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ESP: PubMed Auto Bibliography 24 Apr 2026 at 01:54 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: 2026-04-21
CmpDate: 2026-04-21
Next generation approaches in cancer immunotherapy targeting mechanisms beyond PD1 and PDL1.
Discover oncology, 17(1):.
UNLABELLED: Cancer immunotherapy has revolutionized oncology by leveraging the immune system’s ability to recognize and eliminate tumor cells. Among the most impactful advances are immune checkpoint inhibitors that target the programmed death-1 (PD-1) receptor and its ligand PD-L1, which can restore T cell activity and generate durable responses across several cancer types. However, their effectiveness is limited by both primary and acquired resistance, restricting long-term benefit to a subset of patients. This review highlights current progress in cancer immunotherapy and explores emerging strategies beyond PD-1/PD-L1 blockade. Novel inhibitory and co-stimulatory immune checkpoints such as lymphocyte activation gene-3 (LAG-3), T cell immunoglobulin mucin-3 (TIM-3), T cell immunoreceptor with Ig and ITIM domains (TIGIT), OX40, CD137 (4-1BB), and CD40 are examined for their potential to enhance anti-tumor immunity. The rationale for combining immunotherapy with chemotherapy, radiotherapy, targeted therapies, oncolytic viruses, and neoantigen vaccines is discussed in the context of overcoming resistance. Additional emphasis is placed on modifying the tumor microenvironment, targeting tumor metabolism, and overcoming stromal barriers. Advanced delivery systems such as chimeric antigen receptor (CAR) T cells, bispecific antibodies, and nanoparticle-based platforms offer improved specificity and reduced toxicity. Biomarker-guided precision immuno-oncology using tumor mutational burden, microsatellite instability, and immune gene signatures is advancing clinical decision-making. Gut microbiota modulation and artificial intelligence-based tools are also emerging as critical components in optimizing therapeutic outcomes. Collectively, this review proposes a multidimensional and personalized immunotherapy paradigm aimed at broadening clinical efficacy and overcoming resistance beyond conventional PD-1/PD-L1 inhibition.
GRAPHICAL ABSTRACT: [Image: see text]
Additional Links: PMID-41832248
PubMed:
Citation:
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@article {pmid41832248,
year = {2026},
author = {El-Tanani, M and Satyam, SM and Rabbani, SA and Rangraze, IR and Matalka, IIA and Muhana, F and El-Tanani, Y and Aljabali, AAA and Khan, MA and Parvez, S and Porntaveetus, T},
title = {Next generation approaches in cancer immunotherapy targeting mechanisms beyond PD1 and PDL1.},
journal = {Discover oncology},
volume = {17},
number = {1},
pages = {},
pmid = {41832248},
issn = {2730-6011},
abstract = {UNLABELLED: Cancer immunotherapy has revolutionized oncology by leveraging the immune system’s ability to recognize and eliminate tumor cells. Among the most impactful advances are immune checkpoint inhibitors that target the programmed death-1 (PD-1) receptor and its ligand PD-L1, which can restore T cell activity and generate durable responses across several cancer types. However, their effectiveness is limited by both primary and acquired resistance, restricting long-term benefit to a subset of patients. This review highlights current progress in cancer immunotherapy and explores emerging strategies beyond PD-1/PD-L1 blockade. Novel inhibitory and co-stimulatory immune checkpoints such as lymphocyte activation gene-3 (LAG-3), T cell immunoglobulin mucin-3 (TIM-3), T cell immunoreceptor with Ig and ITIM domains (TIGIT), OX40, CD137 (4-1BB), and CD40 are examined for their potential to enhance anti-tumor immunity. The rationale for combining immunotherapy with chemotherapy, radiotherapy, targeted therapies, oncolytic viruses, and neoantigen vaccines is discussed in the context of overcoming resistance. Additional emphasis is placed on modifying the tumor microenvironment, targeting tumor metabolism, and overcoming stromal barriers. Advanced delivery systems such as chimeric antigen receptor (CAR) T cells, bispecific antibodies, and nanoparticle-based platforms offer improved specificity and reduced toxicity. Biomarker-guided precision immuno-oncology using tumor mutational burden, microsatellite instability, and immune gene signatures is advancing clinical decision-making. Gut microbiota modulation and artificial intelligence-based tools are also emerging as critical components in optimizing therapeutic outcomes. Collectively, this review proposes a multidimensional and personalized immunotherapy paradigm aimed at broadening clinical efficacy and overcoming resistance beyond conventional PD-1/PD-L1 inhibition.
GRAPHICAL ABSTRACT: [Image: see text]},
}
RevDate: 2026-04-22
Geophagy in Gibraltar Barbary macaques is a primate tradition anthropogenically induced.
Scientific reports, 16(1):.
UNLABELLED: We report, for the first time, geophagy – the deliberate consumption of earth – in the Barbary macaque (Macaca sylvanus) population living at the human-primate interface in Gibraltar. We evaluate potential adaptive functions of this behavior in an anthropogenic context, drawing on predictions from the protection and supplementation hypotheses. Geophagy occurred at exceptionally high rates compared to other macaque species and locations, and it was more common in summer when tourist numbers peak. It was also more likely when macaques consumed greater amounts of tourist-derived food, supporting a protective function. Local ecological factors contributed as well, with the distribution of red soil (terra rossa) influencing geophagy frequency. Although the behavior was not linked to female reproductive status, supplementation cannot be fully dismissed given the very limited insectivory in this population. We propose that tourist-derived foods may disrupt gut microbiome composition, producing discomfort that individuals mitigate through soil ingestion. Geophagy is likely socially learned, as groups showed consistent preferences for specific soil types, and its practice in presence of conspecifics offered opportunities for social learning. Reports from other sites indicate that geophagy is not unique to Gibraltar, but in this population it appears to be anthropogenically induced and socially transmitted, forming a locally maintained tradition.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-44607-0.
Additional Links: PMID-41857116
PubMed:
Citation:
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@article {pmid41857116,
year = {2026},
author = {Frater, J and Nicourt, M and Landi, F and Maxwell, B and Thiodet, J and Mestrallet, E and Warr, SJ and Pizarro, M and Fa, JE and Lemoine, S},
title = {Geophagy in Gibraltar Barbary macaques is a primate tradition anthropogenically induced.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {41857116},
issn = {2045-2322},
support = {101034349-6//Marie Skłodowska-Curie Action COFUND - R2STAIR/ ; SRG2223\231596//British Academy Leverhulme Small Research Grant/ ; },
abstract = {UNLABELLED: We report, for the first time, geophagy – the deliberate consumption of earth – in the Barbary macaque (Macaca sylvanus) population living at the human-primate interface in Gibraltar. We evaluate potential adaptive functions of this behavior in an anthropogenic context, drawing on predictions from the protection and supplementation hypotheses. Geophagy occurred at exceptionally high rates compared to other macaque species and locations, and it was more common in summer when tourist numbers peak. It was also more likely when macaques consumed greater amounts of tourist-derived food, supporting a protective function. Local ecological factors contributed as well, with the distribution of red soil (terra rossa) influencing geophagy frequency. Although the behavior was not linked to female reproductive status, supplementation cannot be fully dismissed given the very limited insectivory in this population. We propose that tourist-derived foods may disrupt gut microbiome composition, producing discomfort that individuals mitigate through soil ingestion. Geophagy is likely socially learned, as groups showed consistent preferences for specific soil types, and its practice in presence of conspecifics offered opportunities for social learning. Reports from other sites indicate that geophagy is not unique to Gibraltar, but in this population it appears to be anthropogenically induced and socially transmitted, forming a locally maintained tradition.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-44607-0.},
}
RevDate: 2026-04-21
Identification of bacterial signals that modulate enteric sensory neurons to influence behavior in C. elegans.
Current biology : CB pii:S0960-9822(26)00390-8 [Epub ahead of print].
The bacterial microbiome influences many aspects of animal health and disease. Bacteria can have beneficial functions, for example providing nutrients, whereas others can act as pathogens. Bacteria are sensed by host cells to induce adaptive changes in physiology and behavior. While immune and intestinal cells detect bacterial signals through well-characterized mechanisms, recent studies indicate that neurons can also directly sense bacteria. However, the bacterial sensory mechanisms in neurons are less well understood. In Caenorhabditis elegans, the enteric sensory neuron NSM innervates the pharyngeal lumen and is directly activated by bacterial ingestion; in turn, NSM releases serotonin to induce feeding-related behaviors. However, the molecular identities of the bacterial signals that activate NSM are unknown. To identify them, we probed bacterial macromolecules from nutritive bacteria using biochemical approaches. We find that polysaccharides from bacteria are sufficient to activate NSM. We further identify peptidoglycans from Gram-positive bacteria as specific components capable of activating NSM. NSM responses to polysaccharides require the acid-sensing ion channels DEL-3 and DEL-7, which localize to NSM's sensory dendrite in the pharyngeal lumen. Ingestion of bacterial polysaccharides enhances feeding and reduces locomotion, matching the known effects of NSM on behavior. We also examine signals produced by pathogenic bacteria. This approach identifies prodigiosin, from pathogenic Serratia marcescens, as a metabolite that prevents NSM activation by nutritive bacterial signals. This study identifies molecular signals that underlie neuronal recognition of nutritive bacteria in the alimentary canal and competing signals from a pathogenic bacterial strain that can mask this form of recognition.
Additional Links: PMID-42013859
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PubMed:
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@article {pmid42013859,
year = {2026},
author = {Estrem, CE and Dua, M and Fees, CP and Hoeprich, GJ and Au, M and Goode, BL and Deng, LL and Flavell, SW},
title = {Identification of bacterial signals that modulate enteric sensory neurons to influence behavior in C. elegans.},
journal = {Current biology : CB},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cub.2026.03.070},
pmid = {42013859},
issn = {1879-0445},
abstract = {The bacterial microbiome influences many aspects of animal health and disease. Bacteria can have beneficial functions, for example providing nutrients, whereas others can act as pathogens. Bacteria are sensed by host cells to induce adaptive changes in physiology and behavior. While immune and intestinal cells detect bacterial signals through well-characterized mechanisms, recent studies indicate that neurons can also directly sense bacteria. However, the bacterial sensory mechanisms in neurons are less well understood. In Caenorhabditis elegans, the enteric sensory neuron NSM innervates the pharyngeal lumen and is directly activated by bacterial ingestion; in turn, NSM releases serotonin to induce feeding-related behaviors. However, the molecular identities of the bacterial signals that activate NSM are unknown. To identify them, we probed bacterial macromolecules from nutritive bacteria using biochemical approaches. We find that polysaccharides from bacteria are sufficient to activate NSM. We further identify peptidoglycans from Gram-positive bacteria as specific components capable of activating NSM. NSM responses to polysaccharides require the acid-sensing ion channels DEL-3 and DEL-7, which localize to NSM's sensory dendrite in the pharyngeal lumen. Ingestion of bacterial polysaccharides enhances feeding and reduces locomotion, matching the known effects of NSM on behavior. We also examine signals produced by pathogenic bacteria. This approach identifies prodigiosin, from pathogenic Serratia marcescens, as a metabolite that prevents NSM activation by nutritive bacterial signals. This study identifies molecular signals that underlie neuronal recognition of nutritive bacteria in the alimentary canal and competing signals from a pathogenic bacterial strain that can mask this form of recognition.},
}
RevDate: 2026-04-23
Spleen metabolomics coupled with gut microbiome analysis to elucidate the immunomodulatory mechanisms of longan polysaccharides against cyclophosphamide-induced immunosuppression in mice.
International journal of biological macromolecules, 362:152109 pii:S0141-8130(26)02035-0 [Epub ahead of print].
Longan polysaccharide (LP) has exhibited excellent immunomodulatory activities by modifying gut microbiota but the specific regulatory mechanism remains unclear. Therefore, spleen metabolomics and metagenomic sequencing of gut microbiota were combined to investigate the immunomodulatory mechanism of LP in cyclophosphamide (CPA)-induced immunosuppressed mice with an intact and antibiotic-depleted microbiota. The results indicated that LP significantly restored thymic and splenic indices, increased lymphocyte proliferation, and mitigated damage to immune organs. LP up-regulated the ratio of CD4[+]/CD8[+] in the mouse spleen to modulated cytokine secretion, thereby increasing serum concentrations of IFN-γ, TNF-α, IL-12, and IL-6. The metabolomic analysis indicated that LP alleviated CPA-induced splenic disturbance by coordinately improving amino acid metabolism, unsaturated fatty acid metabolism, and pyrimidine metabolism. Furthermore, LP significantly reshaped the CPA-induced gut microbiota imbalance, particularly by increasing the relative abundance of unclassified_f__Muribaculaceae and Bacteroides. However, antibiotic intervention almost offset the LP-mediated alleviation of immunosuppression. Our findings provide novel insights into the mechanisms underlying the immunosuppression-alleviating effects of natural polysaccharides.
Additional Links: PMID-42014006
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PubMed:
Citation:
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@article {pmid42014006,
year = {2026},
author = {Liu, H and Luo, J and Yang, Y and Yang, R and Li, W},
title = {Spleen metabolomics coupled with gut microbiome analysis to elucidate the immunomodulatory mechanisms of longan polysaccharides against cyclophosphamide-induced immunosuppression in mice.},
journal = {International journal of biological macromolecules},
volume = {362},
number = {},
pages = {152109},
doi = {10.1016/j.ijbiomac.2026.152109},
pmid = {42014006},
issn = {1879-0003},
abstract = {Longan polysaccharide (LP) has exhibited excellent immunomodulatory activities by modifying gut microbiota but the specific regulatory mechanism remains unclear. Therefore, spleen metabolomics and metagenomic sequencing of gut microbiota were combined to investigate the immunomodulatory mechanism of LP in cyclophosphamide (CPA)-induced immunosuppressed mice with an intact and antibiotic-depleted microbiota. The results indicated that LP significantly restored thymic and splenic indices, increased lymphocyte proliferation, and mitigated damage to immune organs. LP up-regulated the ratio of CD4[+]/CD8[+] in the mouse spleen to modulated cytokine secretion, thereby increasing serum concentrations of IFN-γ, TNF-α, IL-12, and IL-6. The metabolomic analysis indicated that LP alleviated CPA-induced splenic disturbance by coordinately improving amino acid metabolism, unsaturated fatty acid metabolism, and pyrimidine metabolism. Furthermore, LP significantly reshaped the CPA-induced gut microbiota imbalance, particularly by increasing the relative abundance of unclassified_f__Muribaculaceae and Bacteroides. However, antibiotic intervention almost offset the LP-mediated alleviation of immunosuppression. Our findings provide novel insights into the mechanisms underlying the immunosuppression-alleviating effects of natural polysaccharides.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Precursors of sea star wasting: immune and microbial disruption during initial disease outbreak in southeast Alaska.
Proceedings. Biological sciences, 293(2069):.
Sea star wasting (SSW) disease has devastated sea star populations along the North American Pacific coast with some recovery since 2013. Though Vibrio pectenicida has recently been implicated as a causative agent, the dynamics of disease progression and host response in natural environments remain understudied. Here, we integrate transcriptomic and microbial data from wild Pycnopodia helianthoides sampled across sites affected and unaffected by SSW in southeast Alaska during the initial outbreak recorded in the region in 2016. Individuals exposed to SSW but lacking visible signs of disease showed elevated expression of complement system components, pathogen recognition and immune regulatory pathways relative to naive individuals. Differential expression of extracellular matrix and tissue remodelling genes suggests disruption of tissue homeostasis preceding visible signs of disease. Furthermore, network analyses revealed certain microbial abundances, including Vibrio spp., correlated with immune response and tissue integrity gene expression. Although V. pectenicida was detected in some samples, its rarity prevented detailed analysis. Nevertheless, higher prevalence in exposed samples is consistent with growing evidence implicating Vibrio infection as an agent of SSW. Together, our findings offer insight into early host-pathogen dynamics in wild populations, underscoring links between immune activation and microbial shifts with the onset of SSW disease.
Additional Links: PMID-42014077
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PubMed:
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@article {pmid42014077,
year = {2026},
author = {McCracken, AR and Rodger, A and Saratkar, C and Mariani Sularz, S and Brusch, S and Nunez, JCB and Pespeni, MH},
title = {Precursors of sea star wasting: immune and microbial disruption during initial disease outbreak in southeast Alaska.},
journal = {Proceedings. Biological sciences},
volume = {293},
number = {2069},
pages = {},
doi = {10.1098/rspb.2025.2947},
pmid = {42014077},
issn = {1471-2954},
support = {//National Science Foundation/ ; },
mesh = {*Starfish/microbiology/immunology ; Animals ; Alaska ; *Vibrio/physiology ; Disease Outbreaks/veterinary ; Transcriptome ; },
abstract = {Sea star wasting (SSW) disease has devastated sea star populations along the North American Pacific coast with some recovery since 2013. Though Vibrio pectenicida has recently been implicated as a causative agent, the dynamics of disease progression and host response in natural environments remain understudied. Here, we integrate transcriptomic and microbial data from wild Pycnopodia helianthoides sampled across sites affected and unaffected by SSW in southeast Alaska during the initial outbreak recorded in the region in 2016. Individuals exposed to SSW but lacking visible signs of disease showed elevated expression of complement system components, pathogen recognition and immune regulatory pathways relative to naive individuals. Differential expression of extracellular matrix and tissue remodelling genes suggests disruption of tissue homeostasis preceding visible signs of disease. Furthermore, network analyses revealed certain microbial abundances, including Vibrio spp., correlated with immune response and tissue integrity gene expression. Although V. pectenicida was detected in some samples, its rarity prevented detailed analysis. Nevertheless, higher prevalence in exposed samples is consistent with growing evidence implicating Vibrio infection as an agent of SSW. Together, our findings offer insight into early host-pathogen dynamics in wild populations, underscoring links between immune activation and microbial shifts with the onset of SSW disease.},
}
MeSH Terms:
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hide MeSH Terms
*Starfish/microbiology/immunology
Animals
Alaska
*Vibrio/physiology
Disease Outbreaks/veterinary
Transcriptome
RevDate: 2026-04-21
Phytochemicals in MASLD: A Focused Review of Gut Microbiome-Linked Mechanisms.
Phytotherapy research : PTR [Epub ahead of print].
Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a major global health burden, yet effective pharmacological options remain limited. Recent advances highlight the gut microbiome as a key modulator of liver metabolism, inflammation, and fibrosis, making it a promising therapeutic target. Among various non-pharmacologic strategies, phytochemicals have drawn growing attention for their ability to influence the gut-liver axis through natural, multitarget mechanisms. This mini-review summarizes preclinical and clinical evidence on phytochemicals that demonstrate metabolic benefits in MASLD, with a focus on their microbiome-mediated effects. To this end, we classify these mechanistic pathways into three major continuums: restoration of gut microbial composition (causation), modulation of signaling mediators, i.e., gut microbial metabolites (mediation), and the resulting functional outcomes derived from these causal links (outcome). While early pre-clinical data are encouraging, translation is challenged by issues such as mechanistic complexity, microbiome-dependent heterogeneity, and regulatory ambiguity. Future studies incorporating multi-omics analysis, mechanism-linked trial designs, and stratified patient populations will be critical to advancing phytochemicals as safe, effective, and personalized interventions for MASLD.
Additional Links: PMID-42014181
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@article {pmid42014181,
year = {2026},
author = {Seo, JI and Kim, SM and Yoo, HH},
title = {Phytochemicals in MASLD: A Focused Review of Gut Microbiome-Linked Mechanisms.},
journal = {Phytotherapy research : PTR},
volume = {},
number = {},
pages = {},
doi = {10.1002/ptr.70352},
pmid = {42014181},
issn = {1099-1573},
support = {RS-2023-00217123//National Research Foundation of Korea/ ; },
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a major global health burden, yet effective pharmacological options remain limited. Recent advances highlight the gut microbiome as a key modulator of liver metabolism, inflammation, and fibrosis, making it a promising therapeutic target. Among various non-pharmacologic strategies, phytochemicals have drawn growing attention for their ability to influence the gut-liver axis through natural, multitarget mechanisms. This mini-review summarizes preclinical and clinical evidence on phytochemicals that demonstrate metabolic benefits in MASLD, with a focus on their microbiome-mediated effects. To this end, we classify these mechanistic pathways into three major continuums: restoration of gut microbial composition (causation), modulation of signaling mediators, i.e., gut microbial metabolites (mediation), and the resulting functional outcomes derived from these causal links (outcome). While early pre-clinical data are encouraging, translation is challenged by issues such as mechanistic complexity, microbiome-dependent heterogeneity, and regulatory ambiguity. Future studies incorporating multi-omics analysis, mechanism-linked trial designs, and stratified patient populations will be critical to advancing phytochemicals as safe, effective, and personalized interventions for MASLD.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Gut Microbiota Signatures of Sarcopenia: A Comparative 16S rRNA Sequencing Study in Older Indian Adults.
Geriatrics & gerontology international, 26(4):e70500.
AIM: Emerging evidence suggests that alterations in gut microbiota composition may contribute to the onset and progression of sarcopenia through mechanisms involving systemic inflammation, metabolic dysregulation, and reduced production of short-chain fatty acids (SCFAs). However, data from Indian older adults-who exhibit diverse diets and microbiota profiles-are lacking.
METHODS: This hospital-based cross-sectional pilot study enrolled 30 older adults aged ≥ 60 years, including 15 with sarcopenic and 15 age- and sex-matched nonsarcopenic. Sarcopenia was classified according to the Asian Working Group for Sarcopenia (AWGS-2019) criteria. Stool samples were analyzed using 16S ribosomal RNA (rRNA) sequencing (V3-V4 region, Illumina MiSeq). Taxonomic classification and diversity indices (Chao1, Shannon, UniFrac) were compared between groups.
RESULTS: The mean age (S.D.) of study participants was 73.27 ± 5.96 years. A total of 251 315 high-quality sequences were generated from 30 fresh human fecal samples. The dominant phylum in the nonsarcopenic group was Firmicutes (41.2%), followed by Bacteroidetes (36.0%), whereas in the sarcopenic group, Bacteroidetes (39.2%) was most common, followed by Firmicutes (37.8%). A decrease in Operational Taxonomic Units (OTUs) of genus Bifidobacterium (2.21% vs. 3.71%), Bacteroides (8.50% vs. 11.11%) was observed in the sarcopenic group. An increase in OTUs of genus Faecalibacterium (10.64% vs. 8.23%) in the sarcopenic group was observed. The alpha-diversity index Chao1, Shannon was reduced in sarcopenic population.
CONCLUSIONS: Exploratory differences in microbial diversity and relative abundance were observed between sarcopenic and nonsarcopenic older adults. These findings are descriptive and hypothesis-generating and warrant confirmation in larger, adequately powered studies.
Additional Links: PMID-42014206
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@article {pmid42014206,
year = {2026},
author = {George, SM and Chatterjee, P and Chaudhry, R and Bamola, VD and Khan, MA and Purohit, A and Suroliya, V and Muley, R and Chakrawarty, A},
title = {Gut Microbiota Signatures of Sarcopenia: A Comparative 16S rRNA Sequencing Study in Older Indian Adults.},
journal = {Geriatrics & gerontology international},
volume = {26},
number = {4},
pages = {e70500},
doi = {10.1111/ggi.70500},
pmid = {42014206},
issn = {1447-0594},
support = {//National Programme for Health Care of the Elderly, Government of India (NPHCE)/ ; },
mesh = {Humans ; *Sarcopenia/microbiology ; *Gastrointestinal Microbiome/genetics ; Male ; Aged ; Female ; Cross-Sectional Studies ; India ; *RNA, Ribosomal, 16S/genetics ; Pilot Projects ; Middle Aged ; Feces/microbiology ; Aged, 80 and over ; },
abstract = {AIM: Emerging evidence suggests that alterations in gut microbiota composition may contribute to the onset and progression of sarcopenia through mechanisms involving systemic inflammation, metabolic dysregulation, and reduced production of short-chain fatty acids (SCFAs). However, data from Indian older adults-who exhibit diverse diets and microbiota profiles-are lacking.
METHODS: This hospital-based cross-sectional pilot study enrolled 30 older adults aged ≥ 60 years, including 15 with sarcopenic and 15 age- and sex-matched nonsarcopenic. Sarcopenia was classified according to the Asian Working Group for Sarcopenia (AWGS-2019) criteria. Stool samples were analyzed using 16S ribosomal RNA (rRNA) sequencing (V3-V4 region, Illumina MiSeq). Taxonomic classification and diversity indices (Chao1, Shannon, UniFrac) were compared between groups.
RESULTS: The mean age (S.D.) of study participants was 73.27 ± 5.96 years. A total of 251 315 high-quality sequences were generated from 30 fresh human fecal samples. The dominant phylum in the nonsarcopenic group was Firmicutes (41.2%), followed by Bacteroidetes (36.0%), whereas in the sarcopenic group, Bacteroidetes (39.2%) was most common, followed by Firmicutes (37.8%). A decrease in Operational Taxonomic Units (OTUs) of genus Bifidobacterium (2.21% vs. 3.71%), Bacteroides (8.50% vs. 11.11%) was observed in the sarcopenic group. An increase in OTUs of genus Faecalibacterium (10.64% vs. 8.23%) in the sarcopenic group was observed. The alpha-diversity index Chao1, Shannon was reduced in sarcopenic population.
CONCLUSIONS: Exploratory differences in microbial diversity and relative abundance were observed between sarcopenic and nonsarcopenic older adults. These findings are descriptive and hypothesis-generating and warrant confirmation in larger, adequately powered studies.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Sarcopenia/microbiology
*Gastrointestinal Microbiome/genetics
Male
Aged
Female
Cross-Sectional Studies
India
*RNA, Ribosomal, 16S/genetics
Pilot Projects
Middle Aged
Feces/microbiology
Aged, 80 and over
RevDate: 2026-04-21
CmpDate: 2026-04-21
Microbiome Modulation with Lactobacillus rhamnosus GG Potentiates Curcumin's Efficacy in Reversing Gemcitabine Resistance of Gallbladder Cancer through Gut Microbiota-PI3K/AKT Axis.
Journal of microbiology and biotechnology, 36:e2601007.
Gemcitabine (GEM) resistance remains a major challenge in the treatment of gallbladder cancer (GBC). This study investigated the synergistic effect of curcumin (CUR) combined with the probiotic Lactobacillus rhamnosus GG (LGG) in reversing chemoresistance through modulation of the gut microbiota. In GEM-resistant GBC-SD cells, the CUR-LGG combination significantly inhibited cell proliferation, suppressed migration and invasion, and induced apoptosis, as demonstrated by CCK-8, wound healing, Transwell, and flow cytometry assays. Western blot analysis revealed corresponding regulation of proliferation markers (Ki67, PCNA), apoptosis-related proteins (Bcl-2, Bax, cleaved Caspase-3), and epithelial-mesenchymal transition markers. In xenograft models, the combined treatment markedly suppressed tumor growth and altered gut microbial composition, increasing beneficial bacteria (Lactobacillus, Bifidobacterium) while reducing pathogenic taxa. LC-MS analysis further demonstrated restoration of bile acid homeostasis, characterized by elevated primary bile acids (GCA, CDCA) and decreased secondary bile acids (DCA, LCA). Mechanistically, the intervention significantly inhibited PI3K/AKT signaling, as confirmed by Western blot and immunohistochemistry. Bioinformatic analysis further identified PI3K/AKT as a central regulatory pathway. These findings indicate that probiotic-assisted CUR therapy reverses GEM resistance by remodeling the gut microbiota and its metabolic outputs, thereby suppressing oncogenic signaling pathways. This strategy provides a promising microbiota-based approach for improving therapeutic outcomes in GBC.
Additional Links: PMID-42014368
PubMed:
Citation:
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@article {pmid42014368,
year = {2026},
author = {Li, Y and Niu, S and Wang, H and Li, J},
title = {Microbiome Modulation with Lactobacillus rhamnosus GG Potentiates Curcumin's Efficacy in Reversing Gemcitabine Resistance of Gallbladder Cancer through Gut Microbiota-PI3K/AKT Axis.},
journal = {Journal of microbiology and biotechnology},
volume = {36},
number = {},
pages = {e2601007},
pmid = {42014368},
issn = {1738-8872},
mesh = {*Lacticaseibacillus rhamnosus/physiology ; *Curcumin/pharmacology ; Humans ; *Gastrointestinal Microbiome/drug effects ; Gemcitabine ; Phosphatidylinositol 3-Kinases/metabolism ; *Gallbladder Neoplasms/drug therapy/microbiology/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; *Deoxycytidine/analogs & derivatives/pharmacology ; *Drug Resistance, Neoplasm/drug effects ; Animals ; Cell Proliferation/drug effects ; Probiotics/pharmacology ; Cell Line, Tumor ; Signal Transduction/drug effects ; Mice ; Apoptosis/drug effects ; Xenograft Model Antitumor Assays ; },
abstract = {Gemcitabine (GEM) resistance remains a major challenge in the treatment of gallbladder cancer (GBC). This study investigated the synergistic effect of curcumin (CUR) combined with the probiotic Lactobacillus rhamnosus GG (LGG) in reversing chemoresistance through modulation of the gut microbiota. In GEM-resistant GBC-SD cells, the CUR-LGG combination significantly inhibited cell proliferation, suppressed migration and invasion, and induced apoptosis, as demonstrated by CCK-8, wound healing, Transwell, and flow cytometry assays. Western blot analysis revealed corresponding regulation of proliferation markers (Ki67, PCNA), apoptosis-related proteins (Bcl-2, Bax, cleaved Caspase-3), and epithelial-mesenchymal transition markers. In xenograft models, the combined treatment markedly suppressed tumor growth and altered gut microbial composition, increasing beneficial bacteria (Lactobacillus, Bifidobacterium) while reducing pathogenic taxa. LC-MS analysis further demonstrated restoration of bile acid homeostasis, characterized by elevated primary bile acids (GCA, CDCA) and decreased secondary bile acids (DCA, LCA). Mechanistically, the intervention significantly inhibited PI3K/AKT signaling, as confirmed by Western blot and immunohistochemistry. Bioinformatic analysis further identified PI3K/AKT as a central regulatory pathway. These findings indicate that probiotic-assisted CUR therapy reverses GEM resistance by remodeling the gut microbiota and its metabolic outputs, thereby suppressing oncogenic signaling pathways. This strategy provides a promising microbiota-based approach for improving therapeutic outcomes in GBC.},
}
MeSH Terms:
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hide MeSH Terms
*Lacticaseibacillus rhamnosus/physiology
*Curcumin/pharmacology
Humans
*Gastrointestinal Microbiome/drug effects
Gemcitabine
Phosphatidylinositol 3-Kinases/metabolism
*Gallbladder Neoplasms/drug therapy/microbiology/metabolism
Proto-Oncogene Proteins c-akt/metabolism
*Deoxycytidine/analogs & derivatives/pharmacology
*Drug Resistance, Neoplasm/drug effects
Animals
Cell Proliferation/drug effects
Probiotics/pharmacology
Cell Line, Tumor
Signal Transduction/drug effects
Mice
Apoptosis/drug effects
Xenograft Model Antitumor Assays
RevDate: 2026-04-21
CmpDate: 2026-04-21
Habitual coffee intake shapes the gut microbiome and modifies host physiology and cognition.
