = {4},
pages = {},
pmid = {42042868},
issn = {2218-1989},
support = {CSTB2022NSCQ-MSX0163//Natural Science Foundation of Chongqing (General Program)/ ; },
abstract = {BACKGROUND: The gut microbiota and plasma metabolites have been shown to contribute to the etiology of post-traumatic stress disorder (PTSD). The relationship between the gut microbiome and plasma metabolome in PTSD is poorly understood. This study aims to integrate the gut microbiome data and plasma metabolome data to elucidate microbial-metabolite associations specific for PTSD in a mouse model.
METHODS: A PTSD mouse model was induced by single prolonged stress and electric foot shock (SPS&S). We sequenced the gut microbiota composition by 16S rRNA gene sequencing and used ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) for the plasma metabolomic profiling to explore the association between the gut microbiota and the plasma metabolites in mice with PTSD.
RESULTS: The PTSD mice exhibited robust anxiety-like behaviors, significantly elevated plasma IL-1β and TNF-α, and profound gut dysbiosis characterized by a marked depletion of Muribaculaceae and Akkermansia and expansion of the Lachnospiraceae_NK4A136_group. The plasma metabolomics identified 24 significantly dysregulated metabolites, including upregulated L-arginine, palmitic acid, and oleic acid, and downregulated uridine. The pathway enrichment analysis revealed coordinated perturbations in arginine biosynthesis, pyrimidine metabolism, unsaturated fatty acid biosynthesis, and glycerophospholipid metabolism. Critically, genus-level correlation analysis uncovered biologically coherent associations. The Muribaculaceae abundance showed strong negative correlations with L-arginine and palmitic acid and positive correlations with L-glutamine and thymidine.
CONCLUSIONS: This study provides an exploratory investigation into the association network between the gut microbiota and the plasma metabolites in a PTSD mouse model, offering preliminary insights into potential microbe-metabolite interactions in PTSD.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Age-Specific Ex Vivo Modulation of Gut-Brain Axis-Associated Metabolites by Galacto-Oligosaccharides and Nutrient Blends in Early Childhood.
Metabolites, 16(4):.
Background: Gut microbiome-derived metabolites, particularly short-chain fatty acids (SCFA) and tryptophan derivatives, are central mediators of the gut-brain axis. This ex vivo study assessed how nutritional interventions impact such metabolites during early life, a critical period for neurodevelopment. Methods: The effects of galacto-oligosaccharides (GOS), nutrient blends (vitamins, minerals and amino acids) and their combinations were evaluated in the gut microbiomes of infants (2-4 months, n = 6) and young children (2-3 years old, n = 6) using the ex vivo SIFR[®] technology. Results: Baseline microbiome composition was age-dependent, with infants displaying lower α-diversity and greater interpersonal variability. After ex vivo incubation, nutrient blends increased the propionate/butyrate ratio and branched-chain fatty acids in young children and elevated several B-vitamins and amino acid-derived metabolites, including indole-3-carboxaldehyde, imidazoleacetic acid and pipecolinic acid. Combining nutrient blends with GOS exhibited potential synergistic effects on propionate (infants) and 2-hydroxyisocaproic acid (HICA, both age groups). GOS strongly stimulated Bifidobacteriaceae and increased metabolites linked to bifidobacterial metabolism like acetate, HICA, N-acetylated amino acids, aromatic lactic acids and acetylagmatine; in young children, butyrate and γ-aminobutyric acid (GABA) also increased. Conclusions: Combinations of GOS with nutrient blends impacted microbiome-derived metabolites associated with the gut-brain axis, with potential synergistic increases of metabolites with emerging roles in neurodevelopment, including GABA, acetylagmatine and HICA. Despite shared bifidogenic effects, differences between age groups indicate that microbiome maturity may influence responses to nutritional intervention. Future clinical studies are needed to determine whether these metabolite changes translate into neurodevelopmental benefits in vivo.
Additional Links: PMID-42042900
PubMed:
Citation:
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@article {pmid42042900,
year = {2026},
author = {Ferrier, L and Dogra, SK and Vu, LD and Kanellopoulos, AK and Poppe, J and Biehl, L and Baudot, A and Van den Abbeele, P},
title = {Age-Specific Ex Vivo Modulation of Gut-Brain Axis-Associated Metabolites by Galacto-Oligosaccharides and Nutrient Blends in Early Childhood.},
journal = {Metabolites},
volume = {16},
number = {4},
pages = {},
pmid = {42042900},
issn = {2218-1989},
abstract = {Background: Gut microbiome-derived metabolites, particularly short-chain fatty acids (SCFA) and tryptophan derivatives, are central mediators of the gut-brain axis. This ex vivo study assessed how nutritional interventions impact such metabolites during early life, a critical period for neurodevelopment. Methods: The effects of galacto-oligosaccharides (GOS), nutrient blends (vitamins, minerals and amino acids) and their combinations were evaluated in the gut microbiomes of infants (2-4 months, n = 6) and young children (2-3 years old, n = 6) using the ex vivo SIFR[®] technology. Results: Baseline microbiome composition was age-dependent, with infants displaying lower α-diversity and greater interpersonal variability. After ex vivo incubation, nutrient blends increased the propionate/butyrate ratio and branched-chain fatty acids in young children and elevated several B-vitamins and amino acid-derived metabolites, including indole-3-carboxaldehyde, imidazoleacetic acid and pipecolinic acid. Combining nutrient blends with GOS exhibited potential synergistic effects on propionate (infants) and 2-hydroxyisocaproic acid (HICA, both age groups). GOS strongly stimulated Bifidobacteriaceae and increased metabolites linked to bifidobacterial metabolism like acetate, HICA, N-acetylated amino acids, aromatic lactic acids and acetylagmatine; in young children, butyrate and γ-aminobutyric acid (GABA) also increased. Conclusions: Combinations of GOS with nutrient blends impacted microbiome-derived metabolites associated with the gut-brain axis, with potential synergistic increases of metabolites with emerging roles in neurodevelopment, including GABA, acetylagmatine and HICA. Despite shared bifidogenic effects, differences between age groups indicate that microbiome maturity may influence responses to nutritional intervention. Future clinical studies are needed to determine whether these metabolite changes translate into neurodevelopmental benefits in vivo.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
A Dual-Target Microbial Therapeutic Strategy for Treating Metabolic Diseases: Complementary Mechanisms and Clinical Prospects of Lactiplantibacillus plantarum and Akkermansia muciniphila.
Metabolites, 16(4):.
Metabolic diseases, including obesity, type 2 diabetes, and their related complications, have emerged as major global public health challenges. Increasing evidence indicates that gut microbiota dysbiosis contributes to disrupted metabolic homeostasis, chronic low-grade inflammation, and progression of metabolic disorders. Among candidate microbiome-based interventions, Lactiplantibacillus plantarum (L. plantarum) and Akkermansia muciniphila (A. muciniphila) have attracted particular attention because they regulate host metabolism through partially distinct yet potentially complementary mechanisms. L. plantarum has been associated with modulation of appetite-related hormones, adipose tissue remodeling, reinforcement of intestinal barrier function, and attenuation of inflammatory signaling. A. muciniphila has been linked to strengthening of the mucus barrier, production of beneficial metabolites, and improvement in immune and metabolic homeostasis. However, current evidence remains fragmented across strain-specific studies, heterogeneous formulations, and predominantly single-strain experimental designs, and direct comparative evidence for combined administration is still limited. This review synthesizes current epidemiological, mechanistic, preclinical, and clinical evidence on L. plantarum and A. muciniphila, with emphasis on their physiological traits, gut ecological adaptability, pathway-based metabolic effects, and translational challenges in obesity, type 2 diabetes, and related complications. We further highlight the ecological rationale for their functional complementarity and discuss priorities for future combination studies and precision implementation. Overall, the available literature supports functional complementarity and possible additive metabolic benefits, but synergistic effects in humans remain unconfirmed. A clearer understanding of strain identity, active therapeutic entities, delivery strategies, and host context will be essential for advancing this dual-target microbial strategy toward clinically meaningful applications.
Additional Links: PMID-42042904
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Citation:
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@article {pmid42042904,
year = {2026},
author = {Liu, S and Wang, M and Sun, X and Jia, Z and Huang, K},
title = {A Dual-Target Microbial Therapeutic Strategy for Treating Metabolic Diseases: Complementary Mechanisms and Clinical Prospects of Lactiplantibacillus plantarum and Akkermansia muciniphila.},
journal = {Metabolites},
volume = {16},
number = {4},
pages = {},
pmid = {42042904},
issn = {2218-1989},
support = {KJQN202401144//Chongqing Municipality Education Commission/ ; },
abstract = {Metabolic diseases, including obesity, type 2 diabetes, and their related complications, have emerged as major global public health challenges. Increasing evidence indicates that gut microbiota dysbiosis contributes to disrupted metabolic homeostasis, chronic low-grade inflammation, and progression of metabolic disorders. Among candidate microbiome-based interventions, Lactiplantibacillus plantarum (L. plantarum) and Akkermansia muciniphila (A. muciniphila) have attracted particular attention because they regulate host metabolism through partially distinct yet potentially complementary mechanisms. L. plantarum has been associated with modulation of appetite-related hormones, adipose tissue remodeling, reinforcement of intestinal barrier function, and attenuation of inflammatory signaling. A. muciniphila has been linked to strengthening of the mucus barrier, production of beneficial metabolites, and improvement in immune and metabolic homeostasis. However, current evidence remains fragmented across strain-specific studies, heterogeneous formulations, and predominantly single-strain experimental designs, and direct comparative evidence for combined administration is still limited. This review synthesizes current epidemiological, mechanistic, preclinical, and clinical evidence on L. plantarum and A. muciniphila, with emphasis on their physiological traits, gut ecological adaptability, pathway-based metabolic effects, and translational challenges in obesity, type 2 diabetes, and related complications. We further highlight the ecological rationale for their functional complementarity and discuss priorities for future combination studies and precision implementation. Overall, the available literature supports functional complementarity and possible additive metabolic benefits, but synergistic effects in humans remain unconfirmed. A clearer understanding of strain identity, active therapeutic entities, delivery strategies, and host context will be essential for advancing this dual-target microbial strategy toward clinically meaningful applications.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Kidney Function Modulates Gut Microbial Metabolism.
Toxins, 18(4):.
Growing evidence suggests that chronic kidney disease (CKD) profoundly disrupts gut microbiome and its activity. This study explores how CKD affects colon microbial metabolism, focusing on (1) the representativeness of fecal metabolomics, (2) saccharolytic and proteolytic fermentation metabolites, and (3) the gut microbiome's role in the partitioning of tryptophan in its metabolic pathways. Tryptophan's main metabolic pathways include the indolic and the kynurenine pathways, which lead, respectively, to the formation of indoxyl sulfate and kynurenine, both contributing to uremic toxicity. Using a rat model of CKD, we evaluated whether fecal concentrations of microbial compounds, on which most studies are based, reflect the colonic concentrations in contact with the gut mucosa. Thus, we quantified the concentration and content of amino acids, indole, p-cresol, and also short-chain fatty acids, in different colon sections. We demonstrated that CKD promotes increased proteolytic fermentation and an augmented tryptophan partitioning into both the indolic and kynurenine pathways. Depletion of the indolic pathway obtained upon antibiotic treatment leads to a further enhancement of the kynurenine pathway.
Additional Links: PMID-42043039
PubMed:
Citation:
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@article {pmid42043039,
year = {2026},
author = {Lauriola, M and Valkenburg, S and Dejongh, S and Zadora, W and Krukowski, H and Evenepoel, P and Raes, J and Farré, R and Glorieux, G and Meijers, B},
title = {Kidney Function Modulates Gut Microbial Metabolism.},
journal = {Toxins},
volume = {18},
number = {4},
pages = {},
pmid = {42043039},
issn = {2072-6651},
support = {860329//European Union's Horizon 2020 research and innovation program/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Renal Insufficiency, Chronic/metabolism/microbiology/physiopathology ; *Colon/microbiology/metabolism ; Male ; Tryptophan/metabolism ; Feces/microbiology/chemistry ; *Kidney/physiopathology ; Fatty Acids, Volatile/metabolism ; Indoles/metabolism ; Kynurenine/metabolism ; Rats ; Amino Acids/metabolism ; Fermentation ; Rats, Wistar ; Cresols/metabolism ; *Bacteria/metabolism ; },
abstract = {Growing evidence suggests that chronic kidney disease (CKD) profoundly disrupts gut microbiome and its activity. This study explores how CKD affects colon microbial metabolism, focusing on (1) the representativeness of fecal metabolomics, (2) saccharolytic and proteolytic fermentation metabolites, and (3) the gut microbiome's role in the partitioning of tryptophan in its metabolic pathways. Tryptophan's main metabolic pathways include the indolic and the kynurenine pathways, which lead, respectively, to the formation of indoxyl sulfate and kynurenine, both contributing to uremic toxicity. Using a rat model of CKD, we evaluated whether fecal concentrations of microbial compounds, on which most studies are based, reflect the colonic concentrations in contact with the gut mucosa. Thus, we quantified the concentration and content of amino acids, indole, p-cresol, and also short-chain fatty acids, in different colon sections. We demonstrated that CKD promotes increased proteolytic fermentation and an augmented tryptophan partitioning into both the indolic and kynurenine pathways. Depletion of the indolic pathway obtained upon antibiotic treatment leads to a further enhancement of the kynurenine pathway.},
}
MeSH Terms:
show MeSH Terms
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Animals
*Gastrointestinal Microbiome
*Renal Insufficiency, Chronic/metabolism/microbiology/physiopathology
*Colon/microbiology/metabolism
Male
Tryptophan/metabolism
Feces/microbiology/chemistry
*Kidney/physiopathology
Fatty Acids, Volatile/metabolism
Indoles/metabolism
Kynurenine/metabolism
Rats
Amino Acids/metabolism
Fermentation
Rats, Wistar
Cresols/metabolism
*Bacteria/metabolism
RevDate: 2026-04-27
CmpDate: 2026-04-27
Physiological Stress Signatures of Waterborne Glyphosate Exposure in Apostichopus japonicus: Insights for Aquatic Ecotoxicology.
Toxics, 14(4):.
Glyphosate is a widely used herbicide with increasing concern regarding its non-target impacts in coastal ecosystems and mariculture species. Here, we profiled acute physiological stress signatures of waterborne glyphosate exposure in the sea cucumber Apostichopus japonicus, integrating measured exposure concentrations, tissue residues, digestive and oxidative/innate immune biomarkers, and gut microbiota. After 24 h exposure, measured waterborne glyphosate confirmed the intended gradient (0.09 ± 0.02, 1.26 ± 0.09, and 4.49 ± 1.12 mg/L for low-, medium-, and high-dose treatments, respectively), and overt stress phenotypes with mortality occurred only at the high dose (36.67%), enabling separation of high-dose survivors (HS) and high-dose dead (HD) for downstream analyses. Tissue measurements showed low/background levels in controls, with compartment-specific distribution: the respiratory tree exhibited higher burdens at the medium dose, whereas coelomic fluid showed the highest burdens in HS at the 24 h endpoint. Functionally, most intestinal digestive enzymes were unchanged, but trypsin activity was consistently suppressed across exposed groups (p < 0.05). In coelomic fluid, oxidative stress responses were evident, with elevated MDA (L and M), reduced CAT (L, M, and HS), and reduced GSH-PX in HS (all p < 0.05), while SOD, GR, and lysozyme showed no significant changes. Gene sequencing of 16S rRNA (n = 3 per group) revealed significant shifts in community diversity/evenness (Shannon p = 0.0497; Simpson p = 0.0484) and beta diversity (PCo1 = 30.08%, PCo2 = 26.30%; PERMANOVA F = 1.816, p = 0.008), with LEfSe indicating discriminative taxa associated with exposure/outcomes. Collectively, these multi-level endpoints define an acute glyphosate stress signature in A. japonicus, linking internal dose distribution to oxidative disruption, impaired intestinal proteolysis, and microbiome restructuring.
Additional Links: PMID-42043109
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@article {pmid42043109,
year = {2026},
author = {Sun, J and Kuang, S and Yang, H},
title = {Physiological Stress Signatures of Waterborne Glyphosate Exposure in Apostichopus japonicus: Insights for Aquatic Ecotoxicology.},
journal = {Toxics},
volume = {14},
number = {4},
pages = {},
pmid = {42043109},
issn = {2305-6304},
support = {2023YFE0106200//the National Key R&D Program of China/ ; },
abstract = {Glyphosate is a widely used herbicide with increasing concern regarding its non-target impacts in coastal ecosystems and mariculture species. Here, we profiled acute physiological stress signatures of waterborne glyphosate exposure in the sea cucumber Apostichopus japonicus, integrating measured exposure concentrations, tissue residues, digestive and oxidative/innate immune biomarkers, and gut microbiota. After 24 h exposure, measured waterborne glyphosate confirmed the intended gradient (0.09 ± 0.02, 1.26 ± 0.09, and 4.49 ± 1.12 mg/L for low-, medium-, and high-dose treatments, respectively), and overt stress phenotypes with mortality occurred only at the high dose (36.67%), enabling separation of high-dose survivors (HS) and high-dose dead (HD) for downstream analyses. Tissue measurements showed low/background levels in controls, with compartment-specific distribution: the respiratory tree exhibited higher burdens at the medium dose, whereas coelomic fluid showed the highest burdens in HS at the 24 h endpoint. Functionally, most intestinal digestive enzymes were unchanged, but trypsin activity was consistently suppressed across exposed groups (p < 0.05). In coelomic fluid, oxidative stress responses were evident, with elevated MDA (L and M), reduced CAT (L, M, and HS), and reduced GSH-PX in HS (all p < 0.05), while SOD, GR, and lysozyme showed no significant changes. Gene sequencing of 16S rRNA (n = 3 per group) revealed significant shifts in community diversity/evenness (Shannon p = 0.0497; Simpson p = 0.0484) and beta diversity (PCo1 = 30.08%, PCo2 = 26.30%; PERMANOVA F = 1.816, p = 0.008), with LEfSe indicating discriminative taxa associated with exposure/outcomes. Collectively, these multi-level endpoints define an acute glyphosate stress signature in A. japonicus, linking internal dose distribution to oxidative disruption, impaired intestinal proteolysis, and microbiome restructuring.},
}
RevDate: 2026-04-27
CmpDate: 2026-04-27
Functional Portability of a Hyperaccumulator-Derived Core Microbiome: Enhancing Cadmium Phytoextraction in Brassica juncea L. Through Molecular Reprogramming.
Toxics, 14(4):.
Soil cadmium (Cd) contamination is a persistent threat to global food security, requiring sustainable in situ remediation strategies. While hyperaccumulating plants possess specialized traits for metal extraction, their low biomass limits large-scale application. This study investigates the potential of a core endophytic synthetic community (SynCom-NS)-characterized by heavy metal tolerance and growth-promoting traits, originally derived from the hyperaccumulator Sedum alfredii-by assessing its ability to modulate the remediation phenotype of a high-biomass non-host crop, Brassica juncea. Pot experiments revealed that SynCom-NS root-zone application significantly alleviated Cd toxicity, increasing total fresh weight by 82% and chlorophyll content by 33%. Crucially, the consortium bypassed the "growth-dilution" trade-off, facilitating a 4.07-fold increase in shoot Cd accumulation. Multi-omics analysis demonstrated a systemic modulation of the host's defense machinery, marked by a >3-fold surge in glutathione (GSH) levels and the induction of phenylpropanoid biosynthesis for cell wall reinforcement. SynCom-NS application also mediated tissue-specific regulation of the key metal transporter HMA4, upregulating its expression in roots to accelerate long-distance translocation while downregulating it in shoots. These findings demonstrate that specialized core microbiomes function as potent bio-inoculants, offering a promising biological strategy for engineering high-efficiency phytoremediation systems.
Additional Links: PMID-42043130
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Citation:
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@article {pmid42043130,
year = {2026},
author = {Huang, L and Fu, S and Du, S and Feng, Y},
title = {Functional Portability of a Hyperaccumulator-Derived Core Microbiome: Enhancing Cadmium Phytoextraction in Brassica juncea L. Through Molecular Reprogramming.},
journal = {Toxics},
volume = {14},
number = {4},
pages = {},
pmid = {42043130},
issn = {2305-6304},
support = {LQN26D010019//Zhejiang Province Natural Science Foundation/ ; 42507020//National Natural Science Foundation of China/ ; },
abstract = {Soil cadmium (Cd) contamination is a persistent threat to global food security, requiring sustainable in situ remediation strategies. While hyperaccumulating plants possess specialized traits for metal extraction, their low biomass limits large-scale application. This study investigates the potential of a core endophytic synthetic community (SynCom-NS)-characterized by heavy metal tolerance and growth-promoting traits, originally derived from the hyperaccumulator Sedum alfredii-by assessing its ability to modulate the remediation phenotype of a high-biomass non-host crop, Brassica juncea. Pot experiments revealed that SynCom-NS root-zone application significantly alleviated Cd toxicity, increasing total fresh weight by 82% and chlorophyll content by 33%. Crucially, the consortium bypassed the "growth-dilution" trade-off, facilitating a 4.07-fold increase in shoot Cd accumulation. Multi-omics analysis demonstrated a systemic modulation of the host's defense machinery, marked by a >3-fold surge in glutathione (GSH) levels and the induction of phenylpropanoid biosynthesis for cell wall reinforcement. SynCom-NS application also mediated tissue-specific regulation of the key metal transporter HMA4, upregulating its expression in roots to accelerate long-distance translocation while downregulating it in shoots. These findings demonstrate that specialized core microbiomes function as potent bio-inoculants, offering a promising biological strategy for engineering high-efficiency phytoremediation systems.},
}
RevDate: 2026-04-23
The network structure of cross-feeding impacts microbial community diversity under growth-inhibiting stresses.
Nature communications pii:10.1038/s41467-026-71097-5 [Epub ahead of print].
Perturbations such as dietary shifts and drug treatment can reduce gut microbiome diversity, with negative consequences for host health, yet predicting diversity responses remains challenging because microbial species interact through multiple mechanisms. While nutrient competition and cross-feeding both influence microbiota assembly, environmental stresses such as antibiotics are typically studied experimentally in monoculture, and most theoretical frameworks consider nutrient competition alone. To investigate how these processes jointly shape community structure, we develop a consumer-resource model that incorporates nutrient competition, growth-inhibiting stress, and metabolite cross-feeding with a unified framework spanning varied cross-feeding architectures. For three-species communities, coexistence during narrow-spectrum growth inhibition is maximized by cyclic cross-feeding networks, whereas fully connected cross-feeding networks maximize coexistence during broad-spectrum growth inhibition. However, the benefits of cyclic cross-feeding depend strongly on community size and stress targeting: in communities with more than six species and six resources, cyclic networks can destabilize coexistence. These results are robust to inefficient leakage, dead-end metabolites, and embedding in larger communities, and large communities generalize to random leakage architectures in which connectivity determines the response to stress. Together, this framework shows that cross-feeding network architecture can fundamentally reshape how microbial communities respond to growth-inhibiting stresses.
Additional Links: PMID-42026051
Publisher:
PubMed:
Citation:
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@article {pmid42026051,
year = {2026},
author = {Newton, DP and Ho, PY and Huang, KC},
title = {The network structure of cross-feeding impacts microbial community diversity under growth-inhibiting stresses.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-71097-5},
pmid = {42026051},
issn = {2041-1723},
support = {RM1 GM135102/GM/NIGMS NIH HHS/United States ; F32 GM143859/GM/NIGMS NIH HHS/United States ; },
abstract = {Perturbations such as dietary shifts and drug treatment can reduce gut microbiome diversity, with negative consequences for host health, yet predicting diversity responses remains challenging because microbial species interact through multiple mechanisms. While nutrient competition and cross-feeding both influence microbiota assembly, environmental stresses such as antibiotics are typically studied experimentally in monoculture, and most theoretical frameworks consider nutrient competition alone. To investigate how these processes jointly shape community structure, we develop a consumer-resource model that incorporates nutrient competition, growth-inhibiting stress, and metabolite cross-feeding with a unified framework spanning varied cross-feeding architectures. For three-species communities, coexistence during narrow-spectrum growth inhibition is maximized by cyclic cross-feeding networks, whereas fully connected cross-feeding networks maximize coexistence during broad-spectrum growth inhibition. However, the benefits of cyclic cross-feeding depend strongly on community size and stress targeting: in communities with more than six species and six resources, cyclic networks can destabilize coexistence. These results are robust to inefficient leakage, dead-end metabolites, and embedding in larger communities, and large communities generalize to random leakage architectures in which connectivity determines the response to stress. Together, this framework shows that cross-feeding network architecture can fundamentally reshape how microbial communities respond to growth-inhibiting stresses.},
}
RevDate: 2026-04-23
Seasonality of composition, genomic potential and activity of coniferous forest soil microbiomes.
Scientific data pii:10.1038/s41597-026-07163-w [Epub ahead of print].
Coniferous forest soils represent a globally important carbon sink, where the microbiome is essential for carbon flux between tree roots, rhizosphere, litter and soil. Soil habitats, such as roots, rhizosphere, bulk soil and litter differ in physicochemical properties and composition of highly specialized microbial communities, whose activity reflects the seasonality of temperature and tree activity of these mid- to high-latitude biomes. Here we present a multi-omic dataset encompassing 160 samples collected from four coniferous forest soil habitats in the Czech Republic and Norway, sampled in early summer, late summer, early winter and late winter that characterize the composition, genomic potential and activity of tree roots and microbiome. For each sample, we provide metabarcoding-based composition of bacterial, fungal and eukaryotic communities, results of shotgun DNA sequencing (metagenomes) and shotgun RNA sequencing (metatranscriptomes) illustrating the functional potential and activity within habitats. This dataset enables analyses of the temporal variation of taxonomic composition, functional potential and transcription across seasons in a temperate and boreal coniferous forest.
Additional Links: PMID-42026082
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@article {pmid42026082,
year = {2026},
author = {Human, ZR and Štursová, M and Odriozola, I and Větrovský, T and Howe, A and Navrátilová, D and López-Mondéjar, R and Žifčáková, L and Brabcová, V and Mundra, S and Thoen, E and Morgado, L and Fiore-Donno, AM and Bonkowski, M and Adamczyk, B and Kohout, P and Lipton, MS and Calhoun, S and LaButti, K and Lipzen, A and Keymanesh, K and Tejomurthula, S and Pennacchio, C and Grigoriev, IV and Martin, F and Kauserud, H and Baldrian, P},
title = {Seasonality of composition, genomic potential and activity of coniferous forest soil microbiomes.},
journal = {Scientific data},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41597-026-07163-w},
pmid = {42026082},
issn = {2052-4463},
support = {240859//Norges Forskningsråd (Research Council of Norway)/ ; },
abstract = {Coniferous forest soils represent a globally important carbon sink, where the microbiome is essential for carbon flux between tree roots, rhizosphere, litter and soil. Soil habitats, such as roots, rhizosphere, bulk soil and litter differ in physicochemical properties and composition of highly specialized microbial communities, whose activity reflects the seasonality of temperature and tree activity of these mid- to high-latitude biomes. Here we present a multi-omic dataset encompassing 160 samples collected from four coniferous forest soil habitats in the Czech Republic and Norway, sampled in early summer, late summer, early winter and late winter that characterize the composition, genomic potential and activity of tree roots and microbiome. For each sample, we provide metabarcoding-based composition of bacterial, fungal and eukaryotic communities, results of shotgun DNA sequencing (metagenomes) and shotgun RNA sequencing (metatranscriptomes) illustrating the functional potential and activity within habitats. This dataset enables analyses of the temporal variation of taxonomic composition, functional potential and transcription across seasons in a temperate and boreal coniferous forest.},
}
RevDate: 2026-04-26
Rumen bacteria, feed utilization, and milk production of Damascus goats fed different levels of azolla meal.
Scientific reports, 16(1):.
UNLABELLED: Azolla could be a promising alternative feed as it is a rich source of nutrients and bioactive compounds that can modulate rumen microbiota and improve animal productivity. This study evaluated the effects of inclusion dietary Azolla (Azolla pinnata) as a partial replacement of concentrate feed mixture (CFM) on rumen bacteria, nutrient digestibility, and milk production in lactating Damascus goats. Thirty-two goats were assigned to four groups (n = 8): a control group (C), A10, A20, and A30 to receive 0, 10%, 20%, and 30% of Azolla as a replacement of CFM, respectively. Microbial diversity increased in Azolla-fed goats, with enrichment of phylum Firmicutes in Azolla-supplemented groups C=13.36%, A10= 31.09%, A20= 25.15%, and A30= 29.85%. Fiber-degrading bacterial genera such as Prevotella, Ruminococcus, and Christensenellaceae R-7 group. .Crude protein digestibility was declined in supplemented groups and was found in order 74.76>69.11>68.24>63.93 %. Total volatile fatty acids (TVFA) and the concentration of acetate, propionate, and butyrate were higher in supplemented groups (p < 0.01). Fat-corrected milk (FCM) was higher in A20 (1139 mL/head) compared to other groups (C=992, A10=1050, A30=888 mL/head and feed efficiency followed the same trend (p < 0.05). Azolla could replace 20% of CFM in goats’ diet, and it is a viable alternative feed resource, particularly under challenges associated with the availability of conventional concentrate mixtures.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-38113-6.
Additional Links: PMID-42026105
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@article {pmid42026105,
year = {2026},
author = {Abd-Elgwad, AFA and Bakr, SA and Sabra, EA and Khorshed, MM and Metwally, HM and Rabee, AE},
title = {Rumen bacteria, feed utilization, and milk production of Damascus goats fed different levels of azolla meal.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {42026105},
issn = {2045-2322},
abstract = {UNLABELLED: Azolla could be a promising alternative feed as it is a rich source of nutrients and bioactive compounds that can modulate rumen microbiota and improve animal productivity. This study evaluated the effects of inclusion dietary Azolla (Azolla pinnata) as a partial replacement of concentrate feed mixture (CFM) on rumen bacteria, nutrient digestibility, and milk production in lactating Damascus goats. Thirty-two goats were assigned to four groups (n = 8): a control group (C), A10, A20, and A30 to receive 0, 10%, 20%, and 30% of Azolla as a replacement of CFM, respectively. Microbial diversity increased in Azolla-fed goats, with enrichment of phylum Firmicutes in Azolla-supplemented groups C=13.36%, A10= 31.09%, A20= 25.15%, and A30= 29.85%. Fiber-degrading bacterial genera such as Prevotella, Ruminococcus, and Christensenellaceae R-7 group. .Crude protein digestibility was declined in supplemented groups and was found in order 74.76>69.11>68.24>63.93 %. Total volatile fatty acids (TVFA) and the concentration of acetate, propionate, and butyrate were higher in supplemented groups (p < 0.01). Fat-corrected milk (FCM) was higher in A20 (1139 mL/head) compared to other groups (C=992, A10=1050, A30=888 mL/head and feed efficiency followed the same trend (p < 0.05). Azolla could replace 20% of CFM in goats’ diet, and it is a viable alternative feed resource, particularly under challenges associated with the availability of conventional concentrate mixtures.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-38113-6.},
}
RevDate: 2026-04-23
The long-lived immune system of centenarians.
Nature reviews. Immunology [Epub ahead of print].
Centenarians - individuals aged 100 years or older - constitute a biologically distinct human population that achieves exceptional longevity while frequently retaining functional independence and avoiding major age-related diseases or postponing their onset. Despite their advanced age, many centenarians show relatively preserved immune function and resistance to conditions linked to immunosenescence and chronic low-grade inflammation (inflammageing). These features are especially pronounced in semi-supercentenarians (105-109 years) and supercentenarians (≥110 years), whose immune profiles often resemble those of much younger individuals. In this Review, we explore how centenarians modulate key hallmarks of immune ageing across innate and adaptive immune compartments. We discuss evidence that they limit the pathological effects of inflammageing, potentially through reduced NLRP3 inflammasome activation, enhanced autophagy and a tempered senescence-associated secretory phenotype. Omics studies further reveal transcriptomic, epigenetic and microbial signatures consistent with preserved immune function, including youth-like gene expression patterns in circulating immune cells and beneficial shifts in gut microbiome composition. Together, these findings suggest that centenarians achieve longevity through coordinated adaptations that maintain immune homeostasis and disease resistance and may inform strategies to enhance healthspan in ageing societies.
Additional Links: PMID-42026253
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@article {pmid42026253,
year = {2026},
author = {Plaza-Florido, A and Carrera-Bastos, P and Pérez-Prieto, I and Fiuza-Luces, C and Radom-Aizik, S and Del Pozo Cruz, B and Franceschi, C and López-Soto, A and López-Otín, C and Lucia, A},
title = {The long-lived immune system of centenarians.},
journal = {Nature reviews. Immunology},
volume = {},
number = {},
pages = {},
pmid = {42026253},
issn = {1474-1741},
abstract = {Centenarians - individuals aged 100 years or older - constitute a biologically distinct human population that achieves exceptional longevity while frequently retaining functional independence and avoiding major age-related diseases or postponing their onset. Despite their advanced age, many centenarians show relatively preserved immune function and resistance to conditions linked to immunosenescence and chronic low-grade inflammation (inflammageing). These features are especially pronounced in semi-supercentenarians (105-109 years) and supercentenarians (≥110 years), whose immune profiles often resemble those of much younger individuals. In this Review, we explore how centenarians modulate key hallmarks of immune ageing across innate and adaptive immune compartments. We discuss evidence that they limit the pathological effects of inflammageing, potentially through reduced NLRP3 inflammasome activation, enhanced autophagy and a tempered senescence-associated secretory phenotype. Omics studies further reveal transcriptomic, epigenetic and microbial signatures consistent with preserved immune function, including youth-like gene expression patterns in circulating immune cells and beneficial shifts in gut microbiome composition. Together, these findings suggest that centenarians achieve longevity through coordinated adaptations that maintain immune homeostasis and disease resistance and may inform strategies to enhance healthspan in ageing societies.},
}
RevDate: 2026-04-23
Patterns in Marine Fungal Diversity and Community Structure on Native Versus Invasive Macroalgae at a Local Geographic Scale.
Microbial ecology pii:10.1007/s00248-026-02781-8 [Epub ahead of print].
Additional Links: PMID-42026383
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PubMed:
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@article {pmid42026383,
year = {2026},
author = {Owen, EAM and Griffiths, RI and Golyshin, PN and Chernikova, TN and Kurr, M},
title = {Patterns in Marine Fungal Diversity and Community Structure on Native Versus Invasive Macroalgae at a Local Geographic Scale.},
journal = {Microbial ecology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00248-026-02781-8},
pmid = {42026383},
issn = {1432-184X},
support = {81280//European Regional Development Fund (ERDF)/ ; 81280//European Regional Development Fund (ERDF)/ ; },
}
RevDate: 2026-04-23
Functional remodeling of the gut microbiome and metabolome in primary idiopathic male infertility.
BMC microbiology pii:10.1186/s12866-026-05064-x [Epub ahead of print].
Additional Links: PMID-42026467
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PubMed:
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@article {pmid42026467,
year = {2026},
author = {Luo, C and Yao, H and Xian, Y and Yang, T and Xiao, X and Ying, L and Xu, J and Luo, X and Qiu, D and Liu, Y and Liu, B and Li, F},
title = {Functional remodeling of the gut microbiome and metabolome in primary idiopathic male infertility.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05064-x},
pmid = {42026467},
issn = {1471-2180},
support = {2024NSFSC0647//Sichuan Provincial Science and Technology Support Program/ ; 24SYJS01//Health Commission of Sichuan Province Medical Science and Technology Program/ ; SCU2025J4183//the Fundamental Research Funds for the Central Universities/ ; },
}
RevDate: 2026-04-23
Apple replant disease resistance in different apple rootstocks evaluated using microbiomic and metabolomic analyses.
BMC plant biology pii:10.1186/s12870-026-08844-9 [Epub ahead of print].
Additional Links: PMID-42026475
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PubMed:
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@article {pmid42026475,
year = {2026},
author = {Jia, L and Ren, S and Zhang, J and Ma, J and Yu, Z and Sun, N and Li, B and Zhang, X and Liang, B},
title = {Apple replant disease resistance in different apple rootstocks evaluated using microbiomic and metabolomic analyses.},
journal = {BMC plant biology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12870-026-08844-9},
pmid = {42026475},
issn = {1471-2229},
support = {HBCT2024150205//Hebei Agriculture Research System/ ; 21326308D-02-03//Key Research and Development Project of Hebei Province/ ; C2024204214//Natural Science Foundation of Hebei Province/ ; BJK2022012//Science and Technology Project of Hebei Education Department/ ; },
}
RevDate: 2026-04-24
Application of Gut Microbiota in the Treatment and Efficacy Evaluation of Tic Disorders: A Systematic Review.
Journal of child and adolescent psychopharmacology [Epub ahead of print].
OBJECTIVE: To systematically review existing evidence on the role of gut microbiota in the pathogenesis of tic disorders (TD) and to assess the therapeutic potential of microbiome-targeted interventions such as probiotics and fecal microbiota transplantation in the management of TD.
METHODS: A comprehensive search was conducted in PubMed, Web of Science, EMBASE, and The Cochrane Library (up to May 26, 2025). The review followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines and was registered in PROSPERO (CRD420251067880).
RESULTS: Eleven studies were included, with four focusing on gut microbiome-based therapies and seven studies with gut microbiota and its metabolites as outcome indicators. At the genus level, children with TD exhibited specific alterations in gut microbiota: increased abundance of Bacteroides, Faecalibacterium, and Ruminococcus, alongside decreased levels of Bifidobacterium and Prevotella. This functional dysbiosis may trigger neuroinflammation via disrupted short-chain fatty acid metabolism and impaired intestinal barrier function, ultimately disturbing the glutamate and γ-aminobutyric acid neurotransmitter balance and leading to dysfunction in the cortico-striato-thalamo-cortical circuit. Meanwhile, probiotics as an intervention have been consistently reported to alleviate tic symptoms, although clinical evidence remains limited.
CONCLUSION: Gut microbiota may contribute to TD pathogenesis via immune modulation and neurotransmitter metabolism. While microbiota-based strategies show promise, heterogeneity and methodological limitations in current studies necessitate further high-quality research to validate mechanisms and support clinical application.
Additional Links: PMID-42026738
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PubMed:
Citation:
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@article {pmid42026738,
year = {2026},
author = {Cao, B and Zhou, X and Cao, X and Shi, J and Liu, C and Yuan, B},
title = {Application of Gut Microbiota in the Treatment and Efficacy Evaluation of Tic Disorders: A Systematic Review.},
journal = {Journal of child and adolescent psychopharmacology},
volume = {},
number = {},
pages = {10445463261445906},
doi = {10.1177/10445463261445906},
pmid = {42026738},
issn = {1557-8992},
abstract = {OBJECTIVE: To systematically review existing evidence on the role of gut microbiota in the pathogenesis of tic disorders (TD) and to assess the therapeutic potential of microbiome-targeted interventions such as probiotics and fecal microbiota transplantation in the management of TD.
METHODS: A comprehensive search was conducted in PubMed, Web of Science, EMBASE, and The Cochrane Library (up to May 26, 2025). The review followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines and was registered in PROSPERO (CRD420251067880).
RESULTS: Eleven studies were included, with four focusing on gut microbiome-based therapies and seven studies with gut microbiota and its metabolites as outcome indicators. At the genus level, children with TD exhibited specific alterations in gut microbiota: increased abundance of Bacteroides, Faecalibacterium, and Ruminococcus, alongside decreased levels of Bifidobacterium and Prevotella. This functional dysbiosis may trigger neuroinflammation via disrupted short-chain fatty acid metabolism and impaired intestinal barrier function, ultimately disturbing the glutamate and γ-aminobutyric acid neurotransmitter balance and leading to dysfunction in the cortico-striato-thalamo-cortical circuit. Meanwhile, probiotics as an intervention have been consistently reported to alleviate tic symptoms, although clinical evidence remains limited.
CONCLUSION: Gut microbiota may contribute to TD pathogenesis via immune modulation and neurotransmitter metabolism. While microbiota-based strategies show promise, heterogeneity and methodological limitations in current studies necessitate further high-quality research to validate mechanisms and support clinical application.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Gut microbiome and pregnancy complications: emerging evidence and mechanistic insights.
Gut microbes, 18(1):2661417.
The gut microbiome undergoes significant alterations during pregnancy. Perturbations in these microbial communities are increasingly associated with a range of pregnancy complications, including miscarriage, gestational diabetes mellitus, preeclampsia, preterm birth, and fetal growth restriction, among others. This review synthesizes current evidence on the dynamic changes in the maternal gut microecosystem including bacterial, fungal, and viral communities throughout gestation and examines its relationships with various pregnancy complications. We also summarize the underlying mechanisms driving these interactions, focusing on metabolic regulations involving short-chain fatty acids, bile acids, indoles, sex hormones, intestinal barrier integrity, and the modulation of maternal immune responses essential for fetal tolerance. Additionally, we discuss the lasting impact of the maternal microbiome on offspring health via vertical transmission and developmental programming. This review provides a conceptual framework that integrates mechanistic insights with clinical findings, with the goal of informing future research and supporting the development of microbiome-based interventions to improve maternal and neonatal health outcomes.
Additional Links: PMID-42026776
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@article {pmid42026776,
year = {2026},
author = {Hu, S and Miao, Z and Xiao, C and Fu, Y and Zheng, J and Hu, W and Zheng, JS},
title = {Gut microbiome and pregnancy complications: emerging evidence and mechanistic insights.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2661417},
doi = {10.1080/19490976.2026.2661417},
pmid = {42026776},
issn = {1949-0984},
mesh = {Humans ; Pregnancy ; Female ; *Gastrointestinal Microbiome ; *Pregnancy Complications/microbiology ; Bacteria/classification/genetics/isolation & purification/metabolism ; Animals ; },
abstract = {The gut microbiome undergoes significant alterations during pregnancy. Perturbations in these microbial communities are increasingly associated with a range of pregnancy complications, including miscarriage, gestational diabetes mellitus, preeclampsia, preterm birth, and fetal growth restriction, among others. This review synthesizes current evidence on the dynamic changes in the maternal gut microecosystem including bacterial, fungal, and viral communities throughout gestation and examines its relationships with various pregnancy complications. We also summarize the underlying mechanisms driving these interactions, focusing on metabolic regulations involving short-chain fatty acids, bile acids, indoles, sex hormones, intestinal barrier integrity, and the modulation of maternal immune responses essential for fetal tolerance. Additionally, we discuss the lasting impact of the maternal microbiome on offspring health via vertical transmission and developmental programming. This review provides a conceptual framework that integrates mechanistic insights with clinical findings, with the goal of informing future research and supporting the development of microbiome-based interventions to improve maternal and neonatal health outcomes.},
}
MeSH Terms:
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Humans
Pregnancy
Female
*Gastrointestinal Microbiome
*Pregnancy Complications/microbiology
Bacteria/classification/genetics/isolation & purification/metabolism
Animals
RevDate: 2026-04-24
CmpDate: 2026-04-24
Calorie-restricted oat diet is associated with zonulin and short-chain fatty acid response in metabolic syndrome: a randomized controlled trial.
Gut microbes, 18(1):2662687.
Oats are associated with positive effects on gut health, but human studies are largely lacking. Therefore, we investigated the effects of two different oat diets on gut permeability makers in individuals with metabolic syndrome, each in a randomized, controlled parallel design. Participants either consumed 3 × 100 g oatmeal/d for 2 d or an adapted control diet, or they integrated 1 × 80 g oatmeal/d into their habitual diet for 6 weeks or maintained it unchanged. Serum zonulin decreased upon 2-d calorie-restricted oat diet compared to baseline, while plasma butyric acid increased compared to the control (n = 27). Zonulin reduction correlated inversely with changes in short-chain fatty acids (SCFAs), particularly valeric and butyric acids, which were associated with shifts in microbial composition. During the 6-week isocaloric oat diet, these parameters remained stable (n = 22). Our data suggests that alterations in microbiome and related effects on SCFAs upon a short-term calorie-restricted diet with high-dose oats are contributing factors to changes in gut permeability markers. Thus, an intense oat intake might be a suitable and feasible approach to improve obesity-related intestinal barrier dysfunction in metabolic syndrome.German Clinical Trials Register: 07/28/2020, identifier: DRKS00022169.
Additional Links: PMID-42026801
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@article {pmid42026801,
year = {2026},
author = {Klümpen, L and Mantri, A and Donkers, A and Seel, W and Stoffel-Wagner, B and Coenen, M and Schmid, M and Weinhold, L and Grein, F and Newels, P and Bedarf, J and Wüllner, U and Stehle, P and Simon, MC},
title = {Calorie-restricted oat diet is associated with zonulin and short-chain fatty acid response in metabolic syndrome: a randomized controlled trial.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2662687},
doi = {10.1080/19490976.2026.2662687},
pmid = {42026801},
issn = {1949-0984},
mesh = {Humans ; *Avena/metabolism ; *Metabolic Syndrome/diet therapy/microbiology/metabolism/blood ; Haptoglobins ; Male ; *Fatty Acids, Volatile/metabolism/blood ; Middle Aged ; Female ; *Protein Precursors/blood ; Gastrointestinal Microbiome ; Adult ; *Cholera Toxin/blood ; *Caloric Restriction ; Permeability ; Bacteria/classification/isolation & purification/genetics/metabolism ; },
abstract = {Oats are associated with positive effects on gut health, but human studies are largely lacking. Therefore, we investigated the effects of two different oat diets on gut permeability makers in individuals with metabolic syndrome, each in a randomized, controlled parallel design. Participants either consumed 3 × 100 g oatmeal/d for 2 d or an adapted control diet, or they integrated 1 × 80 g oatmeal/d into their habitual diet for 6 weeks or maintained it unchanged. Serum zonulin decreased upon 2-d calorie-restricted oat diet compared to baseline, while plasma butyric acid increased compared to the control (n = 27). Zonulin reduction correlated inversely with changes in short-chain fatty acids (SCFAs), particularly valeric and butyric acids, which were associated with shifts in microbial composition. During the 6-week isocaloric oat diet, these parameters remained stable (n = 22). Our data suggests that alterations in microbiome and related effects on SCFAs upon a short-term calorie-restricted diet with high-dose oats are contributing factors to changes in gut permeability markers. Thus, an intense oat intake might be a suitable and feasible approach to improve obesity-related intestinal barrier dysfunction in metabolic syndrome.German Clinical Trials Register: 07/28/2020, identifier: DRKS00022169.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Avena/metabolism
*Metabolic Syndrome/diet therapy/microbiology/metabolism/blood
Haptoglobins
Male
*Fatty Acids, Volatile/metabolism/blood
Middle Aged
Female
*Protein Precursors/blood
Gastrointestinal Microbiome
Adult
*Cholera Toxin/blood
*Caloric Restriction
Permeability
Bacteria/classification/isolation & purification/genetics/metabolism
RevDate: 2026-04-24
CmpDate: 2026-04-24
Gene-level gut microbiome signatures as predictive biomarkers for response to immune checkpoint inhibitors across multiple cancer types.
Gut microbes, 18(1):2662690.