Nature communications, 17(1):.
Coffee influences multiple physiological processes, including gut function, stress, cognition, and the microbiome. However, the mechanisms underlying these effects remain poorly understood. In this study, we examined coffee's impact on the microbiota-gut-brain axis-a bidirectional communication pathway between the gut microbiome and the brain-and assessed whether these effects occur independently of caffeine in healthy participants. Our primary outcome was microbiota composition and function, whereas the secondary outcome was gut microbial metabolites and coffee-related metabolites (NCT05927038 and NCT05927103). Significant group differences emerged in faecal microbiome composition, with coffee drinkers showing increased relative abundance of Cryptobacterium and Eggerthella species, alongside reduced levels of the metabolite's indole-3-propionic acid, indole-3-carboxyaldehyde, and the neurotransmitter γ-aminobutyric acid. Behaviourally, coffee drinkers exhibited greater impulsivity and emotional reactivity, whereas non-coffee drinkers demonstrated better memory performance. Some alterations in the faecal metabolome were reversible following coffee abstinence, and reintroduction triggered acute microbiome changes independent of caffeine. An integrated model identified nine key metabolites-including theophylline, caffeine, and selected phenolic acids-strongly linked to microbial species and cognitive measures. These findings reveal previously unrecognised effects of coffee on the microbiota-gut-brain axis, suggesting that microbiome profiles could potentially predict coffee consumption patterns and highlighting a close association between coffee intake and gut microbial composition.
Additional Links: PMID-42014402
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@article {pmid42014402,
year = {2026},
author = {Boscaini, S and Bastiaanssen, TFS and Moloney, GM and Bergamo, F and Zeraik, L and O'Leary, C and Ferri, A and Irfan, M and van der Rhee, M and Lindemann, TIF and Schneider, E and Meyyappan, AC and Harold, KB and Long-Smith, CM and Carbia, C and O'Riordan, KJ and de Alvarenga, JFR and Tosi, N and Del Rio, D and Rosi, A and Bresciani, L and Mena, P and Clarke, G and Cryan, JF},
title = {Habitual coffee intake shapes the gut microbiome and modifies host physiology and cognition.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42014402},
issn = {2041-1723},
support = {950050//EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects/physiology ; *Coffee/metabolism ; *Cognition/drug effects/physiology ; Male ; Adult ; Feces/microbiology ; Female ; Caffeine/pharmacology/metabolism ; Young Adult ; Brain/physiology ; Metabolome ; },
abstract = {Coffee influences multiple physiological processes, including gut function, stress, cognition, and the microbiome. However, the mechanisms underlying these effects remain poorly understood. In this study, we examined coffee's impact on the microbiota-gut-brain axis-a bidirectional communication pathway between the gut microbiome and the brain-and assessed whether these effects occur independently of caffeine in healthy participants. Our primary outcome was microbiota composition and function, whereas the secondary outcome was gut microbial metabolites and coffee-related metabolites (NCT05927038 and NCT05927103). Significant group differences emerged in faecal microbiome composition, with coffee drinkers showing increased relative abundance of Cryptobacterium and Eggerthella species, alongside reduced levels of the metabolite's indole-3-propionic acid, indole-3-carboxyaldehyde, and the neurotransmitter γ-aminobutyric acid. Behaviourally, coffee drinkers exhibited greater impulsivity and emotional reactivity, whereas non-coffee drinkers demonstrated better memory performance. Some alterations in the faecal metabolome were reversible following coffee abstinence, and reintroduction triggered acute microbiome changes independent of caffeine. An integrated model identified nine key metabolites-including theophylline, caffeine, and selected phenolic acids-strongly linked to microbial species and cognitive measures. These findings reveal previously unrecognised effects of coffee on the microbiota-gut-brain axis, suggesting that microbiome profiles could potentially predict coffee consumption patterns and highlighting a close association between coffee intake and gut microbial composition.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/drug effects/physiology
*Coffee/metabolism
*Cognition/drug effects/physiology
Male
Adult
Feces/microbiology
Female
Caffeine/pharmacology/metabolism
Young Adult
Brain/physiology
Metabolome
RevDate: 2026-04-21
The microbial metabolome: remodeling the therapeutic landscape in hematologic malignancies.
NPJ biofilms and microbiomes pii:10.1038/s41522-026-00972-2 [Epub ahead of print].
The gut microbiome's metabolome critically shapes drug efficacy and toxicity in hematologic malignancies. This review explores how microbial metabolites influence chemotherapy, immunotherapy, and transplant outcomes, and how they can be harnessed as biomarkers and therapeutic targets. Moving from association to intervention, we outline a pathway toward metabolome-informed precision oncology, transforming the "second genome" into a actionable ally for improved cancer therapy.
Additional Links: PMID-42014413
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PubMed:
Citation:
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@article {pmid42014413,
year = {2026},
author = {Zhang, L and Soleimani Samarkhazan, H and Almajidi, Y and Gafarov, R},
title = {The microbial metabolome: remodeling the therapeutic landscape in hematologic malignancies.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-00972-2},
pmid = {42014413},
issn = {2055-5008},
abstract = {The gut microbiome's metabolome critically shapes drug efficacy and toxicity in hematologic malignancies. This review explores how microbial metabolites influence chemotherapy, immunotherapy, and transplant outcomes, and how they can be harnessed as biomarkers and therapeutic targets. Moving from association to intervention, we outline a pathway toward metabolome-informed precision oncology, transforming the "second genome" into a actionable ally for improved cancer therapy.},
}
RevDate: 2026-04-21
Navigating multi-omic integration methods for human microbiome research.
Nature microbiology [Epub ahead of print].
Multi-omic studies in human microbiome research hold great potential for advancing our understanding of host-microbiome interactions. However, despite the growing availability of multi-omic datasets, analysing such data remains a major conceptual, analytical and computational challenge. Introduction of new multi-omic integration methods to address these challenges further complicates researchers' efforts to navigate this expanding field. In this Review, we outline the landscape of multi-omic integration methods in the context of human microbiome research. In contrast to previous reviews, we specifically emphasize the different biological questions addressed by various integration approaches, including questions related to interactions between different molecular layers, molecular shifts that occur in disease, subgrouping of patients based on molecular profiles, and identification of biological mechanisms that underlie such associations. Our aim is to provide a timely, convenient and comprehensive resource for the microbiome research community, allowing researchers to identify the multi-omic integration approach that is best suited to their data and objectives.
Additional Links: PMID-42014454
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Citation:
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@article {pmid42014454,
year = {2026},
author = {Muller, E and Bamberger, T and Borenstein, E},
title = {Navigating multi-omic integration methods for human microbiome research.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {42014454},
issn = {2058-5276},
support = {U19AG057377//U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging)/ ; U19AG057377//U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging)/ ; U19AG057377//U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging)/ ; 2266/25//Israel Science Foundation (ISF)/ ; },
abstract = {Multi-omic studies in human microbiome research hold great potential for advancing our understanding of host-microbiome interactions. However, despite the growing availability of multi-omic datasets, analysing such data remains a major conceptual, analytical and computational challenge. Introduction of new multi-omic integration methods to address these challenges further complicates researchers' efforts to navigate this expanding field. In this Review, we outline the landscape of multi-omic integration methods in the context of human microbiome research. In contrast to previous reviews, we specifically emphasize the different biological questions addressed by various integration approaches, including questions related to interactions between different molecular layers, molecular shifts that occur in disease, subgrouping of patients based on molecular profiles, and identification of biological mechanisms that underlie such associations. Our aim is to provide a timely, convenient and comprehensive resource for the microbiome research community, allowing researchers to identify the multi-omic integration approach that is best suited to their data and objectives.},
}
RevDate: 2026-04-21
Genomic-microbial coevolution in human development: chromosome 2 fusion, and human accelerated regions.
Mammalian genome : official journal of the International Mammalian Genome Society, 37(1):.
Additional Links: PMID-42014606
PubMed:
Citation:
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@article {pmid42014606,
year = {2026},
author = {Singh, S and Shahadab, M and Sachin, K and Pandey, RK and Trivedi, P and Mishra, AK and Jha, HC},
title = {Genomic-microbial coevolution in human development: chromosome 2 fusion, and human accelerated regions.},
journal = {Mammalian genome : official journal of the International Mammalian Genome Society},
volume = {37},
number = {1},
pages = {},
pmid = {42014606},
issn = {1432-1777},
}
RevDate: 2026-04-21
A case-series of oral acetate supplementation for gut microbiota alteration and metabolic improvement in patients with affective disorders on psychotropics.
Translational psychiatry pii:10.1038/s41398-026-04046-x [Epub ahead of print].
Mental illnesses affect one in five Canadians and often require psychotropic medications. While effective, many psychotropic medications can cause weight gain and metabolic side effects. The gut microbiota, influenced by short-chain fatty acids like acetate, plays a role in mental health via the gut-brain axis and may be disrupted as a result of medication use. This case-series explored the feasibility of acetate supplementation contained in delayed-release capsules as an intervention to alter the gut microbiota and reduce metabolic side effects in people taking psychotropic medication for mood and anxiety disorders. Eleven participants aged 22-32 with medication-related weight gain were evaluated at baseline, across three months of delayed-release acetate supplementation, and at one-month follow-up. Adherence was high, with no serious adverse events. Six participants showed signs of metabolic improvements, including clinically-meaningful changes in cholesterol and weight. Mood and anxiety symptoms meaningfully improved in two participants. 16S rRNA gene sequencing revealed alterations in the gut microbiota at both the individual and group levels following the intervention, including increased relative abundance of butyrate-producing bacteria and functional changes potentially influencing cholesterol metabolism. Microbiota differences were also noted between participants with and without metabolic improvements, both pre- and post-intervention, suggesting a potential "responder" phenotype. These findings support further exploration of the effectiveness of delayed-release acetate as a safe adjunctive therapy to offset metabolic concerns and gut microbiome changes in people on psychotropic medication. Larger studies with longer follow-up are needed to confirm these effects and validate responder subgroups.
Additional Links: PMID-42014676
Publisher:
PubMed:
Citation:
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@article {pmid42014676,
year = {2026},
author = {Al, KF and Wammes, M and Warren, M and Lee, JE and Walton, DM and O'Connor, C and Cameron, L and Burton, JP and Osuch, EA},
title = {A case-series of oral acetate supplementation for gut microbiota alteration and metabolic improvement in patients with affective disorders on psychotropics.},
journal = {Translational psychiatry},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41398-026-04046-x},
pmid = {42014676},
issn = {2158-3188},
support = {NA//London Community Foundation (LCF)/ ; },
abstract = {Mental illnesses affect one in five Canadians and often require psychotropic medications. While effective, many psychotropic medications can cause weight gain and metabolic side effects. The gut microbiota, influenced by short-chain fatty acids like acetate, plays a role in mental health via the gut-brain axis and may be disrupted as a result of medication use. This case-series explored the feasibility of acetate supplementation contained in delayed-release capsules as an intervention to alter the gut microbiota and reduce metabolic side effects in people taking psychotropic medication for mood and anxiety disorders. Eleven participants aged 22-32 with medication-related weight gain were evaluated at baseline, across three months of delayed-release acetate supplementation, and at one-month follow-up. Adherence was high, with no serious adverse events. Six participants showed signs of metabolic improvements, including clinically-meaningful changes in cholesterol and weight. Mood and anxiety symptoms meaningfully improved in two participants. 16S rRNA gene sequencing revealed alterations in the gut microbiota at both the individual and group levels following the intervention, including increased relative abundance of butyrate-producing bacteria and functional changes potentially influencing cholesterol metabolism. Microbiota differences were also noted between participants with and without metabolic improvements, both pre- and post-intervention, suggesting a potential "responder" phenotype. These findings support further exploration of the effectiveness of delayed-release acetate as a safe adjunctive therapy to offset metabolic concerns and gut microbiome changes in people on psychotropic medication. Larger studies with longer follow-up are needed to confirm these effects and validate responder subgroups.},
}
RevDate: 2026-04-21
Microbiota-derived metabolites as modulators of cancer immunotherapy response.
Nature communications pii:10.1038/s41467-026-72178-1 [Epub ahead of print].
The microbiome is a key regulator of host homeostasis and immune activity, in part through the production of metabolites. These microbiota-derived metabolites can modulate both the innate and adaptive immune system, as well as directly target tumour cells, thereby regulating anti-tumour immunity and response to immunotherapy. Here, we describe the current mechanistic knowledge on how these metabolites exert their effects and outline the methodologies used to detect and assess these metabolites. Finally, we summarize microbiota-targeted therapies capable of improving microbial functionality to ultimately enhance immunotherapy responses and improve patient survival.
Additional Links: PMID-42014741
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PubMed:
Citation:
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@article {pmid42014741,
year = {2026},
author = {Toner-Bartelds, C and Mimpen, IL and Parra-Martinez, M and Burgering, BMT and Voest, EE},
title = {Microbiota-derived metabolites as modulators of cancer immunotherapy response.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-72178-1},
pmid = {42014741},
issn = {2041-1723},
abstract = {The microbiome is a key regulator of host homeostasis and immune activity, in part through the production of metabolites. These microbiota-derived metabolites can modulate both the innate and adaptive immune system, as well as directly target tumour cells, thereby regulating anti-tumour immunity and response to immunotherapy. Here, we describe the current mechanistic knowledge on how these metabolites exert their effects and outline the methodologies used to detect and assess these metabolites. Finally, we summarize microbiota-targeted therapies capable of improving microbial functionality to ultimately enhance immunotherapy responses and improve patient survival.},
}
RevDate: 2026-04-21
A Wolbachia lineage likely representing a new supergroup (Y) dominates the microbiome of the quill mite Syringophilus bipectinatus Heller, 1880 (Acariformes: Syringophilidae).
Scientific reports pii:10.1038/s41598-026-48644-7 [Epub ahead of print].
The microbiome plays a key role in animal biology, including host reproduction. Quill mites (Acariformes: Syringophilidae) are understudied ectoparasites of birds, with many species exhibiting strongly female-biased sex ratios. Previous studies have identified unique strains of Wolbachia and Spiroplasma in quill mites, both known to manipulate host reproduction in other arthropods. To further investigate this association, we analyzed the microbiome of Syringophilus bipectinatus Heller, 1880, a relatively early-diverging quill mite species parasitizing the Red Junglefowl (domestic type) (Galliformes: Phasianidae), using 16S rRNA gene profiling. We categorized mite specimens by sex and developmental stage to test for potential associations between microbiome composition and sex ratios. We report the first detection of Wolbachia in S. bipectinatus with a single amplicon sequence variant (ASV) consistently detected across all analyzed samples, accounting for 56-99% of total bacterial sequence reads. Phylogenetic analysis based on 16S rRNA gene and four protein-coding genes (fbpA, ftsZ, gatB, hcpA) recovered this strain as a deeply divergent Wolbachia lineage that does not cluster with any previously described supergroup. This lineage is therefore interpreted as likely representing a novel Wolbachia supergroup (Y), although its formal status requires further validation using genome-scale data. Its consistent presence across both sexes and all developmental stages suggests a stable and potentially obligate association, although its functional role remains to be determined. In addition, we identified bacterial taxa also reported from avian hosts, including potentially pathogenic genera such as Arcobacter, highlighting the complex microbial ecology of quill mites.
Additional Links: PMID-42014792
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PubMed:
Citation:
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@article {pmid42014792,
year = {2026},
author = {Głowska-Patyniak, E and Ostrowska, K and Olechnowicz, J and Hubert, J and Konecka, E and Sharma, AK and Som, A and Dabert, M and Trzebny, A},
title = {A Wolbachia lineage likely representing a new supergroup (Y) dominates the microbiome of the quill mite Syringophilus bipectinatus Heller, 1880 (Acariformes: Syringophilidae).},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-48644-7},
pmid = {42014792},
issn = {2045-2322},
support = {UMO-2021/03/Y/NZ8/00060//The National Science Centre of Poland/ ; },
abstract = {The microbiome plays a key role in animal biology, including host reproduction. Quill mites (Acariformes: Syringophilidae) are understudied ectoparasites of birds, with many species exhibiting strongly female-biased sex ratios. Previous studies have identified unique strains of Wolbachia and Spiroplasma in quill mites, both known to manipulate host reproduction in other arthropods. To further investigate this association, we analyzed the microbiome of Syringophilus bipectinatus Heller, 1880, a relatively early-diverging quill mite species parasitizing the Red Junglefowl (domestic type) (Galliformes: Phasianidae), using 16S rRNA gene profiling. We categorized mite specimens by sex and developmental stage to test for potential associations between microbiome composition and sex ratios. We report the first detection of Wolbachia in S. bipectinatus with a single amplicon sequence variant (ASV) consistently detected across all analyzed samples, accounting for 56-99% of total bacterial sequence reads. Phylogenetic analysis based on 16S rRNA gene and four protein-coding genes (fbpA, ftsZ, gatB, hcpA) recovered this strain as a deeply divergent Wolbachia lineage that does not cluster with any previously described supergroup. This lineage is therefore interpreted as likely representing a novel Wolbachia supergroup (Y), although its formal status requires further validation using genome-scale data. Its consistent presence across both sexes and all developmental stages suggests a stable and potentially obligate association, although its functional role remains to be determined. In addition, we identified bacterial taxa also reported from avian hosts, including potentially pathogenic genera such as Arcobacter, highlighting the complex microbial ecology of quill mites.},
}
RevDate: 2026-04-21
Soil management strategies shape bacterial and eukaryotic community structure in organic and inorganic systems of Malus × domestica production.
Scientific reports pii:10.1038/s41598-026-49450-x [Epub ahead of print].
Understanding the temporal dynamics of soil microbial communities is crucial for assessing the stability of orchard soils. We analyzed bacterial and eukaryotic communities in the rhizosphere of apple trees under seven mulching treatments across two growing seasons (2020 and 2023). To account for potential batch effects between separate sequencing runs, results from each year were juxtaposed to identify recurring microbial patterns. High-throughput 16S and ITS sequencing revealed that management-specific signatures persisted over time despite inter-run variability. Bacterial alpha diversity varied significantly among individual treatments, while beta diversity consistently distinguished management regimes across both years. Fungal alpha diversity remained largely unaffected, but beta diversity revealed significant compositional shifts between organic and inorganic groups. Organic mulching (shredded Miscanthus straw and spent mushroom compost) consistently enriched bacterial families linked to organic matter turnover (Sphingomonadaceae, Flavobacteriaceae, Moraxellaceae), whereas inorganic systems favored Comamonadaceae and Nitrosomonadaceae. Organic soils were also enriched in saprotrophic fungi (Lasiosphaeriaceae) and broader eukaryotes (Ciliophora), while inorganic - Mortierellaceae. Network analyses identified a cohesive bacterial core, whereas fungal/eukaryotic communities were more modular and responsive to mulching type. These findings demonstrate that sustained organic mulching promotes stable microbial configurations associated with soil functioning, highlighting the consistency of management-associated microbial signatures under long-term agricultural practices.
Additional Links: PMID-42014833
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PubMed:
Citation:
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@article {pmid42014833,
year = {2026},
author = {Bokszczanin, KŁ and Chojnacka, A and Suchocka, M and Kalaji, HM and Malinowski, R and Kubus, M},
title = {Soil management strategies shape bacterial and eukaryotic community structure in organic and inorganic systems of Malus × domestica production.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-49450-x},
pmid = {42014833},
issn = {2045-2322},
abstract = {Understanding the temporal dynamics of soil microbial communities is crucial for assessing the stability of orchard soils. We analyzed bacterial and eukaryotic communities in the rhizosphere of apple trees under seven mulching treatments across two growing seasons (2020 and 2023). To account for potential batch effects between separate sequencing runs, results from each year were juxtaposed to identify recurring microbial patterns. High-throughput 16S and ITS sequencing revealed that management-specific signatures persisted over time despite inter-run variability. Bacterial alpha diversity varied significantly among individual treatments, while beta diversity consistently distinguished management regimes across both years. Fungal alpha diversity remained largely unaffected, but beta diversity revealed significant compositional shifts between organic and inorganic groups. Organic mulching (shredded Miscanthus straw and spent mushroom compost) consistently enriched bacterial families linked to organic matter turnover (Sphingomonadaceae, Flavobacteriaceae, Moraxellaceae), whereas inorganic systems favored Comamonadaceae and Nitrosomonadaceae. Organic soils were also enriched in saprotrophic fungi (Lasiosphaeriaceae) and broader eukaryotes (Ciliophora), while inorganic - Mortierellaceae. Network analyses identified a cohesive bacterial core, whereas fungal/eukaryotic communities were more modular and responsive to mulching type. These findings demonstrate that sustained organic mulching promotes stable microbial configurations associated with soil functioning, highlighting the consistency of management-associated microbial signatures under long-term agricultural practices.},
}
RevDate: 2026-04-21
Construction of an engineered Escherichia coli strain with enhanced intestinal colonization and anti-inflammatory efficacy in colitis.
Cellular & molecular immunology [Epub ahead of print].
Engineered probiotics are considered effective and safe therapeutic strategies for the treatment of various diseases. Escherichia coli Nissle 1917 (EcN) has been widely used as a chassis strain because of its safety and well-established genetic manipulation system. However, the limited intestinal colonization ability of EcN limits its potential as a chassis for the construction of synthetic probiotics. Here, an engineered EcN strain (EcN-CPM) with enhanced gastric acid and bile salt tolerance and improved intestinal adhesion was constructed. Oral administration of EcN-CPM to mice with colitis alleviated disease severity and reshaped the disordered gut microbiome by decreasing the abundance of Escherichia-Shigella while increasing the abundance of norank_f_Muribaculaceae. Mechanistically, the EcN-CPM supernatant directly promoted the proliferation of norank_f_Muribaculaceae, a short-chain fatty acid (SCFA)-producing genus. Targeted metabolomics revealed that EcN-CPM restored the DSS-induced depletion of SCFAs, which were negatively correlated with the abundance of Escherichia-Shigella and positively correlated with the abundance of norank_f_Muribaculaceae. Consistent with these findings, EcN-CPM treatment upregulated the expression of Treg-associated markers (Foxp3, Ctla4, and Cd25) and downregulated the expression of Th17-related genes (IL-17A and Roryt) in colonic tissues, restoring the IL-17A/Foxp3 ratio to homeostasis. Untargeted metabolomics further demonstrated that EcN-CPM uniquely restored the levels of seven anti-inflammatory metabolites depleted by DSS treatment. Collectively, these findings demonstrate that EcN-CPM alleviates intestinal inflammation by remodeling the gut microbiota to increase the production of SCFAs and anti-inflammatory metabolites, thereby driving a shift in Th17- and Treg-associated transcriptional signatures. This study establishes a platform for precision-designed synthetic probiotics with enhanced probiotic properties.
Additional Links: PMID-42014845
PubMed:
Citation:
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@article {pmid42014845,
year = {2026},
author = {Yu, P and Zhou, W and Li, C and Sun, Q and Yang, Y},
title = {Construction of an engineered Escherichia coli strain with enhanced intestinal colonization and anti-inflammatory efficacy in colitis.},
journal = {Cellular & molecular immunology},
volume = {},
number = {},
pages = {},
pmid = {42014845},
issn = {2042-0226},
abstract = {Engineered probiotics are considered effective and safe therapeutic strategies for the treatment of various diseases. Escherichia coli Nissle 1917 (EcN) has been widely used as a chassis strain because of its safety and well-established genetic manipulation system. However, the limited intestinal colonization ability of EcN limits its potential as a chassis for the construction of synthetic probiotics. Here, an engineered EcN strain (EcN-CPM) with enhanced gastric acid and bile salt tolerance and improved intestinal adhesion was constructed. Oral administration of EcN-CPM to mice with colitis alleviated disease severity and reshaped the disordered gut microbiome by decreasing the abundance of Escherichia-Shigella while increasing the abundance of norank_f_Muribaculaceae. Mechanistically, the EcN-CPM supernatant directly promoted the proliferation of norank_f_Muribaculaceae, a short-chain fatty acid (SCFA)-producing genus. Targeted metabolomics revealed that EcN-CPM restored the DSS-induced depletion of SCFAs, which were negatively correlated with the abundance of Escherichia-Shigella and positively correlated with the abundance of norank_f_Muribaculaceae. Consistent with these findings, EcN-CPM treatment upregulated the expression of Treg-associated markers (Foxp3, Ctla4, and Cd25) and downregulated the expression of Th17-related genes (IL-17A and Roryt) in colonic tissues, restoring the IL-17A/Foxp3 ratio to homeostasis. Untargeted metabolomics further demonstrated that EcN-CPM uniquely restored the levels of seven anti-inflammatory metabolites depleted by DSS treatment. Collectively, these findings demonstrate that EcN-CPM alleviates intestinal inflammation by remodeling the gut microbiota to increase the production of SCFAs and anti-inflammatory metabolites, thereby driving a shift in Th17- and Treg-associated transcriptional signatures. This study establishes a platform for precision-designed synthetic probiotics with enhanced probiotic properties.},
}
RevDate: 2026-04-22
Host matters: coral reef fish species show distinct skin microbiome responses to upwelling-driven environmental changes.
BMC microbiology pii:10.1186/s12866-026-05036-1 [Epub ahead of print].
Additional Links: PMID-42014976
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PubMed:
Citation:
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@article {pmid42014976,
year = {2026},
author = {Lardinois, LL and Hinojosa, NA and Quintero-Arrieta, H and Sellers, AJ and Leray, M and Barrett, RDH},
title = {Host matters: coral reef fish species show distinct skin microbiome responses to upwelling-driven environmental changes.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05036-1},
pmid = {42014976},
issn = {1471-2180},
support = {doi: 10.69777/330691//Fonds de recherche du Québec/ ; 2019-04549//Natural Sciences and Engineering Research Council of Canada/ ; },
}
RevDate: 2026-04-22
Multi-omics integration analyses reveal microbiome and metabolome features in pregnant sow diarrhea induced by porcine epidemic diarrhea virus.
BMC microbiology pii:10.1186/s12866-026-05043-2 [Epub ahead of print].
Additional Links: PMID-42014993
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PubMed:
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@article {pmid42014993,
year = {2026},
author = {Dong, X and Yi, J and Wang, Y and Zhou, A and Zhang, J and Shi, L and Wang, C},
title = {Multi-omics integration analyses reveal microbiome and metabolome features in pregnant sow diarrhea induced by porcine epidemic diarrhea virus.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05043-2},
pmid = {42014993},
issn = {1471-2180},
}
RevDate: 2026-04-22
Modular biosynthesis of microbiome-derived polyketides and nonribosomal peptides: insights and opportunities for Lactobacillaceae.
Microbial cell factories pii:10.1186/s12934-026-03008-8 [Epub ahead of print].
Additional Links: PMID-42015254
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PubMed:
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@article {pmid42015254,
year = {2026},
author = {Dillen, J and Eilers, T and Dricot, CEMK and Van Hee, M and Vandenheuvel, D and Masschelein, J and Lebeer, S},
title = {Modular biosynthesis of microbiome-derived polyketides and nonribosomal peptides: insights and opportunities for Lactobacillaceae.},
journal = {Microbial cell factories},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12934-026-03008-8},
pmid = {42015254},
issn = {1475-2859},
support = {1S28622N//Fonds Wetenschappelijk Onderzoek/ ; 1158725N//Fonds Wetenschappelijk Onderzoek/ ; G049022N//Fonds Wetenschappelijk Onderzoek/ ; 852600//HORIZON EUROPE European Research Council/ ; },
}
RevDate: 2026-04-22
Alleviation of heat stress-induced microbial dysbiosis in pigs through dietary supplementation with vitamins and trace elements.
Animal microbiome pii:10.1186/s42523-026-00575-4 [Epub ahead of print].
BACKGROUND: Chronic heat stress (HS) is known to impair animal health and productivity, in part by altering gut microbiota. This study investigated how HS affects the pig gut microbiome and whether dietary supplementation with antioxidants and trace elements (vitamins E, C, selenium, and zinc) at moderate (D1) or high (D2) doses can mitigate these effects.
RESULTS: During the adaptation phase, feed efficiency was similar across groups, but as the experiment progressed, the thermoneutral control improved while the heat-stressed control deteriorated. Supplemented diets (D1/D2) partially alleviated this efficiency loss. Microbiome analysis revealed that HS progressively reduced diversity, reaching the lowest Shannon index during exposure. High-dose supplementation markedly increased richness, exceeding control levels. Total microbial abundance declined under HS, with opportunistic pathogens enriched particularly during early exposure. Guild-level indices further indicated a shift under HS. Aerotolerance indices decreased (ATi: TC > D1 > D2 > HSC), reflecting hypoxia-prone conditions favoring obligate anaerobes and SCFA producers. Among supplemented groups, D1 most closely stabilized aerotolerance toward control levels, while D2 maintained an SCFA-dominant community and enhanced butyrate capacity. Genus-level correlations with qPCR-based host gene-expression markers were assessed across all groups. HSP70 was the dominant correlate, and the most extreme associations were confined to a few taxa, indicating marked group specificity.
CONCLUSION: Chronic HS in pigs induced microbial dysbiosis characterized by reduced diversity, loss of beneficial SCFA producers, and expansion of opportunistic pathogens. Dietary supplementation counteracted these adverse changes in a dose-dependent manner. While moderate supplementation provided partial stabilization, high-dose supplementation more effectively restored microbial diversity and enriched beneficial taxa, making it the more effective strategy for mitigating HS-induced microbiome disruption.
Additional Links: PMID-42015325
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PubMed:
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@article {pmid42015325,
year = {2026},
author = {Fauszt, P and Szilagyi, E and Mikolas, M and Szilagyi-Tolnai, E and David, P and Kovacs-Forgacs, IN and Csernus, B and Gal, F and Stundl, L and Biro, S and Szabo, C and Remenyik, J and Babinszky, L and Paholcsek, M},
title = {Alleviation of heat stress-induced microbial dysbiosis in pigs through dietary supplementation with vitamins and trace elements.},
journal = {Animal microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s42523-026-00575-4},
pmid = {42015325},
issn = {2524-4671},
abstract = {BACKGROUND: Chronic heat stress (HS) is known to impair animal health and productivity, in part by altering gut microbiota. This study investigated how HS affects the pig gut microbiome and whether dietary supplementation with antioxidants and trace elements (vitamins E, C, selenium, and zinc) at moderate (D1) or high (D2) doses can mitigate these effects.
RESULTS: During the adaptation phase, feed efficiency was similar across groups, but as the experiment progressed, the thermoneutral control improved while the heat-stressed control deteriorated. Supplemented diets (D1/D2) partially alleviated this efficiency loss. Microbiome analysis revealed that HS progressively reduced diversity, reaching the lowest Shannon index during exposure. High-dose supplementation markedly increased richness, exceeding control levels. Total microbial abundance declined under HS, with opportunistic pathogens enriched particularly during early exposure. Guild-level indices further indicated a shift under HS. Aerotolerance indices decreased (ATi: TC > D1 > D2 > HSC), reflecting hypoxia-prone conditions favoring obligate anaerobes and SCFA producers. Among supplemented groups, D1 most closely stabilized aerotolerance toward control levels, while D2 maintained an SCFA-dominant community and enhanced butyrate capacity. Genus-level correlations with qPCR-based host gene-expression markers were assessed across all groups. HSP70 was the dominant correlate, and the most extreme associations were confined to a few taxa, indicating marked group specificity.
CONCLUSION: Chronic HS in pigs induced microbial dysbiosis characterized by reduced diversity, loss of beneficial SCFA producers, and expansion of opportunistic pathogens. Dietary supplementation counteracted these adverse changes in a dose-dependent manner. While moderate supplementation provided partial stabilization, high-dose supplementation more effectively restored microbial diversity and enriched beneficial taxa, making it the more effective strategy for mitigating HS-induced microbiome disruption.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Gut microbiome and metabolic health: mechanisms and precision interventions.
Gut microbes, 18(1):2644677.
The gut microbiome is increasingly recognized as a fundamental regulator of metabolic health, shaping energy balance, insulin sensitivity, inflammatory tone, and inter-organ communication through a broad spectrum of microbial metabolites that engage host signaling pathways. In this review, we synthesize current mechanistic insights into how gut microbial communities shape metabolic function, with particular emphasis on short-chain fatty acids, secondary bile acid signaling, gut barrier integrity, immune modulation, and the microbiota-gut-brain-pancreas axis. We further summarize disease-associated alterations in microbial composition and function across obesity, type 2 diabetes, metabolic dysfunction-associated steatotic liver disease, and metabolic syndrome, highlighting key microbial and metabolic features that contribute to metabolic dysfunction. Evidence from germ-free models, fecal microbiota transplantation studies, and strain-level interventions suggests that shifts in microbial ecology may causally shape metabolic outcomes. We also critically evaluate emerging microbiome-centered therapeutic strategies, including targeted probiotics, prebiotics, dietary modulation, and fecal microbiota transplantation, while addressing factors that underlie inter-individual variability in treatment responses. In addition, we discuss the growing influence of multi-omics technologies, microbial metabolic modeling, and machine learning approaches in advancing precision microbiome medicine. To integrate these advances within a coherent framework, we outline a precision microbiome intervention pipeline linking multidimensional profiling to functional stratification and targeted therapeutic design. We also introduce a conceptual Precision Microbiome Intervention Triangle to mechanistically explain heterogeneity in responses to microbiome-targeted therapies. Collectively, these insights establish and position the gut microbiome as both a mechanistic driver and a modifiable therapeutic target in metabolic disease, and highlight key challenges and future directions for the development of personalized microbiome-based metabolic interventions.
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@article {pmid42015346,
year = {2026},
author = {Li, Z and Samui, S and Liu, J and Yang, Y and Liu, X and Chen, Q and Li, J and Gopinath, D and Luo, P and Shan, D},
title = {Gut microbiome and metabolic health: mechanisms and precision interventions.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2644677},
doi = {10.1080/19490976.2026.2644677},
pmid = {42015346},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Animals ; Fecal Microbiota Transplantation ; Probiotics ; Precision Medicine ; *Metabolic Diseases/microbiology/metabolism/therapy ; Prebiotics/administration & dosage ; Obesity/microbiology/metabolism ; Diabetes Mellitus, Type 2/microbiology/metabolism ; Metabolic Syndrome/microbiology/metabolism ; },
abstract = {The gut microbiome is increasingly recognized as a fundamental regulator of metabolic health, shaping energy balance, insulin sensitivity, inflammatory tone, and inter-organ communication through a broad spectrum of microbial metabolites that engage host signaling pathways. In this review, we synthesize current mechanistic insights into how gut microbial communities shape metabolic function, with particular emphasis on short-chain fatty acids, secondary bile acid signaling, gut barrier integrity, immune modulation, and the microbiota-gut-brain-pancreas axis. We further summarize disease-associated alterations in microbial composition and function across obesity, type 2 diabetes, metabolic dysfunction-associated steatotic liver disease, and metabolic syndrome, highlighting key microbial and metabolic features that contribute to metabolic dysfunction. Evidence from germ-free models, fecal microbiota transplantation studies, and strain-level interventions suggests that shifts in microbial ecology may causally shape metabolic outcomes. We also critically evaluate emerging microbiome-centered therapeutic strategies, including targeted probiotics, prebiotics, dietary modulation, and fecal microbiota transplantation, while addressing factors that underlie inter-individual variability in treatment responses. In addition, we discuss the growing influence of multi-omics technologies, microbial metabolic modeling, and machine learning approaches in advancing precision microbiome medicine. To integrate these advances within a coherent framework, we outline a precision microbiome intervention pipeline linking multidimensional profiling to functional stratification and targeted therapeutic design. We also introduce a conceptual Precision Microbiome Intervention Triangle to mechanistically explain heterogeneity in responses to microbiome-targeted therapies. Collectively, these insights establish and position the gut microbiome as both a mechanistic driver and a modifiable therapeutic target in metabolic disease, and highlight key challenges and future directions for the development of personalized microbiome-based metabolic interventions.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Gastrointestinal Microbiome/physiology
Animals
Fecal Microbiota Transplantation
Probiotics
Precision Medicine
*Metabolic Diseases/microbiology/metabolism/therapy
Prebiotics/administration & dosage
Obesity/microbiology/metabolism
Diabetes Mellitus, Type 2/microbiology/metabolism
Metabolic Syndrome/microbiology/metabolism
RevDate: 2026-04-22
Statin-induced gut dysbiosis and sleep disturbances: Mechanistic insights into microbiota-brain-circadian interactions and chronotherapeutic implications.
Chronobiology international [Epub ahead of print].
Statins are widely prescribed lipid-lowering agents with well-established efficacy in reducing cardiovascular morbidity and mortality. However, accumulating clinical and experimental evidence suggests that statin therapy may be associated with sleep disturbances, including insomnia, altered sleep architecture, vivid dreams, and reduced sleep quality. Emerging insights implicate the gut microbiota as a key regulator of host circadian rhythms and sleep homeostasis through interconnected pathways involving the tryptophan-serotonin-melatonin axis, short-chain fatty acid (SCFA) production, bile acid signaling, and immune-mediated neuroinflammation. Statins have been shown to modulate gut microbial composition, often reducing SCFA producing taxa and altering bile acid pools, which in turn may disrupt neurochemical signaling and circadian regulation. These microbiota-driven perturbations may contribute to central nervous system effects that underlie sleep-related adverse outcomes. This review integrates current mechanistic and clinical evidence linking statin-induced gut dysbiosis with sleep disturbances, highlighting the role of microbiome-host interactions in mediating off-target drug effects. It further examines implications for vulnerable populations, including shift workers, and discusses the potential of chronotherapy in optimizing statin administration. Finally, microbiota targeted interventions, such as probiotics, prebiotics, and dietary modulation, are proposed as promising strategies to mitigate these adverse effects. A deeper understanding of these interactions may enable personalized therapeutic approaches to enhance both cardiovascular outcomes and sleep health.
Additional Links: PMID-42015619
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PubMed:
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@article {pmid42015619,
year = {2026},
author = {Ganamurali, N and Sabarathinam, S},
title = {Statin-induced gut dysbiosis and sleep disturbances: Mechanistic insights into microbiota-brain-circadian interactions and chronotherapeutic implications.},
journal = {Chronobiology international},
volume = {},
number = {},
pages = {1-11},
doi = {10.1080/07420528.2026.2660826},
pmid = {42015619},
issn = {1525-6073},
abstract = {Statins are widely prescribed lipid-lowering agents with well-established efficacy in reducing cardiovascular morbidity and mortality. However, accumulating clinical and experimental evidence suggests that statin therapy may be associated with sleep disturbances, including insomnia, altered sleep architecture, vivid dreams, and reduced sleep quality. Emerging insights implicate the gut microbiota as a key regulator of host circadian rhythms and sleep homeostasis through interconnected pathways involving the tryptophan-serotonin-melatonin axis, short-chain fatty acid (SCFA) production, bile acid signaling, and immune-mediated neuroinflammation. Statins have been shown to modulate gut microbial composition, often reducing SCFA producing taxa and altering bile acid pools, which in turn may disrupt neurochemical signaling and circadian regulation. These microbiota-driven perturbations may contribute to central nervous system effects that underlie sleep-related adverse outcomes. This review integrates current mechanistic and clinical evidence linking statin-induced gut dysbiosis with sleep disturbances, highlighting the role of microbiome-host interactions in mediating off-target drug effects. It further examines implications for vulnerable populations, including shift workers, and discusses the potential of chronotherapy in optimizing statin administration. Finally, microbiota targeted interventions, such as probiotics, prebiotics, and dietary modulation, are proposed as promising strategies to mitigate these adverse effects. A deeper understanding of these interactions may enable personalized therapeutic approaches to enhance both cardiovascular outcomes and sleep health.},
}
RevDate: 2026-04-23
CmpDate: 2026-04-22
Tongue-coating microbiome as a predictor of solid tumors: an updated scoping review of clinical studies.
Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan, 46(2):501-508.
This study explores the potential of tongue coating microbiota as a non-invasive biomarker for cancer and precancerous lesions by integrating insights from multi-omics technologies and Traditional Chinese Medicine (TCM) tongue diagnosis. By bridging modern molecular research with TCM diagnostic principles, this study systematically reviewed the relationship between tongue microbiota and oncological conditions, identifying 18 eligible studies through searches in PubMed, Embase, and Web of Science. The analysis reveals significant differences in microbial diversity, abundance, metabolic pathways, and functional characteristics, which enable the partial differentiation of cancer patients from healthy individuals. However, existing research remains constrained by limited sample sizes, inconsistent analytical approaches, and a lack of integrated multi-dimensional datasets. This review highlights the promising diagnostic potential of the tongue coating microbiota in cancer detection, while suggesting that future studies should focus on standardizing methodologies and employing integrated multi-omics approaches to elucidate underlying mechanisms and advance clinical applications.
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@article {pmid42015788,
year = {2026},
author = {Kexin, LI and Jinzu, Y and Kunlin, X and Shaojie, D and Kunmin, X},
title = {Tongue-coating microbiome as a predictor of solid tumors: an updated scoping review of clinical studies.},
journal = {Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan},
volume = {46},
number = {2},
pages = {501-508},
pmid = {42015788},
issn = {2589-451X},
mesh = {Humans ; *Microbiota ; *Neoplasms/microbiology/diagnosis ; *Tongue/microbiology ; Medicine, Chinese Traditional ; },
abstract = {This study explores the potential of tongue coating microbiota as a non-invasive biomarker for cancer and precancerous lesions by integrating insights from multi-omics technologies and Traditional Chinese Medicine (TCM) tongue diagnosis. By bridging modern molecular research with TCM diagnostic principles, this study systematically reviewed the relationship between tongue microbiota and oncological conditions, identifying 18 eligible studies through searches in PubMed, Embase, and Web of Science. The analysis reveals significant differences in microbial diversity, abundance, metabolic pathways, and functional characteristics, which enable the partial differentiation of cancer patients from healthy individuals. However, existing research remains constrained by limited sample sizes, inconsistent analytical approaches, and a lack of integrated multi-dimensional datasets. This review highlights the promising diagnostic potential of the tongue coating microbiota in cancer detection, while suggesting that future studies should focus on standardizing methodologies and employing integrated multi-omics approaches to elucidate underlying mechanisms and advance clinical applications.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Microbiota
*Neoplasms/microbiology/diagnosis
*Tongue/microbiology
Medicine, Chinese Traditional
RevDate: 2026-04-22
The microbiome landscape of oral cancer in young patients.
JNCI cancer spectrum pii:8660647 [Epub ahead of print].
BACKGROUND: The incidence of oral squamous cell carcinoma (OSCC) is rising in patients under the age of 50, without smoking or alcohol abuse. Viruses are not a causative factor of OSCC in younger patients. The oral microbiome has not been evaluated in this unique patient cohort for a potential bacterial aetiology.
METHODS: We report the bacterial diversity and composition of the largest cohort of OSCC patients with whole genome sequencing (WGS) (n = 72) and compare it with oral mucosa from healthy controls (n = 10) using the Strengthening the Organization and Reporting of Microbiome Studies guidelines.
RESULTS: The microbial diversity between tumour, normal mucosa from cancer patients and healthy control mucosa is significantly different, with specific species (Streptococcus mitis, Haemophilus haemolyticus and Cutibacterium acnes) reduced in normal mucosa of cancer patients as compared to healthy controls (adjusted p < 0.05). The microbial diversity is significantly higher in younger patients as compared to older patients (p < 0.001), with a reduced abundance of anaerobes in older patients (Aggregatibacter segnis, Gemella morbillorum, Peptostreptococcus stomatis, Filifactor alocis and Porphyromonas endodontalis; adjusted p < 0.05).
CONCLUSION: The OSCC tissue of younger patients is significantly more polymicrobial, and their OSCC microbiomes harbour more anaerobic bacteria as compared to older patients. This compositional difference builds the hypothesis that the oral microbiome of younger OSCC patients may have a more hypoxic, immunosuppressive tumour microenvironment with its associated implications for treatment resistance and a potential link to baseline poor dentition.
Additional Links: PMID-42015892
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PubMed:
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@article {pmid42015892,
year = {2026},
author = {Satgunaseelan, L and Strbenac, D and Palme, C and Low, TH and Wykes, J and Manzie, T and Clark, JR and Yang, JYH and Gupta, R},
title = {The microbiome landscape of oral cancer in young patients.},
journal = {JNCI cancer spectrum},
volume = {},
number = {},
pages = {},
doi = {10.1093/jncics/pkag022},
pmid = {42015892},
issn = {2515-5091},
abstract = {BACKGROUND: The incidence of oral squamous cell carcinoma (OSCC) is rising in patients under the age of 50, without smoking or alcohol abuse. Viruses are not a causative factor of OSCC in younger patients. The oral microbiome has not been evaluated in this unique patient cohort for a potential bacterial aetiology.
METHODS: We report the bacterial diversity and composition of the largest cohort of OSCC patients with whole genome sequencing (WGS) (n = 72) and compare it with oral mucosa from healthy controls (n = 10) using the Strengthening the Organization and Reporting of Microbiome Studies guidelines.
RESULTS: The microbial diversity between tumour, normal mucosa from cancer patients and healthy control mucosa is significantly different, with specific species (Streptococcus mitis, Haemophilus haemolyticus and Cutibacterium acnes) reduced in normal mucosa of cancer patients as compared to healthy controls (adjusted p < 0.05). The microbial diversity is significantly higher in younger patients as compared to older patients (p < 0.001), with a reduced abundance of anaerobes in older patients (Aggregatibacter segnis, Gemella morbillorum, Peptostreptococcus stomatis, Filifactor alocis and Porphyromonas endodontalis; adjusted p < 0.05).
CONCLUSION: The OSCC tissue of younger patients is significantly more polymicrobial, and their OSCC microbiomes harbour more anaerobic bacteria as compared to older patients. This compositional difference builds the hypothesis that the oral microbiome of younger OSCC patients may have a more hypoxic, immunosuppressive tumour microenvironment with its associated implications for treatment resistance and a potential link to baseline poor dentition.},
}
RevDate: 2026-04-22
Faecal Attraction: 40 Years of Research in Gut Microbiology.
Nutrition bulletin [Epub ahead of print].
This article summarises the 2025 British Nutrition Foundation Annual Lecture given on 25/11/25. It overviews aspects of research in anaerobic microbiology, principally involving the human gut. Until October 2025, Gibson was Professor of Food Microbiology at the University of Reading. His research investigated gut microbiome interactions and dietary intervention. The latter included human studies in healthy persons, patients with gut-related disorders, at-risk populations and specialist groups like sportspersons and those in the military. Initial principles such as the type of intervention, dose, duration and outcomes were tested using in vitro models of the human gut.
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@article {pmid42015905,
year = {2026},
author = {Gibson, GR},
title = {Faecal Attraction: 40 Years of Research in Gut Microbiology.},
journal = {Nutrition bulletin},
volume = {},
number = {},
pages = {},
doi = {10.1111/nbu.70052},
pmid = {42015905},
issn = {1467-3010},
abstract = {This article summarises the 2025 British Nutrition Foundation Annual Lecture given on 25/11/25. It overviews aspects of research in anaerobic microbiology, principally involving the human gut. Until October 2025, Gibson was Professor of Food Microbiology at the University of Reading. His research investigated gut microbiome interactions and dietary intervention. The latter included human studies in healthy persons, patients with gut-related disorders, at-risk populations and specialist groups like sportspersons and those in the military. Initial principles such as the type of intervention, dose, duration and outcomes were tested using in vitro models of the human gut.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Multi-Target Mechanisms of Whey Protein Against NAFLD: Integrating Bile Acid Metabolism, Gut Microbiota and Hepatic Inflammation.
Food science & nutrition, 14(3):e71655.
This study elucidates the protective mechanisms of whey protein (WP) in treating high-fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) in mice, emphasizing its role in bile acid regulation, intestinal flora homeostasis, and inflammatory suppression. ICR mice were subjected to a 12-week HFD to establish NAFLD, followed by WP intervention (200 g/kg). Comprehensive analyses included histopathological assessment (HE staining), serum biomarkers, hepatic gene expression (qPCR), gut microbial profiling (16S rRNA sequencing), quantitative bile acid and short-chain fatty acid (SCFA) analysis, and serum metabolomics. Core targets were predicted via network pharmacology and validated through molecular docking. WP administration markedly alleviated NAFLD progression by targeting multiple pathways: (1) It suppressed hepatic lipid deposition and inflammatory injury, downregulating NLRP3, NF-κB, and TNF-α (p < 0.05) while enhancing Nrf2/HO-1-mediated antioxidant defenses; (2) Network pharmacology prioritized IL-1β, STAT3, and MMP9 as pivotal targets, with β-lactoglobulin exhibiting high binding potentials (STAT3: -1.42 kcal/mol); (3) WP restored gut microbial balance, enriching beneficial taxa (e.g., Lactobacillus) and fecal SCFAs; (4) It reprogrammed bile acid metabolism, elevating cholesterol-cleaving enzymes (CYP7A1/CYP27A1) but inhibiting FXR/SHP (p < 0.05), alongside increased hepatoprotective bile acids (TDCA/TUDCA). Metabolomics identified WP-induced anti-inflammatory mediators (e.g., eicosapentaenoic acid) and perturbations in arginine and unsaturated fatty acid pathways, synergistically attenuating steatosis and fibrosis. WP counters NAFLD via a tripartite mechanism: gut microbiome-directed SCFA synthesis, bile acid-driven cholesterol disposal, and dual modulation of inflammation (NLRP3/NF-κB) and oxidative stress (Nrf2/HO-1). These insights position WP as a promising dietary strategy targeting the gut-liver axis.
Additional Links: PMID-42016247
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Citation:
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@article {pmid42016247,
year = {2026},
author = {Xu, D and Qiu, B and Dong, X and Tan, J and Xie, Y and Wan, Y and Chu, C and Miao, C and Ali, A and Chen, M and He, J and Wu, L and Xie, J},
title = {Multi-Target Mechanisms of Whey Protein Against NAFLD: Integrating Bile Acid Metabolism, Gut Microbiota and Hepatic Inflammation.},
journal = {Food science & nutrition},
volume = {14},
number = {3},
pages = {e71655},
pmid = {42016247},
issn = {2048-7177},
abstract = {This study elucidates the protective mechanisms of whey protein (WP) in treating high-fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) in mice, emphasizing its role in bile acid regulation, intestinal flora homeostasis, and inflammatory suppression. ICR mice were subjected to a 12-week HFD to establish NAFLD, followed by WP intervention (200 g/kg). Comprehensive analyses included histopathological assessment (HE staining), serum biomarkers, hepatic gene expression (qPCR), gut microbial profiling (16S rRNA sequencing), quantitative bile acid and short-chain fatty acid (SCFA) analysis, and serum metabolomics. Core targets were predicted via network pharmacology and validated through molecular docking. WP administration markedly alleviated NAFLD progression by targeting multiple pathways: (1) It suppressed hepatic lipid deposition and inflammatory injury, downregulating NLRP3, NF-κB, and TNF-α (p < 0.05) while enhancing Nrf2/HO-1-mediated antioxidant defenses; (2) Network pharmacology prioritized IL-1β, STAT3, and MMP9 as pivotal targets, with β-lactoglobulin exhibiting high binding potentials (STAT3: -1.42 kcal/mol); (3) WP restored gut microbial balance, enriching beneficial taxa (e.g., Lactobacillus) and fecal SCFAs; (4) It reprogrammed bile acid metabolism, elevating cholesterol-cleaving enzymes (CYP7A1/CYP27A1) but inhibiting FXR/SHP (p < 0.05), alongside increased hepatoprotective bile acids (TDCA/TUDCA). Metabolomics identified WP-induced anti-inflammatory mediators (e.g., eicosapentaenoic acid) and perturbations in arginine and unsaturated fatty acid pathways, synergistically attenuating steatosis and fibrosis. WP counters NAFLD via a tripartite mechanism: gut microbiome-directed SCFA synthesis, bile acid-driven cholesterol disposal, and dual modulation of inflammation (NLRP3/NF-κB) and oxidative stress (Nrf2/HO-1). These insights position WP as a promising dietary strategy targeting the gut-liver axis.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Targeted Next-Generation Sequencing Analysis of BALF Microbiota and Clinical Characteristics in Severe versus Non-Severe Community-Acquired Pneumonia.
Infection and drug resistance, 19:588781.
BACKGROUND: Severe community-acquired pneumonia (SCAP) is associated with high mortality. However, data on the bronchoalveolar lavage fluid (BALF) microbiota in Chinese SCAP patients remain limited. This study aimed to characterize the clinical features and BALF microbiome composition in patients with SCAP compared to non-severe CAP using targeted next-generation sequencing (tNGS).
METHODS: We conducted a retrospective study involving 224 CAP and 97 SCAP patients from two hospitals in Shanxi, China (January 2023-January 2025). Clinical characteristics and inflammatory cytokines were compared between groups. BALF samples were analyzed via tNGS to evaluate microbial alpha and beta diversity. Differentially abundant taxa were identified using Linear Discriminant Analysis Effect Size (LEfSe).
RESULTS: Compared to the CAP group, SCAP patients were significantly older, had a higher prevalence of comorbidities (hypertension, coronary heart disease, diabetes), and exhibited elevated inflammatory indices (CRP, IL-6, PCT, ESR). SCAP patients also demonstrated a higher likelihood of mixed infections, and the number of detected pathogens showed a positive correlation with the length of hospital stay. tNGS analysis revealed significant differences in alpha diversity and distinct beta diversity clustering between the two groups. LEfSe analysis identified Pseudomonas as a potential biomarker enriched in SCAP, whereas Streptococcus was predominant in CAP.
CONCLUSION: In patients with SCAP, the BALF microbiota showed a significant increase in alpha diversity, which appears to be closely associated with inflammatory cytokine production and correlates with disease severity. There were pronounced differences between SCAP and CAP in both clinical characteristics and microbiome profiles, highlighting the necessity of integrated diagnostic approaches in pneumonia care. Future research should prioritize delineating the dynamic shifts of microbial communities and their influence on pneumonia severity, with the goal of refining and optimizing treatment strategies.
Additional Links: PMID-42016370
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@article {pmid42016370,
year = {2026},
author = {Fan, Y and Ren, Y and An, J and Wang, X},
title = {Targeted Next-Generation Sequencing Analysis of BALF Microbiota and Clinical Characteristics in Severe versus Non-Severe Community-Acquired Pneumonia.},
journal = {Infection and drug resistance},
volume = {19},
number = {},
pages = {588781},
pmid = {42016370},
issn = {1178-6973},
abstract = {BACKGROUND: Severe community-acquired pneumonia (SCAP) is associated with high mortality. However, data on the bronchoalveolar lavage fluid (BALF) microbiota in Chinese SCAP patients remain limited. This study aimed to characterize the clinical features and BALF microbiome composition in patients with SCAP compared to non-severe CAP using targeted next-generation sequencing (tNGS).
METHODS: We conducted a retrospective study involving 224 CAP and 97 SCAP patients from two hospitals in Shanxi, China (January 2023-January 2025). Clinical characteristics and inflammatory cytokines were compared between groups. BALF samples were analyzed via tNGS to evaluate microbial alpha and beta diversity. Differentially abundant taxa were identified using Linear Discriminant Analysis Effect Size (LEfSe).
RESULTS: Compared to the CAP group, SCAP patients were significantly older, had a higher prevalence of comorbidities (hypertension, coronary heart disease, diabetes), and exhibited elevated inflammatory indices (CRP, IL-6, PCT, ESR). SCAP patients also demonstrated a higher likelihood of mixed infections, and the number of detected pathogens showed a positive correlation with the length of hospital stay. tNGS analysis revealed significant differences in alpha diversity and distinct beta diversity clustering between the two groups. LEfSe analysis identified Pseudomonas as a potential biomarker enriched in SCAP, whereas Streptococcus was predominant in CAP.
CONCLUSION: In patients with SCAP, the BALF microbiota showed a significant increase in alpha diversity, which appears to be closely associated with inflammatory cytokine production and correlates with disease severity. There were pronounced differences between SCAP and CAP in both clinical characteristics and microbiome profiles, highlighting the necessity of integrated diagnostic approaches in pneumonia care. Future research should prioritize delineating the dynamic shifts of microbial communities and their influence on pneumonia severity, with the goal of refining and optimizing treatment strategies.},
}
RevDate: 2026-04-23
Bayesian Modeling on Microbiome Data Analysis: Application to Subgingival Microbiome Study.
Statistics in biosciences, 16(3):556-577.
The study of microbiome data has been widely used to investigate associations between the abundance of microbial taxa and human diseases. Identifying and understanding these relationships precisely gives the microbiome a key role in human health, disease status, and the development of new diagnostics and targeted therapeutics. Due to its unique features such as compositional data, excessive zero counts, overdispersion, and complexed structure between taxa, undertaking effective microbiome data analytics presents numerous obstacles. To quantify covariate-taxa effects on the subgingival microbiome study, we proposed a refined Bayesian zero-inflated negative binomial (ZINB) regression model with random subject effects. This proposed approach not only accommodates inflated zero counts and overdispersion similar to the existing ZINB model developed by Jiang et al. (Biostatistics 22(3):522-540, 2021), but also accounts for subject-level heterogeneity through the inclusion of random subject effects. In addition, an efficient Markov chain Monte Carlo (MCMC) sampling algorithm was developed for Bayesian computation. Overall effects of pre-selected group variables on predicted taxa abundance were estimated and tested under the proposed model. We conduct simulation studies and demonstrate that the proposed model outperforms the competing models in achieving a better power with controlling the type I error. The usefulness of the proposed model is applied to a real subgingival microbiome study.