Targeting programmed cell death protein 1 (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) with immune checkpoint inhibitors (ICIs) has improved survival across multiple cancer types, but the variability in patient response highlights the need for better predictive biomarkers. Existing studies rely on taxonomic abundance derived from reference genome databases, limiting the discovery and functional interpretation of uncharacterized microbes. Here, we integrated metagenomic data from multiple ICI-treated cohorts spanning diverse cancer types and geographic regions and developed a deep learning model, named BioP-VAE, that incorporates biological prior knowledge via protein sequence embeddings and uses gene-level microbial abundance features as input. Gene-level microbial abundance outperformed taxonomy abundance in predicting both ICI response and 12-month progression-free survival (PFS). In patients receiving combination immune checkpoint blockade (CICB), BioP-VAE achieved a mean AUC of 0.89 in intracohort and 0.88 in cross-cohort evaluation. Notably, in the monotherapy-treated intracohorts, BioP-VAE achieved a mean AUC of 0.97. Feature attribution analysis revealed key microbial genes. Additionally, we identified distinct predictive microbial signatures via age-stratified analysis, suggesting that host age may modulate microbiome‒immune interactions. Importantly, this is the first large-scale study to evaluate gene-level microbial abundance features for ICI response prediction across multiple cancer types by deep learning. Our findings demonstrate that incorporating biological prior knowledge into deep learning models can improve the discovery of microbial biomarkers that can be generalized across cancer types and treatment settings, offering a novel strategy for patient stratification in immunotherapy.
Additional Links: PMID-42026803
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PubMed:
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@article {pmid42026803,
year = {2026},
author = {Zhang, F and Hu, K and Sun, C and Chen, R and Ni, G and Liu, X and Wei, L and Su, R},
title = {Gene-level gut microbiome signatures as predictive biomarkers for response to immune checkpoint inhibitors across multiple cancer types.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2662690},
doi = {10.1080/19490976.2026.2662690},
pmid = {42026803},
issn = {1949-0984},
mesh = {Humans ; *Immune Checkpoint Inhibitors/therapeutic use ; *Gastrointestinal Microbiome/genetics/drug effects ; *Neoplasms/drug therapy/microbiology ; Deep Learning ; Biomarkers, Tumor/genetics ; *Bacteria/classification/genetics/isolation & purification ; Female ; Male ; Metagenomics ; },
abstract = {Targeting programmed cell death protein 1 (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) with immune checkpoint inhibitors (ICIs) has improved survival across multiple cancer types, but the variability in patient response highlights the need for better predictive biomarkers. Existing studies rely on taxonomic abundance derived from reference genome databases, limiting the discovery and functional interpretation of uncharacterized microbes. Here, we integrated metagenomic data from multiple ICI-treated cohorts spanning diverse cancer types and geographic regions and developed a deep learning model, named BioP-VAE, that incorporates biological prior knowledge via protein sequence embeddings and uses gene-level microbial abundance features as input. Gene-level microbial abundance outperformed taxonomy abundance in predicting both ICI response and 12-month progression-free survival (PFS). In patients receiving combination immune checkpoint blockade (CICB), BioP-VAE achieved a mean AUC of 0.89 in intracohort and 0.88 in cross-cohort evaluation. Notably, in the monotherapy-treated intracohorts, BioP-VAE achieved a mean AUC of 0.97. Feature attribution analysis revealed key microbial genes. Additionally, we identified distinct predictive microbial signatures via age-stratified analysis, suggesting that host age may modulate microbiome‒immune interactions. Importantly, this is the first large-scale study to evaluate gene-level microbial abundance features for ICI response prediction across multiple cancer types by deep learning. Our findings demonstrate that incorporating biological prior knowledge into deep learning models can improve the discovery of microbial biomarkers that can be generalized across cancer types and treatment settings, offering a novel strategy for patient stratification in immunotherapy.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Immune Checkpoint Inhibitors/therapeutic use
*Gastrointestinal Microbiome/genetics/drug effects
*Neoplasms/drug therapy/microbiology
Deep Learning
Biomarkers, Tumor/genetics
*Bacteria/classification/genetics/isolation & purification
Female
Male
Metagenomics
RevDate: 2026-04-24
Ketogenic diet modulates gut microbiota composition in an experimental model of cerebral palsy.
Nutritional neuroscience [Epub ahead of print].
BACKGROUND: Cerebral palsy (CPa) is a neurodevelopmental disorder often accompanied by gastrointestinal dysfunction and dysbiosis of the gut microbiota (GM). The ketogenic diet (KD) has demonstrated neuroprotective and anti-inflammatory properties in neurological diseases, yet its effects on GM in CPa remain poorly understood.
OBJECTIVE: This study aimed to evaluate the impact of KD on the GM composition in an experimental model of CPa.
METHODS: Male Wistar rats were assigned to four groups (n = 10) according to healthy status and KD intervention: healthy control (C), healthy ketogenic diet (K), cerebral palsy (P), and cerebral palsy with ketogenic diet (PK). CPa was induced by perinatal anoxia and sensorimotor restriction, and, from postnatal day 25-65, animals received a standard or a KD. Body weight, food, and energy intake were monitored. Fecal samples were collected at day 65 for 16S rRNA sequencing and bioinformatics analyses.
RESULTS: The CPa condition was associated with reduced body weight, decreased food intake, and marked alterations in GM composition, characterized by increased abundance of Proteobacteria, Enterobacteriaceae, and Escherichia-Shigella, along with reduced levels of Bifidobacterium and Lactobacillus. KD intervention in animals with CPa was associated with coordinated shifts in GM structure, including reduced representation of taxa linked to inflammatory profiles and increased abundance of short-chain fatty acid-producing bacterial groups, such as members of the Lachnospiraceae and Ruminococcaceae families.
CONCLUSION: Overall, these findings suggest that modulation of GM may contribute to the neuroprotective and anti-inflammatory effects of the KD, highlighting GM as a potential therapeutic target for CPa-associated comorbidities.
Additional Links: PMID-42026999
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PubMed:
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@article {pmid42026999,
year = {2026},
author = {Dantas Alves, JS and De Oliveira Melo, NC and Toscano, AE and Manhães-De-Castro, R and Fraga Filho, CX and Cruz Neto, JPR and De Brito Alves, JL and Muniz, GS},
title = {Ketogenic diet modulates gut microbiota composition in an experimental model of cerebral palsy.},
journal = {Nutritional neuroscience},
volume = {},
number = {},
pages = {1-11},
doi = {10.1080/1028415X.2026.2656403},
pmid = {42026999},
issn = {1476-8305},
abstract = {BACKGROUND: Cerebral palsy (CPa) is a neurodevelopmental disorder often accompanied by gastrointestinal dysfunction and dysbiosis of the gut microbiota (GM). The ketogenic diet (KD) has demonstrated neuroprotective and anti-inflammatory properties in neurological diseases, yet its effects on GM in CPa remain poorly understood.
OBJECTIVE: This study aimed to evaluate the impact of KD on the GM composition in an experimental model of CPa.
METHODS: Male Wistar rats were assigned to four groups (n = 10) according to healthy status and KD intervention: healthy control (C), healthy ketogenic diet (K), cerebral palsy (P), and cerebral palsy with ketogenic diet (PK). CPa was induced by perinatal anoxia and sensorimotor restriction, and, from postnatal day 25-65, animals received a standard or a KD. Body weight, food, and energy intake were monitored. Fecal samples were collected at day 65 for 16S rRNA sequencing and bioinformatics analyses.
RESULTS: The CPa condition was associated with reduced body weight, decreased food intake, and marked alterations in GM composition, characterized by increased abundance of Proteobacteria, Enterobacteriaceae, and Escherichia-Shigella, along with reduced levels of Bifidobacterium and Lactobacillus. KD intervention in animals with CPa was associated with coordinated shifts in GM structure, including reduced representation of taxa linked to inflammatory profiles and increased abundance of short-chain fatty acid-producing bacterial groups, such as members of the Lachnospiraceae and Ruminococcaceae families.
CONCLUSION: Overall, these findings suggest that modulation of GM may contribute to the neuroprotective and anti-inflammatory effects of the KD, highlighting GM as a potential therapeutic target for CPa-associated comorbidities.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Characterization of the Gut Virome in Patients with Inflammatory Bowel Disease and Non-Alcoholic Fatty Liver Disease.
Journal of inflammation research, 19:581751.
OBJECTIVE: The dysbiosis of the gut microbiota is a well-known correlate in the pathogenesis of inflammatory bowel disease (IBD). However, the microbiome characteristics of patients with IBD who also have non-alcoholic fatty liver disease (NAFLD) are understudied, particularly the potential pathogenic mechanisms of the gut virome.
MATERIALS AND METHODS: In this study, we conducted a comprehensive gut virome correlation study, along with serum metabolomics analysis, by performing virus-like particle (VLP) and metagenomic sequencing on fecal samples from patients with inflammatory bowel disease and non-alcoholic fatty liver disease (IBD-NAFLD) and NAFLD (MASLD) controls without gastrointestinal diseases.
RESULTS: The results showed that changes in the fecal virome were associated with IBD-NAFLD (MASLD), particularly with an increase in the abundance of Caudovirales in IBD-NAFLD (MASLD) patients. Subsequent analysis of the gut virome identified Bacteroides as the top predicted host for the viruses. Additionally, we identified the pathways involved in all differential metabolites through KEGG annotation analysis, with the highest correlation being the galactose metabolism pathway.
CONCLUSION: In conclusion, by using a customized integrated gut virome catalog tailored for IBD, we revealed the fundamental changes in the gut virome of IBD-NAFLD (MASLD) patients. This study is the first to uncover the specificity of the gut virome in IBD-NAFLD (MASLD) patients and predict Bacteroides as a potential host, suggesting a microbial signature primarily influenced by intestinal inflammation.
Additional Links: PMID-42027256
PubMed:
Citation:
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@article {pmid42027256,
year = {2026},
author = {Lu, S and Xia, Y and Sun, Q and Sun, Y and Chen, R and Jin, H and Zhang, J and Liu, W and Huang, J},
title = {Characterization of the Gut Virome in Patients with Inflammatory Bowel Disease and Non-Alcoholic Fatty Liver Disease.},
journal = {Journal of inflammation research},
volume = {19},
number = {},
pages = {581751},
pmid = {42027256},
issn = {1178-7031},
abstract = {OBJECTIVE: The dysbiosis of the gut microbiota is a well-known correlate in the pathogenesis of inflammatory bowel disease (IBD). However, the microbiome characteristics of patients with IBD who also have non-alcoholic fatty liver disease (NAFLD) are understudied, particularly the potential pathogenic mechanisms of the gut virome.
MATERIALS AND METHODS: In this study, we conducted a comprehensive gut virome correlation study, along with serum metabolomics analysis, by performing virus-like particle (VLP) and metagenomic sequencing on fecal samples from patients with inflammatory bowel disease and non-alcoholic fatty liver disease (IBD-NAFLD) and NAFLD (MASLD) controls without gastrointestinal diseases.
RESULTS: The results showed that changes in the fecal virome were associated with IBD-NAFLD (MASLD), particularly with an increase in the abundance of Caudovirales in IBD-NAFLD (MASLD) patients. Subsequent analysis of the gut virome identified Bacteroides as the top predicted host for the viruses. Additionally, we identified the pathways involved in all differential metabolites through KEGG annotation analysis, with the highest correlation being the galactose metabolism pathway.
CONCLUSION: In conclusion, by using a customized integrated gut virome catalog tailored for IBD, we revealed the fundamental changes in the gut virome of IBD-NAFLD (MASLD) patients. This study is the first to uncover the specificity of the gut virome in IBD-NAFLD (MASLD) patients and predict Bacteroides as a potential host, suggesting a microbial signature primarily influenced by intestinal inflammation.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Immune fitness and biomarkers of immune function: Relationships with the oral and gut microbiome composition.
Brain, behavior, & immunity - health, 54:101239.
BACKGROUND: Immune fitness refers to the body's capacity to respond to health challenges, such as infections, by activating an appropriate immune response. The aim of the current study was to investigate the relationship between oral and gut microbiota community structure and immune fitness scores.
METHODS: Stool and saliva samples were collected to assess compositions of both oral and gut microbiota. Immune fitness was assessed with a single-item scale ranging from 0 (very poor) to 10 (excellent). Additionally, saliva samples were analyzed to measure the concentrations (pg/ml) of pro-inflammatory biomarkers interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-alpha (TNF-α). Spearman's correlations were computed between microbiota abundance, immune fitness, and salivary biomarker levels. Bootstrapping was used to adjust for the relatively small sample size in the correlation analysis.
RESULTS: A total of 29 healthy participants (15 males; 14 females) enrolled in the study, with a mean age of 21.1 years old. Analysis of the salivary microbiota revealed significant negative correlations between self-reported immune fitness scores and the relative abundances of putative oral proinflammatory genera Selenomonas (r = -0.610), and Lachnospiraceae uncultured (r = -0.501). In the fecal microbiota, immune fitness scores showed a significant positive correlation with the relative abundance of putative beneficial butyrate-producing genus Lachnoclostridium (r = 0.513), and significant negative correlations with commensal gut bacterial genera Colidextribacter (r = -0.582) and Lachnospiraceae FCS020 group (r = -0.504).
CONCLUSION: Self-reported immune fitness is associated with the oral and gut microbiota community. The findings demonstrate the importance of microbiota in immune function and support the use of self-assessment scales to evaluate immune fitness.
Additional Links: PMID-42027356
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Citation:
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@article {pmid42027356,
year = {2026},
author = {Ulijn, GA and Išerić, E and van de Loo, AJAE and Garssen, J and Engen, PA and Naqib, A and Green, SJ and Keshavarzian, A and Verster, JC},
title = {Immune fitness and biomarkers of immune function: Relationships with the oral and gut microbiome composition.},
journal = {Brain, behavior, & immunity - health},
volume = {54},
number = {},
pages = {101239},
pmid = {42027356},
issn = {2666-3546},
abstract = {BACKGROUND: Immune fitness refers to the body's capacity to respond to health challenges, such as infections, by activating an appropriate immune response. The aim of the current study was to investigate the relationship between oral and gut microbiota community structure and immune fitness scores.
METHODS: Stool and saliva samples were collected to assess compositions of both oral and gut microbiota. Immune fitness was assessed with a single-item scale ranging from 0 (very poor) to 10 (excellent). Additionally, saliva samples were analyzed to measure the concentrations (pg/ml) of pro-inflammatory biomarkers interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-alpha (TNF-α). Spearman's correlations were computed between microbiota abundance, immune fitness, and salivary biomarker levels. Bootstrapping was used to adjust for the relatively small sample size in the correlation analysis.
RESULTS: A total of 29 healthy participants (15 males; 14 females) enrolled in the study, with a mean age of 21.1 years old. Analysis of the salivary microbiota revealed significant negative correlations between self-reported immune fitness scores and the relative abundances of putative oral proinflammatory genera Selenomonas (r = -0.610), and Lachnospiraceae uncultured (r = -0.501). In the fecal microbiota, immune fitness scores showed a significant positive correlation with the relative abundance of putative beneficial butyrate-producing genus Lachnoclostridium (r = 0.513), and significant negative correlations with commensal gut bacterial genera Colidextribacter (r = -0.582) and Lachnospiraceae FCS020 group (r = -0.504).
CONCLUSION: Self-reported immune fitness is associated with the oral and gut microbiota community. The findings demonstrate the importance of microbiota in immune function and support the use of self-assessment scales to evaluate immune fitness.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
The eye's coral reef: toward a planetary-health agenda for ocular-microbiome stewardship.
Frontiers in microbiology, 17:1816460.
Coral reefs and the human ocular surface represent ecologically distinct yet structurally comparable microbial ecosystems in which resilience depends on finely regulated host-microbe interactions. In coral reef science, microbial shifts precede visible bleaching and ecosystem collapse, enabling the development of predictive stress indices such as Degree Heating Weeks (DHW). Comparable principles are emerging in host-associated, low-biomass microbiomes, where subtle perturbations may trigger disproportionate functional consequences. Here, we propose a systems-level conceptual framework linking coral reef holobionts and the ocular surface as sentinel ecosystems governed by cumulative stress, threshold dynamics, and microbial instability. We introduce two heuristic constructs-the Cumulative Desiccating Load (CDL) and the Ocular Dysbiosis Sentinel Index (ODSI)-to frame dysbiosis as a trajectory of resilience loss driven by cumulative perturbations. Aging-related conditions such as age-related macular degeneration are discussed as examples of microbial and metabolic senescence within the human holobiont, conceptually paralleling coral reef decline under chronic sublethal stress. By integrating environmental and host-associated microbiome research within a planetary-health perspective, this article advances a resilience-oriented systems framework applicable across biological scales.
Additional Links: PMID-42027463
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@article {pmid42027463,
year = {2026},
author = {Drago, L and De La Motte, LR},
title = {The eye's coral reef: toward a planetary-health agenda for ocular-microbiome stewardship.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1816460},
pmid = {42027463},
issn = {1664-302X},
abstract = {Coral reefs and the human ocular surface represent ecologically distinct yet structurally comparable microbial ecosystems in which resilience depends on finely regulated host-microbe interactions. In coral reef science, microbial shifts precede visible bleaching and ecosystem collapse, enabling the development of predictive stress indices such as Degree Heating Weeks (DHW). Comparable principles are emerging in host-associated, low-biomass microbiomes, where subtle perturbations may trigger disproportionate functional consequences. Here, we propose a systems-level conceptual framework linking coral reef holobionts and the ocular surface as sentinel ecosystems governed by cumulative stress, threshold dynamics, and microbial instability. We introduce two heuristic constructs-the Cumulative Desiccating Load (CDL) and the Ocular Dysbiosis Sentinel Index (ODSI)-to frame dysbiosis as a trajectory of resilience loss driven by cumulative perturbations. Aging-related conditions such as age-related macular degeneration are discussed as examples of microbial and metabolic senescence within the human holobiont, conceptually paralleling coral reef decline under chronic sublethal stress. By integrating environmental and host-associated microbiome research within a planetary-health perspective, this article advances a resilience-oriented systems framework applicable across biological scales.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Th17/treg balance in Inflammatory Bowel Disease: the role of microbial, and genetic regulators in disease modulation.
Frontiers in cell and developmental biology, 14:1774790.
Inflammatory Bowel Disease (IBD) is a chronic condition characterized by persistent mucosal inflammation driven by complex interactions among the gut microbiome, host immune genetics, and cellular metabolism. Emerging evidence highlights the central role of the Th17/Treg cell balance in maintaining intestinal immune tolerance, which is tightly regulated by microbe-derived metabolites and host metabolic pathways. In IBD, microbial dysbiosis and altered metabolite profiles disrupt this equilibrium, favoring pro-inflammatory responses. Moreover, genetic variants affecting immune regulation modulate individual susceptibility and disease course. Understanding how microbiome modulation, metabolic reprogramming, and genetic predisposition converge in IBD pathogenesis opens new avenues for precision medicine. This minireview discusses recent advances in this field, emphasizing novel microbiome-targeted strategies, metabolic interventions, and personalized immunomodulatory therapies aimed at restoring Th17/Treg homeostasis. Integrating microbiome, metabolome, and immunogenetic profiling may ultimately guide tailored treatments and improve long-term outcomes in IBD.
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@article {pmid42027582,
year = {2026},
author = {Giudice, A and Brescia, C and Morano, D and Viglietto, G and Luzza, F and Amato, R and Spagnuolo, R},
title = {Th17/treg balance in Inflammatory Bowel Disease: the role of microbial, and genetic regulators in disease modulation.},
journal = {Frontiers in cell and developmental biology},
volume = {14},
number = {},
pages = {1774790},
pmid = {42027582},
issn = {2296-634X},
abstract = {Inflammatory Bowel Disease (IBD) is a chronic condition characterized by persistent mucosal inflammation driven by complex interactions among the gut microbiome, host immune genetics, and cellular metabolism. Emerging evidence highlights the central role of the Th17/Treg cell balance in maintaining intestinal immune tolerance, which is tightly regulated by microbe-derived metabolites and host metabolic pathways. In IBD, microbial dysbiosis and altered metabolite profiles disrupt this equilibrium, favoring pro-inflammatory responses. Moreover, genetic variants affecting immune regulation modulate individual susceptibility and disease course. Understanding how microbiome modulation, metabolic reprogramming, and genetic predisposition converge in IBD pathogenesis opens new avenues for precision medicine. This minireview discusses recent advances in this field, emphasizing novel microbiome-targeted strategies, metabolic interventions, and personalized immunomodulatory therapies aimed at restoring Th17/Treg homeostasis. Integrating microbiome, metabolome, and immunogenetic profiling may ultimately guide tailored treatments and improve long-term outcomes in IBD.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
The Gut-Brain Axis as a Mediator of Environmental Endocrine Disruptors in Attention-Deficit/Hyperactivity Disorder: A Systematic Review and Mechanistic Synthesis.
Biological psychiatry global open science, 6(3):100717.
The rising global prevalence of attention-deficit/hyperactivity disorder (ADHD) underscores the importance of environmental factors, particularly environmental endocrine-disrupting chemicals (EEDs), whose mechanistic links to ADHD remain unclear. The gut-brain axis, a key modulator of neurodevelopment, is susceptible to EEDs and is altered in ADHD, suggesting a potential mediating pathway. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and PROSPERO registration (CRD420251152480), we systematically searched PubMed, Web of Science, and Embase (January 2014-July 2025) for studies on EEDs, gut microbiota, and ADHD. Data from 127 included studies (observational, experimental, interventional) were narratively synthesized to evaluate the gut-brain axis as a mediator. We found 1) consistent epidemiological associations between prenatal/childhood EED exposure (e.g., phthalates, bisphenol A, pesticides) and increased ADHD risk; 2) a distinct gut microbial signature in ADHD featuring reduced alpha diversity, elevated Firmicutes/Bacteroidetes ratio, depletion of beneficial taxa (Lactobacillus, Bifidobacterium), and impaired short-chain fatty acid (SCFA) production; 3) evidence that EED exposure induces convergent gut dysbiosis; and 4) interventional studies indicating that modulating the microbiota (via probiotics, synbiotics, fecal microbiota transplantation) can ameliorate ADHD-related behaviors. These findings support a novel mechanistic model wherein EEDs disrupt gut microbiota homeostasis, thereby contributing to ADHD pathogenesis via immune-inflammatory, microbial metabolite (e.g., SCFA), and neuroendocrine pathways along the gut-brain axis. This review synthesizes evidence positioning the gut-brain axis as a critical mediator linking EED exposure to ADHD. It proposes a unifying etiological framework and highlights the microbiome as a promising target for preventive and therapeutic strategies. Future longitudinal and intervention studies are needed to establish causality.
Additional Links: PMID-42027687
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Citation:
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@article {pmid42027687,
year = {2026},
author = {Wu, H and Yu, M and Huang, S and Peng, Y and Wei, G and Huang, C},
title = {The Gut-Brain Axis as a Mediator of Environmental Endocrine Disruptors in Attention-Deficit/Hyperactivity Disorder: A Systematic Review and Mechanistic Synthesis.},
journal = {Biological psychiatry global open science},
volume = {6},
number = {3},
pages = {100717},
pmid = {42027687},
issn = {2667-1743},
abstract = {The rising global prevalence of attention-deficit/hyperactivity disorder (ADHD) underscores the importance of environmental factors, particularly environmental endocrine-disrupting chemicals (EEDs), whose mechanistic links to ADHD remain unclear. The gut-brain axis, a key modulator of neurodevelopment, is susceptible to EEDs and is altered in ADHD, suggesting a potential mediating pathway. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and PROSPERO registration (CRD420251152480), we systematically searched PubMed, Web of Science, and Embase (January 2014-July 2025) for studies on EEDs, gut microbiota, and ADHD. Data from 127 included studies (observational, experimental, interventional) were narratively synthesized to evaluate the gut-brain axis as a mediator. We found 1) consistent epidemiological associations between prenatal/childhood EED exposure (e.g., phthalates, bisphenol A, pesticides) and increased ADHD risk; 2) a distinct gut microbial signature in ADHD featuring reduced alpha diversity, elevated Firmicutes/Bacteroidetes ratio, depletion of beneficial taxa (Lactobacillus, Bifidobacterium), and impaired short-chain fatty acid (SCFA) production; 3) evidence that EED exposure induces convergent gut dysbiosis; and 4) interventional studies indicating that modulating the microbiota (via probiotics, synbiotics, fecal microbiota transplantation) can ameliorate ADHD-related behaviors. These findings support a novel mechanistic model wherein EEDs disrupt gut microbiota homeostasis, thereby contributing to ADHD pathogenesis via immune-inflammatory, microbial metabolite (e.g., SCFA), and neuroendocrine pathways along the gut-brain axis. This review synthesizes evidence positioning the gut-brain axis as a critical mediator linking EED exposure to ADHD. It proposes a unifying etiological framework and highlights the microbiome as a promising target for preventive and therapeutic strategies. Future longitudinal and intervention studies are needed to establish causality.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Predictors of sensitivity to immune therapies in classic Hodgkin lymphoma.