Additional Links: PMID-42016555
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Citation:
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@article {pmid42016555,
year = {2024},
author = {Gwon, Y and Yu, F and Payne, JB and Mikuls, TR},
title = {Bayesian Modeling on Microbiome Data Analysis: Application to Subgingival Microbiome Study.},
journal = {Statistics in biosciences},
volume = {16},
number = {3},
pages = {556-577},
pmid = {42016555},
issn = {1867-1764},
support = {I01 CX000896/CX/CSRD VA/United States ; U54 GM115458/GM/NIGMS NIH HHS/United States ; },
abstract = {The study of microbiome data has been widely used to investigate associations between the abundance of microbial taxa and human diseases. Identifying and understanding these relationships precisely gives the microbiome a key role in human health, disease status, and the development of new diagnostics and targeted therapeutics. Due to its unique features such as compositional data, excessive zero counts, overdispersion, and complexed structure between taxa, undertaking effective microbiome data analytics presents numerous obstacles. To quantify covariate-taxa effects on the subgingival microbiome study, we proposed a refined Bayesian zero-inflated negative binomial (ZINB) regression model with random subject effects. This proposed approach not only accommodates inflated zero counts and overdispersion similar to the existing ZINB model developed by Jiang et al. (Biostatistics 22(3):522-540, 2021), but also accounts for subject-level heterogeneity through the inclusion of random subject effects. In addition, an efficient Markov chain Monte Carlo (MCMC) sampling algorithm was developed for Bayesian computation. Overall effects of pre-selected group variables on predicted taxa abundance were estimated and tested under the proposed model. We conduct simulation studies and demonstrate that the proposed model outperforms the competing models in achieving a better power with controlling the type I error. The usefulness of the proposed model is applied to a real subgingival microbiome study.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Restoring low-fiber diets-induced Lachnospiraceae bacterium loss partially recovers fiber digestion and immune function in mammals.
Current research in food science, 12:101401.
Mammals rely on their gut microbiota to degrade cellulose, the major component of dietary fiber. Westernized populations harbor a depleted microbiome with reduced fiber-digesting capacity and impaired immune regulation due to prolonged consumption of low-fiber diets. Comparable patterns are evident in other mammals, including Western commercial pigs raised on high-energy, low-fiber diets, exhibiting reduced diversity and abundance of fiber-degrading bacteria. In contrast, semi-free-ranging Chinese indigenous pigs consuming fiber-rich diets retain a more diverse and functionally resilient microbiota, reflecting divergent trajectories of host-microbiota co-evolution. However, the specific cellulose-degrading species lost and strategies to restore these functions remain unclear in mammals. By analyzing 473 human stool metagenomes spanning non-westernized and westernized diets, together with 251 fecal 16S rRNA datasets and 95 metagenomes from Western commercial pigs, Chinese indigenous pigs, and their crossbred progeny, we identified the Lachnospiraceae bacterium as a key symbiont enriched in non-westernized guts. This bacterium possesses an extensive Carbohydrate-Active Enzymes repertoire conferring strong fiber-degrading capacity. Notably, low-fiber diets leave a genetic signature on this keystone gut symbiont, which cannot be reversed by short-term dietary interventions alone. Reintroduction of Lachnospiraceae bacterium to germ-free mice improved feed efficiency and increased acetic acid production. Intestinal transcriptomics and peripheral blood flow cytometry revealed that it activates a broad adaptive immune response, promoting CD4[+] T cell accumulation, B cell activation, and anti-inflammatory cytokine induction. Reintroduction of this bacterium also alleviated dextran sodium sulfate-induced colitis. These findings highlight the preclinical functional potential of this Lachnospiraceae bacterium in mitigating low-fiber diets-induced dysfunction in mammals.
Additional Links: PMID-42016568
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@article {pmid42016568,
year = {2026},
author = {Liu, L and Xu, C and Liu, Y and Yang, J and Ye, Y and Yao, Z and Lin, D and Qiu, H and Ruan, D and Qiu, Y and Wang, S and Lin, M and Zhang, Z and Huang, S and Meng, F and Zheng, E and Cai, G and Wu, Z and Wu, JJ},
title = {Restoring low-fiber diets-induced Lachnospiraceae bacterium loss partially recovers fiber digestion and immune function in mammals.},
journal = {Current research in food science},
volume = {12},
number = {},
pages = {101401},
pmid = {42016568},
issn = {2665-9271},
abstract = {Mammals rely on their gut microbiota to degrade cellulose, the major component of dietary fiber. Westernized populations harbor a depleted microbiome with reduced fiber-digesting capacity and impaired immune regulation due to prolonged consumption of low-fiber diets. Comparable patterns are evident in other mammals, including Western commercial pigs raised on high-energy, low-fiber diets, exhibiting reduced diversity and abundance of fiber-degrading bacteria. In contrast, semi-free-ranging Chinese indigenous pigs consuming fiber-rich diets retain a more diverse and functionally resilient microbiota, reflecting divergent trajectories of host-microbiota co-evolution. However, the specific cellulose-degrading species lost and strategies to restore these functions remain unclear in mammals. By analyzing 473 human stool metagenomes spanning non-westernized and westernized diets, together with 251 fecal 16S rRNA datasets and 95 metagenomes from Western commercial pigs, Chinese indigenous pigs, and their crossbred progeny, we identified the Lachnospiraceae bacterium as a key symbiont enriched in non-westernized guts. This bacterium possesses an extensive Carbohydrate-Active Enzymes repertoire conferring strong fiber-degrading capacity. Notably, low-fiber diets leave a genetic signature on this keystone gut symbiont, which cannot be reversed by short-term dietary interventions alone. Reintroduction of Lachnospiraceae bacterium to germ-free mice improved feed efficiency and increased acetic acid production. Intestinal transcriptomics and peripheral blood flow cytometry revealed that it activates a broad adaptive immune response, promoting CD4[+] T cell accumulation, B cell activation, and anti-inflammatory cytokine induction. Reintroduction of this bacterium also alleviated dextran sodium sulfate-induced colitis. These findings highlight the preclinical functional potential of this Lachnospiraceae bacterium in mitigating low-fiber diets-induced dysfunction in mammals.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Investigating the role of bacterial raw milk community members in chlorate reduction.
Access microbiology, 8(4):.
Chlorine-based detergents, used in the dairy industry for cleaning, often degrade into chlorate, contaminating milk and dairy products. Consumption of chlorate has been linked to thyroid dysfunction in adults and impaired neurological development in infants. Despite the ban on chlorine-based detergents in Ireland since 2021, chlorate contamination remains a problem in the dairy supply chain. A recent study identified chlorate-reducing bacteria naturally present in raw milk, highlighting their potential for mitigating chlorate. In this study, shotgun metagenomic sequencing was applied to determine the effects of chlorate concentration and incubation conditions on the raw milk microbiome, specifically focusing on chlorate-reducing bacteria within the community. Chlorate-spiked milk samples from different farms showed reductions in chlorate levels over time, from day 10 onwards when stored at 4 °C and after 24 h when incubated at 25 °C. Pseudomonas and Lactococcus were observed as the most dominant taxa in raw milk samples stored at 4 °C and 25 °C, respectively. High abundances of ydeP and narG genes were observed for 4 °C samples and were attributed to Pseudomonas and various low-abundance genera, respectively. High abundances of the napA gene were noted in 25 °C samples and were attributed to the Lactococcus genus. Overall, this study highlights the presence of naturally occurring chlorate-reducing bacteria as part of the raw milk microbiome and identifies multiple genes linked to various pathways potentially involved in chlorate reduction. Furthermore, incomplete pathways potentially involved in chlorate reduction were found, suggesting metabolic cross-feeding and underscoring the community roles bacteria play in chlorate reduction in raw milk. Additionally, a few previously uncharacterized genes, such as ydeP, belonging to the DMSO reductase gene family were identified at high abundances in samples that showed chlorate reduction, emphasizing the need for further biochemical characterization of these genes to better understand the pathways involved in chlorate reduction in milk.
Additional Links: PMID-42016597
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@article {pmid42016597,
year = {2026},
author = {Srinivas, M and O'Sullivan, O and Cotter, PD and van Sinderen, D and Kenny, JG},
title = {Investigating the role of bacterial raw milk community members in chlorate reduction.},
journal = {Access microbiology},
volume = {8},
number = {4},
pages = {},
pmid = {42016597},
issn = {2516-8290},
abstract = {Chlorine-based detergents, used in the dairy industry for cleaning, often degrade into chlorate, contaminating milk and dairy products. Consumption of chlorate has been linked to thyroid dysfunction in adults and impaired neurological development in infants. Despite the ban on chlorine-based detergents in Ireland since 2021, chlorate contamination remains a problem in the dairy supply chain. A recent study identified chlorate-reducing bacteria naturally present in raw milk, highlighting their potential for mitigating chlorate. In this study, shotgun metagenomic sequencing was applied to determine the effects of chlorate concentration and incubation conditions on the raw milk microbiome, specifically focusing on chlorate-reducing bacteria within the community. Chlorate-spiked milk samples from different farms showed reductions in chlorate levels over time, from day 10 onwards when stored at 4 °C and after 24 h when incubated at 25 °C. Pseudomonas and Lactococcus were observed as the most dominant taxa in raw milk samples stored at 4 °C and 25 °C, respectively. High abundances of ydeP and narG genes were observed for 4 °C samples and were attributed to Pseudomonas and various low-abundance genera, respectively. High abundances of the napA gene were noted in 25 °C samples and were attributed to the Lactococcus genus. Overall, this study highlights the presence of naturally occurring chlorate-reducing bacteria as part of the raw milk microbiome and identifies multiple genes linked to various pathways potentially involved in chlorate reduction. Furthermore, incomplete pathways potentially involved in chlorate reduction were found, suggesting metabolic cross-feeding and underscoring the community roles bacteria play in chlorate reduction in raw milk. Additionally, a few previously uncharacterized genes, such as ydeP, belonging to the DMSO reductase gene family were identified at high abundances in samples that showed chlorate reduction, emphasizing the need for further biochemical characterization of these genes to better understand the pathways involved in chlorate reduction in milk.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Nonsurgical periodontal therapy remodels oral microbiome-metabolome networks and associates with glycemic and inflammatory improvements in type 2 diabetes mellitus with periodontitis: a 6-month longitudinal study.
Journal of oral microbiology, 18(1):2660482.
BACKGROUND: Periodontitis and type 2 diabetes mellitus (T2DM) have a bidirectional relationship, yet how nonsurgical periodontal therapy (NSPT) affects oral microbiome-metabolome interactions in this comorbidity remains unclear.
OBJECTIVE: To longitudinally characterize oral microbiome and metabolome shifts following NSPT in patients with T2DM and periodontitis, and to relate these shifts to periodontal and systemic outcomes.
DESIGN: A total of 42 participants completed the 6-month follow-up. At baseline, they were randomly assigned to NSPT (supragingival scaling plus scaling and root planning, n = 24) or supragingival scaling alone (n = 18). Periodontal parameters, glycated hemoglobin (HbA1c), C-reactive protein (CRP), and glucose/lipid markers were measured at baseline, at 3 and 6 months. Oral samples were collected at each visit for microbiome profiling and metabolomics. Microbe-metabolite-clinical features and associations were explored using correlation analyses and pathway annotation.
RESULTS: NSPT improved periodontal inflammation and was accompanied by favorable changes in systemic inflammation and glucose/lipid indices; HbA1c reduction was more pronounced in those with poorer baseline glycemic control. Both groups showed temporal variability in microbiome and metabolome profiles, but the taxa/metabolites that changed differed between groups. Changes in bleeding index correlated positively with 13-eicosenoic acid, xylose, Rothia aeria, and Alloprevotella tannerae, whereas changes in CRP correlated positively with sorbitol, galactitol, Prevotella nigrescens, and Treponema denticola. Selected microbe-metabolite pairs mapped to glutathione and purine metabolism.
CONCLUSION: NSPT reshapes oral microbe-metabolite networks in T2DM with periodontitis, implicating redox-related pathways that may link periodontal therapy to systemic inflammation and glycemic control.
Additional Links: PMID-42016708
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@article {pmid42016708,
year = {2026},
author = {Diao, J and Li, H and Zheng, S and Niu, J and Yuan, C},
title = {Nonsurgical periodontal therapy remodels oral microbiome-metabolome networks and associates with glycemic and inflammatory improvements in type 2 diabetes mellitus with periodontitis: a 6-month longitudinal study.},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2660482},
pmid = {42016708},
issn = {2000-2297},
abstract = {BACKGROUND: Periodontitis and type 2 diabetes mellitus (T2DM) have a bidirectional relationship, yet how nonsurgical periodontal therapy (NSPT) affects oral microbiome-metabolome interactions in this comorbidity remains unclear.
OBJECTIVE: To longitudinally characterize oral microbiome and metabolome shifts following NSPT in patients with T2DM and periodontitis, and to relate these shifts to periodontal and systemic outcomes.
DESIGN: A total of 42 participants completed the 6-month follow-up. At baseline, they were randomly assigned to NSPT (supragingival scaling plus scaling and root planning, n = 24) or supragingival scaling alone (n = 18). Periodontal parameters, glycated hemoglobin (HbA1c), C-reactive protein (CRP), and glucose/lipid markers were measured at baseline, at 3 and 6 months. Oral samples were collected at each visit for microbiome profiling and metabolomics. Microbe-metabolite-clinical features and associations were explored using correlation analyses and pathway annotation.
RESULTS: NSPT improved periodontal inflammation and was accompanied by favorable changes in systemic inflammation and glucose/lipid indices; HbA1c reduction was more pronounced in those with poorer baseline glycemic control. Both groups showed temporal variability in microbiome and metabolome profiles, but the taxa/metabolites that changed differed between groups. Changes in bleeding index correlated positively with 13-eicosenoic acid, xylose, Rothia aeria, and Alloprevotella tannerae, whereas changes in CRP correlated positively with sorbitol, galactitol, Prevotella nigrescens, and Treponema denticola. Selected microbe-metabolite pairs mapped to glutathione and purine metabolism.
CONCLUSION: NSPT reshapes oral microbe-metabolite networks in T2DM with periodontitis, implicating redox-related pathways that may link periodontal therapy to systemic inflammation and glycemic control.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Development of a multi-targeted metabolomics platform for semi-quantification of faecal metabolites: a proof-of-concept analysis in human faeces.
Microbiome research reports, 5(1):7.
Objectives: Targeted metabolomic analysis of faecal samples has been limited by narrow chemical coverage. Here, we established a multiplexed, triple quadrupole mass spectrometry (TQMS)-based targeted metabolomics workflow. This workflow allows accurate detection and semi-quantification of diverse faecal metabolites and provides a methodological platform for studying host-microbiome metabolic interactions. Methods: Faecal metabolomes from germ-free (GF) mice, ex-germ-free (Ex-GF) mice, and human participants were analysed using TQMS-based targeted metabolomics. The analysis comprised multiple methods targeting amino acids and their derivatives, carbohydrates, short-chain fatty acids, bile acids, lipid mediators, and phospholipids. Results: In total, 607 low-molecular-weight metabolites in 44 chemical categories were detected and semi-quantified. Faecal metabolomes of GF and Ex-GF mice were analysed, uncovering 341 intestinal microbiome-dependent metabolites. A proof-of-concept analysis using faecal samples from five patients with colorectal cancer demonstrated the successful application of this platform to human clinical material, highlighting its strong potential for future disease-oriented metabolomic investigations. Conclusion: We developed a multi-targeted faecal metabolomics platform that substantially expands the chemical space accessible to targeted analysis. This workflow provides a methodological foundation for future large-scale and translational studies.
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@article {pmid42016721,
year = {2026},
author = {Ikuta, K and Kunisawa, A and Dekio, I and Ito, A and Wang, Q and Kawamura, K and Yamada, M and Nakamura, S and Hayakawa, Y and Higurashi, T and Iida, J and Fukusaki, E and Suzuki, T and Matsumoto, M},
title = {Development of a multi-targeted metabolomics platform for semi-quantification of faecal metabolites: a proof-of-concept analysis in human faeces.},
journal = {Microbiome research reports},
volume = {5},
number = {1},
pages = {7},
pmid = {42016721},
issn = {2771-5965},
abstract = {Objectives: Targeted metabolomic analysis of faecal samples has been limited by narrow chemical coverage. Here, we established a multiplexed, triple quadrupole mass spectrometry (TQMS)-based targeted metabolomics workflow. This workflow allows accurate detection and semi-quantification of diverse faecal metabolites and provides a methodological platform for studying host-microbiome metabolic interactions. Methods: Faecal metabolomes from germ-free (GF) mice, ex-germ-free (Ex-GF) mice, and human participants were analysed using TQMS-based targeted metabolomics. The analysis comprised multiple methods targeting amino acids and their derivatives, carbohydrates, short-chain fatty acids, bile acids, lipid mediators, and phospholipids. Results: In total, 607 low-molecular-weight metabolites in 44 chemical categories were detected and semi-quantified. Faecal metabolomes of GF and Ex-GF mice were analysed, uncovering 341 intestinal microbiome-dependent metabolites. A proof-of-concept analysis using faecal samples from five patients with colorectal cancer demonstrated the successful application of this platform to human clinical material, highlighting its strong potential for future disease-oriented metabolomic investigations. Conclusion: We developed a multi-targeted faecal metabolomics platform that substantially expands the chemical space accessible to targeted analysis. This workflow provides a methodological foundation for future large-scale and translational studies.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Bacterial clusters are associated with the risk of severe disease progression in inflammatory bowel disease irrespective of conventional disease categories.
Microbiome research reports, 5(1):4.
Background: Inflammatory bowel diseases (IBDs) are complex conditions marked by chronic inflammation in the gastrointestinal tract. Traditional classification separates IBD into Crohn's disease and ulcerative colitis, but this division may not fully capture disease heterogeneity. Here, we examine whether microbiome-driven subtyping can describe novel clinical IBD phenotypes. To achieve this, we applied unsupervised clustering to fecal microbiota profiles from the population-based Inflammatory Bowel Disease in South-Eastern Norway III (IBSEN III) cohort. Methods: A Gaussian Mixture Model (GMM) was used to cluster participants with IBD based on microbiome composition and examine associations between clusters and clinical outcomes, including inflammatory markers and disease severity during the first year after inclusion. Results: Three microbiome-based clusters were identified: CLO (dominated by Clostridia UCG-014), ALF (Agathobacter, Lachnoclostridium, and Faecalibacterium), and RUM (Ruminococcus gnavus). Participants in the RUM cluster had a higher risk of future severe disease than those in the CLO cluster, even among participants with remission-to-mild disease at inclusion (21% vs. 6%, P < 0.00001). This association could not be explained by antibiotic use or baseline disease severity. Cluster membership alone performed comparably to fecal calprotectin in distinguishing severe disease, and a combined model significantly improved accuracy (P < 0.0001). Conclusion: Our findings demonstrate a connection between microbiome composition and the risk of severe disease development, which is partly independent of inflammation levels at the time of sampling. Microbiome-informed subgrouping could lead to more personalized treatment strategies. Further validation is needed to determine the clinical utility of these clusters.
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@article {pmid42016722,
year = {2026},
author = {Hansen, SH and Bhattacharjee, N and Hu, C and Maseng, MG and Grannö, O and Bang, C and Olbjørn, C and Perminow, G and Valeur, J and Bengtson, MB and Frigstad, SO and Andersen, S and Aabrekk, TB and Detlie, TE and Franke, A and Kristensen, VA and Halfvarson, J and Høivik, ML and Iyer, RK and Hov, J},
title = {Bacterial clusters are associated with the risk of severe disease progression in inflammatory bowel disease irrespective of conventional disease categories.},
journal = {Microbiome research reports},
volume = {5},
number = {1},
pages = {4},
pmid = {42016722},
issn = {2771-5965},
abstract = {Background: Inflammatory bowel diseases (IBDs) are complex conditions marked by chronic inflammation in the gastrointestinal tract. Traditional classification separates IBD into Crohn's disease and ulcerative colitis, but this division may not fully capture disease heterogeneity. Here, we examine whether microbiome-driven subtyping can describe novel clinical IBD phenotypes. To achieve this, we applied unsupervised clustering to fecal microbiota profiles from the population-based Inflammatory Bowel Disease in South-Eastern Norway III (IBSEN III) cohort. Methods: A Gaussian Mixture Model (GMM) was used to cluster participants with IBD based on microbiome composition and examine associations between clusters and clinical outcomes, including inflammatory markers and disease severity during the first year after inclusion. Results: Three microbiome-based clusters were identified: CLO (dominated by Clostridia UCG-014), ALF (Agathobacter, Lachnoclostridium, and Faecalibacterium), and RUM (Ruminococcus gnavus). Participants in the RUM cluster had a higher risk of future severe disease than those in the CLO cluster, even among participants with remission-to-mild disease at inclusion (21% vs. 6%, P < 0.00001). This association could not be explained by antibiotic use or baseline disease severity. Cluster membership alone performed comparably to fecal calprotectin in distinguishing severe disease, and a combined model significantly improved accuracy (P < 0.0001). Conclusion: Our findings demonstrate a connection between microbiome composition and the risk of severe disease development, which is partly independent of inflammation levels at the time of sampling. Microbiome-informed subgrouping could lead to more personalized treatment strategies. Further validation is needed to determine the clinical utility of these clusters.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Multi-modal machine learning and gut microbiome pathway analysis for Alzheimer's risk prediction.
Alzheimer's & dementia (Amsterdam, Netherlands), 18:e70340.
INTRODUCTION: Early Alzheimer's disease (AD) risk assessment requires accessible alternatives to invasive biomarkers. We developed a multi-modal machine learning framework using questionnaire metadata from participants with concurrent microbiome sequencing data.
METHODS: We analyzed 9832 participants with 120 metadata features across five categories (demographic, dietary, lifestyle, nutritional, medical). Features were selected via Pearson correlation and chi-squared tests. Four algorithms were trained using 10-fold cross-validation with synthetic minority oversampling technique (SMOTE), validated on 1967 samples. The 16S rRNA sequencing data from the same cohort with 2000 samples enabled microbiome composition analysis.
RESULTS: Medical history (area under the curve [AUC] = 0.871) and dietary patterns (AUC = 0.874) achieved best performance, outperforming demographic (0.795), lifestyle (0.660), and nutritional (0.569) domains (p < 0.001). Microbiome analysis revealed dysbiosis markers (Prevotella/Bacteroides ratio: 1.921) linking dietary factors to potential neuroinflammatory pathways.
DISCUSSION: These findings support non-invasive, multi-modal screening combining medical and dietary evaluation for AD risk stratification, with preliminary microbiome evidence suggesting gut-brain axis dysbiosis as a mechanistic pathway warranting validation in larger cohorts.
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@article {pmid42016780,
year = {2026},
author = {Jabeen, T and Karimi, F and Zomorrodi, AR and Khalilpour, K},
title = {Multi-modal machine learning and gut microbiome pathway analysis for Alzheimer's risk prediction.},
journal = {Alzheimer's & dementia (Amsterdam, Netherlands)},
volume = {18},
number = {},
pages = {e70340},
pmid = {42016780},
issn = {2352-8729},
abstract = {INTRODUCTION: Early Alzheimer's disease (AD) risk assessment requires accessible alternatives to invasive biomarkers. We developed a multi-modal machine learning framework using questionnaire metadata from participants with concurrent microbiome sequencing data.
METHODS: We analyzed 9832 participants with 120 metadata features across five categories (demographic, dietary, lifestyle, nutritional, medical). Features were selected via Pearson correlation and chi-squared tests. Four algorithms were trained using 10-fold cross-validation with synthetic minority oversampling technique (SMOTE), validated on 1967 samples. The 16S rRNA sequencing data from the same cohort with 2000 samples enabled microbiome composition analysis.
RESULTS: Medical history (area under the curve [AUC] = 0.871) and dietary patterns (AUC = 0.874) achieved best performance, outperforming demographic (0.795), lifestyle (0.660), and nutritional (0.569) domains (p < 0.001). Microbiome analysis revealed dysbiosis markers (Prevotella/Bacteroides ratio: 1.921) linking dietary factors to potential neuroinflammatory pathways.
DISCUSSION: These findings support non-invasive, multi-modal screening combining medical and dietary evaluation for AD risk stratification, with preliminary microbiome evidence suggesting gut-brain axis dysbiosis as a mechanistic pathway warranting validation in larger cohorts.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Lipid stress evolved, microbiome-based probiotics reduce lipid uptake in mice.
Bioengineering & translational medicine, 11(2):e70122.
Controlling the molecular transport of nutrients through the gut is an attractive strategy to modulate host metabolism. Herein, a technique of stress-based evolution of an individual's own microbiota to enhance lipid metabolism is presented, which is based on sequential culture of these bacteria in higher concentrations of lipids. Using this technique, a probiotic formulation of bacterial colonies that exhibit increased lipid metabolism was generated from oral microbiota samples from mice, canine, and human sources. Mice fed a high-fat diet (HFD) and administered lipid stress evolved (LSE) probiotics excreted increased lipids in stool and reduced triglyceride transport into the blood by three-fold till 3 h post-oral gavage of soybean oil, as compared to controls. In addition, these enhanced probiotics prevented weight gain in mice fed a HFD five-fold better than controls and induced weight loss in mice with diet change three-fold faster than diet change alone. In these mice, there was a marked change in appearance with a more healthy, less oily coat. Controlled metabolic cage experiments demonstrated that the total movement, food intake, and water intake were not significantly different between mice receiving LSE probiotic versus a control probiotic formulation, suggesting that important health measures are unchanged with LSE probiotic administration. Overall, this facile stress-based culture technique can be utilized to modulate bacterial metabolism and applied to different industrial processes of probiotic generation and to affect different disease outcomes such as obesity.
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@article {pmid42016853,
year = {2026},
author = {Acharya, AP and Borrelli, MA and Jurczak, MJ and Krakoff, J and Little, SR},
title = {Lipid stress evolved, microbiome-based probiotics reduce lipid uptake in mice.},
journal = {Bioengineering & translational medicine},
volume = {11},
number = {2},
pages = {e70122},
pmid = {42016853},
issn = {2380-6761},
abstract = {Controlling the molecular transport of nutrients through the gut is an attractive strategy to modulate host metabolism. Herein, a technique of stress-based evolution of an individual's own microbiota to enhance lipid metabolism is presented, which is based on sequential culture of these bacteria in higher concentrations of lipids. Using this technique, a probiotic formulation of bacterial colonies that exhibit increased lipid metabolism was generated from oral microbiota samples from mice, canine, and human sources. Mice fed a high-fat diet (HFD) and administered lipid stress evolved (LSE) probiotics excreted increased lipids in stool and reduced triglyceride transport into the blood by three-fold till 3 h post-oral gavage of soybean oil, as compared to controls. In addition, these enhanced probiotics prevented weight gain in mice fed a HFD five-fold better than controls and induced weight loss in mice with diet change three-fold faster than diet change alone. In these mice, there was a marked change in appearance with a more healthy, less oily coat. Controlled metabolic cage experiments demonstrated that the total movement, food intake, and water intake were not significantly different between mice receiving LSE probiotic versus a control probiotic formulation, suggesting that important health measures are unchanged with LSE probiotic administration. Overall, this facile stress-based culture technique can be utilized to modulate bacterial metabolism and applied to different industrial processes of probiotic generation and to affect different disease outcomes such as obesity.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Embryonic sheep placenta alleviates muscle-fat wasting symptoms and improves gut microbiome dysbiosis in cachexia mice.
Biochemistry and biophysics reports, 46:102590.
Cachexia is a multifactorial wasting syndrome characterized by muscle-fat depletion, accompanied by significant gut microbiome disturbances. Embryonic sheep placenta (ESP), a functional food known to modulate immunity and gut microbiome, represents a potential intervention substance. By in vitro and in vivo experiments combined with multi-omics analysis, this study provides experimental evidence for the effect of ESP on cachexia. These studies have found that ESP and its extract alleviate cachexia by increasing 91.80% (P < 0.0001) muscle tube diameter, 19.56% (P < 0.01) muscle cross-sectional area and 37.56% (P < 0.05) fat mass. Western blot shows that ESP downregulates the expression of TRIM63 and inhibits the expression of the HSL protein in the AMPK signaling pathway. Integrated multi-omics analysis suggests that ESP reshapes the gut microbiota structure of cachexia mice, restores their gut homeostasis and improves energy metabolism pathways. In conclusion, ESP plays a protective role in cachexia mice by alleviating the symptoms of muscle-fat atrophy, maintaining gut homeostasis and improving energy metabolism pathway.
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@article {pmid42016931,
year = {2026},
author = {Sun, M and Tu, L and Zhou, Z and Ma, Y and Zhang, H and Jiang, X and Tu, H and Lu, J and Niu, Y and Yue, Y and Yang, R and Chen, M and Fang, H and Si, Z and Chen, P},
title = {Embryonic sheep placenta alleviates muscle-fat wasting symptoms and improves gut microbiome dysbiosis in cachexia mice.},
journal = {Biochemistry and biophysics reports},
volume = {46},
number = {},
pages = {102590},
pmid = {42016931},
issn = {2405-5808},
abstract = {Cachexia is a multifactorial wasting syndrome characterized by muscle-fat depletion, accompanied by significant gut microbiome disturbances. Embryonic sheep placenta (ESP), a functional food known to modulate immunity and gut microbiome, represents a potential intervention substance. By in vitro and in vivo experiments combined with multi-omics analysis, this study provides experimental evidence for the effect of ESP on cachexia. These studies have found that ESP and its extract alleviate cachexia by increasing 91.80% (P < 0.0001) muscle tube diameter, 19.56% (P < 0.01) muscle cross-sectional area and 37.56% (P < 0.05) fat mass. Western blot shows that ESP downregulates the expression of TRIM63 and inhibits the expression of the HSL protein in the AMPK signaling pathway. Integrated multi-omics analysis suggests that ESP reshapes the gut microbiota structure of cachexia mice, restores their gut homeostasis and improves energy metabolism pathways. In conclusion, ESP plays a protective role in cachexia mice by alleviating the symptoms of muscle-fat atrophy, maintaining gut homeostasis and improving energy metabolism pathway.},
}
RevDate: 2026-04-23
Inorganic arsenic exposure and modifying factors: a systematic evidence map.
Human and ecological risk assessment : HERA, 31(9-10):1525-1542.
Evidence maps employing systematic review screening tools have been used for identifying and categorizing chemical-specific literature that may be potentially relevant to scientific assessment. Inorganic arsenic (iAs), naturally distributed throughout the Earth's crust, is found in water, food, soil, and air. The epidemiologic evidence shows that iAs is associated with cancer and noncancer human health outcomes. Increased susceptibility to iAs-related disease is associated both with intrinsic and extrinsic factors. Our objective was to explore the use and feasibility of the systematic evidence map (SEM) approach to provide a clearer picture of the available literature on modifying factors that may alter the relationship between iAs exposure and health effects. A literature search (2014-2022) was conducted using PubMed, Web of Science, and Toxnet to identify studies with modifying factors of iAs health effects defined in Populations, Exposures, Comparators, Outcomes (PECO) criteria. Where applicable, health effects were also categorized. The literature search identified 584 studies with modifying factors that met the PECO criteria. Studies on the following modifying factors were identified: alcohol consumption (n= 8), chemical co-exposure (n= 104), genetic polymorphisms (n= 172), lifestages (n=228), microbiome (n=6), nutritional deficiencies (n=150), pre-existing conditions (n= 9), sex (n=65), smoking (n= 45), and other (e.g., arsenic metabolism, epigenetics, UV/sun exposure, DNA damage/repair, coffee consumption) (n=227). The SEM method was effectively utilized to identify studies on modifying factors for inorganic arsenic.
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@article {pmid42017169,
year = {2025},
author = {Lee, JS and Fleming, D and Vulimiri, SV and Powers, M and Davis, JA and Gift, JS and Druwe, IL and Jones, R and Keshava, C and Toledo, M and Cote, I and Persad, AS},
title = {Inorganic arsenic exposure and modifying factors: a systematic evidence map.},
journal = {Human and ecological risk assessment : HERA},
volume = {31},
number = {9-10},
pages = {1525-1542},
pmid = {42017169},
issn = {1080-7039},
support = {EPA999999/ImEPA/Intramural EPA/United States ; },
abstract = {Evidence maps employing systematic review screening tools have been used for identifying and categorizing chemical-specific literature that may be potentially relevant to scientific assessment. Inorganic arsenic (iAs), naturally distributed throughout the Earth's crust, is found in water, food, soil, and air. The epidemiologic evidence shows that iAs is associated with cancer and noncancer human health outcomes. Increased susceptibility to iAs-related disease is associated both with intrinsic and extrinsic factors. Our objective was to explore the use and feasibility of the systematic evidence map (SEM) approach to provide a clearer picture of the available literature on modifying factors that may alter the relationship between iAs exposure and health effects. A literature search (2014-2022) was conducted using PubMed, Web of Science, and Toxnet to identify studies with modifying factors of iAs health effects defined in Populations, Exposures, Comparators, Outcomes (PECO) criteria. Where applicable, health effects were also categorized. The literature search identified 584 studies with modifying factors that met the PECO criteria. Studies on the following modifying factors were identified: alcohol consumption (n= 8), chemical co-exposure (n= 104), genetic polymorphisms (n= 172), lifestages (n=228), microbiome (n=6), nutritional deficiencies (n=150), pre-existing conditions (n= 9), sex (n=65), smoking (n= 45), and other (e.g., arsenic metabolism, epigenetics, UV/sun exposure, DNA damage/repair, coffee consumption) (n=227). The SEM method was effectively utilized to identify studies on modifying factors for inorganic arsenic.},
}
RevDate: 2026-04-22
DNA Methylation Shapes Seed-Borne Microbiome and Proteome Responses During Early Maize-Beneficial Bacteria Interactions.
Plant, cell & environment [Epub ahead of print].
Microorganism and plant interactions are crucial for development and environmental adaptation. Plant growth promoting bacteria enhance agricultural productivity in a sustainable manner, while epigenetic modifications such as DNA methylation regulate gene expression and adaptive responses. The objective of this study is to determine how DNA hypomethylation influences early interactions between maize (Zea mays) and the endophytic diazotrophic bacterium Herbaspirillum seropedicae, particularly regarding plant growth, metabolism, and the root microbiome. Treatment with the hypomethylating agent 5-azacytidine (5-azaC) altered maize root morphology without affecting bacterial growth. Inoculation with H. seropedicae promoted plant growth and bacterial colonisation in root mucilage, with higher accumulation in 5-azaC treated roots. Global methylation analysis showed that bacterial inoculation modulates cytosine methylation in a manner similar to 5-azaC, suggesting a role in epigenetic regulation. Gene expression analysis of DNA methylation machinery confirmed that hypomethylation drives plant-microbe interactions. Root microbiome profiling revealed that 5-azaC disrupted microbial composition, which was partially restored by bacterial inoculation. Proteomic analysis identified 1,818 proteins and highlighted significant changes in metabolic pathways, especially carbon metabolism and the citric acid cycle. These findings demonstrate that DNA hypomethylation combined with bacterial interaction profoundly affects cellular and metabolic processes and provide insights for sustainable agricultural practices through epigenetic and microbial modulation.
Additional Links: PMID-42017455
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PubMed:
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@article {pmid42017455,
year = {2026},
author = {Zocateli, PI and de OlÃmpio, GV and de Almeida, FA and da Rocha, LO and de Sena Martins, DV and Sangi, S and Olivares, FL and de Matos, EM and Siqueira, J and Viccini, LF and da Paschoa, RP and Silveira, V and Grativol, C},
title = {DNA Methylation Shapes Seed-Borne Microbiome and Proteome Responses During Early Maize-Beneficial Bacteria Interactions.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.70552},
pmid = {42017455},
issn = {1365-3040},
support = {//Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro/ ; //Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; 001//Coordenação de Aperfeiçoamento de Pessoal de Nível Superior/ ; PAPIC-2024//Universidade Estadual do Norte Fluminense Darcy Ribeiro/ ; },
abstract = {Microorganism and plant interactions are crucial for development and environmental adaptation. Plant growth promoting bacteria enhance agricultural productivity in a sustainable manner, while epigenetic modifications such as DNA methylation regulate gene expression and adaptive responses. The objective of this study is to determine how DNA hypomethylation influences early interactions between maize (Zea mays) and the endophytic diazotrophic bacterium Herbaspirillum seropedicae, particularly regarding plant growth, metabolism, and the root microbiome. Treatment with the hypomethylating agent 5-azacytidine (5-azaC) altered maize root morphology without affecting bacterial growth. Inoculation with H. seropedicae promoted plant growth and bacterial colonisation in root mucilage, with higher accumulation in 5-azaC treated roots. Global methylation analysis showed that bacterial inoculation modulates cytosine methylation in a manner similar to 5-azaC, suggesting a role in epigenetic regulation. Gene expression analysis of DNA methylation machinery confirmed that hypomethylation drives plant-microbe interactions. Root microbiome profiling revealed that 5-azaC disrupted microbial composition, which was partially restored by bacterial inoculation. Proteomic analysis identified 1,818 proteins and highlighted significant changes in metabolic pathways, especially carbon metabolism and the citric acid cycle. These findings demonstrate that DNA hypomethylation combined with bacterial interaction profoundly affects cellular and metabolic processes and provide insights for sustainable agricultural practices through epigenetic and microbial modulation.},
}
RevDate: 2026-04-22
Systematic evaluation of TCGA tumor microbiota reveals context-dependent reliability.
mSystems [Epub ahead of print].
UNLABELLED: Microbial profiles from The Cancer Genome Atlas (TCGA) are widely used to study the tumor microbiota, a key component of the cancer ecosystem, yet their reliability remains unclear. Here, we systematically benchmarked two leading TCGA microbial profiles (TMPs) to define their consistency, accuracy, and reliability in host-microbe association studies across 24 cancer types, with a primary focus on the bacterial component. We found that while the TMPs showed substantial agreement in microbial composition, their accuracy in detecting known oncomicrobes was variable, ranging from excellent for human papillomavirus (HPV) to poor for Helicobacter pylori. The concordance of downstream host-microbe associations was moderate for gene expression but nearly absent for methylation and protein data. Our permutation-based framework revealed that while most individual associations were statistically reliable, those involving cell type composition and patient survival were statistically spurious. To empower future research with these insights, we introduced Multi-Omics and Microbiome Associations in Cancer 2 (MOMAC2), an interactive web portal that stratifies all associations by confidence level. We demonstrated its utility by using high-confidence associations to confirm HPV-driven methylation-gene expression axes and guide a novel experimental investigation. Co-culture with Streptococcus anginosus not only validated its predicted gene expression changes in oral cancer cells but also revealed a significant promotion of cancer cell proliferation and migration. Our study provides a rigorous framework for interpreting TCGA's tumor microbiome and highlights that these data require careful, multi-layered validation to yield robust biological insights.
IMPORTANCE: Bacteria living inside tumors can influence how cancer grows and responds to treatment, but the field has been hampered by controversy over the reliability of the data. Our study provides a much-needed road map for researchers. We rigorously tested the massive Cancer Genome Atlas data set and developed a statistical framework to separate true biological signals from random noise. We discovered that many widely reported links are statistically unreliable and likely false leads. Importantly, our framework successfully pinpoints trustworthy signals. We used it to identify a specific bacterium, Streptococcus anginosus, and proved in the lab that it makes oral cancer cells grow faster and spread. Our publicly available Multi-Omics and Microbiome Associations in Cancer 2 (MOMAC2) web portal now allows scientists to use these reliability-graded findings to accelerate robust cancer microbiome research.
Additional Links: PMID-42017663
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PubMed:
Citation:
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@article {pmid42017663,
year = {2026},
author = {Ma, C and Su, C and Li, J and Wang, J and Liao, J and Cheng, L and Qu, J and Zhang, G and Jiang, J and Shuai, S},
title = {Systematic evaluation of TCGA tumor microbiota reveals context-dependent reliability.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0018026},
doi = {10.1128/msystems.00180-26},
pmid = {42017663},
issn = {2379-5077},
abstract = {UNLABELLED: Microbial profiles from The Cancer Genome Atlas (TCGA) are widely used to study the tumor microbiota, a key component of the cancer ecosystem, yet their reliability remains unclear. Here, we systematically benchmarked two leading TCGA microbial profiles (TMPs) to define their consistency, accuracy, and reliability in host-microbe association studies across 24 cancer types, with a primary focus on the bacterial component. We found that while the TMPs showed substantial agreement in microbial composition, their accuracy in detecting known oncomicrobes was variable, ranging from excellent for human papillomavirus (HPV) to poor for Helicobacter pylori. The concordance of downstream host-microbe associations was moderate for gene expression but nearly absent for methylation and protein data. Our permutation-based framework revealed that while most individual associations were statistically reliable, those involving cell type composition and patient survival were statistically spurious. To empower future research with these insights, we introduced Multi-Omics and Microbiome Associations in Cancer 2 (MOMAC2), an interactive web portal that stratifies all associations by confidence level. We demonstrated its utility by using high-confidence associations to confirm HPV-driven methylation-gene expression axes and guide a novel experimental investigation. Co-culture with Streptococcus anginosus not only validated its predicted gene expression changes in oral cancer cells but also revealed a significant promotion of cancer cell proliferation and migration. Our study provides a rigorous framework for interpreting TCGA's tumor microbiome and highlights that these data require careful, multi-layered validation to yield robust biological insights.
IMPORTANCE: Bacteria living inside tumors can influence how cancer grows and responds to treatment, but the field has been hampered by controversy over the reliability of the data. Our study provides a much-needed road map for researchers. We rigorously tested the massive Cancer Genome Atlas data set and developed a statistical framework to separate true biological signals from random noise. We discovered that many widely reported links are statistically unreliable and likely false leads. Importantly, our framework successfully pinpoints trustworthy signals. We used it to identify a specific bacterium, Streptococcus anginosus, and proved in the lab that it makes oral cancer cells grow faster and spread. Our publicly available Multi-Omics and Microbiome Associations in Cancer 2 (MOMAC2) web portal now allows scientists to use these reliability-graded findings to accelerate robust cancer microbiome research.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Cosmetics and their role in modulating skin microbiome health. A narrative review.
JPMA. The Journal of the Pakistan Medical Association, 76(3):417-423.
The skin microbiome plays a vital role in immune regulation, barrier function, and protection against pathogens. Cosmetics, traditionally used for aesthetic purposes, also influence skin microbiomes. Depending on their formulation, they can support microbial balance through probiotics, prebiotics and postbiotics, or disrupt it, leading to dysbiosis and conditions such as eczema and acne. Advances in nanotechnology have further altered cosmetic efficacy and microbial interactions. The current narrative review was planned to highlight the dual role of cosmetics in modulating skin microbiome health, to emphasise the need for regulatory oversight, and to explore strategies for developing safe, microbiome friendly skincare products.
Additional Links: PMID-42017723
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PubMed:
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@article {pmid42017723,
year = {2026},
author = {Fatima, M and Omer, H and Nadeem, N and Imtiaz, S},
title = {Cosmetics and their role in modulating skin microbiome health. A narrative review.},
journal = {JPMA. The Journal of the Pakistan Medical Association},
volume = {76},
number = {3},
pages = {417-423},
doi = {10.47391/JPMA.30352},
pmid = {42017723},
issn = {0030-9982},
mesh = {Humans ; *Cosmetics/pharmacology/adverse effects ; *Microbiota/drug effects ; *Skin/microbiology/drug effects ; Probiotics ; Prebiotics ; Dysbiosis ; Skin Microbiome ; },
abstract = {The skin microbiome plays a vital role in immune regulation, barrier function, and protection against pathogens. Cosmetics, traditionally used for aesthetic purposes, also influence skin microbiomes. Depending on their formulation, they can support microbial balance through probiotics, prebiotics and postbiotics, or disrupt it, leading to dysbiosis and conditions such as eczema and acne. Advances in nanotechnology have further altered cosmetic efficacy and microbial interactions. The current narrative review was planned to highlight the dual role of cosmetics in modulating skin microbiome health, to emphasise the need for regulatory oversight, and to explore strategies for developing safe, microbiome friendly skincare products.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Cosmetics/pharmacology/adverse effects
*Microbiota/drug effects
*Skin/microbiology/drug effects
Probiotics
Prebiotics
Dysbiosis
Skin Microbiome
RevDate: 2026-04-22
Inflammatory bowel disease and Primary sclerosing cholangitis: immunological links and clinical outlook.
Expert review of clinical immunology [Epub ahead of print].
INTRODUCTION: Primary sclerosing cholangitis (PSC) represents a progressive fibroinflammatory cholangiopathy intricately linked to inflammatory bowel disease (IBD), forming a distinctive overlap syndrome driven by immune dysregulation and gut - liver axis disruption and characterized by a markedly increased risk of colorectal and hepatobiliary cancers.
AREAS COVERED: This review summarizes current understanding of the immunopathogenesis and clinical spectrum of PSC - IBD. Key mechanisms include aberrant lymphocyte homing through the α4β7/MAdCAM-1 axis, shared genetic susceptibility loci, alterations in bile acid metabolism, and gut microbial dysbiosis. The clinical course and malignancy risk of PSC - IBD are contrasted with those of isolated PSC and IBD, and surveillance strategies are discussed. Therapeutic approaches under investigation, such as advanced therapies and microbiome-targeted interventions including oral vancomycin, are critically appraised based on recent translational and clinical studies.
EXPERT OPINION: PSC - IBD demands multidisciplinary, risk-stratified management and intensive cancer surveillance. Although no medical therapy currently halts disease progression, novel agents modulating immune and microbial pathways represent promising avenues. In the future, integration of hepatology, gastroenterology, and immunology within a precision-medicine framework is expected to reshape disease stratification and therapeutic decision-making for this complex overlap syndrome.
Additional Links: PMID-42017751
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PubMed:
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@article {pmid42017751,
year = {2026},
author = {Massironi, S and Fanizzi, F and Invernizzi, F and Furfaro, F and Ciocca, L and Arcari, I and Allocca, M and Peyrin-Biroulet, L and Danese, S},
title = {Inflammatory bowel disease and Primary sclerosing cholangitis: immunological links and clinical outlook.},
journal = {Expert review of clinical immunology},
volume = {},
number = {},
pages = {},
doi = {10.1080/1744666X.2026.2664055},
pmid = {42017751},
issn = {1744-8409},
abstract = {INTRODUCTION: Primary sclerosing cholangitis (PSC) represents a progressive fibroinflammatory cholangiopathy intricately linked to inflammatory bowel disease (IBD), forming a distinctive overlap syndrome driven by immune dysregulation and gut - liver axis disruption and characterized by a markedly increased risk of colorectal and hepatobiliary cancers.
AREAS COVERED: This review summarizes current understanding of the immunopathogenesis and clinical spectrum of PSC - IBD. Key mechanisms include aberrant lymphocyte homing through the α4β7/MAdCAM-1 axis, shared genetic susceptibility loci, alterations in bile acid metabolism, and gut microbial dysbiosis. The clinical course and malignancy risk of PSC - IBD are contrasted with those of isolated PSC and IBD, and surveillance strategies are discussed. Therapeutic approaches under investigation, such as advanced therapies and microbiome-targeted interventions including oral vancomycin, are critically appraised based on recent translational and clinical studies.
EXPERT OPINION: PSC - IBD demands multidisciplinary, risk-stratified management and intensive cancer surveillance. Although no medical therapy currently halts disease progression, novel agents modulating immune and microbial pathways represent promising avenues. In the future, integration of hepatology, gastroenterology, and immunology within a precision-medicine framework is expected to reshape disease stratification and therapeutic decision-making for this complex overlap syndrome.},
}
RevDate: 2026-04-22
Conserved glycan-utilization strategies shape Akkermansiaceae success across aquatic and gut ecosystems.
The ISME journal pii:8660835 [Epub ahead of print].
Elucidating interaction mechanisms and substrate specialization is central to understanding bacterial adaptation across ecological niches. Specialized mucin-degrading bacteria of the genus Akkermansia are widely recognized for their beneficial roles in the human gut, yet it remains unclear whether this specialization is unique to the gut or reflects a conserved ecological strategy across different hosts and environments. Here, we show that members of the family Akkermansiaceae share a deeply conserved genetic and mechanistic framework enabling colonization across gut and aquatic ecosystems. Comparative genomics of Akkermansiaceae representatives revealed niche-specific gene repertoires tightly adapted to substrate source and availability. Marine representatives encode distinct combinations of CAZymes and comparatively expanded sulfatase repertoires that enable the degradation of sulfated polysaccharides such as fucoidan, a recalcitrant substrate linked to carbon sequestration. Structural predictions and comparisons identified a conserved molecular system centered on a type IV-like pilus that mediates attachment to complex, fucose-rich glycans. The genes underlying this system are syntenic with the recently described mucin utilization locus in Akkermansia muciniphila, revealing an evolutionary continuity between aquatic and gut lineages. Seawater incubations with fluorescently labeled substrates confirmed fucoidan uptake and degradation by marine Akkermansiaceae. Together, these results reveal a unified glycan-utilization strategy spanning the environmental breadth of Akkermansiaceae and provide a mechanistic framework linking ecological success in marine environments to traits associated with probiotic functions in the human gut.
Additional Links: PMID-42017823
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PubMed:
Citation:
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@article {pmid42017823,
year = {2026},
author = {Wilkie, I and Von Possel, N and Sauma-Sánchez, T and Reintjes, G and Orellana, LH},
title = {Conserved glycan-utilization strategies shape Akkermansiaceae success across aquatic and gut ecosystems.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag096},
pmid = {42017823},
issn = {1751-7370},
abstract = {Elucidating interaction mechanisms and substrate specialization is central to understanding bacterial adaptation across ecological niches. Specialized mucin-degrading bacteria of the genus Akkermansia are widely recognized for their beneficial roles in the human gut, yet it remains unclear whether this specialization is unique to the gut or reflects a conserved ecological strategy across different hosts and environments. Here, we show that members of the family Akkermansiaceae share a deeply conserved genetic and mechanistic framework enabling colonization across gut and aquatic ecosystems. Comparative genomics of Akkermansiaceae representatives revealed niche-specific gene repertoires tightly adapted to substrate source and availability. Marine representatives encode distinct combinations of CAZymes and comparatively expanded sulfatase repertoires that enable the degradation of sulfated polysaccharides such as fucoidan, a recalcitrant substrate linked to carbon sequestration. Structural predictions and comparisons identified a conserved molecular system centered on a type IV-like pilus that mediates attachment to complex, fucose-rich glycans. The genes underlying this system are syntenic with the recently described mucin utilization locus in Akkermansia muciniphila, revealing an evolutionary continuity between aquatic and gut lineages. Seawater incubations with fluorescently labeled substrates confirmed fucoidan uptake and degradation by marine Akkermansiaceae. Together, these results reveal a unified glycan-utilization strategy spanning the environmental breadth of Akkermansiaceae and provide a mechanistic framework linking ecological success in marine environments to traits associated with probiotic functions in the human gut.},
}
RevDate: 2026-04-22
Taxonomy, tissue, and habitat influence mollusc microbial communities.
The ISME journal pii:8660834 [Epub ahead of print].
Microbes play a crucial role in the health, development, and resilience of molluscs, yet the ecological and evolutionary factors shaping their microbial communities remain poorly understood. To uncover the drivers of microbial community composition of molluscs, we conducted a systematic review of 85 studies, including 45 on bivalves from marine and freshwater habitats; 33 on gastropods from marine, freshwater, and terrestrial habitats; and seven on cephalopods. Our synthesis reveals that both intrinsic (e.g., host phylogeny, tissue type) and extrinsic (e.g., environment, geography, and seasonality) factors influence microbial community structure, but the effects are highly taxon- and context-dependent. Although studies of bivalves often emphasize environmental drivers, those of cephalopods more frequently highlight intrinsic host features. Despite growing interest in molluscan microbiomes, we identified significant taxonomic and methodological biases, including a predominant focus on economically important species and gut tissues. We advocate for a broader, integrative approach that includes underrepresented molluscan groups, diverse tissue types, and testing of both intrinsic and extrinsic variables across spatial and temporal gradients. This review highlights the need for standardized, multi-factorial research to better understand and predict microbial community responses to environmental change of one of the most diverse and ecologically important invertebrate phyla.
Additional Links: PMID-42017830
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PubMed:
Citation:
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@article {pmid42017830,
year = {2026},
author = {Vergara-Florez, DC and Duda, TF},
title = {Taxonomy, tissue, and habitat influence mollusc microbial communities.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag092},
pmid = {42017830},
issn = {1751-7370},
abstract = {Microbes play a crucial role in the health, development, and resilience of molluscs, yet the ecological and evolutionary factors shaping their microbial communities remain poorly understood. To uncover the drivers of microbial community composition of molluscs, we conducted a systematic review of 85 studies, including 45 on bivalves from marine and freshwater habitats; 33 on gastropods from marine, freshwater, and terrestrial habitats; and seven on cephalopods. Our synthesis reveals that both intrinsic (e.g., host phylogeny, tissue type) and extrinsic (e.g., environment, geography, and seasonality) factors influence microbial community structure, but the effects are highly taxon- and context-dependent. Although studies of bivalves often emphasize environmental drivers, those of cephalopods more frequently highlight intrinsic host features. Despite growing interest in molluscan microbiomes, we identified significant taxonomic and methodological biases, including a predominant focus on economically important species and gut tissues. We advocate for a broader, integrative approach that includes underrepresented molluscan groups, diverse tissue types, and testing of both intrinsic and extrinsic variables across spatial and temporal gradients. This review highlights the need for standardized, multi-factorial research to better understand and predict microbial community responses to environmental change of one of the most diverse and ecologically important invertebrate phyla.},
}
RevDate: 2026-04-22
Impact of Probiotic-Adjunctive Vonoprazan-Amoxicillin Dual Therapy on Gut Microbiota and Clinical Symptoms in Helicobacter pylori Eradication.
Tissue engineering and regenerative medicine [Epub ahead of print].
BACKGROUND: This study evaluates the impact of Bacillus subtilis dual-strain enteric-coated capsules combined with vonoprazan-amoxicillin (VA) therapy on Helicobacter pylori (Hp) eradication rates, gastrointestinal symptoms, adverse events (AEs), and gut microbiota.
METHODS: 60 Hp-positive adults were enrolled, allocated to probiotic (n = 30) or placebo (n = 30) groups. Both groups received a 14-day VA dual therapy, with the probiotic group additionally receiving a 28-day Bacillus subtilis dual-strain capsule regimen and the placebo group receiving matched placebos. Outcomes included Hp eradication rates (intention-to-treat [ITT]/per-protocol [PP] analyses), Gastrointestinal Symptom Rating Scale (GSRS) scores, AEs, antibiotic susceptibility, and gut microbiota changes (16S rRNA sequencing).
RESULTS: ITT analysis showed identical eradication rates (93.33%) in both groups; PP analysis revealed 96.67% (probiotic) versus 93.33% (placebo). The probiotic group exhibited significantly lower GSRS scores at weeks 4 (T2) and 8 (T3), particularly for diarrhea and acid reflux, with milder AEs (severity score: 5). Probiotic supplementation reduced Hp resistance to metronidazole (26.67% vs. 60.00%) without affecting other antibiotics. Microbiota analysis demonstrated post-eradication reductions in gastric pathogens (e.g., Helicobacter) and increased beneficial bacteria (e.g., Lactobacillus). The probiotic group showed faster restoration of gut α-diversity (higher at T2), enriched butyrate producers (e.g., Blautia, Anaerobutyricum), and decreased opportunistic pathogens (e.g., Klebsiella).
CONCLUSIONS: Although Bacillus subtilis supplementation did not enhance Hp eradication rates, it significantly improved gastrointestinal symptoms, reduced AEs, increased Hp susceptibility to metronidazole, and accelerated microbiota recovery, supporting its role in microbiome modulation during Hp eradication therapy.
Additional Links: PMID-42018226
PubMed:
Citation:
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@article {pmid42018226,
year = {2026},
author = {Yang, Y and Lan, C and Jiang, Z},
title = {Impact of Probiotic-Adjunctive Vonoprazan-Amoxicillin Dual Therapy on Gut Microbiota and Clinical Symptoms in Helicobacter pylori Eradication.},
journal = {Tissue engineering and regenerative medicine},
volume = {},
number = {},
pages = {},
pmid = {42018226},
issn = {2212-5469},
abstract = {BACKGROUND: This study evaluates the impact of Bacillus subtilis dual-strain enteric-coated capsules combined with vonoprazan-amoxicillin (VA) therapy on Helicobacter pylori (Hp) eradication rates, gastrointestinal symptoms, adverse events (AEs), and gut microbiota.
METHODS: 60 Hp-positive adults were enrolled, allocated to probiotic (n = 30) or placebo (n = 30) groups. Both groups received a 14-day VA dual therapy, with the probiotic group additionally receiving a 28-day Bacillus subtilis dual-strain capsule regimen and the placebo group receiving matched placebos. Outcomes included Hp eradication rates (intention-to-treat [ITT]/per-protocol [PP] analyses), Gastrointestinal Symptom Rating Scale (GSRS) scores, AEs, antibiotic susceptibility, and gut microbiota changes (16S rRNA sequencing).
RESULTS: ITT analysis showed identical eradication rates (93.33%) in both groups; PP analysis revealed 96.67% (probiotic) versus 93.33% (placebo). The probiotic group exhibited significantly lower GSRS scores at weeks 4 (T2) and 8 (T3), particularly for diarrhea and acid reflux, with milder AEs (severity score: 5). Probiotic supplementation reduced Hp resistance to metronidazole (26.67% vs. 60.00%) without affecting other antibiotics. Microbiota analysis demonstrated post-eradication reductions in gastric pathogens (e.g., Helicobacter) and increased beneficial bacteria (e.g., Lactobacillus). The probiotic group showed faster restoration of gut α-diversity (higher at T2), enriched butyrate producers (e.g., Blautia, Anaerobutyricum), and decreased opportunistic pathogens (e.g., Klebsiella).
CONCLUSIONS: Although Bacillus subtilis supplementation did not enhance Hp eradication rates, it significantly improved gastrointestinal symptoms, reduced AEs, increased Hp susceptibility to metronidazole, and accelerated microbiota recovery, supporting its role in microbiome modulation during Hp eradication therapy.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Interspecies interaction controls Escherichia coli growth in human gut microbiome samples.
Proceedings of the National Academy of Sciences of the United States of America, 123(17):e2527793123.
Gut microbial community composition varies from one person to another. Potentially, this means the ecological interactions experienced by individual strains or species also vary among microbiomes of different people. However, testing this directly in human microbiomes and identifying ecological drivers involved are challenging. Here, we use replicated anaerobic microcosms to quantify variability of population growth for a key commensal species among microbiome samples from different individuals and to identify underlying intra- and interspecific interactions. In a reciprocal transplant experiment, both absolute and relative growth performance of different Escherichia coli strains varied among gut microbiome samples from healthy individuals. This was partly explained by intraspecific competition: growth performance of individual E. coli strains was associated with displacement of resident conspecifics. However, the determinants of E. coli growth varied among samples. In one microbiome sample with a distinctive taxonomic composition, culture acidification by resident microbes impaired growth of all E. coli strains. We identified a strain of Clostridium butyricum contributing to this effect and showed that transferring it into other microbiomes predictably altered pH, fermentation product profiles (butyrate accumulation and acetate/lactate depletion), and population growth of other species including E. coli, thereby reshaping overall taxonomic composition. Our results suggest natural interindividual gut microbiome variation translates to variable ecological interactions with incoming bacteria, but these dynamics can be manipulated by a generalizable interspecies interaction.