Blood neoplasia, 3(2):100207.
Immune checkpoint blockade, particularly programmed cell death protein 1 inhibition, has redefined the management of classic Hodgkin lymphoma (cHL), achieving unprecedented efficacy in relapsed/refractory settings. Yet, durable benefit is not universal, because mechanisms of primary and acquired resistance remain incompletely understood. This review integrates current knowledge on predictors of sensitivity to immune therapies in cHL across clinical, biological, and technological dimensions. Established predictors, including disease burden, previous treatment exposure, CD30 intensity, programmed death-ligand 1 (PD-L1)/PD-L2 copy number gains, and loss of major histocompatibility complex expression, offer valuable but incomplete prognostic information. Tumor microenvironmental features such as macrophage polarization, T-cell exhaustion, and immune spatial organization further refine response prediction, whereas circulating biomarkers such as soluble PD-L1, circulating tumor DNA kinetics, and cytokine profiles provide noninvasive insights. Molecular and cellular pathways underlying resistance encompass genetic and epigenetic alterations, immune editing, and adaptive checkpoint upregulation. Emerging predictive frameworks, spanning multiomics and spatial profiling, radiomics, artificial intelligence, and microbiome-host cross talk, promise to enhance precision in patient stratification. Finally, the review outlines key challenges and research priorities for translating these multidimensional biomarkers into clinical trials and practice. A unified predictive framework integrating clinical, molecular, and computational indicators may ultimately enable personalized immunotherapy and overcome resistance in cHL.
Additional Links: PMID-42027746
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@article {pmid42027746,
year = {2026},
author = {Alibrahim, MN and Carbone, A and Gloghini, A},
title = {Predictors of sensitivity to immune therapies in classic Hodgkin lymphoma.},
journal = {Blood neoplasia},
volume = {3},
number = {2},
pages = {100207},
pmid = {42027746},
issn = {2950-3280},
abstract = {Immune checkpoint blockade, particularly programmed cell death protein 1 inhibition, has redefined the management of classic Hodgkin lymphoma (cHL), achieving unprecedented efficacy in relapsed/refractory settings. Yet, durable benefit is not universal, because mechanisms of primary and acquired resistance remain incompletely understood. This review integrates current knowledge on predictors of sensitivity to immune therapies in cHL across clinical, biological, and technological dimensions. Established predictors, including disease burden, previous treatment exposure, CD30 intensity, programmed death-ligand 1 (PD-L1)/PD-L2 copy number gains, and loss of major histocompatibility complex expression, offer valuable but incomplete prognostic information. Tumor microenvironmental features such as macrophage polarization, T-cell exhaustion, and immune spatial organization further refine response prediction, whereas circulating biomarkers such as soluble PD-L1, circulating tumor DNA kinetics, and cytokine profiles provide noninvasive insights. Molecular and cellular pathways underlying resistance encompass genetic and epigenetic alterations, immune editing, and adaptive checkpoint upregulation. Emerging predictive frameworks, spanning multiomics and spatial profiling, radiomics, artificial intelligence, and microbiome-host cross talk, promise to enhance precision in patient stratification. Finally, the review outlines key challenges and research priorities for translating these multidimensional biomarkers into clinical trials and practice. A unified predictive framework integrating clinical, molecular, and computational indicators may ultimately enable personalized immunotherapy and overcome resistance in cHL.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
From dysbacteriosis to ecological remodeling: A new breakthrough in microbial treatment of inflammatory bowel disease.
iScience, 29(5):115483.
Inflammatory bowel disease (IBD) is a group of chronic and recurrent inflammatory conditions of the gastrointestinal tract, arising from complex interactions among genetic susceptibility, environmental factors, immune dysregulation, and alterations in the gut microbiota. Increasing evidence suggests that gut microbiota dysbiosis is closely associated with IBD pathogenesis and disease progression, providing a promising target for microbiome-oriented therapeutic strategies. However, due to the multi-factorial and dynamic nature of microbial alterations in IBD, single-intervention approaches often show limited efficacy and durability. On this basis, this review highlights emerging strategies based on engineered microbial ecosystems, which aim to systematically modulate microbial composition and function, reinforce intestinal barrier integrity, and regulate host immune responses. While these approaches hold significant potential, their therapeutic value should be interpreted in the context of current preclinical and early clinical evidence, and further validation is required to determine their long-term efficacy and safety in patients with IBD.
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@article {pmid42028017,
year = {2026},
author = {Xie, J and Deng, S and Zhang, X and Zhang, L and Jia, X},
title = {From dysbacteriosis to ecological remodeling: A new breakthrough in microbial treatment of inflammatory bowel disease.},
journal = {iScience},
volume = {29},
number = {5},
pages = {115483},
pmid = {42028017},
issn = {2589-0042},
abstract = {Inflammatory bowel disease (IBD) is a group of chronic and recurrent inflammatory conditions of the gastrointestinal tract, arising from complex interactions among genetic susceptibility, environmental factors, immune dysregulation, and alterations in the gut microbiota. Increasing evidence suggests that gut microbiota dysbiosis is closely associated with IBD pathogenesis and disease progression, providing a promising target for microbiome-oriented therapeutic strategies. However, due to the multi-factorial and dynamic nature of microbial alterations in IBD, single-intervention approaches often show limited efficacy and durability. On this basis, this review highlights emerging strategies based on engineered microbial ecosystems, which aim to systematically modulate microbial composition and function, reinforce intestinal barrier integrity, and regulate host immune responses. While these approaches hold significant potential, their therapeutic value should be interpreted in the context of current preclinical and early clinical evidence, and further validation is required to determine their long-term efficacy and safety in patients with IBD.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Postbiotics and phage synergy in precision oral microbiome engineering: systems biology strategies targeting Streptococcus mutans in dental caries.
Frontiers in molecular biosciences, 13:1766853.
Dental caries continues to represent a major global public health concern and arises from complex ecological shifts within oral biofilms. The dominance of Streptococcus mutans, in combination with broader microbial imbalance and interactions involving the oral virome, plays a central role in disease progression. Although established preventive measures such as fluoride therapy and mechanical plaque control reduce enamel demineralization and microbial load, they do not comprehensively address dysbiosis, virulence regulation, or host-microbial signaling dynamics. Postbiotics are non-viable microbial products or metabolic derivatives with biological activity, are gaining attention as targeted modulators of the oral ecosystem. These agents include organic acids, exopolysaccharides, bacteriocins, and structural components derived from inactivated probiotic cells. Through diverse mechanisms, postbiotics can reduce acidogenic potential, weaken extracellular matrix integrity within biofilms, disrupt bacterial communication systems, and modulate mucosal immune pathways. Such effects may limit colonization efficiency and pathogenic behavior of S. mutans while preserving commensal balance. Emerging strategies propose combining postbiotics with bacteriophage-based approaches, immunomodulatory platforms, and innovative delivery systems such as nanoformulations and bioadhesive matrices to improve site-specific efficacy. Advances in multi-omics technologies, systems biology modeling, and artificial intelligence-driven diagnostics further support the development of personalized interventions tailored to individual microbial signatures. In addition, postbiotic-mediated modulation of viral-bacterial interactions and horizontal gene exchange may contribute to restoring ecological stability and reducing antimicrobial resistance dissemination. This review integrates current knowledge on postbiotic-driven regulation of the oral microbiome and virome and examines their potential role in precision-oriented caries management. Addressing translational challenges, including formulation stability, safety evaluation, regulatory pathways, and comprehensive virome profiling, will be critical for future clinical application.
Additional Links: PMID-42028131
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@article {pmid42028131,
year = {2026},
author = {Radhamanalan, G},
title = {Postbiotics and phage synergy in precision oral microbiome engineering: systems biology strategies targeting Streptococcus mutans in dental caries.},
journal = {Frontiers in molecular biosciences},
volume = {13},
number = {},
pages = {1766853},
pmid = {42028131},
issn = {2296-889X},
abstract = {Dental caries continues to represent a major global public health concern and arises from complex ecological shifts within oral biofilms. The dominance of Streptococcus mutans, in combination with broader microbial imbalance and interactions involving the oral virome, plays a central role in disease progression. Although established preventive measures such as fluoride therapy and mechanical plaque control reduce enamel demineralization and microbial load, they do not comprehensively address dysbiosis, virulence regulation, or host-microbial signaling dynamics. Postbiotics are non-viable microbial products or metabolic derivatives with biological activity, are gaining attention as targeted modulators of the oral ecosystem. These agents include organic acids, exopolysaccharides, bacteriocins, and structural components derived from inactivated probiotic cells. Through diverse mechanisms, postbiotics can reduce acidogenic potential, weaken extracellular matrix integrity within biofilms, disrupt bacterial communication systems, and modulate mucosal immune pathways. Such effects may limit colonization efficiency and pathogenic behavior of S. mutans while preserving commensal balance. Emerging strategies propose combining postbiotics with bacteriophage-based approaches, immunomodulatory platforms, and innovative delivery systems such as nanoformulations and bioadhesive matrices to improve site-specific efficacy. Advances in multi-omics technologies, systems biology modeling, and artificial intelligence-driven diagnostics further support the development of personalized interventions tailored to individual microbial signatures. In addition, postbiotic-mediated modulation of viral-bacterial interactions and horizontal gene exchange may contribute to restoring ecological stability and reducing antimicrobial resistance dissemination. This review integrates current knowledge on postbiotic-driven regulation of the oral microbiome and virome and examines their potential role in precision-oriented caries management. Addressing translational challenges, including formulation stability, safety evaluation, regulatory pathways, and comprehensive virome profiling, will be critical for future clinical application.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Characteristics of CD4[+]T-cell reduction and pulmonary infections in critically ill immunocompromised patients.
Journal of intensive medicine, 6(2):157-165.
BACKGROUND: The CD4[+]T-cell count is a key indicator for evaluating immunosuppression. Infections significantly influence the survival and prognosis of critically ill patients. This study aims to systematically evaluate the association between reduced CD4[+] T-cell counts and lung infections in immunosuppressed ICU patients, offering clinical evidence to guide the management of lung infections in this population.
METHODS: This retrospective, single-center study included 40 immunocompromised patients admitted to the ICU from January 1, 2021, to June 30, 2023. All participants underwent metagenomic next-generation sequencing. Patients with suspected lung infections based on their CD4[+]T-cell counts were divided into mild (350/µL
RESULTS: Amang these forty immunosuppressed patients, 8 were assigned to the mild group, 16 to the moderate group, and 16 to the severe group. Streptococcus pneumoniae was almost all distributed in moderate patients (75.0%), while severe patients had a higher proportion of fungi detected (25.7%). Respiratory microbiome analysis identified Acinetobacter baumannii, Human alphaherpesvirus 1, and Klebsiella pneumoniae as the most abundant species. Although no significant difference in the alpha diversity index was found among the groups, index values were lower in the severe group than in the moderate group. Beta diversity analysis showed that the microbial community structure did not significantly differ among the three groups. A total of 27 microbial markers were obtained, with multiple streptococcal species showing enrichment in moderate group and Candida tropicalis in severe group. By day 28, four patients (50.0%) in the mild group had died compared with six (37.5%) in the moderate group and nine (56.3%) in the severe group. There were no significant difference in the duration of ICU or hospital stays.
CONCLUSIONS: This study on ICU-admitted immunocompromised patients identified the prevalent pathogens and microbiome features associated with pulmonary infections, as well as their relationship with CD4[+]T-cell depletion. These findings are valuable for optimizing clinical diagnosis and treatment strategies and may contribute to improving patient outcomes.
Additional Links: PMID-42028145
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@article {pmid42028145,
year = {2026},
author = {Chen, Y and Zhang, L and Wang, T and Pan, X and Chen, D and Liu, J},
title = {Characteristics of CD4[+]T-cell reduction and pulmonary infections in critically ill immunocompromised patients.},
journal = {Journal of intensive medicine},
volume = {6},
number = {2},
pages = {157-165},
pmid = {42028145},
issn = {2667-100X},
abstract = {BACKGROUND: The CD4[+]T-cell count is a key indicator for evaluating immunosuppression. Infections significantly influence the survival and prognosis of critically ill patients. This study aims to systematically evaluate the association between reduced CD4[+] T-cell counts and lung infections in immunosuppressed ICU patients, offering clinical evidence to guide the management of lung infections in this population.
METHODS: This retrospective, single-center study included 40 immunocompromised patients admitted to the ICU from January 1, 2021, to June 30, 2023. All participants underwent metagenomic next-generation sequencing. Patients with suspected lung infections based on their CD4[+]T-cell counts were divided into mild (350/µL
RESULTS: Amang these forty immunosuppressed patients, 8 were assigned to the mild group, 16 to the moderate group, and 16 to the severe group. Streptococcus pneumoniae was almost all distributed in moderate patients (75.0%), while severe patients had a higher proportion of fungi detected (25.7%). Respiratory microbiome analysis identified Acinetobacter baumannii, Human alphaherpesvirus 1, and Klebsiella pneumoniae as the most abundant species. Although no significant difference in the alpha diversity index was found among the groups, index values were lower in the severe group than in the moderate group. Beta diversity analysis showed that the microbial community structure did not significantly differ among the three groups. A total of 27 microbial markers were obtained, with multiple streptococcal species showing enrichment in moderate group and Candida tropicalis in severe group. By day 28, four patients (50.0%) in the mild group had died compared with six (37.5%) in the moderate group and nine (56.3%) in the severe group. There were no significant difference in the duration of ICU or hospital stays.
CONCLUSIONS: This study on ICU-admitted immunocompromised patients identified the prevalent pathogens and microbiome features associated with pulmonary infections, as well as their relationship with CD4[+]T-cell depletion. These findings are valuable for optimizing clinical diagnosis and treatment strategies and may contribute to improving patient outcomes.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Mode of birth and risk of inflammatory bowel disease in offspring: an updated systematic review and meta-analysis.
Frontiers in reproductive health, 8:1776110.
BACKGROUND: Cesarean section (CS) rates continue rising worldwide, raising concerns about long-term offspring health consequences, including inflammatory bowel disease (IBD). This systematic review and meta-analysis evaluate the association between CS and risk of IBD, Crohn's disease (CD), and ulcerative colitis (UC).
METHODS: PubMed, Scopus, CENTRAL, and Web of Science were searched through June 2025. Eligible studies included observational cohorts and case-control studies reporting CS vs. vaginal delivery (VD) and IBD outcomes. Data extraction and risk of bias assessment were performed independently. Pooled relative risks (RRs), hazard ratios (HRs), and odds ratios (ORs) were calculated using fixed or random-effects models. Subgroup analyses and publication bias assessment were conducted.
RESULTS: Twenty-two studies comprising over 13 million births were included. Unadjusted analyses showed no association between CS and IBD (RR: 0.98, 95% CI: 0.88-1.08), CD (RR: 0.99, 95% CI: 0.88-1.12), however, an inverse association was observed for UC (RR: 0.82, 95% CI: 0.72-0.95). Regional variation was observed, with CS associated with reduced IBD risk in Denmark, Switzerland, and Norway, but increased risk in Germany and Australia. Adjusted analyses consistently demonstrated no association: IBD (HR: 1.14, 95% CI: 0.99-1.30; OR: 0.91, 95% CI: 0.65-1.25), CD (HR: 1.07, 95% CI: 0.90-1.28; OR: 1.11, 95% CI: 0.98-1.26), and UC (HR: 0.96, 95% CI: 0.87-1.05; OR: 1.05, 95% CI: 0.86-1.27). No publication bias was detected.
CONCLUSION: Across over 13 million births, delivery mode was not associated with IBD, CD, or UC risk. Despite biologically plausible mechanisms linking CS to altered microbiome patterns, epidemiological evidence does not support CS as an independent IBD risk factor. These findings provide reassurance for clinical counseling regarding CS and long-term IBD risk.
https://www.crd.york.ac.uk/PROSPERO/view/CRD420251237413, PROSPERO CRD420251237413.
Additional Links: PMID-42028273
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@article {pmid42028273,
year = {2026},
author = {Taha, H and Al-Shalalfeh, M and Khalil, A and Khasawneh, Y and Abu Ata, A and AbuEin, H and Issa, A and Alhawamdeh, T and BaniMustafa, M and Al-Sabbagh, MQ and Jönsson, L},
title = {Mode of birth and risk of inflammatory bowel disease in offspring: an updated systematic review and meta-analysis.},
journal = {Frontiers in reproductive health},
volume = {8},
number = {},
pages = {1776110},
pmid = {42028273},
issn = {2673-3153},
abstract = {BACKGROUND: Cesarean section (CS) rates continue rising worldwide, raising concerns about long-term offspring health consequences, including inflammatory bowel disease (IBD). This systematic review and meta-analysis evaluate the association between CS and risk of IBD, Crohn's disease (CD), and ulcerative colitis (UC).
METHODS: PubMed, Scopus, CENTRAL, and Web of Science were searched through June 2025. Eligible studies included observational cohorts and case-control studies reporting CS vs. vaginal delivery (VD) and IBD outcomes. Data extraction and risk of bias assessment were performed independently. Pooled relative risks (RRs), hazard ratios (HRs), and odds ratios (ORs) were calculated using fixed or random-effects models. Subgroup analyses and publication bias assessment were conducted.
RESULTS: Twenty-two studies comprising over 13 million births were included. Unadjusted analyses showed no association between CS and IBD (RR: 0.98, 95% CI: 0.88-1.08), CD (RR: 0.99, 95% CI: 0.88-1.12), however, an inverse association was observed for UC (RR: 0.82, 95% CI: 0.72-0.95). Regional variation was observed, with CS associated with reduced IBD risk in Denmark, Switzerland, and Norway, but increased risk in Germany and Australia. Adjusted analyses consistently demonstrated no association: IBD (HR: 1.14, 95% CI: 0.99-1.30; OR: 0.91, 95% CI: 0.65-1.25), CD (HR: 1.07, 95% CI: 0.90-1.28; OR: 1.11, 95% CI: 0.98-1.26), and UC (HR: 0.96, 95% CI: 0.87-1.05; OR: 1.05, 95% CI: 0.86-1.27). No publication bias was detected.
CONCLUSION: Across over 13 million births, delivery mode was not associated with IBD, CD, or UC risk. Despite biologically plausible mechanisms linking CS to altered microbiome patterns, epidemiological evidence does not support CS as an independent IBD risk factor. These findings provide reassurance for clinical counseling regarding CS and long-term IBD risk.
https://www.crd.york.ac.uk/PROSPERO/view/CRD420251237413, PROSPERO CRD420251237413.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Investigating microbiota and biochemical changes in vaginal fluid toward point-of-care microbial monitoring using surface-enhanced Raman spectroscopy.
Biophotonics discovery, 2(4):042102.
SIGNIFICANCE: Vaginal health is maintained by the vaginal microbiome, and dysbiosis of this community can have lifelong negative consequences for women. Current clinical techniques for detecting bacteria in the vagina rely on subjective visual and microscopic analysis or untimely microbial culturing. Surface-enhanced Raman spectroscopy (SERS), a biochemical fingerprinting technique, shows potential for filling this gap as it can identify bacterial species and strains.
AIM: In this study, SERS was used to investigate biochemical changes in vaginal fluid when common vaginal bacteria were present and absent. Subsequently, the performance of a portable Raman spectrometer to detect these biochemical changes was evaluated.
APPROACH: Vaginal fluid was collected from participants attending routine gynecology exams, and SERS spectra were collected using a Raman microscope and a portable spectrometer. Partial least squares, peak intensity, and peak ratio analysis were used to investigate biochemical differences. Quantitative polymerase chain reaction was performed for characterization of Lactobacillus iners, Lactobacillus crispatus, Gardnerella vaginalis, and Streptococcus agalactiae content.
RESULTS: Gardnerella vaginalis presence was characterized by a significant increase in protein and lipid-related features and a decrease in organic acid peaks. The presence of Lactobacillus iners was represented by increased organic acid peaks and a reduction of protein, amino acid, and polysaccharide-related features. Similar trends with little loss of significance were observed when comparing the performance of a Raman microscope and a portable spectrometer.
CONCLUSION: We highlight the feasibility of SERS for detecting differences in bacterial species presence in vaginal fluid and showcase the potential for clinical translation.
Additional Links: PMID-42028293
PubMed:
Citation:
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@article {pmid42028293,
year = {2025},
author = {Rourke-Funderburg, AS and Francisco, VA and Nelson, DJ and Goncalves, KL and Haselton, FR and Elsamadicy, E and Locke, AK},
title = {Investigating microbiota and biochemical changes in vaginal fluid toward point-of-care microbial monitoring using surface-enhanced Raman spectroscopy.},
journal = {Biophotonics discovery},
volume = {2},
number = {4},
pages = {042102},
pmid = {42028293},
issn = {3005-4745},
abstract = {SIGNIFICANCE: Vaginal health is maintained by the vaginal microbiome, and dysbiosis of this community can have lifelong negative consequences for women. Current clinical techniques for detecting bacteria in the vagina rely on subjective visual and microscopic analysis or untimely microbial culturing. Surface-enhanced Raman spectroscopy (SERS), a biochemical fingerprinting technique, shows potential for filling this gap as it can identify bacterial species and strains.
AIM: In this study, SERS was used to investigate biochemical changes in vaginal fluid when common vaginal bacteria were present and absent. Subsequently, the performance of a portable Raman spectrometer to detect these biochemical changes was evaluated.
APPROACH: Vaginal fluid was collected from participants attending routine gynecology exams, and SERS spectra were collected using a Raman microscope and a portable spectrometer. Partial least squares, peak intensity, and peak ratio analysis were used to investigate biochemical differences. Quantitative polymerase chain reaction was performed for characterization of Lactobacillus iners, Lactobacillus crispatus, Gardnerella vaginalis, and Streptococcus agalactiae content.
RESULTS: Gardnerella vaginalis presence was characterized by a significant increase in protein and lipid-related features and a decrease in organic acid peaks. The presence of Lactobacillus iners was represented by increased organic acid peaks and a reduction of protein, amino acid, and polysaccharide-related features. Similar trends with little loss of significance were observed when comparing the performance of a Raman microscope and a portable spectrometer.
CONCLUSION: We highlight the feasibility of SERS for detecting differences in bacterial species presence in vaginal fluid and showcase the potential for clinical translation.},
}
RevDate: 2026-04-26
CmpDate: 2026-04-24
Emerging Therapeutic Strategies in Oral Cancer: Epigenetic, Mitochondrial and Immunotherapy Approaches.
Journal of cellular and molecular medicine, 30(8):e71107.
Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer and poses treatment challenges owing to genetic, epigenetic and environmental factors. Conventional treatments, including surgery, chemotherapy and radiation therapy, often have limitations in terms of efficacy and tolerability. Advances in epigenetic therapies such as DNA methyltransferase and histone deacetylase inhibitors offer promising avenues for reversing abnormal gene expression in OSCC. Mitochondria-targeted therapies leverage metabolic disruption and reactive oxygen species modulation to induce apoptosis. Immunotherapy, particularly with immune checkpoint inhibitors and cancer vaccines, enhances the immune response against cancer cells. This review explores the interplay between the tumour microenvironment and oral microbiome in OSCC progression and treatment response. Additionally, RNA interference therapy and nanoparticle-based drug delivery systems enable targeted therapeutic strategies, reduce off-target effects and improve efficacy. Although these approaches show potential, challenges in clinical translation remain. The integration of precision medicine with innovative drug delivery systems can significantly improve patient outcomes in oral cancer management.
Additional Links: PMID-42028862
PubMed:
Citation:
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@article {pmid42028862,
year = {2026},
author = {Shanmugam, G and Singh, CD and Thiruvengadam, R and Thiruvengadam, M and Morozov, V and Kolesnikov, R and Alkaladi, A and Saleh, R and Shariati, MA},
title = {Emerging Therapeutic Strategies in Oral Cancer: Epigenetic, Mitochondrial and Immunotherapy Approaches.},
journal = {Journal of cellular and molecular medicine},
volume = {30},
number = {8},
pages = {e71107},
pmid = {42028862},
issn = {1582-4934},
mesh = {Humans ; *Mouth Neoplasms/therapy/genetics/immunology/pathology ; *Epigenesis, Genetic/drug effects ; *Mitochondria/drug effects/metabolism/genetics ; *Immunotherapy/methods ; Tumor Microenvironment/drug effects ; Animals ; },
abstract = {Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer and poses treatment challenges owing to genetic, epigenetic and environmental factors. Conventional treatments, including surgery, chemotherapy and radiation therapy, often have limitations in terms of efficacy and tolerability. Advances in epigenetic therapies such as DNA methyltransferase and histone deacetylase inhibitors offer promising avenues for reversing abnormal gene expression in OSCC. Mitochondria-targeted therapies leverage metabolic disruption and reactive oxygen species modulation to induce apoptosis. Immunotherapy, particularly with immune checkpoint inhibitors and cancer vaccines, enhances the immune response against cancer cells. This review explores the interplay between the tumour microenvironment and oral microbiome in OSCC progression and treatment response. Additionally, RNA interference therapy and nanoparticle-based drug delivery systems enable targeted therapeutic strategies, reduce off-target effects and improve efficacy. Although these approaches show potential, challenges in clinical translation remain. The integration of precision medicine with innovative drug delivery systems can significantly improve patient outcomes in oral cancer management.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Mouth Neoplasms/therapy/genetics/immunology/pathology
*Epigenesis, Genetic/drug effects
*Mitochondria/drug effects/metabolism/genetics
*Immunotherapy/methods
Tumor Microenvironment/drug effects
Animals
RevDate: 2026-04-24
Decoding Microbial Reductive Dechlorination of 209 Polychlorinated Biphenyl Congeners through Experiment-Aided Quantum Chemistry and Machine Learning.
Environmental science & technology [Epub ahead of print].
Polychlorinated biphenyls (PCBs) persist globally as legacy pollutants with a complex structural diversity that complicates the understanding of their microbial conversion processes and remediation. In this study, high-throughput enzymatic assays, quantum chemical calculations, and machine learning were integrated to elucidate the reductive dechlorination pathways and reactivity of all 209 PCB congeners. By coupling Hirshfeld charge analysis with empirically derived steric effects, 98.3% accuracy was achieved in predicting dechlorination pathways across diverse Dehalococcoides isolates and enrichment cultures containing distinct organohalide-respiring bacteria. Furthermore, XGBoost models incorporating electronic, steric, and physicochemical descriptors were developed to quantify the dechlorination reactivity of PCBs, revealing that the steric effect-corrected Hirshfeld charge and PCB solubility primarily control microbial reductive dechlorination potential. The model successfully captured the observed trends in the dechlorination reactivity of PCBs across multiple dechlorinating cultures and predicted that 11 of the 12 dioxin-like PCB congeners were susceptible to microbial reductive dechlorination, highlighting intrinsic microbial detoxification potential under anaerobic conditions. This integrative framework unveils the first full picture of microbial dechlorination pathways and reactivity for the entire PCB family, providing mechanistic insight into how molecular properties dictate halogen removal. The findings advance the predictive understanding of organohalide respiration and offer a roadmap for designing microbiome-based bioremediation strategies for persistent halogenated pollutants like PCBs.
Additional Links: PMID-42028897
Publisher:
PubMed:
Citation:
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@article {pmid42028897,
year = {2026},
author = {Wang, S and He, H and Zhang, S and Tian, L and Lu, Q and Mai, B and Adrian, L and Dolfing, J and Xu, G},
title = {Decoding Microbial Reductive Dechlorination of 209 Polychlorinated Biphenyl Congeners through Experiment-Aided Quantum Chemistry and Machine Learning.},
journal = {Environmental science & technology},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.est.5c16226},
pmid = {42028897},
issn = {1520-5851},
abstract = {Polychlorinated biphenyls (PCBs) persist globally as legacy pollutants with a complex structural diversity that complicates the understanding of their microbial conversion processes and remediation. In this study, high-throughput enzymatic assays, quantum chemical calculations, and machine learning were integrated to elucidate the reductive dechlorination pathways and reactivity of all 209 PCB congeners. By coupling Hirshfeld charge analysis with empirically derived steric effects, 98.3% accuracy was achieved in predicting dechlorination pathways across diverse Dehalococcoides isolates and enrichment cultures containing distinct organohalide-respiring bacteria. Furthermore, XGBoost models incorporating electronic, steric, and physicochemical descriptors were developed to quantify the dechlorination reactivity of PCBs, revealing that the steric effect-corrected Hirshfeld charge and PCB solubility primarily control microbial reductive dechlorination potential. The model successfully captured the observed trends in the dechlorination reactivity of PCBs across multiple dechlorinating cultures and predicted that 11 of the 12 dioxin-like PCB congeners were susceptible to microbial reductive dechlorination, highlighting intrinsic microbial detoxification potential under anaerobic conditions. This integrative framework unveils the first full picture of microbial dechlorination pathways and reactivity for the entire PCB family, providing mechanistic insight into how molecular properties dictate halogen removal. The findings advance the predictive understanding of organohalide respiration and offer a roadmap for designing microbiome-based bioremediation strategies for persistent halogenated pollutants like PCBs.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
[Cutaneous pre- and probiotics: Modulating the axillary microbiome to control body odors].
Medecine sciences : M/S, 42(4):398-401.
Additional Links: PMID-42028948
Publisher:
PubMed:
Citation:
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@article {pmid42028948,
year = {2026},
author = {Joncour, G and Saghbini, S},
title = {[Cutaneous pre- and probiotics: Modulating the axillary microbiome to control body odors].},
journal = {Medecine sciences : M/S},
volume = {42},
number = {4},
pages = {398-401},
doi = {10.1051/medsci/2026062},
pmid = {42028948},
issn = {1958-5381},
mesh = {*Probiotics/administration & dosage/therapeutic use ; Humans ; *Microbiota/drug effects/physiology ; *Axilla/microbiology ; *Odorants/prevention & control/analysis ; *Skin/microbiology ; *Prebiotics/administration & dosage ; Administration, Cutaneous ; },
}
MeSH Terms:
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*Probiotics/administration & dosage/therapeutic use
Humans
*Microbiota/drug effects/physiology
*Axilla/microbiology
*Odorants/prevention & control/analysis
*Skin/microbiology
*Prebiotics/administration & dosage
Administration, Cutaneous
RevDate: 2026-04-24
Bacillus aerius synergizes with coal gangue to enhance Medicago sativa growth via soil microbiome and gene regulation.
Applied and environmental microbiology [Epub ahead of print].
UNLABELLED: The extensive accumulation of coal gangue poses significant environmental threats through water contamination, soil degradation, and atmospheric pollution, necessitating the urgent development of ecological utilization strategies. This study elucidates the mechanistic basis by which the thermophilic bacterium Bacillus aerius (B. aerius) enhances plant growth in coal gangue-amended sandy soils. Through integrated analysis of nutrient dynamics, phytohormonal activities, soil enzymatic profiles, and metagenomic functional profiling, we demonstrate significant synergy between coal gangue and B. aerius. When applied together in sandy soils, the germination rate, plant height, root length, and fresh biomass of Medicago sativa (alfalfa) increased by 1.18-2.06 times. The levels of soil nitrogen, phosphorus, and potassium also significantly increased, resulting in notable improvements in soil fertility. The bacterial treatment enhanced the activities of indole-3-acetic acid, 1-aminocyclopropane-1-carboxylate (ACC) deaminase, and various soil enzyme activities while also optimizing the microbial community structure and increasing the abundance of beneficial bacteria, including Bacillus. Metagenomic analysis revealed the upregulation of growth-promoting genes such as acdS, nifK, and phnG, which collectively drive plant growth through multiple pathways, including enhanced soil nutrient availability, hormone regulation, soil enzyme activities, and nutrient cycling. Collectively, this work deciphers molecular-scale bacteria-gangue synergism, providing a theoretical foundation for sustainable coal gangue utilization and ecological restoration of degraded soils.
IMPORTANCE: The accumulation of coal gangue poses significant environmental challenges, necessitating the development of eco-friendly utilization strategies. This study demonstrates that the thermophilic bacterium Bacillus aerius acts synergistically with coal gangue to promote alfalfa growth in sandy soils while improving soil fertility. The combined treatment enhanced plant morphological traits, soil nutrient availability, beneficial microbial communities, and associated biological activities, with these effects supported by molecular evidence. As the first study to verify this growth-promoting mechanism, our findings address a critical knowledge gap and provide a theoretical foundation for the sustainable utilization of coal gangue in the ecological restoration of degraded soils.
Additional Links: PMID-42028995
Publisher:
PubMed:
Citation:
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@article {pmid42028995,
year = {2026},
author = {Liu, M and Du, M and Xi, Z and Tastambek, KT and Bao, Y and Song, X and Zhou, A and Wang, Y},
title = {Bacillus aerius synergizes with coal gangue to enhance Medicago sativa growth via soil microbiome and gene regulation.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0026826},
doi = {10.1128/aem.00268-26},
pmid = {42028995},
issn = {1098-5336},
abstract = {UNLABELLED: The extensive accumulation of coal gangue poses significant environmental threats through water contamination, soil degradation, and atmospheric pollution, necessitating the urgent development of ecological utilization strategies. This study elucidates the mechanistic basis by which the thermophilic bacterium Bacillus aerius (B. aerius) enhances plant growth in coal gangue-amended sandy soils. Through integrated analysis of nutrient dynamics, phytohormonal activities, soil enzymatic profiles, and metagenomic functional profiling, we demonstrate significant synergy between coal gangue and B. aerius. When applied together in sandy soils, the germination rate, plant height, root length, and fresh biomass of Medicago sativa (alfalfa) increased by 1.18-2.06 times. The levels of soil nitrogen, phosphorus, and potassium also significantly increased, resulting in notable improvements in soil fertility. The bacterial treatment enhanced the activities of indole-3-acetic acid, 1-aminocyclopropane-1-carboxylate (ACC) deaminase, and various soil enzyme activities while also optimizing the microbial community structure and increasing the abundance of beneficial bacteria, including Bacillus. Metagenomic analysis revealed the upregulation of growth-promoting genes such as acdS, nifK, and phnG, which collectively drive plant growth through multiple pathways, including enhanced soil nutrient availability, hormone regulation, soil enzyme activities, and nutrient cycling. Collectively, this work deciphers molecular-scale bacteria-gangue synergism, providing a theoretical foundation for sustainable coal gangue utilization and ecological restoration of degraded soils.
IMPORTANCE: The accumulation of coal gangue poses significant environmental challenges, necessitating the development of eco-friendly utilization strategies. This study demonstrates that the thermophilic bacterium Bacillus aerius acts synergistically with coal gangue to promote alfalfa growth in sandy soils while improving soil fertility. The combined treatment enhanced plant morphological traits, soil nutrient availability, beneficial microbial communities, and associated biological activities, with these effects supported by molecular evidence. As the first study to verify this growth-promoting mechanism, our findings address a critical knowledge gap and provide a theoretical foundation for the sustainable utilization of coal gangue in the ecological restoration of degraded soils.},
}
RevDate: 2026-04-24
Applying microbial ecology frameworks to microbial therapies for wildlife.
mSystems [Epub ahead of print].
Microbial ecology is increasingly incorporated into human and animal medicine via the study and purposeful manipulation of host-associated microbiomes. Microbial therapies-treatments with the aim of beneficially modulating microbiomes-are a burgeoning area of research and industry. These microbial therapies include prebiotic dietary items, live probiotics, and whole microbiota transplants (e.g., fecal microbiota transplants). Although microbial therapies for humans and domestic animals are now widely produced for commercial use and application, evidence supporting the efficacy of commercial microbial therapies is mixed. We suggest that microbial therapies are most effective when paired with concepts from ecology and rigorous empirical research. This is particularly relevant for the development and use of microbial therapies in wildlife animal species, in which we see large-scale variation in microbial communities across hosts of varying ecologies. Identifying and developing microbial therapies that can simultaneously be accessible and effective in a variety of hosts poses a novel challenge for microbial ecologists, animal scientists, and human and animal medical professionals. In addition to pre- and probiotics, we suggest that whole microbiota transplants provide a method of microbial supplementation that may better align with species-specific microbial ecology. Moving forward, emerging methods used in human medicine such as machine learning, network analysis, and microbiome engineering using high-throughput culturomics will likely be key to identifying and applying functionally relevant (e.g., disease suppressive) microbial taxa for wildlife therapies.
Additional Links: PMID-42029022
Publisher:
PubMed:
Citation:
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@article {pmid42029022,
year = {2026},
author = {Bornbusch, SL and Muletz-Wolz, CR},
title = {Applying microbial ecology frameworks to microbial therapies for wildlife.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0059825},
doi = {10.1128/msystems.00598-25},
pmid = {42029022},
issn = {2379-5077},
abstract = {Microbial ecology is increasingly incorporated into human and animal medicine via the study and purposeful manipulation of host-associated microbiomes. Microbial therapies-treatments with the aim of beneficially modulating microbiomes-are a burgeoning area of research and industry. These microbial therapies include prebiotic dietary items, live probiotics, and whole microbiota transplants (e.g., fecal microbiota transplants). Although microbial therapies for humans and domestic animals are now widely produced for commercial use and application, evidence supporting the efficacy of commercial microbial therapies is mixed. We suggest that microbial therapies are most effective when paired with concepts from ecology and rigorous empirical research. This is particularly relevant for the development and use of microbial therapies in wildlife animal species, in which we see large-scale variation in microbial communities across hosts of varying ecologies. Identifying and developing microbial therapies that can simultaneously be accessible and effective in a variety of hosts poses a novel challenge for microbial ecologists, animal scientists, and human and animal medical professionals. In addition to pre- and probiotics, we suggest that whole microbiota transplants provide a method of microbial supplementation that may better align with species-specific microbial ecology. Moving forward, emerging methods used in human medicine such as machine learning, network analysis, and microbiome engineering using high-throughput culturomics will likely be key to identifying and applying functionally relevant (e.g., disease suppressive) microbial taxa for wildlife therapies.},
}
RevDate: 2026-04-24
The Paradoxical Toxicity of Microplastics under Predation Risk: The Driving Role of Gut Microbiota-Mediated Tolerance.
Environmental science & technology [Epub ahead of print].
Accurate predictions of the ecological risks of microplastics require understanding of their interplay with natural stressors. Here, we revealed that predation risk fundamentally altered the microplastics ecotoxicity on the keystone species Daphnia magna. The microplastics alone were toxic (e.g., reduced growth rate, body size, spine length, and delayed maturity) and became more toxic under predation risk. For instance, the maturation delay at high MP concentrations increased 6.67-fold. Paradoxically, microplastics also enhanced inducible defenses, with fish cues offsetting microplastics that induced reductions in spine length and somatic growth. Contrasting Daphnia genotypes revealed that the fish-adapted clone exhibited superior tolerance to combined exposure to stressors, maintaining robust growth and defensive integrity, unlike the fish-naïve clone. The gut microbiome was identified as a key mechanistic driver. The fish-adapted clone maintained a more stable microbial community structure with functions enriched in carbohydrate metabolism and immune defense. A reciprocal transplantation experiment provided causal evidence: transplanting the adapted microbiota into the predator-naïve clone reduced mortality by 39% and increased intrinsic growth by 22% under combined stress. These findings highlight that microplastics risk assessment may be flawed if they ignore the eco-evolutionary context of natural stressors.
Additional Links: PMID-42029232
Publisher:
PubMed:
Citation:
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@article {pmid42029232,
year = {2026},
author = {Li, J and Zhang, C and Zhang, H and Xu, W and Protopopov, M and Chang, M and Stoks, R},
title = {The Paradoxical Toxicity of Microplastics under Predation Risk: The Driving Role of Gut Microbiota-Mediated Tolerance.},
journal = {Environmental science & technology},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.est.6c01355},
pmid = {42029232},
issn = {1520-5851},
abstract = {Accurate predictions of the ecological risks of microplastics require understanding of their interplay with natural stressors. Here, we revealed that predation risk fundamentally altered the microplastics ecotoxicity on the keystone species Daphnia magna. The microplastics alone were toxic (e.g., reduced growth rate, body size, spine length, and delayed maturity) and became more toxic under predation risk. For instance, the maturation delay at high MP concentrations increased 6.67-fold. Paradoxically, microplastics also enhanced inducible defenses, with fish cues offsetting microplastics that induced reductions in spine length and somatic growth. Contrasting Daphnia genotypes revealed that the fish-adapted clone exhibited superior tolerance to combined exposure to stressors, maintaining robust growth and defensive integrity, unlike the fish-naïve clone. The gut microbiome was identified as a key mechanistic driver. The fish-adapted clone maintained a more stable microbial community structure with functions enriched in carbohydrate metabolism and immune defense. A reciprocal transplantation experiment provided causal evidence: transplanting the adapted microbiota into the predator-naïve clone reduced mortality by 39% and increased intrinsic growth by 22% under combined stress. These findings highlight that microplastics risk assessment may be flawed if they ignore the eco-evolutionary context of natural stressors.},
}
RevDate: 2026-04-24
A urinary three-metabolite signature enables non-invasive identification of high-risk ovarian cancer patients.
Clinical cancer research : an official journal of the American Association for Cancer Research pii:784360 [Epub ahead of print].
BACKGROUND: Reliable prognostic tools in ovarian cancer are urgently needed to guide risk-adapted treatment decisions, yet the clinical utility of urinary metabolites for non-invasive risk stratification remains largely undefined. Here, we define a clinically relevant urinary metabolite signature that enables non-invasive prognostic risk stratification in ovarian cancer.
METHODS: Using targeted ¹H NMR spectroscopy, we profiled 149 metabolites involved in energy metabolism, oxidative stress, mitochondrial function, nitrogen metabolism, amino acid degradation, gut microbiome activity and inflammation in pre-operative urine from 199 consecutive patients with newly diagnosed ovarian cancer treated in routine clinical practice between 2013 and 2022.
RESULTS: Unsupervised clustering revealed biologically heterogeneous subgroups but lacked prognostic resolution and alignment with overt clinical phenotypes. However, single-metabolite analysis identified a condensed three-metabolite prognostic signature comprising glycine, alanine and citrate. A final parsimonious model integrating this metabolite-signature with clinical covariates outperformed established risk factors alone (FIGO-stage, surgical outcome), accurately predicted 60-month overall survival (AUC = 0.839) and stratified risk. Patients in the highest-risk quartile (Q4) had markedly shorter progression-free survival (Δmedian ≈ 56 months; HR = 2.63, 95% CI: 1.54-4.52, p < 0.001) and overall survival (Δmedian ≈ 86 months; HR = 2.49, 95% CI: 1.39-4.46, p = 0.009) compared to the lowest-risk group (Q1).
CONCLUSION: We define a urinary three-metabolite signature that enables non-invasive identification of high-risk ovarian cancer patients beyond established clinical factors and may support molecular stratification and risk-adapted clinical decisions, thereby supporting the clinical scalability of urine as a matrix for metabolic risk profiling in ovarian cancer.
Additional Links: PMID-42029478
Publisher:
PubMed:
Citation:
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@article {pmid42029478,
year = {2026},
author = {Funk, AM and Brieske, M and Schwarz, FM and Link, T and Jonas, S and Wimberger, P and Freitag, L and Klimova, A and Chavakis, T and Mirtschink, P and Kuhlmann, JD},
title = {A urinary three-metabolite signature enables non-invasive identification of high-risk ovarian cancer patients.},
journal = {Clinical cancer research : an official journal of the American Association for Cancer Research},
volume = {},
number = {},
pages = {},
doi = {10.1158/1078-0432.CCR-25-4260},
pmid = {42029478},
issn = {1557-3265},
abstract = {BACKGROUND: Reliable prognostic tools in ovarian cancer are urgently needed to guide risk-adapted treatment decisions, yet the clinical utility of urinary metabolites for non-invasive risk stratification remains largely undefined. Here, we define a clinically relevant urinary metabolite signature that enables non-invasive prognostic risk stratification in ovarian cancer.
METHODS: Using targeted ¹H NMR spectroscopy, we profiled 149 metabolites involved in energy metabolism, oxidative stress, mitochondrial function, nitrogen metabolism, amino acid degradation, gut microbiome activity and inflammation in pre-operative urine from 199 consecutive patients with newly diagnosed ovarian cancer treated in routine clinical practice between 2013 and 2022.
RESULTS: Unsupervised clustering revealed biologically heterogeneous subgroups but lacked prognostic resolution and alignment with overt clinical phenotypes. However, single-metabolite analysis identified a condensed three-metabolite prognostic signature comprising glycine, alanine and citrate. A final parsimonious model integrating this metabolite-signature with clinical covariates outperformed established risk factors alone (FIGO-stage, surgical outcome), accurately predicted 60-month overall survival (AUC = 0.839) and stratified risk. Patients in the highest-risk quartile (Q4) had markedly shorter progression-free survival (Δmedian ≈ 56 months; HR = 2.63, 95% CI: 1.54-4.52, p < 0.001) and overall survival (Δmedian ≈ 86 months; HR = 2.49, 95% CI: 1.39-4.46, p = 0.009) compared to the lowest-risk group (Q1).
CONCLUSION: We define a urinary three-metabolite signature that enables non-invasive identification of high-risk ovarian cancer patients beyond established clinical factors and may support molecular stratification and risk-adapted clinical decisions, thereby supporting the clinical scalability of urine as a matrix for metabolic risk profiling in ovarian cancer.},
}
RevDate: 2026-04-26
CmpDate: 2026-04-24
HBV and the Microbiome-PubMed Database Literature Review.
Infectious disease reports, 18(3):.
OBJECTIVE: Hepatitis B virus (HBV) is a globally distributed infectious disease affecting the liver. This literature review aims to summarize all available relevant information on the PubMed database about HBV's connection to the microbiome and to consider possible treatment adjuncts.
MATERIALS AND METHODS: Database used: PubMed. Keywords used: "HBV", "Hepatitis B", "microbiome". In the PubMed database, 179 research publications were identified using these keywords; 69 studies were excluded as they were irrelevant or retracted. Of the remaining, 110 were analyzed in this literature review, and four additional literature sources were used to supply background information and context. Information was summarized. The analysed studies in total included 14,814 participants (excluding animal studies), of whom 8564 were HBV-infected individuals.
RESULTS: Results characterizing abundance or decrease in specific bacterial, viral, and fungal species are heterogeneous; multiple studies support that the HBV patient oral and fecal microbiome is different from that in healthy controls (HCs) and varies throughout disease progression. The HBV seems to transform the microbiome negatively, leading to dysbiosis and decreased microbial diversity in most studies. Evidence links HBV microbiome changes with influence on HbeAg seroconversion, HBV-DNA load, metabolic pathways, liver cirrhosis, and hepatocellular carcinoma. The research proposes that members of microbiota could potentially promote or protect against liver injury in HBV. Four studies proposed that the plasma virome in HBV patients was primarily composed of members of the Anelloviridae. One study researched a parasite (Entamoeba gingivalis) in HBV patients. Two studies analyzed HBV patients' fungal profiles.