Additional Links: PMID-42018414
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PubMed:
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@article {pmid42018414,
year = {2026},
author = {Boumasmoud, M and León-Sampedro, R and Beusch, V and Benz, F and Arnoldini, M and Hall, AR},
title = {Interspecies interaction controls Escherichia coli growth in human gut microbiome samples.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {17},
pages = {e2527793123},
doi = {10.1073/pnas.2527793123},
pmid = {42018414},
issn = {1091-6490},
support = {310030_192428//Swiss NSF/ ; },
mesh = {Humans ; *Escherichia coli/growth & development ; *Gastrointestinal Microbiome/physiology ; Feces/microbiology ; },
abstract = {Gut microbial community composition varies from one person to another. Potentially, this means the ecological interactions experienced by individual strains or species also vary among microbiomes of different people. However, testing this directly in human microbiomes and identifying ecological drivers involved are challenging. Here, we use replicated anaerobic microcosms to quantify variability of population growth for a key commensal species among microbiome samples from different individuals and to identify underlying intra- and interspecific interactions. In a reciprocal transplant experiment, both absolute and relative growth performance of different Escherichia coli strains varied among gut microbiome samples from healthy individuals. This was partly explained by intraspecific competition: growth performance of individual E. coli strains was associated with displacement of resident conspecifics. However, the determinants of E. coli growth varied among samples. In one microbiome sample with a distinctive taxonomic composition, culture acidification by resident microbes impaired growth of all E. coli strains. We identified a strain of Clostridium butyricum contributing to this effect and showed that transferring it into other microbiomes predictably altered pH, fermentation product profiles (butyrate accumulation and acetate/lactate depletion), and population growth of other species including E. coli, thereby reshaping overall taxonomic composition. Our results suggest natural interindividual gut microbiome variation translates to variable ecological interactions with incoming bacteria, but these dynamics can be manipulated by a generalizable interspecies interaction.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Escherichia coli/growth & development
*Gastrointestinal Microbiome/physiology
Feces/microbiology
RevDate: 2026-04-22
Extensive individual and microorganism-specific circadian oscillations of the upper respiratory tract microbiome.
Cell reports, 45(5):117284 pii:S2211-1247(26)00362-1 [Epub ahead of print].
The upper respiratory tract microbiome (URM) influences host susceptibility and respiratory disease outcomes, but its normal temporal dynamics remain poorly understood. We conducted temporal metagenomic profiling of the URM by collecting oropharyngeal swabs from 22 healthy adults at 4-h intervals over 48 h. We identify significant 24-h cyclic variations in microbial composition and biomass, with two predominant oscillation patterns: "evening-peak" and "morning-peak" patterns. Temporal variation introduces substantial shifts in microbial profiles, leading to false positives in differential analyses. Microbial rhythmicity is linked to phenotypic traits such as oxygen and nutrient requirements. Nonetheless, rhythmic patterns differ across individuals, and regression analysis reveals that host identity contributes more substantially to microbial rhythmicity than species identity. Functional pathway analysis based on metagenomic sequencing data shows similar circadian fluctuations. Additionally, although anatomically adjacent, the oral cavity and oropharynx exhibit divergent rhythmic behaviors, highlighting local environmental influences on microbial rhythmicity. These findings reveal previously unrecognized temporal dynamics of the URM and provide a temporal framework for more accurate biomarker discovery.
Additional Links: PMID-42018438
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PubMed:
Citation:
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@article {pmid42018438,
year = {2026},
author = {Sun, X and Jiang, X and Zhang, L and Li, M},
title = {Extensive individual and microorganism-specific circadian oscillations of the upper respiratory tract microbiome.},
journal = {Cell reports},
volume = {45},
number = {5},
pages = {117284},
doi = {10.1016/j.celrep.2026.117284},
pmid = {42018438},
issn = {2211-1247},
abstract = {The upper respiratory tract microbiome (URM) influences host susceptibility and respiratory disease outcomes, but its normal temporal dynamics remain poorly understood. We conducted temporal metagenomic profiling of the URM by collecting oropharyngeal swabs from 22 healthy adults at 4-h intervals over 48 h. We identify significant 24-h cyclic variations in microbial composition and biomass, with two predominant oscillation patterns: "evening-peak" and "morning-peak" patterns. Temporal variation introduces substantial shifts in microbial profiles, leading to false positives in differential analyses. Microbial rhythmicity is linked to phenotypic traits such as oxygen and nutrient requirements. Nonetheless, rhythmic patterns differ across individuals, and regression analysis reveals that host identity contributes more substantially to microbial rhythmicity than species identity. Functional pathway analysis based on metagenomic sequencing data shows similar circadian fluctuations. Additionally, although anatomically adjacent, the oral cavity and oropharynx exhibit divergent rhythmic behaviors, highlighting local environmental influences on microbial rhythmicity. These findings reveal previously unrecognized temporal dynamics of the URM and provide a temporal framework for more accurate biomarker discovery.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Bacterial tryptophan metabolites in cancer and atherosclerosis: insights for a role in immune checkpoint inhibition.
Essays in biochemistry, 69(6):.
The gut microbiota plays a pivotal role in human health, partly through the production of bioactive metabolites from dietary tryptophan. These indole derivatives have emerged as key modulators of immune function, inflammation, and metabolic health and have been linked to various diseases. In the context of cancer, indole derivatives are increasingly being studied as promising modulators of immune checkpoint inhibitor (ICI) therapy, with accumulating evidence indicating potential for various derivatives to enhance therapeutic efficacy. ICI therapy is associated with various immune-related adverse events, including accelerated progression of atherosclerotic cardiovascular disease. Given their immunomodulatory properties, there is a growing interest in the usage of indole metabolites to mitigate these cardiovascular complications. This mini-review summarizes current knowledge on the roles of microbiota-derived indoles in cancer, ICI therapy, and atherosclerosis. Though direct evidence linking bacterial tryptophan-derived metabolites to ICI-associated atherosclerosis is currently lacking, accumulating evidence indicates that indole derivatives regulate pathways involved in both anti-tumor immunity and atherosclerosis. Advancing our understanding of how the microbiome and its metabolites influence both cancer and cardiovascular disease will be crucial for developing personalized, metabolite-based strategies to improve outcomes in patients undergoing ICI therapy.
Additional Links: PMID-42018480
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@article {pmid42018480,
year = {2025},
author = {Dormans, T and Kroon, J and Rampanelli, E and Nieuwdorp, M and van Es, N},
title = {Bacterial tryptophan metabolites in cancer and atherosclerosis: insights for a role in immune checkpoint inhibition.},
journal = {Essays in biochemistry},
volume = {69},
number = {6},
pages = {},
doi = {10.1042/EBC20253060},
pmid = {42018480},
issn = {1744-1358},
mesh = {Humans ; *Tryptophan/metabolism ; *Atherosclerosis/metabolism/immunology/microbiology ; *Neoplasms/metabolism/drug therapy/immunology/microbiology ; *Immune Checkpoint Inhibitors/therapeutic use/adverse effects/pharmacology ; *Gastrointestinal Microbiome ; Indoles/metabolism ; Animals ; *Bacteria/metabolism ; },
abstract = {The gut microbiota plays a pivotal role in human health, partly through the production of bioactive metabolites from dietary tryptophan. These indole derivatives have emerged as key modulators of immune function, inflammation, and metabolic health and have been linked to various diseases. In the context of cancer, indole derivatives are increasingly being studied as promising modulators of immune checkpoint inhibitor (ICI) therapy, with accumulating evidence indicating potential for various derivatives to enhance therapeutic efficacy. ICI therapy is associated with various immune-related adverse events, including accelerated progression of atherosclerotic cardiovascular disease. Given their immunomodulatory properties, there is a growing interest in the usage of indole metabolites to mitigate these cardiovascular complications. This mini-review summarizes current knowledge on the roles of microbiota-derived indoles in cancer, ICI therapy, and atherosclerosis. Though direct evidence linking bacterial tryptophan-derived metabolites to ICI-associated atherosclerosis is currently lacking, accumulating evidence indicates that indole derivatives regulate pathways involved in both anti-tumor immunity and atherosclerosis. Advancing our understanding of how the microbiome and its metabolites influence both cancer and cardiovascular disease will be crucial for developing personalized, metabolite-based strategies to improve outcomes in patients undergoing ICI therapy.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Tryptophan/metabolism
*Atherosclerosis/metabolism/immunology/microbiology
*Neoplasms/metabolism/drug therapy/immunology/microbiology
*Immune Checkpoint Inhibitors/therapeutic use/adverse effects/pharmacology
*Gastrointestinal Microbiome
Indoles/metabolism
Animals
*Bacteria/metabolism
RevDate: 2026-04-22
Conventional and biodegradable microplastics elicit contrasting taxon-level responses in rhizosphere microbiomes of maize and strawberry.
FEMS microbiology ecology pii:8660973 [Epub ahead of print].
Microplastics (MP) are relevant contaminants in agroecosystems, influencing soil nutrient dynamics and soil-plant-microbial interactions. As agriculture shifts from conventional to biodegradable plastics, their impacts on different crop rhizosphere microbiomes considering both total (DNA-derived) and active (rRNA-derived) communities have not been clearly elaborated. We hypothesized that microbiome impacts would be distinct across different plants and polymer types. Maize and strawberry plants were cultivated with 1% MP by soil weight, including two conventional polymers (LDPE, PET) and one biodegradable polymer (PBAT). Strawberry plants increased biomass across all MP treatments, accompanied by greater soil nitrate depletion. MP-induced impacts on soil prokaryotic communities were mostly additive to plant effects, as determined by 16S rRNA amplicon sequence profiling. PBAT stimulated Cupriavidus spp. and members of Saccharimonadales, suggesting a selection of potential polymer-degraders and microbial interactions, independent of plant species and root proximity. In contrast, conventional MPs induced a less selective response with compositional shifts across a greater number of taxa. MP-induced changes were more apparent in rRNA- than DNA-derived profiles, suggesting a profound response of putative active taxa. Together, we demonstrate that plant species and MP type jointly modulate rhizosphere microbial community response to MP pollution, with direct implications for soil biogeochemistry, rhizosphere functioning, and crop performance.
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@article {pmid42018486,
year = {2026},
author = {Jung, A and Bartnick, R and Thomas, DC and Lehndorff, E and Lueders, T},
title = {Conventional and biodegradable microplastics elicit contrasting taxon-level responses in rhizosphere microbiomes of maize and strawberry.},
journal = {FEMS microbiology ecology},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsec/fiag040},
pmid = {42018486},
issn = {1574-6941},
abstract = {Microplastics (MP) are relevant contaminants in agroecosystems, influencing soil nutrient dynamics and soil-plant-microbial interactions. As agriculture shifts from conventional to biodegradable plastics, their impacts on different crop rhizosphere microbiomes considering both total (DNA-derived) and active (rRNA-derived) communities have not been clearly elaborated. We hypothesized that microbiome impacts would be distinct across different plants and polymer types. Maize and strawberry plants were cultivated with 1% MP by soil weight, including two conventional polymers (LDPE, PET) and one biodegradable polymer (PBAT). Strawberry plants increased biomass across all MP treatments, accompanied by greater soil nitrate depletion. MP-induced impacts on soil prokaryotic communities were mostly additive to plant effects, as determined by 16S rRNA amplicon sequence profiling. PBAT stimulated Cupriavidus spp. and members of Saccharimonadales, suggesting a selection of potential polymer-degraders and microbial interactions, independent of plant species and root proximity. In contrast, conventional MPs induced a less selective response with compositional shifts across a greater number of taxa. MP-induced changes were more apparent in rRNA- than DNA-derived profiles, suggesting a profound response of putative active taxa. Together, we demonstrate that plant species and MP type jointly modulate rhizosphere microbial community response to MP pollution, with direct implications for soil biogeochemistry, rhizosphere functioning, and crop performance.},
}
RevDate: 2026-04-22
CmpDate: 2026-04-22
Perioperative Antibiotic Prophylaxis in Cesarean Section and the Maternal Gut Microbiome: Protocol for a Remote Observational Cohort Study.
JMIR research protocols, 15:e84909.
BACKGROUND: Cesarean section (CS) requires perioperative antibiotic prophylaxis (PAP) for the prevention of surgical site infections. However, systemic antibiotics during the peripartum period may induce compositional perturbations of the maternal gut microbiome, a system already characterized by reduced resilience. Data on maternal gut microbiome dynamics after CS with PAP are scarce, largely due to logistical and feasibility barriers that limit the participation of pregnant women and new mothers in conventional clinical studies.
OBJECTIVE: This protocol primarily aims to evaluate the feasibility of a fully decentralized, remote study design for longitudinal gut microbiome research in the peripartum period. Secondary exploratory objectives include the comparative analyses of microbiome composition between CS with PAP and vaginal delivery (VD) without antibiotic exposure to inform future adequately powered studies.
METHODS: The MAMA (Microbiome Changes Due to Antibiotic Prophylaxis in Mothers at Birth) study is a prospective, 2-arm observational cohort study conducted entirely off-site. Women in the third trimester of pregnancy were recruited at 2 German level-1 perinatal centers and affiliated outpatient facilities. Participants underwent either CS with PAP (single dose cefuroxime 1.5 g intravenously) or VD without antibiotics. Stool samples were self-collected at home and returned by mail at 3 predefined time points: late pregnancy (T0), 2 to 3 days post partum (T1), and 90±10 days post partum (T2). Primary outcomes are feasibility indicators, including recruitment rate, sample and questionnaire return rates at each time point, adherence to sampling windows, and participant retention across follow-up. Secondary outcomes are exploratory microbiome measures based on 16S rRNA gene sequencing (V3-V4), including alpha diversity indices, beta diversity metrics, and relative taxonomic abundances. Microbiome analyses are explicitly compositional and hypothesis-generating. Group comparisons and longitudinal within-individual changes will be assessed using nonparametric diversity metrics and multivariate distance-based methods. No confirmatory hypothesis testing is planned.
RESULTS: Recruitment occurred between May 2022 and October 2023, with 37 women enrolled (25 CSs and 12 VDs). Follow-up was completed with receipt of the final stool sample in March 2024. DNA extraction and sequencing were completed in a single batch in October 2024. Bioinformatic processing and statistical analyses were initiated in June 2025 and are ongoing as of December 2025. Results from the exploratory microbiome analyses are expected to be published in 2026.
CONCLUSIONS: This protocol demonstrates the feasibility of conducting fully decentralized, longitudinal microbiome research in a peripartum population without requiring on-site visits. By integrating study procedures into maternal realities, the remote design reduces participation barriers and addresses a clinically relevant research gap that has remained largely unexamined despite routine use of PAP. While microbiome-related outcomes are exploratory, the methodological framework established here provides a scalable model for future maternal and postpartum research, supporting ethically grounded, participant-centered study designs and evidence-informed care strategies.
Additional Links: PMID-42018976
PubMed:
Citation:
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@article {pmid42018976,
year = {2026},
author = {Feles, EA and Mattner, F},
title = {Perioperative Antibiotic Prophylaxis in Cesarean Section and the Maternal Gut Microbiome: Protocol for a Remote Observational Cohort Study.},
journal = {JMIR research protocols},
volume = {15},
number = {},
pages = {e84909},
pmid = {42018976},
issn = {1929-0748},
mesh = {Humans ; Female ; *Antibiotic Prophylaxis/methods ; *Cesarean Section/methods/adverse effects ; *Gastrointestinal Microbiome/drug effects ; Pregnancy ; Prospective Studies ; *Anti-Bacterial Agents/administration & dosage/therapeutic use ; Adult ; *Surgical Wound Infection/prevention & control ; Cohort Studies ; Observational Studies as Topic ; Perioperative Care/methods ; },
abstract = {BACKGROUND: Cesarean section (CS) requires perioperative antibiotic prophylaxis (PAP) for the prevention of surgical site infections. However, systemic antibiotics during the peripartum period may induce compositional perturbations of the maternal gut microbiome, a system already characterized by reduced resilience. Data on maternal gut microbiome dynamics after CS with PAP are scarce, largely due to logistical and feasibility barriers that limit the participation of pregnant women and new mothers in conventional clinical studies.
OBJECTIVE: This protocol primarily aims to evaluate the feasibility of a fully decentralized, remote study design for longitudinal gut microbiome research in the peripartum period. Secondary exploratory objectives include the comparative analyses of microbiome composition between CS with PAP and vaginal delivery (VD) without antibiotic exposure to inform future adequately powered studies.
METHODS: The MAMA (Microbiome Changes Due to Antibiotic Prophylaxis in Mothers at Birth) study is a prospective, 2-arm observational cohort study conducted entirely off-site. Women in the third trimester of pregnancy were recruited at 2 German level-1 perinatal centers and affiliated outpatient facilities. Participants underwent either CS with PAP (single dose cefuroxime 1.5 g intravenously) or VD without antibiotics. Stool samples were self-collected at home and returned by mail at 3 predefined time points: late pregnancy (T0), 2 to 3 days post partum (T1), and 90±10 days post partum (T2). Primary outcomes are feasibility indicators, including recruitment rate, sample and questionnaire return rates at each time point, adherence to sampling windows, and participant retention across follow-up. Secondary outcomes are exploratory microbiome measures based on 16S rRNA gene sequencing (V3-V4), including alpha diversity indices, beta diversity metrics, and relative taxonomic abundances. Microbiome analyses are explicitly compositional and hypothesis-generating. Group comparisons and longitudinal within-individual changes will be assessed using nonparametric diversity metrics and multivariate distance-based methods. No confirmatory hypothesis testing is planned.
RESULTS: Recruitment occurred between May 2022 and October 2023, with 37 women enrolled (25 CSs and 12 VDs). Follow-up was completed with receipt of the final stool sample in March 2024. DNA extraction and sequencing were completed in a single batch in October 2024. Bioinformatic processing and statistical analyses were initiated in June 2025 and are ongoing as of December 2025. Results from the exploratory microbiome analyses are expected to be published in 2026.
CONCLUSIONS: This protocol demonstrates the feasibility of conducting fully decentralized, longitudinal microbiome research in a peripartum population without requiring on-site visits. By integrating study procedures into maternal realities, the remote design reduces participation barriers and addresses a clinically relevant research gap that has remained largely unexamined despite routine use of PAP. While microbiome-related outcomes are exploratory, the methodological framework established here provides a scalable model for future maternal and postpartum research, supporting ethically grounded, participant-centered study designs and evidence-informed care strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
*Antibiotic Prophylaxis/methods
*Cesarean Section/methods/adverse effects
*Gastrointestinal Microbiome/drug effects
Pregnancy
Prospective Studies
*Anti-Bacterial Agents/administration & dosage/therapeutic use
Adult
*Surgical Wound Infection/prevention & control
Cohort Studies
Observational Studies as Topic
Perioperative Care/methods
RevDate: 2026-04-22
6PPD-Quinone Triggers Oxidative Stress, Metabolic Reprogramming, and Rhizosphere Microbiota Shifts in Wheat.
Journal of agricultural and food chemistry [Epub ahead of print].
The highly toxic tire-derived compound N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-Q) poses emerging environmental risks, yet its fate within the soil-plant system remains unclear. This study reveals that 6PPD-Q induces significant oxidative stress in wheat (Triticum aestivum L.), increasing reactive oxygen species (ROS) by 259% in shoots and 217% in roots and malondialdehyde (MDA) by 57 and 59%, respectively, at a concentration of 200 ng/g compared to the control. This oxidative stress disrupted key antioxidant enzymes (SOD and POD) and reduced the uptake of essential nutrients (Fe, Cu, Mg, Mn, and P). Metabolomic analysis showed perturbation in central carbon metabolism, fatty acid turnover, and amino acid biosynthesis. 16S rRNA sequencing indicated reduced rhizosphere bacterial diversity and shifts in key phyla, linked to nutrient cycling. This work provides mechanistic insights into tire-derived contaminant toxicity in soil-plant systems and highlights the need for further ecological risk assessment.
Additional Links: PMID-42019076
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PubMed:
Citation:
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@article {pmid42019076,
year = {2026},
author = {Baig, AM and Iqbal, H and Shi, R and Zeb, A and Khan, S and Tariq, H and Li, X and Irshad, F and Miao, X and Hussain, S and Liu, W},
title = {6PPD-Quinone Triggers Oxidative Stress, Metabolic Reprogramming, and Rhizosphere Microbiota Shifts in Wheat.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.6c01118},
pmid = {42019076},
issn = {1520-5118},
abstract = {The highly toxic tire-derived compound N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-Q) poses emerging environmental risks, yet its fate within the soil-plant system remains unclear. This study reveals that 6PPD-Q induces significant oxidative stress in wheat (Triticum aestivum L.), increasing reactive oxygen species (ROS) by 259% in shoots and 217% in roots and malondialdehyde (MDA) by 57 and 59%, respectively, at a concentration of 200 ng/g compared to the control. This oxidative stress disrupted key antioxidant enzymes (SOD and POD) and reduced the uptake of essential nutrients (Fe, Cu, Mg, Mn, and P). Metabolomic analysis showed perturbation in central carbon metabolism, fatty acid turnover, and amino acid biosynthesis. 16S rRNA sequencing indicated reduced rhizosphere bacterial diversity and shifts in key phyla, linked to nutrient cycling. This work provides mechanistic insights into tire-derived contaminant toxicity in soil-plant systems and highlights the need for further ecological risk assessment.},
}
RevDate: 2026-04-22
Enterolactone mitigates atherosclerosis by facilitating resolution of ferroptosis-associated intimal inflammation via the Keap1/Nrf2/GPX4 pathway.
Phytomedicine : international journal of phytotherapy and phytopharmacology, 155:158178 pii:S0944-7113(26)00412-5 [Epub ahead of print].
BACKGROUND: Atherosclerosis is the inflammatory consequence of lipid accumulation with plaque formation in the vascular intima and is a common condition to develop into various cardiovascular diseases. Current therapies do not always lead to satisfactory treatment outcomes. Enterolactone, a mammalian lignan produced by bacterial transformation from plant lignans, has a preventive effect against cardiovascular disease. However, its effect on atherosclerosis and the underlying mechanism of action remain unclear.
PURPOSE: To explore the therapeutic effect of ENL on atherosclerosis and elucidate the underlying mechanism.
METHODS: We established a model of atherosclerosis on ApoE-/- C57BL/6 mice by high fat diet. The aortic root was collected and sectioned to assess arterial plaque area, collagen fibrillar proliferation, and lipid content. RT-qPCR was used to determine the inflammatory response in the artery of mice. The serum from mice was isolated to measure lipid levels, and the fecal microbiota was analyzed by 16S rDNA. H2O2 was used to induce HUVEC injury and ferroptosis to mimic endothelial cell dysfunction in atherosclerosis, and the inhibitory effect of ENL on HUVEC ferroptosis was appraised by monitoring ferroptosis indexes and levels of iron-related proteins.
RESULTS: In the animals, enterolactone significantly improved lipid metabolism, attenuated ferroptosis occurring in the intima, facilitated the antioxidant mechanisms, and promoted healing of the endothelial lesions, by interacting with Nrf2. Of great importance, enterolactone massively altered the gut microbiota toward a curative outcome by elevating the abundance of beneficial bacteria, such as the SCFA-producing taxa. Additionally, ENL suppresses lipid peroxidation and inflammatory activation in HUVECs by regulating the Keap1/Nrf2/GPX4 pathway, and knocking down Nrf2 attenuates the treatment effect of ENL.
CONCLUSION: Enterolactone effectively resolves intimal inflammation and redresses atherosclerosis by ameliorating the gut microbiome and modulating lipid metabolism via the Keap1/Nrf2/GPX4 pathway.
Additional Links: PMID-42019202
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PubMed:
Citation:
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@article {pmid42019202,
year = {2026},
author = {Chai, S and Zhang, Y and Guo, Y and Cao, D and Wang, J and Yan, Y and Shi, Y and Yuan, Z and Wang, X and Tong, T and Zhen, Z and Huo, Y and Zhang, K and Wang, F and Liu, GR and Li, W and Xu, X and Ban, T and Liu, SL and Liu, H},
title = {Enterolactone mitigates atherosclerosis by facilitating resolution of ferroptosis-associated intimal inflammation via the Keap1/Nrf2/GPX4 pathway.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {155},
number = {},
pages = {158178},
doi = {10.1016/j.phymed.2026.158178},
pmid = {42019202},
issn = {1618-095X},
abstract = {BACKGROUND: Atherosclerosis is the inflammatory consequence of lipid accumulation with plaque formation in the vascular intima and is a common condition to develop into various cardiovascular diseases. Current therapies do not always lead to satisfactory treatment outcomes. Enterolactone, a mammalian lignan produced by bacterial transformation from plant lignans, has a preventive effect against cardiovascular disease. However, its effect on atherosclerosis and the underlying mechanism of action remain unclear.
PURPOSE: To explore the therapeutic effect of ENL on atherosclerosis and elucidate the underlying mechanism.
METHODS: We established a model of atherosclerosis on ApoE-/- C57BL/6 mice by high fat diet. The aortic root was collected and sectioned to assess arterial plaque area, collagen fibrillar proliferation, and lipid content. RT-qPCR was used to determine the inflammatory response in the artery of mice. The serum from mice was isolated to measure lipid levels, and the fecal microbiota was analyzed by 16S rDNA. H2O2 was used to induce HUVEC injury and ferroptosis to mimic endothelial cell dysfunction in atherosclerosis, and the inhibitory effect of ENL on HUVEC ferroptosis was appraised by monitoring ferroptosis indexes and levels of iron-related proteins.
RESULTS: In the animals, enterolactone significantly improved lipid metabolism, attenuated ferroptosis occurring in the intima, facilitated the antioxidant mechanisms, and promoted healing of the endothelial lesions, by interacting with Nrf2. Of great importance, enterolactone massively altered the gut microbiota toward a curative outcome by elevating the abundance of beneficial bacteria, such as the SCFA-producing taxa. Additionally, ENL suppresses lipid peroxidation and inflammatory activation in HUVECs by regulating the Keap1/Nrf2/GPX4 pathway, and knocking down Nrf2 attenuates the treatment effect of ENL.
CONCLUSION: Enterolactone effectively resolves intimal inflammation and redresses atherosclerosis by ameliorating the gut microbiome and modulating lipid metabolism via the Keap1/Nrf2/GPX4 pathway.},
}
RevDate: 2026-04-22
Lakes and lagoons used for drinking water supply and fisheries as sources of potentially pathogenic bacteria and antimicrobial resistance.
Journal of environmental management, 405:129718 pii:S0301-4797(26)01178-3 [Epub ahead of print].
Drinking water supplies and water basins used for fisheries represent two essential water sources for humans. Despite the growing accessibility of metagenomic approaches, their routine use for water quality monitoring is still limited. Many key water resources have yet to be fully characterized in terms of microbiome, pathobiome, and antimicrobial resistome. In this study, surface water samples were collected over one year from the artificial Lake Bidighinzu (drinking water supply) and the coastal lagoon Cabras (fisheries) located in the western Mediterranean area. Samples were analyzed for physical and chemical properties, and 16S rRNA gene amplicon and shotgun sequencing were used to characterize bacterial communities, pathobiomes, and antimicrobial resistomes. Physical and chemical properties were generally similar between sites, except for higher salinity in Cabras Lagoon. In Cabras Lagoon, richness of the bacterial community and pathobiome was generally higher in the largest trophic fraction (>20 μm), while in both sites the abundance of potentially pathogenic bacteria (PPB) increased at this fraction. PPB, including ESKAPE pathogens, were more abundant in Lake Bidighinzu. The overall antimicrobial resistome was similar across sites, with high-risk antimicrobial resistance genes (ARGs) such as emrB prevalent. Lake Bidighinzu also had more contigs where ARGs co-occurred with mobile genetic elements. This study highlights microbiological risks in two aquatic systems, particularly Lake Bidighinzu, and underscores the need to integrate metagenomic approaches, possibly with cultivation-based methods, to monitor water quality and assess health risks in drinking water supplies and fisheries.
Additional Links: PMID-42019335
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PubMed:
Citation:
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@article {pmid42019335,
year = {2026},
author = {Sabatino, R and Pulina, S and Sbaffi, T and Kamburska, L and Titocci, J and Cherchi, M and Pittalis, C and Piscia, R and Vaccarelli, I and Rosati, I and Padedda, BM and Allemanno, F and Casiddu, P and Di Cesare, A},
title = {Lakes and lagoons used for drinking water supply and fisheries as sources of potentially pathogenic bacteria and antimicrobial resistance.},
journal = {Journal of environmental management},
volume = {405},
number = {},
pages = {129718},
doi = {10.1016/j.jenvman.2026.129718},
pmid = {42019335},
issn = {1095-8630},
abstract = {Drinking water supplies and water basins used for fisheries represent two essential water sources for humans. Despite the growing accessibility of metagenomic approaches, their routine use for water quality monitoring is still limited. Many key water resources have yet to be fully characterized in terms of microbiome, pathobiome, and antimicrobial resistome. In this study, surface water samples were collected over one year from the artificial Lake Bidighinzu (drinking water supply) and the coastal lagoon Cabras (fisheries) located in the western Mediterranean area. Samples were analyzed for physical and chemical properties, and 16S rRNA gene amplicon and shotgun sequencing were used to characterize bacterial communities, pathobiomes, and antimicrobial resistomes. Physical and chemical properties were generally similar between sites, except for higher salinity in Cabras Lagoon. In Cabras Lagoon, richness of the bacterial community and pathobiome was generally higher in the largest trophic fraction (>20 μm), while in both sites the abundance of potentially pathogenic bacteria (PPB) increased at this fraction. PPB, including ESKAPE pathogens, were more abundant in Lake Bidighinzu. The overall antimicrobial resistome was similar across sites, with high-risk antimicrobial resistance genes (ARGs) such as emrB prevalent. Lake Bidighinzu also had more contigs where ARGs co-occurred with mobile genetic elements. This study highlights microbiological risks in two aquatic systems, particularly Lake Bidighinzu, and underscores the need to integrate metagenomic approaches, possibly with cultivation-based methods, to monitor water quality and assess health risks in drinking water supplies and fisheries.},
}
RevDate: 2026-04-22
Correlation analysis of heavy metal, antibiotics accumulation, and antibiotic resistance genes induced by long-term biogas slurry application.
Journal of environmental management, 405:129745 pii:S0301-4797(26)01205-3 [Epub ahead of print].