CONCLUSIONS: Microbiota research, although promising, at the present moment is heterogeneous. HBV patients' microbiota is distinguishable from HCs, and multiple studies have tried to identify the HBV characteristic microbiome; however, more precise information is needed to draw conclusions. Fecal microbiota transplantation and probiotics have the potential to be therapy adjuncts for HBV patients, but more research is needed.
Additional Links: PMID-42029644
PubMed:
Citation:
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@article {pmid42029644,
year = {2026},
author = {Prince, AM and Zeltiņa, I and Reinis, A and Valciņa, O and Krūmiņa, A},
title = {HBV and the Microbiome-PubMed Database Literature Review.},
journal = {Infectious disease reports},
volume = {18},
number = {3},
pages = {},
pmid = {42029644},
issn = {2036-7430},
abstract = {OBJECTIVE: Hepatitis B virus (HBV) is a globally distributed infectious disease affecting the liver. This literature review aims to summarize all available relevant information on the PubMed database about HBV's connection to the microbiome and to consider possible treatment adjuncts.
MATERIALS AND METHODS: Database used: PubMed. Keywords used: "HBV", "Hepatitis B", "microbiome". In the PubMed database, 179 research publications were identified using these keywords; 69 studies were excluded as they were irrelevant or retracted. Of the remaining, 110 were analyzed in this literature review, and four additional literature sources were used to supply background information and context. Information was summarized. The analysed studies in total included 14,814 participants (excluding animal studies), of whom 8564 were HBV-infected individuals.
RESULTS: Results characterizing abundance or decrease in specific bacterial, viral, and fungal species are heterogeneous; multiple studies support that the HBV patient oral and fecal microbiome is different from that in healthy controls (HCs) and varies throughout disease progression. The HBV seems to transform the microbiome negatively, leading to dysbiosis and decreased microbial diversity in most studies. Evidence links HBV microbiome changes with influence on HbeAg seroconversion, HBV-DNA load, metabolic pathways, liver cirrhosis, and hepatocellular carcinoma. The research proposes that members of microbiota could potentially promote or protect against liver injury in HBV. Four studies proposed that the plasma virome in HBV patients was primarily composed of members of the Anelloviridae. One study researched a parasite (Entamoeba gingivalis) in HBV patients. Two studies analyzed HBV patients' fungal profiles.
CONCLUSIONS: Microbiota research, although promising, at the present moment is heterogeneous. HBV patients' microbiota is distinguishable from HCs, and multiple studies have tried to identify the HBV characteristic microbiome; however, more precise information is needed to draw conclusions. Fecal microbiota transplantation and probiotics have the potential to be therapy adjuncts for HBV patients, but more research is needed.},
}
RevDate: 2026-04-24
Genomic and Functional Diversity of Pseudoalteromonas Associated with the Tropical Bivalve Anadara Tuberculosa.
Microbial ecology pii:10.1007/s00248-026-02753-y [Epub ahead of print].
Additional Links: PMID-42029730
Publisher:
PubMed:
Citation:
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@article {pmid42029730,
year = {2026},
author = {Restrepo-Benavides, M and Jiménez, P and Figueras, MJ and Restrepo, S and Zambrano, MM and Pujol, I and Guevara-Suarez, M and Fernández-Bravo, A},
title = {Genomic and Functional Diversity of Pseudoalteromonas Associated with the Tropical Bivalve Anadara Tuberculosa.},
journal = {Microbial ecology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00248-026-02753-y},
pmid = {42029730},
issn = {1432-184X},
}
RevDate: 2026-04-27
CmpDate: 2026-04-24
Bacterial diversity in ferruginous duricrust (canga) and the physicochemical variables affecting their prevalence, distribution and predicted metabolic pathways.
Antonie van Leeuwenhoek, 119(5):.
The ferruginous duricrust (canga) in the Iron Quadrangle (IQ), Minas Gerais, Brazil, occurs within the Campo Rupestre and presents remarkable levels of endemism and species richness. Despite the recognized importance of microorganisms for the maintenance of this ecosystem, current molecular-based studies reveal that both the taxonomic composition and the ecological functions of the canga microbiome are undiscovered. In this study, eighteen samples of canga were collected from the Serra da Piedade State Natural Monument, and their taxonomic diversity was investigated using 16S rRNA metabarcoding. Additionally, the influence of physicochemical variables on microbial diversity and community structure was estimated using statistical tools. Most of the 856,667 reads clustered into ASVs corresponded to Bacteria (99.7%), and the most abundant of the 184 identified genera were Conexibacter, Acidothermus and Bryobacter. Microbial diversity was explained by a combination of physicochemical variables, such as organic matter (OM), iron (Fe), aluminum (Al) and pH, whereas microbial community structure was influenced by the concentrations of Fe, Al and the cation exchange capacity (CEC). Functional prediction analysis based on the main genera identified in the samples indicated that the denitrification pathway may play an important role in the ecosystem. The investigation of the genera and their metabolic pathways based on the literature revealed that they are unexplored and emphasized the biodiversity hotspot yet to be explored in ferruginous duricrust. Therefore, our results reinforce the importance of further studies in this environment, both for future biotechnological applications and for appropriate management and preservation actions.
Additional Links: PMID-42029786
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Citation:
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@article {pmid42029786,
year = {2026},
author = {Jotta, VFM and Silva, CA and García, GJY and Marques, AR and Dos Santos Freitas, A and Góes-Neto, A and Badotti, F},
title = {Bacterial diversity in ferruginous duricrust (canga) and the physicochemical variables affecting their prevalence, distribution and predicted metabolic pathways.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {5},
pages = {},
pmid = {42029786},
issn = {1572-9699},
mesh = {*Bacteria/classification/genetics/metabolism/isolation & purification ; RNA, Ribosomal, 16S/genetics ; Brazil ; *Biodiversity ; *Metabolic Networks and Pathways ; Phylogeny ; *Microbiota ; *Soil Microbiology ; Iron/analysis ; DNA, Bacterial/genetics ; },
abstract = {The ferruginous duricrust (canga) in the Iron Quadrangle (IQ), Minas Gerais, Brazil, occurs within the Campo Rupestre and presents remarkable levels of endemism and species richness. Despite the recognized importance of microorganisms for the maintenance of this ecosystem, current molecular-based studies reveal that both the taxonomic composition and the ecological functions of the canga microbiome are undiscovered. In this study, eighteen samples of canga were collected from the Serra da Piedade State Natural Monument, and their taxonomic diversity was investigated using 16S rRNA metabarcoding. Additionally, the influence of physicochemical variables on microbial diversity and community structure was estimated using statistical tools. Most of the 856,667 reads clustered into ASVs corresponded to Bacteria (99.7%), and the most abundant of the 184 identified genera were Conexibacter, Acidothermus and Bryobacter. Microbial diversity was explained by a combination of physicochemical variables, such as organic matter (OM), iron (Fe), aluminum (Al) and pH, whereas microbial community structure was influenced by the concentrations of Fe, Al and the cation exchange capacity (CEC). Functional prediction analysis based on the main genera identified in the samples indicated that the denitrification pathway may play an important role in the ecosystem. The investigation of the genera and their metabolic pathways based on the literature revealed that they are unexplored and emphasized the biodiversity hotspot yet to be explored in ferruginous duricrust. Therefore, our results reinforce the importance of further studies in this environment, both for future biotechnological applications and for appropriate management and preservation actions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Bacteria/classification/genetics/metabolism/isolation & purification
RNA, Ribosomal, 16S/genetics
Brazil
*Biodiversity
*Metabolic Networks and Pathways
Phylogeny
*Microbiota
*Soil Microbiology
Iron/analysis
DNA, Bacterial/genetics
RevDate: 2026-04-27
CmpDate: 2026-04-24
Gut microbiome alterations among Ghanaian children with asymptomatic malaria infections.
PloS one, 21(4):e0348120.
The human gut microbiome, consisting of bacteria, archaea, fungi, and viruses, influences various physiological processes of the body. The gut microbiome composition is shaped by factors such as diet, geography, and antibiotic use. Malaria has been a global health challenge over the years, especially in low- and middle-income countries. This study investigated how asymptomatic malaria infection altered gut microbial communities in Ghanaian children, offering insights for novel malaria control strategies. Standard aseptic phlebotomy procedures were employed to collect venous blood samples for Plasmodium species detection. The gut microbial community was profiled by sequencing the 16S rRNA V4 region, and sequence data were processed using the DADA2 pipeline in R. Asymptomatic malaria infections were predominantly mixed with P. falciparum and P. malariae. Microbiome analysis revealed that Firmicutes and Bacteroidetes comprised nearly 70% of the total microbial population. Asymptomatic individuals showed a decrease in Firmicutes abundance from 52.5% to 44.0% and an increase in Bacteroidetes from 34.7% to 45.6%. There was also a slight increase in the abundance of Proteobacteria from 3.0% to 4.8%. At the genus level, Prevotella_9 was the most abundant and exhibited the highest variability in the infected groups. The Alloprevotella and Streptococcus genera increased in both infected groups, but Escherichia-Shigella was significantly elevated in only those with mixed infections. Faecalibacterium significantly declined in asymptomatic malaria-infected individuals compared to healthy controls, with variability further reduced in mixed infections. Beta-diversity analysis indicated a significant effect of malaria status on microbial composition (PERMANOVA, p < 0.05), explaining approximately 19.1% of the total variation captured by a 2D Principal Component Analysis (PCA) projection. These findings suggest a potential link between malaria infection and gut microbiota alterations and highlight microbial shifts associated with disease status.
Additional Links: PMID-42030348
PubMed:
Citation:
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@article {pmid42030348,
year = {2026},
author = {Larbi, AA and Etsey, M and Brew, O and Koduah, B and Mawuenyega, RE and Amewu, EKA and Essilfie, NK and Wireko, S and Kwarteng, A and Gyan, BA},
title = {Gut microbiome alterations among Ghanaian children with asymptomatic malaria infections.},
journal = {PloS one},
volume = {21},
number = {4},
pages = {e0348120},
pmid = {42030348},
issn = {1932-6203},
mesh = {Humans ; *Gastrointestinal Microbiome/genetics ; Ghana/epidemiology ; *Malaria/microbiology/epidemiology/parasitology ; Child, Preschool ; Male ; Female ; Child ; RNA, Ribosomal, 16S/genetics ; Asymptomatic Infections ; Bacteria/genetics/classification ; Infant ; },
abstract = {The human gut microbiome, consisting of bacteria, archaea, fungi, and viruses, influences various physiological processes of the body. The gut microbiome composition is shaped by factors such as diet, geography, and antibiotic use. Malaria has been a global health challenge over the years, especially in low- and middle-income countries. This study investigated how asymptomatic malaria infection altered gut microbial communities in Ghanaian children, offering insights for novel malaria control strategies. Standard aseptic phlebotomy procedures were employed to collect venous blood samples for Plasmodium species detection. The gut microbial community was profiled by sequencing the 16S rRNA V4 region, and sequence data were processed using the DADA2 pipeline in R. Asymptomatic malaria infections were predominantly mixed with P. falciparum and P. malariae. Microbiome analysis revealed that Firmicutes and Bacteroidetes comprised nearly 70% of the total microbial population. Asymptomatic individuals showed a decrease in Firmicutes abundance from 52.5% to 44.0% and an increase in Bacteroidetes from 34.7% to 45.6%. There was also a slight increase in the abundance of Proteobacteria from 3.0% to 4.8%. At the genus level, Prevotella_9 was the most abundant and exhibited the highest variability in the infected groups. The Alloprevotella and Streptococcus genera increased in both infected groups, but Escherichia-Shigella was significantly elevated in only those with mixed infections. Faecalibacterium significantly declined in asymptomatic malaria-infected individuals compared to healthy controls, with variability further reduced in mixed infections. Beta-diversity analysis indicated a significant effect of malaria status on microbial composition (PERMANOVA, p < 0.05), explaining approximately 19.1% of the total variation captured by a 2D Principal Component Analysis (PCA) projection. These findings suggest a potential link between malaria infection and gut microbiota alterations and highlight microbial shifts associated with disease status.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/genetics
Ghana/epidemiology
*Malaria/microbiology/epidemiology/parasitology
Child, Preschool
Male
Female
Child
RNA, Ribosomal, 16S/genetics
Asymptomatic Infections
Bacteria/genetics/classification
Infant
RevDate: 2026-04-24
Gut microbiota modulation of regulatory DNA elements revealed by massively parallel functional characterization.
Molecular cell pii:S1097-2765(26)00232-7 [Epub ahead of print].
Cis-regulatory elements (CREs) are central to dynamic gene regulation in hepatocytes, yet most functional annotations derive from in vitro models that poorly capture physiological regulation. We systematically profiled 109,386 human liver-derived CREs using massively parallel reporter assays in hepatocytes under matched in vitro and in vivo conditions. In vivo-active functional CREs (fCREs) were enriched for H3K27ac and chromatin accessibility and were regulated by diverse transcription factors in the human liver. We further demonstrate that gut microbiota-derived signals modulate fCRE activity and target gene expression in vivo, in part via the KEAP1/NFE2L2 antioxidant pathway. Specific microbial metabolites directly altered the activity of selected fCREs, and genetic variation within fCREs modified their responsiveness to microbial signals. Together, these findings reveal microbiota-dependent regulation of hepatic CREs and highlight condition-specific gene regulatory mechanisms in vivo.
Additional Links: PMID-42030942
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PubMed:
Citation:
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@article {pmid42030942,
year = {2026},
author = {Zaratiana, C and M, Y and Lee, YA and Ong, ABL and Liu, TZY and Low, SMC and Chang, SMS and Tan, S and Mustafa, DNA and Ganesh, A and Chang, X and Koh, XQ and Tay, SH and Lee, WJJ and Yuan, JM and Khor, CC and Koh, WP and Dorajoo, R and Li, YE and Kasahara, K and Wuestefeld, T and Chen, PB},
title = {Gut microbiota modulation of regulatory DNA elements revealed by massively parallel functional characterization.},
journal = {Molecular cell},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.molcel.2026.03.036},
pmid = {42030942},
issn = {1097-4164},
abstract = {Cis-regulatory elements (CREs) are central to dynamic gene regulation in hepatocytes, yet most functional annotations derive from in vitro models that poorly capture physiological regulation. We systematically profiled 109,386 human liver-derived CREs using massively parallel reporter assays in hepatocytes under matched in vitro and in vivo conditions. In vivo-active functional CREs (fCREs) were enriched for H3K27ac and chromatin accessibility and were regulated by diverse transcription factors in the human liver. We further demonstrate that gut microbiota-derived signals modulate fCRE activity and target gene expression in vivo, in part via the KEAP1/NFE2L2 antioxidant pathway. Specific microbial metabolites directly altered the activity of selected fCREs, and genetic variation within fCREs modified their responsiveness to microbial signals. Together, these findings reveal microbiota-dependent regulation of hepatic CREs and highlight condition-specific gene regulatory mechanisms in vivo.},
}
RevDate: 2026-04-24
Neutrophil-Derived Reactive Oxygen Species and Bystander Tissue Damage in Inflammatory Bowel Disease.
Free radical biology & medicine pii:S0891-5849(26)00446-6 [Epub ahead of print].
Neutrophils (PMNs) are indispensable effectors of innate immunity whose oxidative and proteolytic capabilities permit rapid microbial containment at mucosal surfaces. Nowhere is this more functionally consequential than in the gastrointestinal tract, where PMN recruitment to the intestinal mucosa serves as both a critical antimicrobial safeguard and a primary driver of epithelial injury in inflammatory bowel diseases (IBD). Upon activation, PMNs deploy an intricate oxidative network centered on the phagocyte NADPH oxidase complex-derived superoxide and hydrogen peroxide in conjunction with the halogenating and nitrating chemistries catalyzed by myeloperoxidase (MPO). These pathways generate a rich repertoire of oxidants-including hypochlorous acid (HOCl), hypobromous acid, reactive nitrogen species, and secondary radical products-that interact with proteins, lipids, nucleic acids, and extracellular matrix components with distinct reaction kinetics and spatial preferences. Importantly, the magnitude, composition, and distribution of these oxidants shape tissue outcomes ranging from transient signaling alterations to epithelial barrier dysfunction and mutational injury contributing to dysplasia. Recent advances in redox proteomics, spatial transcriptomics, intravital imaging, and single-cell analyses have expanded our understanding of how PMN oxidative radical pathways operate within specific mucosal microenvironments and how their outputs intersect with epithelial repair pathways, the microbiome, innate immune crosstalk, and disease chronicity. These studies reveal that PMNs do not function as a uniform oxidative manner; rather, distinct subsets specialize in oxidative burst, extracellular trap formation, metabolic adaptation, or reparative functions. Together, these data emphasize that oxidative injury in IBD is not an unavoidable byproduct of inflammation but rather a dynamic, context-dependent process that with significant potential as a therapeutic target. In this review, we synthesize current knowledge of PMN oxidative radical biology with a focus on the gastrointestinal mucosa. We examine the architecture of PMN reactive oxygen species (ROS) systems, delineate mechanisms of oxidative tissue injury, integrate translational and microbiome implications, and evaluate therapeutic strategies aimed at reducing bystander damage while preserving essential host defense. Through this framework, we highlight future directions that may enable the development of selective redox-modulating therapies capable of restoring mucosal integrity without compromising antimicrobial function.
Additional Links: PMID-42031118
Publisher:
PubMed:
Citation:
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@article {pmid42031118,
year = {2026},
author = {Kim, JY and Colgan, SP and Cartwright, IM},
title = {Neutrophil-Derived Reactive Oxygen Species and Bystander Tissue Damage in Inflammatory Bowel Disease.},
journal = {Free radical biology & medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.freeradbiomed.2026.04.146},
pmid = {42031118},
issn = {1873-4596},
abstract = {Neutrophils (PMNs) are indispensable effectors of innate immunity whose oxidative and proteolytic capabilities permit rapid microbial containment at mucosal surfaces. Nowhere is this more functionally consequential than in the gastrointestinal tract, where PMN recruitment to the intestinal mucosa serves as both a critical antimicrobial safeguard and a primary driver of epithelial injury in inflammatory bowel diseases (IBD). Upon activation, PMNs deploy an intricate oxidative network centered on the phagocyte NADPH oxidase complex-derived superoxide and hydrogen peroxide in conjunction with the halogenating and nitrating chemistries catalyzed by myeloperoxidase (MPO). These pathways generate a rich repertoire of oxidants-including hypochlorous acid (HOCl), hypobromous acid, reactive nitrogen species, and secondary radical products-that interact with proteins, lipids, nucleic acids, and extracellular matrix components with distinct reaction kinetics and spatial preferences. Importantly, the magnitude, composition, and distribution of these oxidants shape tissue outcomes ranging from transient signaling alterations to epithelial barrier dysfunction and mutational injury contributing to dysplasia. Recent advances in redox proteomics, spatial transcriptomics, intravital imaging, and single-cell analyses have expanded our understanding of how PMN oxidative radical pathways operate within specific mucosal microenvironments and how their outputs intersect with epithelial repair pathways, the microbiome, innate immune crosstalk, and disease chronicity. These studies reveal that PMNs do not function as a uniform oxidative manner; rather, distinct subsets specialize in oxidative burst, extracellular trap formation, metabolic adaptation, or reparative functions. Together, these data emphasize that oxidative injury in IBD is not an unavoidable byproduct of inflammation but rather a dynamic, context-dependent process that with significant potential as a therapeutic target. In this review, we synthesize current knowledge of PMN oxidative radical biology with a focus on the gastrointestinal mucosa. We examine the architecture of PMN reactive oxygen species (ROS) systems, delineate mechanisms of oxidative tissue injury, integrate translational and microbiome implications, and evaluate therapeutic strategies aimed at reducing bystander damage while preserving essential host defense. Through this framework, we highlight future directions that may enable the development of selective redox-modulating therapies capable of restoring mucosal integrity without compromising antimicrobial function.},
}
RevDate: 2026-04-24
Shared pathogenic mechanisms between systemic lupus erythematosus and autoimmune hepatitis: A unified view of autoimmune convergence.
Biochimica et biophysica acta. Molecular basis of disease pii:S0925-4439(26)00137-7 [Epub ahead of print].
BACKGROUND: Systemic lupus erythematosus (SLE) and autoimmune hepatitis (AIH) are clinically distinct autoimmune disorders characterized by multisystem involvement and liver-restricted inflammation, respectively; nevertheless, they exhibit considerable overlap in their underlying immunopathogenic features.
AIM: To provide a systematic synthesis of recent advances in genetics, immunology, and microbiome science, and to delineate the convergent pathogenic mechanisms that underpin both SLE and AIH.
METHODS: A comprehensive literature review was conducted using PubMed and other databases up to 2025, focusing on shared genetic, cellular, and microbial determinants in SLE and AIH. Core topics included genetic susceptibility loci, breakdown of immune tolerance, T-cell dysregulation, innate immune activation, and alterations in gut microbiota composition and function.
RESULTS: SLE and AIH share several genetic risk variants, including HLA-DRB1*03:01, PTPN22, STAT4, and TNFAIP3. Both diseases are characterized by defective central and peripheral immune tolerance, imbalances in Th17/Treg and Tfh/Tfr compartments, and aberrant B-cell activation. Innate immune pathways-encompassing Toll-like receptor and NLRP3 inflammasome signaling as well as complement dysregulation-further amplify inflammation. Moreover, gut dysbiosis and perturbations in microbial metabolites, such as short-chain fatty acids, bile acids, and tryptophan derivatives, function as key mediators linking intestinal homeostasis to both systemic and hepatic autoimmunity.
CONCLUSION: SLE and AIH represent overlapping entities along a unified autoimmune spectrum, driven by shared genetic susceptibility, convergent immune dysregulation, and microbial influences. This review advances an integrated immunological framework that bridges systemic and organ-specific autoimmunity, underscores the pivotal role of innate immunity and gut-liver crosstalk, and provides a mechanistic rationale for cross-disease therapeutic strategies targeting these common pathways.
Additional Links: PMID-42031176
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PubMed:
Citation:
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@article {pmid42031176,
year = {2026},
author = {Yechen, W and Wang, F and Xiao, L and Chen, Y and Li, L},
title = {Shared pathogenic mechanisms between systemic lupus erythematosus and autoimmune hepatitis: A unified view of autoimmune convergence.},
journal = {Biochimica et biophysica acta. Molecular basis of disease},
volume = {},
number = {},
pages = {168274},
doi = {10.1016/j.bbadis.2026.168274},
pmid = {42031176},
issn = {1879-260X},
abstract = {BACKGROUND: Systemic lupus erythematosus (SLE) and autoimmune hepatitis (AIH) are clinically distinct autoimmune disorders characterized by multisystem involvement and liver-restricted inflammation, respectively; nevertheless, they exhibit considerable overlap in their underlying immunopathogenic features.
AIM: To provide a systematic synthesis of recent advances in genetics, immunology, and microbiome science, and to delineate the convergent pathogenic mechanisms that underpin both SLE and AIH.
METHODS: A comprehensive literature review was conducted using PubMed and other databases up to 2025, focusing on shared genetic, cellular, and microbial determinants in SLE and AIH. Core topics included genetic susceptibility loci, breakdown of immune tolerance, T-cell dysregulation, innate immune activation, and alterations in gut microbiota composition and function.
RESULTS: SLE and AIH share several genetic risk variants, including HLA-DRB1*03:01, PTPN22, STAT4, and TNFAIP3. Both diseases are characterized by defective central and peripheral immune tolerance, imbalances in Th17/Treg and Tfh/Tfr compartments, and aberrant B-cell activation. Innate immune pathways-encompassing Toll-like receptor and NLRP3 inflammasome signaling as well as complement dysregulation-further amplify inflammation. Moreover, gut dysbiosis and perturbations in microbial metabolites, such as short-chain fatty acids, bile acids, and tryptophan derivatives, function as key mediators linking intestinal homeostasis to both systemic and hepatic autoimmunity.
CONCLUSION: SLE and AIH represent overlapping entities along a unified autoimmune spectrum, driven by shared genetic susceptibility, convergent immune dysregulation, and microbial influences. This review advances an integrated immunological framework that bridges systemic and organ-specific autoimmunity, underscores the pivotal role of innate immunity and gut-liver crosstalk, and provides a mechanistic rationale for cross-disease therapeutic strategies targeting these common pathways.},
}
RevDate: 2026-04-24
Arsenic oxidation by root endophytes mediates arsenic speciation within rice (Oryza sativa).
Environmental pollution (Barking, Essex : 1987) pii:S0269-7491(26)00564-6 [Epub ahead of print].
Arsenic (As) uptake through rice consumption is a major exposure pathway that severely threatens the health of over 140 million people. Since flooded cultivation makes rice specifically vulnerable to As contamination, dry rice cultivation has been proposed to reduce As accumulation. While microorganisms play important roles in As biogeochemical cycles, the impact of the root-associated microbiome, especially endophytes, on As uptake and metabolism in rice growing under different water regimes remains elusive. In this study, different water regimes significantly altered As speciation in the rhizosphere but less impacted those in roots, in which As(V) dominated. While the endosphere community was significantly altered, microbial As transformation potentials were less impacted by different water treatments. Within rice roots, As(III) oxidase gene (aioA) abundance was consistently higher than that of the genes for As reduction (As(V) respiratory reductase arrA and As(V) detoxification reductase arsC) under both treatments, indicating that As(III) oxidation might be the major As transformation pathway in planta. Activity measurements of the endosphere microbial community demonstrated that As(III) oxidation was significantly faster compared to reduction processes. The major endosphere microbial communities harboring aioA genes were affiliated with Rhodocyclaceae, Xanthobacteraceae, and Burkholderiaceae under dry conditions, while members of Rhodocyclaceae dominated under flooded conditions. These results suggest that dominant microbial As(III) oxidation in rice roots may contribute to maintaining a higher As(V) proportion in planta and potentially reduce As translocation to edible grains.
Additional Links: PMID-42031199
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PubMed:
Citation:
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@article {pmid42031199,
year = {2026},
author = {Wang, Z and Song, B and Sun, X and Huang, D and Häggblom, MM and Yu, Z and Kong, T and He, B and He, B and Zhang, H and Sun, W},
title = {Arsenic oxidation by root endophytes mediates arsenic speciation within rice (Oryza sativa).},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {128194},
doi = {10.1016/j.envpol.2026.128194},
pmid = {42031199},
issn = {1873-6424},
abstract = {Arsenic (As) uptake through rice consumption is a major exposure pathway that severely threatens the health of over 140 million people. Since flooded cultivation makes rice specifically vulnerable to As contamination, dry rice cultivation has been proposed to reduce As accumulation. While microorganisms play important roles in As biogeochemical cycles, the impact of the root-associated microbiome, especially endophytes, on As uptake and metabolism in rice growing under different water regimes remains elusive. In this study, different water regimes significantly altered As speciation in the rhizosphere but less impacted those in roots, in which As(V) dominated. While the endosphere community was significantly altered, microbial As transformation potentials were less impacted by different water treatments. Within rice roots, As(III) oxidase gene (aioA) abundance was consistently higher than that of the genes for As reduction (As(V) respiratory reductase arrA and As(V) detoxification reductase arsC) under both treatments, indicating that As(III) oxidation might be the major As transformation pathway in planta. Activity measurements of the endosphere microbial community demonstrated that As(III) oxidation was significantly faster compared to reduction processes. The major endosphere microbial communities harboring aioA genes were affiliated with Rhodocyclaceae, Xanthobacteraceae, and Burkholderiaceae under dry conditions, while members of Rhodocyclaceae dominated under flooded conditions. These results suggest that dominant microbial As(III) oxidation in rice roots may contribute to maintaining a higher As(V) proportion in planta and potentially reduce As translocation to edible grains.},
}
RevDate: 2026-04-24
The skin microbiome and affective symptoms: neuroimmune, neuroendocrine, and sensory pathways linking inflammatory dermatoses to mood and anxiety burden.
Frontiers in neuroendocrinology pii:S0091-3022(26)00021-X [Epub ahead of print].
The skin functions as a neuro-immuno-endocrine organ with an extensive microbial interface capable of bidirectional signaling with the central nervous system. While the gut-brain axis is well established, the skin-microbiota-brain (SMB) axis remains underexplored, particularly with respect to affective symptom dimensions (depression, anxiety, stress) that commonly co-occur with chronic inflammatory dermatoses. This review synthesizes evidence across clinical, translational, and experimental studies and organizes it by strength (associational findings, mechanistic plausibility, and limited interventional signals). We outline a systems-level model in which cutaneous microbial dysbiosis is associated with brain-relevant pathways via immune, neuropeptide, and metabolic routes. Candidate mediators include cytokines (IL-6, IL-17, TNF-α), neuropeptides (e.g., substance P, CGRP), and microbial-derived metabolites (e.g., SCFA-like compounds and tryptophan catabolites). These signals are hypothesized to influence neuroimmune tone and neurovascular signaling based largely on broader systemic inflammation and stress biology; direct causal evidence specifically attributing affective outcomes to skin microbiome perturbations in humans remains limited. In parallel, top-down neuroendocrine signaling via hypothalamic-pituitary-adrenal (HPA) axis activation, cortisol-related signaling, and sympathetic outflow can alter skin barrier function, antimicrobial peptide expression, and microbial ecology, potentially contributing to symptom-maintaining loops (e.g., itch-sleep disruption-stress). Importantly, we consider counterarguments (psychosocial burden, reverse causality, treatment effects, and the localized nature of lesions) and identify research priorities required to test causality (longitudinal sampling, mechanistic biomarker panels, and preregistered interventional studies with affective endpoints and mediation analyses). By integrating dermatological, microbiological, and neuroimmunological evidence within a symptom-centered framework, the SMB axis is positioned as a biologically plausible but still evolving model that may help explain affective symptom burden in subsets of patients with inflammatory skin disease and guide mechanism-informed translational research.
Additional Links: PMID-42031220
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PubMed:
Citation:
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@article {pmid42031220,
year = {2026},
author = {Coccurello, R},
title = {The skin microbiome and affective symptoms: neuroimmune, neuroendocrine, and sensory pathways linking inflammatory dermatoses to mood and anxiety burden.},
journal = {Frontiers in neuroendocrinology},
volume = {},
number = {},
pages = {101251},
doi = {10.1016/j.yfrne.2026.101251},
pmid = {42031220},
issn = {1095-6808},
abstract = {The skin functions as a neuro-immuno-endocrine organ with an extensive microbial interface capable of bidirectional signaling with the central nervous system. While the gut-brain axis is well established, the skin-microbiota-brain (SMB) axis remains underexplored, particularly with respect to affective symptom dimensions (depression, anxiety, stress) that commonly co-occur with chronic inflammatory dermatoses. This review synthesizes evidence across clinical, translational, and experimental studies and organizes it by strength (associational findings, mechanistic plausibility, and limited interventional signals). We outline a systems-level model in which cutaneous microbial dysbiosis is associated with brain-relevant pathways via immune, neuropeptide, and metabolic routes. Candidate mediators include cytokines (IL-6, IL-17, TNF-α), neuropeptides (e.g., substance P, CGRP), and microbial-derived metabolites (e.g., SCFA-like compounds and tryptophan catabolites). These signals are hypothesized to influence neuroimmune tone and neurovascular signaling based largely on broader systemic inflammation and stress biology; direct causal evidence specifically attributing affective outcomes to skin microbiome perturbations in humans remains limited. In parallel, top-down neuroendocrine signaling via hypothalamic-pituitary-adrenal (HPA) axis activation, cortisol-related signaling, and sympathetic outflow can alter skin barrier function, antimicrobial peptide expression, and microbial ecology, potentially contributing to symptom-maintaining loops (e.g., itch-sleep disruption-stress). Importantly, we consider counterarguments (psychosocial burden, reverse causality, treatment effects, and the localized nature of lesions) and identify research priorities required to test causality (longitudinal sampling, mechanistic biomarker panels, and preregistered interventional studies with affective endpoints and mediation analyses). By integrating dermatological, microbiological, and neuroimmunological evidence within a symptom-centered framework, the SMB axis is positioned as a biologically plausible but still evolving model that may help explain affective symptom burden in subsets of patients with inflammatory skin disease and guide mechanism-informed translational research.},
}
RevDate: 2026-04-24
CmpDate: 2026-04-24
Fundamentals of Neurogastroenterology: Basic Science.
Gastroenterology, 170(6):1099-1113.
This review highlights major advances in neurogastroenterology since Rome IV, offering a condensed summary of a comprehensive document to appear in the forthcoming Rome V book. Prepared by an international team of experts, it emphasizes pivotal studies that have deepened understanding of the physiological and pathophysiological mechanisms underlying disorders of gut-brain interaction (DGBI). These disorders are inherently complex and multifactorial, shaped by interactions among neuronal, epithelial, immune, smooth muscle, interstitial, and microbial populations. The review outlines cutting-edge technologies advancing the field and explores key themes, including brain-gut interactions, neurobiology, and neuroplasticity of the enteric nervous system, neuroimmune function, microbiome influences, and abnormalities of the gut-brain axis in DGBI. Risk factors for DGBI are considered, with serotonergic signaling presented as a conceptual framework for linking symptomatology and pathophysiology. Finally, we discuss how these scientific advances can translate into novel therapeutic strategies to improve patient care.
Additional Links: PMID-42031436
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@article {pmid42031436,
year = {2026},
author = {Greenwood-Van Meerveld, B and Mawe, GM and Beyder, A and Brierley, SM and Clarke, G and Gulbransen, BD and Margolis, KG},
title = {Fundamentals of Neurogastroenterology: Basic Science.},
journal = {Gastroenterology},
volume = {170},
number = {6},
pages = {1099-1113},
doi = {10.1053/j.gastro.2026.01.040},
pmid = {42031436},
issn = {1528-0012},
mesh = {Humans ; *Enteric Nervous System/physiopathology ; *Gastrointestinal Diseases/physiopathology/therapy/microbiology ; *Gastroenterology/trends ; Gastrointestinal Microbiome ; *Brain-Gut Axis/physiology ; Animals ; *Gastrointestinal Tract/innervation/physiopathology ; Neuronal Plasticity ; Neuroimmunomodulation ; *Brain/physiopathology ; Risk Factors ; },
abstract = {This review highlights major advances in neurogastroenterology since Rome IV, offering a condensed summary of a comprehensive document to appear in the forthcoming Rome V book. Prepared by an international team of experts, it emphasizes pivotal studies that have deepened understanding of the physiological and pathophysiological mechanisms underlying disorders of gut-brain interaction (DGBI). These disorders are inherently complex and multifactorial, shaped by interactions among neuronal, epithelial, immune, smooth muscle, interstitial, and microbial populations. The review outlines cutting-edge technologies advancing the field and explores key themes, including brain-gut interactions, neurobiology, and neuroplasticity of the enteric nervous system, neuroimmune function, microbiome influences, and abnormalities of the gut-brain axis in DGBI. Risk factors for DGBI are considered, with serotonergic signaling presented as a conceptual framework for linking symptomatology and pathophysiology. Finally, we discuss how these scientific advances can translate into novel therapeutic strategies to improve patient care.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Enteric Nervous System/physiopathology
*Gastrointestinal Diseases/physiopathology/therapy/microbiology
*Gastroenterology/trends
Gastrointestinal Microbiome
*Brain-Gut Axis/physiology
Animals
*Gastrointestinal Tract/innervation/physiopathology
Neuronal Plasticity
Neuroimmunomodulation
*Brain/physiopathology
Risk Factors
RevDate: 2026-04-24
CmpDate: 2026-04-24
Sociocultural Aspects of the Pathophysiology, Clinical Presentation, and Management of Disorders of Gut-Brain Interaction.
Gastroenterology, 170(6):1190-1204.
Sociocultural determinants such as cultural norms, diet, and environmental factors, along with their effects on the gastrointestinal microbiome, can modify the risk to develop disorders of gut-brain interaction (DGBI). These factors also shape symptom perception and health care-seeking behaviors, and how society and health care providers respond to patients with DGBI. This document summarizes the knowledge about the role of sociocultural factors in the manifestation of DGBI and the management of these patients. Symptom expression and societal response to DGBI varies across different cultural settings, influencing individual patient outcomes and the overall societal burden of disease. Patients with DGBI are often stigmatized, leading to a bias toward conditions with visible abnormalities and underfunded services for DGBI. Recognizing the role of sociocultural factors for DGBI outcomes presents an opportunity to refine pathophysiologic concepts and improve patient outcomes. This calls for greater awareness and equitable resource allocation for DGBI research and treatment.
Additional Links: PMID-42031439
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@article {pmid42031439,
year = {2026},
author = {Wong, RK and Fang, X and Ghoshal, UC and Kashyap, PC and Mulak, A and Lee, YY and Sperber, AD and Holtmann, G},
title = {Sociocultural Aspects of the Pathophysiology, Clinical Presentation, and Management of Disorders of Gut-Brain Interaction.},
journal = {Gastroenterology},
volume = {170},
number = {6},
pages = {1190-1204},
doi = {10.1053/j.gastro.2026.02.006},
pmid = {42031439},
issn = {1528-0012},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Brain-Gut Axis/physiology ; *Gastrointestinal Diseases/physiopathology/therapy/psychology ; Risk Factors ; *Brain/physiopathology ; Social Stigma ; Diet ; },
abstract = {Sociocultural determinants such as cultural norms, diet, and environmental factors, along with their effects on the gastrointestinal microbiome, can modify the risk to develop disorders of gut-brain interaction (DGBI). These factors also shape symptom perception and health care-seeking behaviors, and how society and health care providers respond to patients with DGBI. This document summarizes the knowledge about the role of sociocultural factors in the manifestation of DGBI and the management of these patients. Symptom expression and societal response to DGBI varies across different cultural settings, influencing individual patient outcomes and the overall societal burden of disease. Patients with DGBI are often stigmatized, leading to a bias toward conditions with visible abnormalities and underfunded services for DGBI. Recognizing the role of sociocultural factors for DGBI outcomes presents an opportunity to refine pathophysiologic concepts and improve patient outcomes. This calls for greater awareness and equitable resource allocation for DGBI research and treatment.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Gastrointestinal Microbiome
*Brain-Gut Axis/physiology
*Gastrointestinal Diseases/physiopathology/therapy/psychology
Risk Factors
*Brain/physiopathology
Social Stigma
Diet
RevDate: 2026-04-24
A pathogenic gut lipoglycan drives systemic thromboinflammation in lupus nephritis.
Annals of the rheumatic diseases pii:S0003-4967(26)00146-9 [Epub ahead of print].
OBJECTIVES: The gut microbiome plays a crucial role in regulating systemic immunity and has been implicated in several chronic inflammatory diseases. Intestinal expansions of Ruminococcus gnavus (RG), a dominant gut commensal, correlate with disease flares in lupus nephritis (LN), but the underlying mechanism remains unknown.
METHODS: In a Pilot cohort of patients with biopsy-proven LN, subsetted by gut microbiota community, immune status was characterised using bulk-blood RNA sequencing libraries, serum levels of representative host proteins, and levels of immunoglobulin (Ig)G antibodies to the novel lipoglycan (LG) produced by pathogenic RG strains. A Validation LN cohort was evaluated for blood transcriptomic profiles and levels of anti-LG antibodies. In murine models, mechanistic hypotheses were tested after RG gut colonisation or after intraperitoneal injection with an LG preparation, with outcomes determined by transcriptomic analyses, platelet functional readouts, and tissue histology.
RESULTS: In a Pilot cohort of patients with LN, RG gut expansions were associated with high-level platelet, neutrophil, and monocyte activation. Serum levels of platelet factor 4 and release of neutrophil extracellular traps (NETs) were significantly higher in patients with high serum IgG antibody against the novel RG-specific LG, a marker of in vivo immune exposure. An LN Validation cohort confirmed these correlates and showed that anti-LG antibodies serve as a surrogate for thromboinflammatory profile in this LN-associated endotype. In mice, gut colonisation with LG-producing RG strains or a single LG injection caused megakaryocytosis and platelet activation; RG colonisation with LG-producing strains induced tubulointerstitial injury with NETosis. In vivo responses to LG toxin were Toll-like receptor 2-dependent.
CONCLUSIONS: Gut expansions of the RG pathobiont may contribute to autoimmune pathogenesis through the LG toxin and cause LN flares through thromboinflammatory mechanisms in this previously unrecognised LN endotype.
Additional Links: PMID-42031645
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PubMed:
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@article {pmid42031645,
year = {2027},
author = {Amarnani, A and Rivera, CF and Cornwell, M and Weinstein, T and Azad, Z and Gottesman, SRS and Loomis, C and Lee, A and Ullah, N and Prasad, J and Yi, M and Cooney, L and Barnes, BJ and Gisch, N and Ruggles, KV and Ramkhelawon, B and Silverman, GJ},
title = {A pathogenic gut lipoglycan drives systemic thromboinflammation in lupus nephritis.},
journal = {Annals of the rheumatic diseases},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ard.2026.03.002},
pmid = {42031645},
issn = {1468-2060},
abstract = {OBJECTIVES: The gut microbiome plays a crucial role in regulating systemic immunity and has been implicated in several chronic inflammatory diseases. Intestinal expansions of Ruminococcus gnavus (RG), a dominant gut commensal, correlate with disease flares in lupus nephritis (LN), but the underlying mechanism remains unknown.
METHODS: In a Pilot cohort of patients with biopsy-proven LN, subsetted by gut microbiota community, immune status was characterised using bulk-blood RNA sequencing libraries, serum levels of representative host proteins, and levels of immunoglobulin (Ig)G antibodies to the novel lipoglycan (LG) produced by pathogenic RG strains. A Validation LN cohort was evaluated for blood transcriptomic profiles and levels of anti-LG antibodies. In murine models, mechanistic hypotheses were tested after RG gut colonisation or after intraperitoneal injection with an LG preparation, with outcomes determined by transcriptomic analyses, platelet functional readouts, and tissue histology.
RESULTS: In a Pilot cohort of patients with LN, RG gut expansions were associated with high-level platelet, neutrophil, and monocyte activation. Serum levels of platelet factor 4 and release of neutrophil extracellular traps (NETs) were significantly higher in patients with high serum IgG antibody against the novel RG-specific LG, a marker of in vivo immune exposure. An LN Validation cohort confirmed these correlates and showed that anti-LG antibodies serve as a surrogate for thromboinflammatory profile in this LN-associated endotype. In mice, gut colonisation with LG-producing RG strains or a single LG injection caused megakaryocytosis and platelet activation; RG colonisation with LG-producing strains induced tubulointerstitial injury with NETosis. In vivo responses to LG toxin were Toll-like receptor 2-dependent.
CONCLUSIONS: Gut expansions of the RG pathobiont may contribute to autoimmune pathogenesis through the LG toxin and cause LN flares through thromboinflammatory mechanisms in this previously unrecognised LN endotype.},
}
RevDate: 2026-04-27
Gut virome-microbiome interactions across hosts and environments.
NPJ biofilms and microbiomes, 12(1):.
The Gut microbiome-virome dynamics and interactions Collection highlights gut viruses, mainly bacteriophages, as determinants of microbial community structure and host-relevant functions across human, animal, and environmental systems. The Collection welcomes studies that quantify virus-microbe interactions, evidence-based linking viruses to microbial hosts, characterise infection dynamics, and connect them to ecological or clinical outcomes. It prioritises methodological rigour and translational relevance in diagnostics, surveillance, and phage-based interventions.
Additional Links: PMID-42031776
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@article {pmid42031776,
year = {2026},
author = {Samson, R and Hassard, F and Dharne, M},
title = {Gut virome-microbiome interactions across hosts and environments.},
journal = {NPJ biofilms and microbiomes},
volume = {12},
number = {1},
pages = {},
pmid = {42031776},
issn = {2055-5008},
abstract = {The Gut microbiome-virome dynamics and interactions Collection highlights gut viruses, mainly bacteriophages, as determinants of microbial community structure and host-relevant functions across human, animal, and environmental systems. The Collection welcomes studies that quantify virus-microbe interactions, evidence-based linking viruses to microbial hosts, characterise infection dynamics, and connect them to ecological or clinical outcomes. It prioritises methodological rigour and translational relevance in diagnostics, surveillance, and phage-based interventions.},
}
RevDate: 2026-04-24
Gut microbiome-metabolome profiling reveals divergent growth performance in the spotted knifejaw (Oplegnathus punctatus).
Scientific reports pii:10.1038/s41598-026-50031-1 [Epub ahead of print].
Additional Links: PMID-42032033
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PubMed:
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@article {pmid42032033,
year = {2026},
author = {Ma, C and Chen, C and Shang, X and Wang, Y and Liu, H and Yu, Y and Wang, Q and Wang, X and Jia, L and Liang, S},
title = {Gut microbiome-metabolome profiling reveals divergent growth performance in the spotted knifejaw (Oplegnathus punctatus).},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-50031-1},
pmid = {42032033},
issn = {2045-2322},
support = {24ZYCGSN00150//Tianjin Science and Technology Plan Project/ ; CARS-47-Z01//Tianjin Comprehensive Experimental Station of the National Marine Fish Industry Technology System/ ; },
}
RevDate: 2026-04-24
Fecal virome transplantation alleviates weaning stress-induced behavioral alterations and intestinal health by reshaping the gut microbiome.
Scientific reports pii:10.1038/s41598-026-49647-0 [Epub ahead of print].
Additional Links: PMID-42032216
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PubMed:
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@article {pmid42032216,
year = {2026},
author = {Choi, Y and Ryu, S and Kang, A and Lee, W and Park, J and Kang, MG and Jang, KB and Kwon, Y and Kwak, MJ and Jeong, KC and Song, M and Kim, Y},
title = {Fecal virome transplantation alleviates weaning stress-induced behavioral alterations and intestinal health by reshaping the gut microbiome.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-49647-0},
pmid = {42032216},
issn = {2045-2322},
support = {RS-2025-16068814//National Research Foundation of Korea/ ; },
}
RevDate: 2026-04-24
Cayman enables large-scale analysis of gut microbiome carbohydrate-active enzyme repertoires.
Nature microbiology [Epub ahead of print].
Carbohydrate-active enzymes (CAZymes) are crucial for digesting glycans, but tools for CAZyme profiling and interpretation of substrate preferences in microbiome data are lacking. Here we develop a CAZyme profiler called Cayman (Carbohydrate Active Enzymes Profiling of Metagenomes) and a hierarchical substrate annotation scheme for use with genomic or shotgun metagenomic datasets. Using these tools, we systematically surveyed CAZymes in human gut microorganisms (n = 107,683 genomes) and identified several putative mucin-foraging bacteria, including Hungatella and Eisenbergiella species, which were confirmed experimentally. We compared CAZymes in gut metagenomes (n = 3,960) from high-income settings versus low- and middle-income settings and found that low- and middle-income setting metagenomes are enriched in fibre-degrading CAZymes, while CAZyme richness is generally higher in high-income setting metagenomes. Additional analysis (n = 1,998) indicated that metagenomes of individuals with colorectal cancer are depleted in fibre-targeting and enriched in glycosaminoglycan-targeting CAZymes. Finally, we inferred CAZyme substrates from genomic co-localization of CAZyme domains. Cayman is broadly applicable and freely available from https://github.com/zellerlab/cayman .