Biogas slurry (BS), as product of animal manure fermentation, is often used as a fertilizer in farmland. However, the long-term application impact on the soil remains not fully understood. Studies have shown that although long-term application of BS does not lead to excessive antibiotic residues in the soil, it increases the abundance of antibiotic resistance genes (ARGs) and promotes their transfer among potential hosts. The complex co-occurrence of bacteria and ARGs implies enhanced horizontal gene transfer, and the increased abundance of the intl1 gene supports this change. Moreover, the distribution of antibiotic-resistant bacteria and ARGs is closely related to the duration of application. Meanwhile, tetracyclines and fluoroquinolones antibiotics, as well as ARGs, are significantly enriched in soils irrigated with BS, and various potentially pathogenic bacterial genera are present. In addition, the application of BS can increase the soil organic carbon stock and alter the soil bacterial and fungal communities. Long-term application of BS results in the accumulation of tetracyclines and the enrichment of ARGs in the soil. It also has an impact on the diversity of soil microbial functional genes. These findings provide a basis for the formulation of relevant policies and sustainable soil management.
Additional Links: PMID-42019337
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@article {pmid42019337,
year = {2026},
author = {Yu, B and Jiang, C and Yang, K and Zhang, Y and Gao, Y and Chen, Z and Qian, X and Ouyang, S},
title = {Correlation analysis of heavy metal, antibiotics accumulation, and antibiotic resistance genes induced by long-term biogas slurry application.},
journal = {Journal of environmental management},
volume = {405},
number = {},
pages = {129745},
doi = {10.1016/j.jenvman.2026.129745},
pmid = {42019337},
issn = {1095-8630},
abstract = {Biogas slurry (BS), as product of animal manure fermentation, is often used as a fertilizer in farmland. However, the long-term application impact on the soil remains not fully understood. Studies have shown that although long-term application of BS does not lead to excessive antibiotic residues in the soil, it increases the abundance of antibiotic resistance genes (ARGs) and promotes their transfer among potential hosts. The complex co-occurrence of bacteria and ARGs implies enhanced horizontal gene transfer, and the increased abundance of the intl1 gene supports this change. Moreover, the distribution of antibiotic-resistant bacteria and ARGs is closely related to the duration of application. Meanwhile, tetracyclines and fluoroquinolones antibiotics, as well as ARGs, are significantly enriched in soils irrigated with BS, and various potentially pathogenic bacterial genera are present. In addition, the application of BS can increase the soil organic carbon stock and alter the soil bacterial and fungal communities. Long-term application of BS results in the accumulation of tetracyclines and the enrichment of ARGs in the soil. It also has an impact on the diversity of soil microbial functional genes. These findings provide a basis for the formulation of relevant policies and sustainable soil management.},
}
RevDate: 2026-04-22
Unveiling the enhancement mechanisms of bio-carriers in anoxic treatment of composite phenolic wastewater: A multi-dimensional comparison from macro-performance to microbiome.
Journal of hazardous materials, 510:142163 pii:S0304-3894(26)01141-6 [Epub ahead of print].
This study conducted a comparative investigation into the enhancement of anoxic biodegradation of composite phenols in simulated coal chemical wastewater using four distinct bio-carriers: activated carbon, ceramsite, iron-carbon, and polyurethane (PU). Five parallel anoxic reactors (R1: blank, R2: activated carbon, R3: ceramsite, R4: iron-carbon, R5: PU) were operated under progressively increasing phenol loads (10-350 mg/L). Results demonstrated that all carriers improved treatment performance compared to the blank reactor (R1). The iron-carbon carrier (R4) exhibited exceptional resilience, maintaining complete phenol degradation up to 300 mg/L, attributed to micro-electrolysis pre-treatment that enhanced biodegradability. The PU carrier (R5) achieved the highest and most stable removal efficiencies for both phenol and COD at the highest loadings, coupled with the most diverse bacterial community and a uniquely enriched fungal genus, Cutaneotrichosporon (76.3%), identified as a key degrader. Microbial community analysis revealed that carrier type significantly shaped the microbial structure. The PU and ceramsite carriers fostered higher biodiversity, while the iron-carbon environment selected for specific functional genera. The findings provide critical insights into the mechanisms-adsorption-biofilm synergy, micro-electrolysis, and targeted microbial enrichment-by which different carriers enhance anoxic treatment, offering a scientific basis for selecting optimal carriers in treating high-strength phenolic wastewater.
Additional Links: PMID-42019448
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PubMed:
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@article {pmid42019448,
year = {2026},
author = {Miao, Z and Huang, Z and Wang, J and Li, Z and Shi, J},
title = {Unveiling the enhancement mechanisms of bio-carriers in anoxic treatment of composite phenolic wastewater: A multi-dimensional comparison from macro-performance to microbiome.},
journal = {Journal of hazardous materials},
volume = {510},
number = {},
pages = {142163},
doi = {10.1016/j.jhazmat.2026.142163},
pmid = {42019448},
issn = {1873-3336},
abstract = {This study conducted a comparative investigation into the enhancement of anoxic biodegradation of composite phenols in simulated coal chemical wastewater using four distinct bio-carriers: activated carbon, ceramsite, iron-carbon, and polyurethane (PU). Five parallel anoxic reactors (R1: blank, R2: activated carbon, R3: ceramsite, R4: iron-carbon, R5: PU) were operated under progressively increasing phenol loads (10-350 mg/L). Results demonstrated that all carriers improved treatment performance compared to the blank reactor (R1). The iron-carbon carrier (R4) exhibited exceptional resilience, maintaining complete phenol degradation up to 300 mg/L, attributed to micro-electrolysis pre-treatment that enhanced biodegradability. The PU carrier (R5) achieved the highest and most stable removal efficiencies for both phenol and COD at the highest loadings, coupled with the most diverse bacterial community and a uniquely enriched fungal genus, Cutaneotrichosporon (76.3%), identified as a key degrader. Microbial community analysis revealed that carrier type significantly shaped the microbial structure. The PU and ceramsite carriers fostered higher biodiversity, while the iron-carbon environment selected for specific functional genera. The findings provide critical insights into the mechanisms-adsorption-biofilm synergy, micro-electrolysis, and targeted microbial enrichment-by which different carriers enhance anoxic treatment, offering a scientific basis for selecting optimal carriers in treating high-strength phenolic wastewater.},
}
RevDate: 2026-04-22
Early-life and lifelong exposure to environmentally relevant enrofloxacin reorganizes a proteobacteria-centered gut-lipid-resistome steady state in marine medaka.
Journal of hazardous materials, 510:142146 pii:S0304-3894(26)01124-6 [Epub ahead of print].
Environmental fluoroquinolone residues such as enrofloxacin (ENR) are increasingly detected in coastal waters, yet the persistence of low-dose effects on gut ecosystem organization remains unclear. We compared an early-life window exposure (5 μg/L ENR, 20-35 days post-hatch; depurated to 150 dph) with a lifelong exposure (5 μg/L ENR from fertilization to 150 dph) in marine medaka (Oryzias melastigma), using an environmentally realistic upper-bound concentration reflecting aquaculture-impacted conditions. We integrated intestinal histology and ultrastructure, inflammatory and lipid-metabolic transcriptional programs, intestinal fatty-acid profiles, 16S rRNA and 2bRAD-M characterization of the gut microbiota and antibiotic-resistance genes. Both regimens increased intestinal hypertrophy or densification and rewired communities into more positively connected, Proteobacteria-centered networks. Lifelong exposure produced a pronounced shift in intestinal lipid programming, marked by enhanced lipogenesis and reduced fatty-acid catabolism, together with selective changes in fatty-acid composition and desaturation balance. Early-life window exposure left persistent, albeit weaker, adult signatures in intestinal morphology, microbial network topology, and lipid-related transcription after prolonged withdrawal. Across cohorts, Proteobacteria indicator taxa covaried with inflammatory and lipid gene modules and with coordinated resistance-gene modules, consistent with a Proteobacteria-rich gut-lipid-resistome steady state. These findings indicate that ENR at an environmentally realistic upper-bound concentration reflecting aquaculture-impacted and hotspot contamination scenarios can durably reorganize host-microbe-resistome linkages, supporting re-evaluation of "no-effect" thresholds for antibiotic pollution from a One Health perspective.
Additional Links: PMID-42019450
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@article {pmid42019450,
year = {2026},
author = {Guo, Z and Wang, Z and Liu, Y and Wang, M and Ma, H and Wang, Z and Zhang, S and Chang, Y and Ge, H and Li, C and Yang, H and Miao, H and Zhang, X and Cui, P},
title = {Early-life and lifelong exposure to environmentally relevant enrofloxacin reorganizes a proteobacteria-centered gut-lipid-resistome steady state in marine medaka.},
journal = {Journal of hazardous materials},
volume = {510},
number = {},
pages = {142146},
doi = {10.1016/j.jhazmat.2026.142146},
pmid = {42019450},
issn = {1873-3336},
abstract = {Environmental fluoroquinolone residues such as enrofloxacin (ENR) are increasingly detected in coastal waters, yet the persistence of low-dose effects on gut ecosystem organization remains unclear. We compared an early-life window exposure (5 μg/L ENR, 20-35 days post-hatch; depurated to 150 dph) with a lifelong exposure (5 μg/L ENR from fertilization to 150 dph) in marine medaka (Oryzias melastigma), using an environmentally realistic upper-bound concentration reflecting aquaculture-impacted conditions. We integrated intestinal histology and ultrastructure, inflammatory and lipid-metabolic transcriptional programs, intestinal fatty-acid profiles, 16S rRNA and 2bRAD-M characterization of the gut microbiota and antibiotic-resistance genes. Both regimens increased intestinal hypertrophy or densification and rewired communities into more positively connected, Proteobacteria-centered networks. Lifelong exposure produced a pronounced shift in intestinal lipid programming, marked by enhanced lipogenesis and reduced fatty-acid catabolism, together with selective changes in fatty-acid composition and desaturation balance. Early-life window exposure left persistent, albeit weaker, adult signatures in intestinal morphology, microbial network topology, and lipid-related transcription after prolonged withdrawal. Across cohorts, Proteobacteria indicator taxa covaried with inflammatory and lipid gene modules and with coordinated resistance-gene modules, consistent with a Proteobacteria-rich gut-lipid-resistome steady state. These findings indicate that ENR at an environmentally realistic upper-bound concentration reflecting aquaculture-impacted and hotspot contamination scenarios can durably reorganize host-microbe-resistome linkages, supporting re-evaluation of "no-effect" thresholds for antibiotic pollution from a One Health perspective.},
}
RevDate: 2026-04-22
Gut microbiota-derived taurolithocholic acid modulates myofiber-type switching via p38 MAPK/PGC-1α signaling underlying breed differences between Arbor Acres and Taoyuan chickens.
Poultry science, 105(7):106914 pii:S0032-5791(26)00542-0 [Epub ahead of print].
It is well-established that the gut microbiota plays a crucial role in skeletal muscle development and homeostasis. However, the contribution of the gut microbiome to the distinct meat quality phenotypes observed between fast-growing commercial broilers and slow-growing local chicken breeds remains poorly understood. Therefore, this study aims to elucidate how the gut microbiota modulates pectoral muscle development by comparing muscle growth phenotypes and gut microbiome dynamics across these breeds. Using the fast-growing commercial Arbor Acres (AA) broiler and the slow-growing local breed Taoyuan (TY) chicken as models, we investigated how breed-specific gut microbiota modulate pectoral muscle fiber composition. AA broilers exhibited faster muscle growth but lower oxidative type I fiber proportion than TY chickens. While small intestinal microbiota succession was similar, cecal communities diverged markedly between breeds. Integrated metagenomic sequencing and metabolomics revealed that cecal Phocaeicola dorei abundance was strongly correlated with serum taurolithocholic acid (TLCA) levels and type I fiber content, especially in TY chickens, which prompted the selection of TLCA for functional validation. Reciprocal intestinal microbiota transplantation (IMT) shifted recipient muscle fiber phenotypes toward those of donors, confirming a causal role of the cecal microbiota. Furthermore, in vitro assays using AA-derived myoblasts demonstrated that TLCA promotes mitochondrial biogenesis and type I fiber formation by enhancing p38 MAPK phosphorylation and PGC-1α activation; this effect was abolished by the p38 inhibitor SB203580. Our study demonstrated that gut microbiota-derived TLCA modulates muscle fiber type transformation via the p38 MAPK/PGC-1α signaling pathway. This finding reveals an intricate mechanism whereby the gut microbiota regulates host muscle development through a metabolite-signaling axis, providing critical insights into the gut microbe-myofiber relationship.
Additional Links: PMID-42019469
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@article {pmid42019469,
year = {2026},
author = {Peng, F and Zeng, YY and Chang, L and Huang, YX and Deng, JT and Liu, YX and He, X and Song, ZH},
title = {Gut microbiota-derived taurolithocholic acid modulates myofiber-type switching via p38 MAPK/PGC-1α signaling underlying breed differences between Arbor Acres and Taoyuan chickens.},
journal = {Poultry science},
volume = {105},
number = {7},
pages = {106914},
doi = {10.1016/j.psj.2026.106914},
pmid = {42019469},
issn = {1525-3171},
abstract = {It is well-established that the gut microbiota plays a crucial role in skeletal muscle development and homeostasis. However, the contribution of the gut microbiome to the distinct meat quality phenotypes observed between fast-growing commercial broilers and slow-growing local chicken breeds remains poorly understood. Therefore, this study aims to elucidate how the gut microbiota modulates pectoral muscle development by comparing muscle growth phenotypes and gut microbiome dynamics across these breeds. Using the fast-growing commercial Arbor Acres (AA) broiler and the slow-growing local breed Taoyuan (TY) chicken as models, we investigated how breed-specific gut microbiota modulate pectoral muscle fiber composition. AA broilers exhibited faster muscle growth but lower oxidative type I fiber proportion than TY chickens. While small intestinal microbiota succession was similar, cecal communities diverged markedly between breeds. Integrated metagenomic sequencing and metabolomics revealed that cecal Phocaeicola dorei abundance was strongly correlated with serum taurolithocholic acid (TLCA) levels and type I fiber content, especially in TY chickens, which prompted the selection of TLCA for functional validation. Reciprocal intestinal microbiota transplantation (IMT) shifted recipient muscle fiber phenotypes toward those of donors, confirming a causal role of the cecal microbiota. Furthermore, in vitro assays using AA-derived myoblasts demonstrated that TLCA promotes mitochondrial biogenesis and type I fiber formation by enhancing p38 MAPK phosphorylation and PGC-1α activation; this effect was abolished by the p38 inhibitor SB203580. Our study demonstrated that gut microbiota-derived TLCA modulates muscle fiber type transformation via the p38 MAPK/PGC-1α signaling pathway. This finding reveals an intricate mechanism whereby the gut microbiota regulates host muscle development through a metabolite-signaling axis, providing critical insights into the gut microbe-myofiber relationship.},
}
RevDate: 2026-04-22
A generative AI framework unifies human multi-omics to model aging, metabolic health, and intervention response.
Cell metabolism pii:S1550-4131(26)00108-7 [Epub ahead of print].
Understanding aging and complex diseases requires diverse data, ranging from molecular profiles to imaging and routine clinical tests. However, most multi-omic datasets measure only a subset of modalities and are confounded by batch effects. Here, we present AURORA (AI unification and reconstruction of omics reassembly atlas), a generative deep-learning platform that integrates seven modalities (including transcriptomics, metabolomics, microbiome, 3D and thermal facial imaging, and clinical laboratory tests) across 581,763 samples from 425,258 individuals. AURORA harmonizes batch effects and reconstructs missing data across modalities, enabling highly accurate multimodal aging clocks and disease risk predictors. It also supports personalized in silico perturbation analyses to predict intervention and drug responses, validated using longitudinal cohorts. As a proof of concept, we provide a prototype AI agent that converts single-input modalities into a multimodal report for users and researchers. Together, AURORA links non-invasive inputs to comprehensive aging biomarkers and therapeutic discovery.
Additional Links: PMID-42019500
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@article {pmid42019500,
year = {2026},
author = {Chen, J and Ren, Y and Zhou, Y and Wang, Z and Mao, K and Yu, Z and Li, J and Guo, X and Xu, H and Wang, Y and Wang, Y and Pang, B and Liu, H and Tang, H and Han, JJ},
title = {A generative AI framework unifies human multi-omics to model aging, metabolic health, and intervention response.},
journal = {Cell metabolism},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmet.2026.03.014},
pmid = {42019500},
issn = {1932-7420},
abstract = {Understanding aging and complex diseases requires diverse data, ranging from molecular profiles to imaging and routine clinical tests. However, most multi-omic datasets measure only a subset of modalities and are confounded by batch effects. Here, we present AURORA (AI unification and reconstruction of omics reassembly atlas), a generative deep-learning platform that integrates seven modalities (including transcriptomics, metabolomics, microbiome, 3D and thermal facial imaging, and clinical laboratory tests) across 581,763 samples from 425,258 individuals. AURORA harmonizes batch effects and reconstructs missing data across modalities, enabling highly accurate multimodal aging clocks and disease risk predictors. It also supports personalized in silico perturbation analyses to predict intervention and drug responses, validated using longitudinal cohorts. As a proof of concept, we provide a prototype AI agent that converts single-input modalities into a multimodal report for users and researchers. Together, AURORA links non-invasive inputs to comprehensive aging biomarkers and therapeutic discovery.},
}
RevDate: 2026-04-22
Dissecting the host transcriptome and microbiota responses to Viral Hemorrhagic Septicemia Virus (VHSV) in the turbot (Scophthalmus maximus) intestine: insights from moribund and asymptomatic phenotypes.
Fish & shellfish immunology pii:S1050-4648(26)00274-3 [Epub ahead of print].
Viral infections profoundly influence host physiology, not only by triggering complex immune responses but also by reshaping the associated microbiota. Conversely, the microbiota can modulate antiviral defenses and disease outcomes through its interactions with the host immune system. This dynamic triad -virus, microbiota, and host immunity- has emerged as a central determinant of infection severity and recovery. Yet, despite growing evidence from mammalian models, its functional implications in fish remain poorly understood. Here, we investigated the effects of viral hemorrhagic septicemia virus (VHSV) infection on the intestinal transcriptomic and microbiota profiles of turbot (Scophthalmus maximus), an aquaculture species highly susceptible to this pathogen. Comparative analyses were conducted among asymptomatic and moribund fish at 10 days post-infection, and uninfected controls. Transcriptomic data revealed that moribund individuals exhibited a dysregulated immune response characterized by a strong induction of complement- and coagulation-related genes and other inflammatory pathways, whereas asymptomatic fish displayed expression patterns more closely resembling those of uninfected controls, indicating a more controlled or resolved immune activation. Microbiota analyses showed that VHSV infection induced widespread, severity-dependent changes in the intestinal microbiota, with progressive shifts in the relative abundance of most bacterial taxa from controls to asymptomatic and moribund fish. Interestingly, a subset of bacterial genera deviated from this general trend, displaying an opposite pattern to that observed in both uninfected and moribund individuals, suggesting their potential involvement in resistance mechanisms. Integrative analyses further revealed significant correlations between specific bacterial genera and host genes differentially expressed between asymptomatic and moribund fish, highlighting functional links between microbial composition and immune regulation. Together, these findings reveal complex interactions between VHSV infection, host immunity, and microbiota composition in turbot, providing novel insights into host-microbe-virus relationships that may inform disease management and selective breeding strategies in aquaculture.
Additional Links: PMID-42019590
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@article {pmid42019590,
year = {2026},
author = {MartÃnez-López, N and Figueras, A and Novoa, B and Pereiro, P},
title = {Dissecting the host transcriptome and microbiota responses to Viral Hemorrhagic Septicemia Virus (VHSV) in the turbot (Scophthalmus maximus) intestine: insights from moribund and asymptomatic phenotypes.},
journal = {Fish & shellfish immunology},
volume = {},
number = {},
pages = {111370},
doi = {10.1016/j.fsi.2026.111370},
pmid = {42019590},
issn = {1095-9947},
abstract = {Viral infections profoundly influence host physiology, not only by triggering complex immune responses but also by reshaping the associated microbiota. Conversely, the microbiota can modulate antiviral defenses and disease outcomes through its interactions with the host immune system. This dynamic triad -virus, microbiota, and host immunity- has emerged as a central determinant of infection severity and recovery. Yet, despite growing evidence from mammalian models, its functional implications in fish remain poorly understood. Here, we investigated the effects of viral hemorrhagic septicemia virus (VHSV) infection on the intestinal transcriptomic and microbiota profiles of turbot (Scophthalmus maximus), an aquaculture species highly susceptible to this pathogen. Comparative analyses were conducted among asymptomatic and moribund fish at 10 days post-infection, and uninfected controls. Transcriptomic data revealed that moribund individuals exhibited a dysregulated immune response characterized by a strong induction of complement- and coagulation-related genes and other inflammatory pathways, whereas asymptomatic fish displayed expression patterns more closely resembling those of uninfected controls, indicating a more controlled or resolved immune activation. Microbiota analyses showed that VHSV infection induced widespread, severity-dependent changes in the intestinal microbiota, with progressive shifts in the relative abundance of most bacterial taxa from controls to asymptomatic and moribund fish. Interestingly, a subset of bacterial genera deviated from this general trend, displaying an opposite pattern to that observed in both uninfected and moribund individuals, suggesting their potential involvement in resistance mechanisms. Integrative analyses further revealed significant correlations between specific bacterial genera and host genes differentially expressed between asymptomatic and moribund fish, highlighting functional links between microbial composition and immune regulation. Together, these findings reveal complex interactions between VHSV infection, host immunity, and microbiota composition in turbot, providing novel insights into host-microbe-virus relationships that may inform disease management and selective breeding strategies in aquaculture.},
}
RevDate: 2026-04-21
Hypnotic and sleep-promoting effects of Limosilactobacillus reuteri LM1063 on pentobarbital-induced sleep and electroencephalogram analysis in mice.
Scientific reports, 16(1):.
UNLABELLED: Sleep disturbances are an increasing health concern, and limitations associated with long-term use of conventional hypnotics have prompted interest in alternative approaches that support sleep health. Growing evidence suggests that the gut–brain axis contributes to sleep regulation; however, the effects of probiotics on objective sleep parameters and their underlying mechanisms remain incompletely understood and may vary across probiotic strains. The present study investigated the sleep–modulating effects of a selected probiotic strain, Limosilactobacillus reuteri LM1063 (LM1063), using murine models. Sleep latency and duration were assessed using a pentobarbital-induced sleep test, and sleep architecture was evaluated by electroencephalogram (EEG) recordings, including rapid eye movement (REM) and non-rapid eye movement (NREM) sleep. To explore potential mechanisms, neurochemical analyses focusing on key neurotransmitters, including gamma-aminobutyric acid (GABA) and serotonin, were conducted. Administration of LM1063 significantly shortened sleep latency and prolonged sleep duration in mice. EEG analysis revealed shifts in overall sleep architecture toward a sleep-favorable state without disruption of normal sleep organization. These sleep-related changes were accompanied by modulation of GABAergic and serotonergic neurochemical pathways. In conclusion, LM1063 exerts strain-specific sleep-modulating effects through neurochemical mechanisms associated with the gut–brain axis. By integrating behavioral sleep assessment, electrophysiological analysis, and neurochemical profiling, this study provides mechanistic insight supporting the potential translational application of microbiome-targeted approaches for promoting sleep health.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-42833-0.
Additional Links: PMID-41803210
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@article {pmid41803210,
year = {2026},
author = {Kim, MG and Seo, E and Eor, JY and Kang, A and Kim, TR and Sohn, M and Kim, Y},
title = {Hypnotic and sleep-promoting effects of Limosilactobacillus reuteri LM1063 on pentobarbital-induced sleep and electroencephalogram analysis in mice.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {41803210},
issn = {2045-2322},
support = {RS-2025-16068814//National Research Foundation of Korea/ ; },
abstract = {UNLABELLED: Sleep disturbances are an increasing health concern, and limitations associated with long-term use of conventional hypnotics have prompted interest in alternative approaches that support sleep health. Growing evidence suggests that the gut–brain axis contributes to sleep regulation; however, the effects of probiotics on objective sleep parameters and their underlying mechanisms remain incompletely understood and may vary across probiotic strains. The present study investigated the sleep–modulating effects of a selected probiotic strain, Limosilactobacillus reuteri LM1063 (LM1063), using murine models. Sleep latency and duration were assessed using a pentobarbital-induced sleep test, and sleep architecture was evaluated by electroencephalogram (EEG) recordings, including rapid eye movement (REM) and non-rapid eye movement (NREM) sleep. To explore potential mechanisms, neurochemical analyses focusing on key neurotransmitters, including gamma-aminobutyric acid (GABA) and serotonin, were conducted. Administration of LM1063 significantly shortened sleep latency and prolonged sleep duration in mice. EEG analysis revealed shifts in overall sleep architecture toward a sleep-favorable state without disruption of normal sleep organization. These sleep-related changes were accompanied by modulation of GABAergic and serotonergic neurochemical pathways. In conclusion, LM1063 exerts strain-specific sleep-modulating effects through neurochemical mechanisms associated with the gut–brain axis. By integrating behavioral sleep assessment, electrophysiological analysis, and neurochemical profiling, this study provides mechanistic insight supporting the potential translational application of microbiome-targeted approaches for promoting sleep health.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-42833-0.},
}
RevDate: 2026-04-20
Porphyromonas gingivalis produces a functional HemH ferrochelatase important for its survival in a heme-limited environment.
Scientific reports, 16(1):.
UNLABELLED: Porphyromonas gingivalis, the keystone pathogen responsible for dysbiosis in the oral microbiome, the development of periodontal diseases, and the contribution to systemic comorbidities, is a heme auxotroph. It encodes only four enzymes in the heme biosynthesis pathway (HemD, HemN, HemG, and HemH). Comparative genomic analyses demonstrated that, while many Bacteroidota members have lost most of the canonical heme biosynthetic enzymes, Porphyromonas species uniquely retained a ferrochelatase (HemH) homolog. This study aimed to functionally characterize the P. gingivalis HemH protein to prove its hypothesized role in heme formation. HemH can bind heme and PPIX and insert iron or manganese ions into the PPIX ring. The deletion of the hemH gene triggers a heme-starvation response characterized by transcriptional activation of heme uptake systems and virulence-associated genes, coupled with repression of transport and surface proteins preferentially expressed in heme-rich conditions. Therefore, it is proposed that HemH may play a role in maintaining proper heme homeostasis. In a heme-limited environment, P. gingivalis may use intracellular iron and PPIX reserves to synthesize heme by HemH, thereby contributing to heme supply.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-41999-x.
Additional Links: PMID-41807505
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@article {pmid41807505,
year = {2026},
author = {Åšmiga, M and Roszkiewicz, E and Wojtal, N and Olczak, T},
title = {Porphyromonas gingivalis produces a functional HemH ferrochelatase important for its survival in a heme-limited environment.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {41807505},
issn = {2045-2322},
support = {2023/51/D/NZ6/00324//Narodowe Centrum Nauki/ ; },
abstract = {UNLABELLED: Porphyromonas gingivalis, the keystone pathogen responsible for dysbiosis in the oral microbiome, the development of periodontal diseases, and the contribution to systemic comorbidities, is a heme auxotroph. It encodes only four enzymes in the heme biosynthesis pathway (HemD, HemN, HemG, and HemH). Comparative genomic analyses demonstrated that, while many Bacteroidota members have lost most of the canonical heme biosynthetic enzymes, Porphyromonas species uniquely retained a ferrochelatase (HemH) homolog. This study aimed to functionally characterize the P. gingivalis HemH protein to prove its hypothesized role in heme formation. HemH can bind heme and PPIX and insert iron or manganese ions into the PPIX ring. The deletion of the hemH gene triggers a heme-starvation response characterized by transcriptional activation of heme uptake systems and virulence-associated genes, coupled with repression of transport and surface proteins preferentially expressed in heme-rich conditions. Therefore, it is proposed that HemH may play a role in maintaining proper heme homeostasis. In a heme-limited environment, P. gingivalis may use intracellular iron and PPIX reserves to synthesize heme by HemH, thereby contributing to heme supply.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-41999-x.},
}
RevDate: 2026-04-21
Akkermansia muciniphila confers renal protection in chronic kidney disease: a multi-omics mechanistic investigation.
BMC microbiology, 26(1):.
BACKGROUND: Akkermansia muciniphila (A. muciniphila) improved serum metabolism and renal fibrosis in the mouse model of chronic kidney disease (CKD) via the gut-kidney axis, slowing renal function decline. However, the biological components and underlying metabolic pathways remain unclear. Using a CKD mouse model, we aimed to identify the biological constituents of A. muciniphila that drive its regulatory effects in renal injury. Integrated microbiome and metabolomics analyses further elucidated the metabolic mechanisms of renoprotection, providing a theoretical foundation for the development of evidence-based clinical interventions.
METHODS: A CKD mouse model was established using 5/6 nephrectomy, with sham-operated mice (n = 7) serving as controls. Twenty-eight CKD mice were randomly assigned to four groups and treated with PBS, A. muciniphila, pasteurised A. muciniphila, or A. muciniphila combined with vancomycin by gavage. Serum and kidney tissues were collected to assess renal function, and histopathology was performed to identify the key biological components of A. muciniphila. Faecal samples were subjected to integrated microbiome and metabolomic analyses to identify the metabolic pathways involved in renoprotection. Behavioural experiments were performed to observe the effect of A. muciniphila on the behaviour of CKD mice. Single-factor analysis of variance and post-hoc tests were used for intergroup comparisons.