Additional Links: PMID-42032279
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@article {pmid42032279,
year = {2026},
author = {Ducarmon, QR and Karcher, N and Giri, S and Tytgat, HLP and Delannoy-Bruno, O and Pekel, S and Springer, F and Wörz, P and Schudoma, C and Typas, A and Zeller, G},
title = {Cayman enables large-scale analysis of gut microbiome carbohydrate-active enzyme repertoires.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {42032279},
issn = {2058-5276},
support = {LUMC Fellowship//Leids Universitair Medisch Centrum (Leiden University Medical Center)/ ; 395357507//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 01KD2102A//Bundesministerium für Bildung und Forschung (Federal Ministry of Education and Research)/ ; ALTF 1030-2022//European Molecular Biology Organization (EMBO)/ ; },
abstract = {Carbohydrate-active enzymes (CAZymes) are crucial for digesting glycans, but tools for CAZyme profiling and interpretation of substrate preferences in microbiome data are lacking. Here we develop a CAZyme profiler called Cayman (Carbohydrate Active Enzymes Profiling of Metagenomes) and a hierarchical substrate annotation scheme for use with genomic or shotgun metagenomic datasets. Using these tools, we systematically surveyed CAZymes in human gut microorganisms (n = 107,683 genomes) and identified several putative mucin-foraging bacteria, including Hungatella and Eisenbergiella species, which were confirmed experimentally. We compared CAZymes in gut metagenomes (n = 3,960) from high-income settings versus low- and middle-income settings and found that low- and middle-income setting metagenomes are enriched in fibre-degrading CAZymes, while CAZyme richness is generally higher in high-income setting metagenomes. Additional analysis (n = 1,998) indicated that metagenomes of individuals with colorectal cancer are depleted in fibre-targeting and enriched in glycosaminoglycan-targeting CAZymes. Finally, we inferred CAZyme substrates from genomic co-localization of CAZyme domains. Cayman is broadly applicable and freely available from https://github.com/zellerlab/cayman .},
}
RevDate: 2026-04-27
Representing dental caries and dysbiosis within the oral microbiome in the Oral Health and Disease Ontology.
Journal of biomedical semantics, 17(1):.
BACKGROUND: Dental caries is an oral health condition in which cariogenic bacteria demineralize and decay teeth. It arises due to interaction between the host, environment, and oral microbiome. Current terminologies and ontologies, however, do not accurately represent the important role that the microbiome has in the formation of carious lesions. Rather, they focus on the anatomical features of carious lesions and often obfuscate the distinctions between dental caries as a disease affecting a tooth, as lesions that are produced because of the disease, and as lesions produced as a result of dysbiosis in the oral microbiome. To capture the current state of evidence and provide flexibility for evolving literature on host-environment-microbiome interactions, there is a need to revise and expand the ontological framework for dental caries.
RESULTS: Several established terminologies and ontologies were reviewed for terms used to represent dental caries and the oral microbiome. We found that they either did not represent or misrepresented the current scientific understanding of caries and its relation to the microbial dysbiosis. As a result of these deficiencies, we added terms and relations to the Oral Health and Disease Ontology (OHD) that more accurately represent how oral microbial dysbiosis influences the development of dental caries.
CONCLUSIONS: The Oral Health and Disease Ontology is an advance over existing ontologies for representing the impact of oral microbial dysbiosis on dental caries. It provides a semantic framework that better serves the needs of cariology researchers and can more easily incorporate new oral microbiome findings.
Additional Links: PMID-42032627
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Citation:
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@article {pmid42032627,
year = {2026},
author = {Duncan, WD and Sabharwal, A and Diehl, AD and Dutta, N and Diller, M and Joachimiak, MP and Chandrasekharan, GM},
title = {Representing dental caries and dysbiosis within the oral microbiome in the Oral Health and Disease Ontology.},
journal = {Journal of biomedical semantics},
volume = {17},
number = {1},
pages = {},
pmid = {42032627},
issn = {2041-1480},
abstract = {BACKGROUND: Dental caries is an oral health condition in which cariogenic bacteria demineralize and decay teeth. It arises due to interaction between the host, environment, and oral microbiome. Current terminologies and ontologies, however, do not accurately represent the important role that the microbiome has in the formation of carious lesions. Rather, they focus on the anatomical features of carious lesions and often obfuscate the distinctions between dental caries as a disease affecting a tooth, as lesions that are produced because of the disease, and as lesions produced as a result of dysbiosis in the oral microbiome. To capture the current state of evidence and provide flexibility for evolving literature on host-environment-microbiome interactions, there is a need to revise and expand the ontological framework for dental caries.
RESULTS: Several established terminologies and ontologies were reviewed for terms used to represent dental caries and the oral microbiome. We found that they either did not represent or misrepresented the current scientific understanding of caries and its relation to the microbial dysbiosis. As a result of these deficiencies, we added terms and relations to the Oral Health and Disease Ontology (OHD) that more accurately represent how oral microbial dysbiosis influences the development of dental caries.
CONCLUSIONS: The Oral Health and Disease Ontology is an advance over existing ontologies for representing the impact of oral microbial dysbiosis on dental caries. It provides a semantic framework that better serves the needs of cariology researchers and can more easily incorporate new oral microbiome findings.},
}
RevDate: 2026-04-25
Rhizosphere microbiome influences fruit quality in citrus.
The New phytologist [Epub ahead of print].
Fruit quality is shaped by both crop genetics and cultivation environments, with soil conditions driving rhizosphere microbiome assembly. While rhizosphere microbes are known to enhance nutrient utilization and plant metabolism, their direct contribution to fruit quality regulation remains poorly understood. In this study, we demonstrate that the Satsuma mandarin (Citrus unshiu Marc.) and Navel orange (Citrus sinensis L. Osbeck) rhizosphere microbiome influence fruit sugar concentration, a key determinant of fruit quality. The rhizosphere core microbiota and soil mineral nutrients were positively correlated with fruit quality indices. Fruit quality-correlated bacterial operational taxonomic units (OTUs) explained an average of 32.6% of the observed variation in quality parameters. Inoculation with three bacterial strains (affiliated with Burkholderia, Pseudomonas, Rhizobium) and two bacterial consortia significantly increased fruit sugar concentrations. Metagenomic analysis linked sugar-associated microbes to iron (Fe) utilization, revealing genomic enrichment of siderophore biosynthesis gene clusters. Consistently, the selected bacterial strains exhibited siderophore secretion capabilities, increased leaf Fe content by 23.3-47.8% in citrus rootstock. Further field application of chelated-Fe fertilizer also increased fruit sugar concentration. Collectively, our results revealed an influence of the rhizosphere microbiome on fruit quality that is related to Fe acquisition optimization and subsequent sugar accumulation in citrus.
Additional Links: PMID-42032888
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PubMed:
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@article {pmid42032888,
year = {2026},
author = {Wu, S and Wang, Y and Li, H and Fang, X and Guo, J and Luo, X and Li, M and Song, F and Tan, Q and Deng, X and Xiao, S and Liu, H and Hu, C and Pan, Z},
title = {Rhizosphere microbiome influences fruit quality in citrus.},
journal = {The New phytologist},
volume = {},
number = {},
pages = {},
doi = {10.1111/nph.71159},
pmid = {42032888},
issn = {1469-8137},
support = {2023YFD2300603//The National Key Research and Development Program of China/ ; 2017YFD0202001//The National Key Research and Development Program of China/ ; 2019YFD1000103//The National Key Research and Development Program of China/ ; },
abstract = {Fruit quality is shaped by both crop genetics and cultivation environments, with soil conditions driving rhizosphere microbiome assembly. While rhizosphere microbes are known to enhance nutrient utilization and plant metabolism, their direct contribution to fruit quality regulation remains poorly understood. In this study, we demonstrate that the Satsuma mandarin (Citrus unshiu Marc.) and Navel orange (Citrus sinensis L. Osbeck) rhizosphere microbiome influence fruit sugar concentration, a key determinant of fruit quality. The rhizosphere core microbiota and soil mineral nutrients were positively correlated with fruit quality indices. Fruit quality-correlated bacterial operational taxonomic units (OTUs) explained an average of 32.6% of the observed variation in quality parameters. Inoculation with three bacterial strains (affiliated with Burkholderia, Pseudomonas, Rhizobium) and two bacterial consortia significantly increased fruit sugar concentrations. Metagenomic analysis linked sugar-associated microbes to iron (Fe) utilization, revealing genomic enrichment of siderophore biosynthesis gene clusters. Consistently, the selected bacterial strains exhibited siderophore secretion capabilities, increased leaf Fe content by 23.3-47.8% in citrus rootstock. Further field application of chelated-Fe fertilizer also increased fruit sugar concentration. Collectively, our results revealed an influence of the rhizosphere microbiome on fruit quality that is related to Fe acquisition optimization and subsequent sugar accumulation in citrus.},
}
RevDate: 2026-04-25
Gut Microbiome and Psychoneurological Symptoms Among Patients With Colorectal Cancer and Their Caregivers: A Pilot Study.
Biological research for nursing [Epub ahead of print].
Purpose: Survivorship in colorectal cancer (CRC) is often accompanied by co-occurring psychoneurological symptoms (PNS, e.g., fatigue, depression, pain), which negatively affect quality of life. Caregivers of individuals with CRC also experience PNS due to caregiving burdens, amplifying distress across the dyad. PNS may be influenced by the activity of the gut microbes. The purpose of this pilot study was to examine gut microbiome diversity and composition, and their association with PNS in CRC patients and their caregivers. Methods: Baseline data from a technology-based dyadic intervention were included in this analysis. Eleven patients and eight caregivers provided stool samples and completed PROMIS measures of PNS at baseline. Gut microbiome profiles were assessed using 16S rRNA gene sequencing. Alpha and beta diversity metrics and differential abundance analyses were used to characterize the gut microbiome and examine its associations with PNS. Results: Patients exhibited significantly lower microbial alpha diversity than caregivers in the full sample (p = 0.033). Dyadic comparisons identified 92 differentially abundant taxa, with patients showing depletion of short-chain fatty acid-producing taxa and enrichment of opportunistic taxa. Microbiome-symptom models revealed significant interactions by group (patient vs. caregiver) and taxa-level effects, with patients showing stronger positive associations between microbial alterations and higher PNS severity. Conclusions: CRC patients actively on chemotherapy demonstrated reduced diversity and depletion of beneficial taxa that may contribute to heightened PNS. Caregivers, despite healthier profiles, reported substantial symptom burden that were linked to gut microbiome features, highlighting dyadic interdependence and the potential for microbiome-targeted, dyadic interventions in survivorship care.
Additional Links: PMID-42032897
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PubMed:
Citation:
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@article {pmid42032897,
year = {2026},
author = {Lin, Y and Barandouzi, ZA and Houser, MC and Xiao, C and Alese, OB and Mathebula, S and Bai, J and Gbolahan, O and Bruner, DW},
title = {Gut Microbiome and Psychoneurological Symptoms Among Patients With Colorectal Cancer and Their Caregivers: A Pilot Study.},
journal = {Biological research for nursing},
volume = {},
number = {},
pages = {10998004261447509},
doi = {10.1177/10998004261447509},
pmid = {42032897},
issn = {1552-4175},
abstract = {Purpose: Survivorship in colorectal cancer (CRC) is often accompanied by co-occurring psychoneurological symptoms (PNS, e.g., fatigue, depression, pain), which negatively affect quality of life. Caregivers of individuals with CRC also experience PNS due to caregiving burdens, amplifying distress across the dyad. PNS may be influenced by the activity of the gut microbes. The purpose of this pilot study was to examine gut microbiome diversity and composition, and their association with PNS in CRC patients and their caregivers. Methods: Baseline data from a technology-based dyadic intervention were included in this analysis. Eleven patients and eight caregivers provided stool samples and completed PROMIS measures of PNS at baseline. Gut microbiome profiles were assessed using 16S rRNA gene sequencing. Alpha and beta diversity metrics and differential abundance analyses were used to characterize the gut microbiome and examine its associations with PNS. Results: Patients exhibited significantly lower microbial alpha diversity than caregivers in the full sample (p = 0.033). Dyadic comparisons identified 92 differentially abundant taxa, with patients showing depletion of short-chain fatty acid-producing taxa and enrichment of opportunistic taxa. Microbiome-symptom models revealed significant interactions by group (patient vs. caregiver) and taxa-level effects, with patients showing stronger positive associations between microbial alterations and higher PNS severity. Conclusions: CRC patients actively on chemotherapy demonstrated reduced diversity and depletion of beneficial taxa that may contribute to heightened PNS. Caregivers, despite healthier profiles, reported substantial symptom burden that were linked to gut microbiome features, highlighting dyadic interdependence and the potential for microbiome-targeted, dyadic interventions in survivorship care.},
}
RevDate: 2026-04-25
The lizard microbiome: patterns, drivers, and functional implications.
FEMS microbiology letters pii:8662450 [Epub ahead of print].
The lizard microbiome is a dynamic community that plays a crucial role in the health and survival of these animals. As global change poses significant threats to lizard populations around the world, understanding the interactions between lizards and their microbial communities is increasingly important. Here, we synthesize a rapidly growing body of research on the composition, diversity, transmission, and functional roles of lizard microbiomes. We discuss the implications of microbiome variation for lizard physiology, as well as the potential for microbiomes to inform conservation strategies for threatened species. Finally, we highlight priorities for future research, which include the need to quantify microbiome diversity and function across additional taxa, as lizards remain underrepresented in the microbiome literature. We also stress the importance of experimental and field research that can reveal the adaptive significance of lizard microbiomes in the face of environmental change. Our synthesis highlights the contributions of lizard microbiome science to the fields of ecology, evolution, and conservation biology and demonstrates how the microbial communities that live in and on lizards enhance our understanding of their biodiversity and inform efforts to protect vulnerable populations.
Additional Links: PMID-42033327
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PubMed:
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@article {pmid42033327,
year = {2026},
author = {Williams, CE and Tacoaman, YFL and Fontaine, SS and Logan, ML},
title = {The lizard microbiome: patterns, drivers, and functional implications.},
journal = {FEMS microbiology letters},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsle/fnag049},
pmid = {42033327},
issn = {1574-6968},
abstract = {The lizard microbiome is a dynamic community that plays a crucial role in the health and survival of these animals. As global change poses significant threats to lizard populations around the world, understanding the interactions between lizards and their microbial communities is increasingly important. Here, we synthesize a rapidly growing body of research on the composition, diversity, transmission, and functional roles of lizard microbiomes. We discuss the implications of microbiome variation for lizard physiology, as well as the potential for microbiomes to inform conservation strategies for threatened species. Finally, we highlight priorities for future research, which include the need to quantify microbiome diversity and function across additional taxa, as lizards remain underrepresented in the microbiome literature. We also stress the importance of experimental and field research that can reveal the adaptive significance of lizard microbiomes in the face of environmental change. Our synthesis highlights the contributions of lizard microbiome science to the fields of ecology, evolution, and conservation biology and demonstrates how the microbial communities that live in and on lizards enhance our understanding of their biodiversity and inform efforts to protect vulnerable populations.},
}
RevDate: 2026-04-25
Comparative analysis of microbial diversity and pathogenic potential in marine litter reveals timber as a key reservoir in sandy beaches ecosystems.
Journal of hazardous materials, 511:141937 pii:S0304-3894(26)00915-5 [Epub ahead of print].
Many materials create new habitats for microbial colonization and the persistence of potentially pathogenic bacteria. Despite this, comparative studies addressing the microbial diversity and pathogenic potential across different types of marine litter remain scarce. This study investigated microbial communities associated with plastics, aluminum, and timber collected from the strandline of two types of beaches. Amplicon sequencing of the 16S rRNA gene revealed that bacterial community structure and diversity varied primarily according to substrate type rather than beach environment. Nevertheless, all types of marine litter evaluated hosted rich and diverse bacterial communities, with several taxa recognized as potential pathogens of both marine organisms and humans. Timber supported the richest, most diverse, and most specific microbiome, including a high number of taxa known to contain potential pathogens. Among these, Flavobacterium, Mycobacterium, Pseudoalteromonas, Acinetobacter, and Staphylococcus were particularly notable, as they are recognized pathogens of both marine organisms and humans, representing potential ecological and sanitary risks. These findings highlight that marine litter on sandy beaches functions as a selective substrate influencing biofilm formation, microbial dispersal, and the persistence of pathogens in coastal ecosystems. Timber, in particular, emerges as an underrecognized reservoir for microbial diversity and resistance genes, warranting greater attention in marine pollution and public health monitoring.
Additional Links: PMID-42033818
Publisher:
PubMed:
Citation:
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hide bibtex listing
@article {pmid42033818,
year = {2026},
author = {Póvoa, AA and Amorim Magalhães, E and Dos Santos, KP and Canellas, AL and Soares-Gomes, A and Dos Santos, HF},
title = {Comparative analysis of microbial diversity and pathogenic potential in marine litter reveals timber as a key reservoir in sandy beaches ecosystems.},
journal = {Journal of hazardous materials},
volume = {511},
number = {},
pages = {141937},
doi = {10.1016/j.jhazmat.2026.141937},
pmid = {42033818},
issn = {1873-3336},
abstract = {Many materials create new habitats for microbial colonization and the persistence of potentially pathogenic bacteria. Despite this, comparative studies addressing the microbial diversity and pathogenic potential across different types of marine litter remain scarce. This study investigated microbial communities associated with plastics, aluminum, and timber collected from the strandline of two types of beaches. Amplicon sequencing of the 16S rRNA gene revealed that bacterial community structure and diversity varied primarily according to substrate type rather than beach environment. Nevertheless, all types of marine litter evaluated hosted rich and diverse bacterial communities, with several taxa recognized as potential pathogens of both marine organisms and humans. Timber supported the richest, most diverse, and most specific microbiome, including a high number of taxa known to contain potential pathogens. Among these, Flavobacterium, Mycobacterium, Pseudoalteromonas, Acinetobacter, and Staphylococcus were particularly notable, as they are recognized pathogens of both marine organisms and humans, representing potential ecological and sanitary risks. These findings highlight that marine litter on sandy beaches functions as a selective substrate influencing biofilm formation, microbial dispersal, and the persistence of pathogens in coastal ecosystems. Timber, in particular, emerges as an underrecognized reservoir for microbial diversity and resistance genes, warranting greater attention in marine pollution and public health monitoring.},
}
RevDate: 2026-04-25
Xenobiotic dynamics in mangroves and peatlands: Microbial mechanisms for nature-based mitigation.
Journal of hazardous materials, 511:142149 pii:S0304-3894(26)01127-1 [Epub ahead of print].
Peatlands and mangroves provide substantial ecosystem services, but are increasingly threatened by xenobiotic contamination, posing escalating ecological risks. Here, we present the first integrative synthesis of the xenobiotic dynamics in these systems, mapping contaminant distributions and identifying emerging research priorities. Over time, research has shifted from oil spills and heavy metal pollution towards persistent organic pollutants, microplastics and climate risks. Peatlands remain substantially understudied compared to mangroves, especially for emerging contaminant classes. Xenobiotics disrupt the environment-biota linkages in these systems by impairing microbiome functionality; yet, subsets of microbial communities persist through adaptation and sharing of genomic traits. These traits enable xenobiotic sequestration, degradation or utilization. We compile a wetland-associated catalogue of microbial mechanisms and cross-environment analogues to guide bioprospecting and nature-based xenobiotic transformations. We recommend coupling wetland restoration with systematic microbiome exploration, positioning wetlands as in-situ buffers and ex-situ reservoirs for scalable, nature-based solutions for xenobiotic mitigation.
Additional Links: PMID-42033825
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PubMed:
Citation:
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@article {pmid42033825,
year = {2026},
author = {Mukhopadhyay, S and Ooi, QE and Mukherjee, A and Bhattacharya, R and Sarkar, P and Tan, ZD and Phang, B and Chey, SL and Lupascu, M and Bandla, A and Swarup, S},
title = {Xenobiotic dynamics in mangroves and peatlands: Microbial mechanisms for nature-based mitigation.},
journal = {Journal of hazardous materials},
volume = {511},
number = {},
pages = {142149},
doi = {10.1016/j.jhazmat.2026.142149},
pmid = {42033825},
issn = {1873-3336},
abstract = {Peatlands and mangroves provide substantial ecosystem services, but are increasingly threatened by xenobiotic contamination, posing escalating ecological risks. Here, we present the first integrative synthesis of the xenobiotic dynamics in these systems, mapping contaminant distributions and identifying emerging research priorities. Over time, research has shifted from oil spills and heavy metal pollution towards persistent organic pollutants, microplastics and climate risks. Peatlands remain substantially understudied compared to mangroves, especially for emerging contaminant classes. Xenobiotics disrupt the environment-biota linkages in these systems by impairing microbiome functionality; yet, subsets of microbial communities persist through adaptation and sharing of genomic traits. These traits enable xenobiotic sequestration, degradation or utilization. We compile a wetland-associated catalogue of microbial mechanisms and cross-environment analogues to guide bioprospecting and nature-based xenobiotic transformations. We recommend coupling wetland restoration with systematic microbiome exploration, positioning wetlands as in-situ buffers and ex-situ reservoirs for scalable, nature-based solutions for xenobiotic mitigation.},
}
RevDate: 2026-04-25
Polyphenols and physical activity stimulate gut microbiota mediated Nrf2 signaling to combat neurodegeneration.
Pathology, research and practice, 283:156478 pii:S0344-0338(26)00131-7 [Epub ahead of print].
Polyphenols and regular physical activity are increasingly recognized as complementary lifestyle interventions that influence the gut-brain axis and contribute to neuroprotection. Emerging evidence highlights the central role of the gut microbiota in mediating these effects by transforming dietary and host-derived substrates into bioactive metabolites. These metabolites can activate the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway, a key regulator of cellular antioxidant defenses, mitochondrial function, and anti-inflammatory responses processes that are critically impaired in neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This review synthesizes current mechanistic insights into how polyphenol-derived metabolites and exercise-induced alterations in gut microbial composition converge to modulate Nrf2 signaling. We discuss the roles of key microbiota-derived metabolites, including short-chain fatty acids, urolithins, and indole derivatives, in regulating oxidative stress, neuroinflammation, and synaptic function. Furthermore, we examine evidence from preclinical models supporting the synergistic effects of dietary polyphenols and physical activity on gut microbiota-mediated neuroprotection. Finally, we address translational challenges and highlight the potential of integrating dietary and exercise-based strategies to harness microbiota-dependent Nrf2 activation. This integrative framework provides a basis for developing personalized, microbiome-informed interventions aimed at delaying or mitigating neurodegeneration.
Additional Links: PMID-42033865
Publisher:
PubMed:
Citation:
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@article {pmid42033865,
year = {2026},
author = {Wang, F},
title = {Polyphenols and physical activity stimulate gut microbiota mediated Nrf2 signaling to combat neurodegeneration.},
journal = {Pathology, research and practice},
volume = {283},
number = {},
pages = {156478},
doi = {10.1016/j.prp.2026.156478},
pmid = {42033865},
issn = {1618-0631},
abstract = {Polyphenols and regular physical activity are increasingly recognized as complementary lifestyle interventions that influence the gut-brain axis and contribute to neuroprotection. Emerging evidence highlights the central role of the gut microbiota in mediating these effects by transforming dietary and host-derived substrates into bioactive metabolites. These metabolites can activate the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway, a key regulator of cellular antioxidant defenses, mitochondrial function, and anti-inflammatory responses processes that are critically impaired in neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This review synthesizes current mechanistic insights into how polyphenol-derived metabolites and exercise-induced alterations in gut microbial composition converge to modulate Nrf2 signaling. We discuss the roles of key microbiota-derived metabolites, including short-chain fatty acids, urolithins, and indole derivatives, in regulating oxidative stress, neuroinflammation, and synaptic function. Furthermore, we examine evidence from preclinical models supporting the synergistic effects of dietary polyphenols and physical activity on gut microbiota-mediated neuroprotection. Finally, we address translational challenges and highlight the potential of integrating dietary and exercise-based strategies to harness microbiota-dependent Nrf2 activation. This integrative framework provides a basis for developing personalized, microbiome-informed interventions aimed at delaying or mitigating neurodegeneration.},
}
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