RESULTS: Serum analysis showed that the levels of serum creatinine, urea nitrogen and cystatin C in mice treated with A. muciniphila combined with vancomycin were significantly decreased. Reverse-transcription polymerase chain reaction showed that the renal injury marker Kim-1 was significantly decreased after A. muciniphila intervention. The levels of the renal injury (Ngal) and fibrosis (Col1a1, TIMP-1 and Fibronectin) markers showed a downward trend. 16 S rRNA analysis revealed that, following A. muciniphila intervention, the health index of the intestinal flora in CKD mice was significantly increased; however, the abundances of Turicibacter, Dubosiella and norank_f_UCG-010 were decreased. Metabolomic analysis revealed a strong correlation between A. muciniphila and the tryptophan metabolic pathway. Behavioural experiments showed that the exercise activity and anxiety-like behaviour of CKD mice were significantly improved after intervention with A. muciniphila, and the effect of A. muciniphila combined with vancomycin was better than that of A. muciniphila or pasteurised A. muciniphila alone.
CONCLUSION: Our findings demonstrate that A. muciniphila combined with vancomycin intervention ameliorates kidney injury, body dysfunction, and anxiety-like behaviour, while delaying disease progression in CKD mice. These effects suggest that bioactive substances secreted by A. muciniphila play a key regulatory role and are closely related to tryptophan metabolism in the intestine. In addition, our results indicate that dysbiosis of the gut microbiota in CKD mice suppresses the regulatory potential of A. muciniphila. This study lays an experimental foundation for future biological mechanism research.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-026-04868-1.
Additional Links: PMID-41820827
PubMed:
Citation:
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@article {pmid41820827,
year = {2026},
author = {Ban, Y and Zhang, H and Xu, Y and Chen, F and Wei, Q and Wen, X and Yin, L and Dong, Z and Zhou, Q and Ge, W},
title = {Akkermansia muciniphila confers renal protection in chronic kidney disease: a multi-omics mechanistic investigation.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {},
pmid = {41820827},
issn = {1471-2180},
support = {202303//Lianyungang Health Science and Technology Project-202303 in Lianyungang City/ ; JOUMIRF010//Research Fund Project, College of Marine Pharmaceutical Industry, Jiangsu Ocean University/ ; },
abstract = {BACKGROUND: Akkermansia muciniphila (A. muciniphila) improved serum metabolism and renal fibrosis in the mouse model of chronic kidney disease (CKD) via the gut-kidney axis, slowing renal function decline. However, the biological components and underlying metabolic pathways remain unclear. Using a CKD mouse model, we aimed to identify the biological constituents of A. muciniphila that drive its regulatory effects in renal injury. Integrated microbiome and metabolomics analyses further elucidated the metabolic mechanisms of renoprotection, providing a theoretical foundation for the development of evidence-based clinical interventions.
METHODS: A CKD mouse model was established using 5/6 nephrectomy, with sham-operated mice (n = 7) serving as controls. Twenty-eight CKD mice were randomly assigned to four groups and treated with PBS, A. muciniphila, pasteurised A. muciniphila, or A. muciniphila combined with vancomycin by gavage. Serum and kidney tissues were collected to assess renal function, and histopathology was performed to identify the key biological components of A. muciniphila. Faecal samples were subjected to integrated microbiome and metabolomic analyses to identify the metabolic pathways involved in renoprotection. Behavioural experiments were performed to observe the effect of A. muciniphila on the behaviour of CKD mice. Single-factor analysis of variance and post-hoc tests were used for intergroup comparisons.
RESULTS: Serum analysis showed that the levels of serum creatinine, urea nitrogen and cystatin C in mice treated with A. muciniphila combined with vancomycin were significantly decreased. Reverse-transcription polymerase chain reaction showed that the renal injury marker Kim-1 was significantly decreased after A. muciniphila intervention. The levels of the renal injury (Ngal) and fibrosis (Col1a1, TIMP-1 and Fibronectin) markers showed a downward trend. 16 S rRNA analysis revealed that, following A. muciniphila intervention, the health index of the intestinal flora in CKD mice was significantly increased; however, the abundances of Turicibacter, Dubosiella and norank_f_UCG-010 were decreased. Metabolomic analysis revealed a strong correlation between A. muciniphila and the tryptophan metabolic pathway. Behavioural experiments showed that the exercise activity and anxiety-like behaviour of CKD mice were significantly improved after intervention with A. muciniphila, and the effect of A. muciniphila combined with vancomycin was better than that of A. muciniphila or pasteurised A. muciniphila alone.
CONCLUSION: Our findings demonstrate that A. muciniphila combined with vancomycin intervention ameliorates kidney injury, body dysfunction, and anxiety-like behaviour, while delaying disease progression in CKD mice. These effects suggest that bioactive substances secreted by A. muciniphila play a key regulatory role and are closely related to tryptophan metabolism in the intestine. In addition, our results indicate that dysbiosis of the gut microbiota in CKD mice suppresses the regulatory potential of A. muciniphila. This study lays an experimental foundation for future biological mechanism research.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-026-04868-1.},
}
RevDate: 2026-04-21
A novel obesity index reveals obesity-associated microbiota changes after weight loss intervention in a Spanish population.
Nutrition journal, 25(1):.
BACKGROUND & OBJECTIVES: Gut microbiota specific taxa influencing a higher or lower risk for developing obesity and related metabolic parameters remain unclear. Here, we aimed to identify gut microbiome fingerprints associated with obesity using an integrated obesity index (OBIndex), and to evaluate how these profiles change after a hypocaloric nutritional intervention with two different diets.
SUBJECTS & METHODS: 295 Spanish adult volunteers participating in the Obekit study were classified into LOW or HIGH degree of obesity according to a novel obesity index (OBIndex), based on the combination of three parameters: body mass index (BMI), fat mass (%), and waist circumference (WC). Differential abundant taxa between the two groups were investigated, at baseline together with the changes in their abundance after a weight-loss intervention with two different hypocaloric diets (Moderately high protein (MHP) and low fat (LF)).
RESULTS: The classification of participants using the OBIndex effectively differentiated obesity status, overcoming the inherent limitations of BMI, WC, and fat mass when considered individually. MHP diet was associated with an improvement in obesity status in women, while LF diet showed better outcomes in men. In relation to these improvements, changes in gut microbiota were observed. We found that Mediterraneibacter levels decreased only in men who experienced a significant improvement in their obesity status. Additionally, Agathobacter levels in participants who improved their physiological condition were reduced to match those of individuals who already exhibited a healthier status at baseline. Alongside these findings, we identified two poorly studied genera, Pseudobutyricicoccus and Intestinimonas, which were associated with a healthier profile at baseline and increased in abundance following the nutritional intervention.
CONCLUSIONS: Our OBIndex helped to achieve a more accurate separation of our volunteers regarding their obesity status and, thus, identifying four obesity strong related bacteria. Particularly, Mediterraneibacter and Agathobacter were related to a worse obesity status whereas Pseudobutyricicoccus and Intestinimonas showed a negative association with obesity status suggesting a potential protective or anti-obesity role.
TRIAL REGISTRATION: The study protocol was approved by the ethical committee at the University of Navarra (Registration No. IR.MUI.RESEARCH.REC.1401.370) and registered online at clinicaltrials.gov (identifier NCT02737267).
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12937-026-01313-x.
Additional Links: PMID-41827016
PubMed:
Citation:
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@article {pmid41827016,
year = {2026},
author = {Alonso-Allende, J and Riezu-Boj, JI and Hualde, AR and Milagro, FI and Aranaz, P},
title = {A novel obesity index reveals obesity-associated microbiota changes after weight loss intervention in a Spanish population.},
journal = {Nutrition journal},
volume = {25},
number = {1},
pages = {},
pmid = {41827016},
issn = {1475-2891},
support = {CB12/03/30002//Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición/ ; 0011-1383-2022-000000//Gobierno de Navarra/ ; PID2022-141766OB-I00//Ministerio de Ciencia, Innovación y Universidades/ ; },
abstract = {BACKGROUND & OBJECTIVES: Gut microbiota specific taxa influencing a higher or lower risk for developing obesity and related metabolic parameters remain unclear. Here, we aimed to identify gut microbiome fingerprints associated with obesity using an integrated obesity index (OBIndex), and to evaluate how these profiles change after a hypocaloric nutritional intervention with two different diets.
SUBJECTS & METHODS: 295 Spanish adult volunteers participating in the Obekit study were classified into LOW or HIGH degree of obesity according to a novel obesity index (OBIndex), based on the combination of three parameters: body mass index (BMI), fat mass (%), and waist circumference (WC). Differential abundant taxa between the two groups were investigated, at baseline together with the changes in their abundance after a weight-loss intervention with two different hypocaloric diets (Moderately high protein (MHP) and low fat (LF)).
RESULTS: The classification of participants using the OBIndex effectively differentiated obesity status, overcoming the inherent limitations of BMI, WC, and fat mass when considered individually. MHP diet was associated with an improvement in obesity status in women, while LF diet showed better outcomes in men. In relation to these improvements, changes in gut microbiota were observed. We found that Mediterraneibacter levels decreased only in men who experienced a significant improvement in their obesity status. Additionally, Agathobacter levels in participants who improved their physiological condition were reduced to match those of individuals who already exhibited a healthier status at baseline. Alongside these findings, we identified two poorly studied genera, Pseudobutyricicoccus and Intestinimonas, which were associated with a healthier profile at baseline and increased in abundance following the nutritional intervention.
CONCLUSIONS: Our OBIndex helped to achieve a more accurate separation of our volunteers regarding their obesity status and, thus, identifying four obesity strong related bacteria. Particularly, Mediterraneibacter and Agathobacter were related to a worse obesity status whereas Pseudobutyricicoccus and Intestinimonas showed a negative association with obesity status suggesting a potential protective or anti-obesity role.
TRIAL REGISTRATION: The study protocol was approved by the ethical committee at the University of Navarra (Registration No. IR.MUI.RESEARCH.REC.1401.370) and registered online at clinicaltrials.gov (identifier NCT02737267).
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12937-026-01313-x.},
}
RevDate: 2026-04-20
CmpDate: 2026-04-20
Microbiome-derived metabolites alleviate chronic pain in a reserpine-induced model of fibromyalgia.
iScience, 29(4):115406.
Fibromyalgia is a chronic pain disorder driven by central sensitization and neuroinflammation, increasingly linked to gut-brain axis dysfunction. Here, we delineate a gut-to-CNS axis for pain modulation, demonstrating that an acetate-producing diet alleviates reserpine-induced-fibromyalgia in a rodent model. We show that diet rich in acetylated high-amylose maize starch shifts the gut microbiome to favor acetate-producing bacteria, increasing systemic acetate levels and reducing pain hypersensitivity. This is associated with reduced spinal microglia activation and anti-inflammatory cytokine gene expression, with elevated IL-10 mRNA in the DRG and IL-10, IL-2, and IL-6 in the spinal cord. Electrophysiologically, we observe reduced hyperexcitability in the dorsal horn and increased inhibitory activity. The mechanism driving this change involves reduced prostaglandin-E2 (PGE2)-mediated suppression of glycinergic inhibition, a direct consequence of maintaining microglia in quiescent state. These findings link dietary metabolites to reduced fibromyalgia-like pathology and identify targeted nutrition as a potential disease-modifying therapy for chronic pain.
Additional Links: PMID-42006347
PubMed:
Citation:
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@article {pmid42006347,
year = {2026},
author = {Chen, S and Shanmuganathan, D and Imlach, WL},
title = {Microbiome-derived metabolites alleviate chronic pain in a reserpine-induced model of fibromyalgia.},
journal = {iScience},
volume = {29},
number = {4},
pages = {115406},
pmid = {42006347},
issn = {2589-0042},
abstract = {Fibromyalgia is a chronic pain disorder driven by central sensitization and neuroinflammation, increasingly linked to gut-brain axis dysfunction. Here, we delineate a gut-to-CNS axis for pain modulation, demonstrating that an acetate-producing diet alleviates reserpine-induced-fibromyalgia in a rodent model. We show that diet rich in acetylated high-amylose maize starch shifts the gut microbiome to favor acetate-producing bacteria, increasing systemic acetate levels and reducing pain hypersensitivity. This is associated with reduced spinal microglia activation and anti-inflammatory cytokine gene expression, with elevated IL-10 mRNA in the DRG and IL-10, IL-2, and IL-6 in the spinal cord. Electrophysiologically, we observe reduced hyperexcitability in the dorsal horn and increased inhibitory activity. The mechanism driving this change involves reduced prostaglandin-E2 (PGE2)-mediated suppression of glycinergic inhibition, a direct consequence of maintaining microglia in quiescent state. These findings link dietary metabolites to reduced fibromyalgia-like pathology and identify targeted nutrition as a potential disease-modifying therapy for chronic pain.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Gut microbial signatures and stability are associated with a co-diagnosis of endometriosis and inflammatory bowel disease.
iScience, 29(4):115437.
Emerging evidence suggests that the gut microbiota plays a crucial role in endometriosis (Endo) and inflammatory bowel disease (IBD). This study aimed to explore gut microbial signatures in women with either or both conditions, compared to healthy controls. Fecal samples underwent 16S rRNA sequencing to profile the gut microbiome. Endo-IBD patients had the most profound alterations including reduced microbial richness and evenness as well as bacterial signature changes. Specific bacteria taxa, including Akkermansia and Alistipes, were notably depleted in Endo-IBD patients, suggesting a compromised gut barrier and heightened inflammatory potential. Conversely, Blautia was enriched in Endo-IBD patients. Longitudinal microbiome assessment indicated a persistent dysbiotic signature in Endo-IBD and IBD groups, with microbial instability correlating with disease severity. The findings highlight an intensified impact of having a diagnosis of both conditions and further highlights the potential for microbiome-based diagnostics and the design of personalized interventions to restore microbial balance.
Additional Links: PMID-42006367
PubMed:
Citation:
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@article {pmid42006367,
year = {2026},
author = {Damm, GK and Zhang, F and Koentgen, S and Jayawardana, T and Houshyar, Y and Read, S and Condous, G and El-Assaad, F and Hold, GL},
title = {Gut microbial signatures and stability are associated with a co-diagnosis of endometriosis and inflammatory bowel disease.},
journal = {iScience},
volume = {29},
number = {4},
pages = {115437},
pmid = {42006367},
issn = {2589-0042},
abstract = {Emerging evidence suggests that the gut microbiota plays a crucial role in endometriosis (Endo) and inflammatory bowel disease (IBD). This study aimed to explore gut microbial signatures in women with either or both conditions, compared to healthy controls. Fecal samples underwent 16S rRNA sequencing to profile the gut microbiome. Endo-IBD patients had the most profound alterations including reduced microbial richness and evenness as well as bacterial signature changes. Specific bacteria taxa, including Akkermansia and Alistipes, were notably depleted in Endo-IBD patients, suggesting a compromised gut barrier and heightened inflammatory potential. Conversely, Blautia was enriched in Endo-IBD patients. Longitudinal microbiome assessment indicated a persistent dysbiotic signature in Endo-IBD and IBD groups, with microbial instability correlating with disease severity. The findings highlight an intensified impact of having a diagnosis of both conditions and further highlights the potential for microbiome-based diagnostics and the design of personalized interventions to restore microbial balance.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
The Uterine Microbiota in Mares With Endometritis: Impacts of Antibiotic Treatment.
Veterinary medicine international, 2026:5270993.
Despite growing interest in the role of the reproductive microbiota, the uterine microbiota of mares has been only scarcely investigated using sequencing approaches. The aims of this study were to describe the uterine microbiota of mares with endometritis and the effects of antibiotic treatment using both 16S rRNA sequencing and culture. Five mares with clinical signs of endometritis and a positive bacteriological culture were enrolled. During the follicular phase (T0), uterine samples were collected using a double-guarded cytobrush and swab for microbiome and bacteriological analysis, respectively. Following the antimicrobial susceptibility test, they were treated with intrauterine infusions of ceftiofur sodium, and samplings were repeated during the subsequent follicular phase (T1). According to bacterial culture, at T0, Streptococcus equi zooepidemicus was identified in 4 mares and Escherichia coli in one. At T1, 3 mares resulted negative, one was positive for Staphylococcus xylosus, and one continued to test positive for E. coli. According to NGS, the most represented genera at T0 were Streptococcus, Escherichia-Shigella, Corynebacterium, Arcanobacterium, Porphyromonas, and Staphylococcus. The first 3 genera dominated the microbiome of 4 mares with a relative abundance ranging from 44% to 99%. At T1, these genera's relative abundance dropped, and the most abundant were Acinetobacter, Staphylococcus, and Pseudomonas. Furthermore, after intrauterine infusion of ceftiofur, the microbiome was more diverse, according to Shannon and Simpson indexes (p < 0.05).
Additional Links: PMID-42006445
PubMed:
Citation:
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@article {pmid42006445,
year = {2026},
author = {Donato, GG and Nebbia, P and Stella, MC and Gionechetti, F and Ala, U and Cristofoli, D and Robino, P and Pallavicini, A and Nervo, T},
title = {The Uterine Microbiota in Mares With Endometritis: Impacts of Antibiotic Treatment.},
journal = {Veterinary medicine international},
volume = {2026},
number = {},
pages = {5270993},
pmid = {42006445},
issn = {2090-8113},
abstract = {Despite growing interest in the role of the reproductive microbiota, the uterine microbiota of mares has been only scarcely investigated using sequencing approaches. The aims of this study were to describe the uterine microbiota of mares with endometritis and the effects of antibiotic treatment using both 16S rRNA sequencing and culture. Five mares with clinical signs of endometritis and a positive bacteriological culture were enrolled. During the follicular phase (T0), uterine samples were collected using a double-guarded cytobrush and swab for microbiome and bacteriological analysis, respectively. Following the antimicrobial susceptibility test, they were treated with intrauterine infusions of ceftiofur sodium, and samplings were repeated during the subsequent follicular phase (T1). According to bacterial culture, at T0, Streptococcus equi zooepidemicus was identified in 4 mares and Escherichia coli in one. At T1, 3 mares resulted negative, one was positive for Staphylococcus xylosus, and one continued to test positive for E. coli. According to NGS, the most represented genera at T0 were Streptococcus, Escherichia-Shigella, Corynebacterium, Arcanobacterium, Porphyromonas, and Staphylococcus. The first 3 genera dominated the microbiome of 4 mares with a relative abundance ranging from 44% to 99%. At T1, these genera's relative abundance dropped, and the most abundant were Acinetobacter, Staphylococcus, and Pseudomonas. Furthermore, after intrauterine infusion of ceftiofur, the microbiome was more diverse, according to Shannon and Simpson indexes (p < 0.05).},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Plant-bacteria hybrid nanovesicles for targeted sonodynamic therapy: A microbiome-friendly precision strike against H. pylori infections.
Materials today. Bio, 38:103085.
Rising antibiotic resistance and adverse effects on commensal gut microbiota severely compromise conventional antibiotic therapies for Helicobacter pylori infection. Sonodynamic therapy (SDT), which employs low-intensity ultrasound to activate sonosensitizers for localized generation of cytotoxic reactive oxygen species (ROS), presents a promising non-antibiotic alternative with minimal resistance development risk. However, the efficacy of SDT is inherently constrained by the short diffusion radius and lifetime of ROS. Herein, we developed a homologous-targeting biomimetic sonosensitizer platform to overcome this limitation: hybrid membrane nanovesicles (TNVs-DMVs) engineered from turmeric plant-derived exosome-like nanovesicles (TNVs) and H. pylori-derived double membrane vesicles (DMVs). TNVs contain sonosensitizer curcumin and improve its solubility, yet SDT efficacy against H. pylori is limited. The DMVs endow TNVs-DMVs with intrinsic homologous targeting capability towards H. pylori, significantly enhancing the intracellular delivery of curcumin and subsequent ROS generation within bacterial cells. As a result, TNVs-DMVs achieved potent eradication of H. pylori in both acidic and neutral conditions without inducing detectable resistance. Moreover, TNVs-DMVs exhibited superior mucus penetration compared to TNVs alone, enabling effective elimination of H. pylori and its biofilms residing within the protective gastric mucus layer. In an H. pylori-infected mouse model, TNVs-DMVs mediated SDT demonstrated efficacy surpassing free TNVs and comparable to standard triple antibiotic therapy. Importantly, unlike triple therapy which depletes commensal flora, TNVs-DMVs treatment not only preserves intestinal microbiota homeostasis but also significantly increases populations of beneficial bacteria. This rationally designed TNVs-DMVs platform represents a transformative therapeutic modality, offering resistance-free eradication of H. pylori while maintaining microbiome health, distinct from conventional antibiotics.
Additional Links: PMID-42006709
PubMed:
Citation:
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@article {pmid42006709,
year = {2026},
author = {Yang, L and Ye, Q and Peng, X and Yu, J and Xiao, X and Wang, L and Yang, YY and Yuan, P and Tian, GB and Ding, X},
title = {Plant-bacteria hybrid nanovesicles for targeted sonodynamic therapy: A microbiome-friendly precision strike against H. pylori infections.},
journal = {Materials today. Bio},
volume = {38},
number = {},
pages = {103085},
pmid = {42006709},
issn = {2590-0064},
abstract = {Rising antibiotic resistance and adverse effects on commensal gut microbiota severely compromise conventional antibiotic therapies for Helicobacter pylori infection. Sonodynamic therapy (SDT), which employs low-intensity ultrasound to activate sonosensitizers for localized generation of cytotoxic reactive oxygen species (ROS), presents a promising non-antibiotic alternative with minimal resistance development risk. However, the efficacy of SDT is inherently constrained by the short diffusion radius and lifetime of ROS. Herein, we developed a homologous-targeting biomimetic sonosensitizer platform to overcome this limitation: hybrid membrane nanovesicles (TNVs-DMVs) engineered from turmeric plant-derived exosome-like nanovesicles (TNVs) and H. pylori-derived double membrane vesicles (DMVs). TNVs contain sonosensitizer curcumin and improve its solubility, yet SDT efficacy against H. pylori is limited. The DMVs endow TNVs-DMVs with intrinsic homologous targeting capability towards H. pylori, significantly enhancing the intracellular delivery of curcumin and subsequent ROS generation within bacterial cells. As a result, TNVs-DMVs achieved potent eradication of H. pylori in both acidic and neutral conditions without inducing detectable resistance. Moreover, TNVs-DMVs exhibited superior mucus penetration compared to TNVs alone, enabling effective elimination of H. pylori and its biofilms residing within the protective gastric mucus layer. In an H. pylori-infected mouse model, TNVs-DMVs mediated SDT demonstrated efficacy surpassing free TNVs and comparable to standard triple antibiotic therapy. Importantly, unlike triple therapy which depletes commensal flora, TNVs-DMVs treatment not only preserves intestinal microbiota homeostasis but also significantly increases populations of beneficial bacteria. This rationally designed TNVs-DMVs platform represents a transformative therapeutic modality, offering resistance-free eradication of H. pylori while maintaining microbiome health, distinct from conventional antibiotics.},
}
RevDate: 2026-04-20
CmpDate: 2026-04-20
Natural carrier-free self-assembled binary polyphenol nanoparticles remodel the gut microenvironment for inflammatory bowel disease prevention.
Materials today. Bio, 38:103063.
Developing biocompatible, multi-target therapeutics remains a critical challenge in the management of inflammatory bowel disease (IBD). Herein, we engineered a carrier-free nanoplatform (Cur-Ant NPs) via the facile self-assembly of two natural polyphenols: curcumin (Cur) and anthocyanin (Ant). Spectroscopic analysis and molecular dynamics simulations confirmed that the assembly is stabilized by robust π-π stacking and hydrogen bonding networks, yielding uniform, spherical nanostructures with integrated functionality. In a dextran sulfate sodium (DSS)-induced colitis model, orally administered Cur-Ant NPs demonstrated superior therapeutic efficacy compared to both free polyphenols and the clinical standard, sulfasalazine (SASP). The nanoparticles' potent anti-inflammatory activity was initially validated in a zebrafish model, where they effectively inhibited neutrophil infiltration and scavenged reactive oxygen species (ROS). These protective effects were further substantiated in a murine model, where multi-omics analysis revealed a tripartite mechanism of action: reinforcing the intestinal epithelial barrier, mitigating pro-inflammatory cytokine responses, and remodeling the dysbiotic gut microbiome. Our findings establish Cur-Ant NPs as a potent, safe candidate for IBD prevention and highlight a scalable, green engineering strategy for designing next-generation nanomedicines based on the supramolecular co-assembly of natural bioactive agents.
Additional Links: PMID-42006721
PubMed:
Citation:
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@article {pmid42006721,
year = {2026},
author = {Xie, Q and Xu, H and Yang, X and Chen, Y and Xu, ZZ},
title = {Natural carrier-free self-assembled binary polyphenol nanoparticles remodel the gut microenvironment for inflammatory bowel disease prevention.},
journal = {Materials today. Bio},
volume = {38},
number = {},
pages = {103063},
pmid = {42006721},
issn = {2590-0064},
abstract = {Developing biocompatible, multi-target therapeutics remains a critical challenge in the management of inflammatory bowel disease (IBD). Herein, we engineered a carrier-free nanoplatform (Cur-Ant NPs) via the facile self-assembly of two natural polyphenols: curcumin (Cur) and anthocyanin (Ant). Spectroscopic analysis and molecular dynamics simulations confirmed that the assembly is stabilized by robust π-π stacking and hydrogen bonding networks, yielding uniform, spherical nanostructures with integrated functionality. In a dextran sulfate sodium (DSS)-induced colitis model, orally administered Cur-Ant NPs demonstrated superior therapeutic efficacy compared to both free polyphenols and the clinical standard, sulfasalazine (SASP). The nanoparticles' potent anti-inflammatory activity was initially validated in a zebrafish model, where they effectively inhibited neutrophil infiltration and scavenged reactive oxygen species (ROS). These protective effects were further substantiated in a murine model, where multi-omics analysis revealed a tripartite mechanism of action: reinforcing the intestinal epithelial barrier, mitigating pro-inflammatory cytokine responses, and remodeling the dysbiotic gut microbiome. Our findings establish Cur-Ant NPs as a potent, safe candidate for IBD prevention and highlight a scalable, green engineering strategy for designing next-generation nanomedicines based on the supramolecular co-assembly of natural bioactive agents.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
The role of gut microbiota mediated ferroptosis in PCOS and the therapeutic potential of Chinese herbal medicine.
Frontiers in medicine, 13:1730795.
Polycystic ovary syndrome (PCOS) is a complex reproductive endocrine metabolic disorder whose pathogenesis remains incompletely understood. In recent years, the role of ferroptosis-a novel form of iron-dependent programmed cell death-in the pathogenesis of PCOS has gradually drawn attention. This review proposes an innovative perspective: gut microbiota dysbiosis may be a potential upstream trigger of ferroptosis in PCOS ovarian granulosa cells. Microbiome dysbiosis disrupts iron homeostasis and reduces the production of antioxidant metabolites such as short-chain fatty acids (SCFAs) and bile acids (BAs), thereby exacerbating systemic and local ovarian oxidative stress. This induces ferroptosis, leading to impaired follicular development and insulin resistance. Traditional Chinese Medicine (TCM) demonstrates significant potential in regulating gut microbiota and inhibiting ferroptosis. Based on this, this study explores the role of the gut microbiota-ferroptosis axis in PCOS, focusing on the scientific rationale and application prospects of treating PCOS by intervening in this axis using TCM monomers and compounds such as berberine and quercetin. With its multi-target regulatory effects and favorable safety profile, TCM may offer benefits as an adjunct or alternative to conventional therapies. This research aims to provide theoretical references for developing novel therapeutic strategies.
Additional Links: PMID-42006870
PubMed:
Citation:
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@article {pmid42006870,
year = {2026},
author = {Lv, Y and Li, D and Ding, N and Kuang, H},
title = {The role of gut microbiota mediated ferroptosis in PCOS and the therapeutic potential of Chinese herbal medicine.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1730795},
pmid = {42006870},
issn = {2296-858X},
abstract = {Polycystic ovary syndrome (PCOS) is a complex reproductive endocrine metabolic disorder whose pathogenesis remains incompletely understood. In recent years, the role of ferroptosis-a novel form of iron-dependent programmed cell death-in the pathogenesis of PCOS has gradually drawn attention. This review proposes an innovative perspective: gut microbiota dysbiosis may be a potential upstream trigger of ferroptosis in PCOS ovarian granulosa cells. Microbiome dysbiosis disrupts iron homeostasis and reduces the production of antioxidant metabolites such as short-chain fatty acids (SCFAs) and bile acids (BAs), thereby exacerbating systemic and local ovarian oxidative stress. This induces ferroptosis, leading to impaired follicular development and insulin resistance. Traditional Chinese Medicine (TCM) demonstrates significant potential in regulating gut microbiota and inhibiting ferroptosis. Based on this, this study explores the role of the gut microbiota-ferroptosis axis in PCOS, focusing on the scientific rationale and application prospects of treating PCOS by intervening in this axis using TCM monomers and compounds such as berberine and quercetin. With its multi-target regulatory effects and favorable safety profile, TCM may offer benefits as an adjunct or alternative to conventional therapies. This research aims to provide theoretical references for developing novel therapeutic strategies.},
}
RevDate: 2026-04-21
Cats on dry kibble diet have significantly different microbiome than those on canned wet food.
npj veterinary sciences, 1(1):1.
Domestic cats (Felis catus) are understudied regarding how commercial diets impact their gut microbiomes. Here, we reanalyzed the 16S rRNA gene (V4) amplicon sequencing Kittybiome dataset, using new tools and techniques. Results demonstrated significant microbial composition differences between cats eating commercial dry kibble diets and those eating canned wet food. Kibble-fed cats showed enriched Prevotella, Bifidobacterium, and Megamonas amplicon sequencing variants (ASVs), linked to carbohydrate metabolism and metabolic disease.
Additional Links: PMID-42006912
PubMed:
Citation:
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@article {pmid42006912,
year = {2026},
author = {Allaband, C and Ganz, HH and Rojas, CA and Knight, R},
title = {Cats on dry kibble diet have significantly different microbiome than those on canned wet food.},
journal = {npj veterinary sciences},
volume = {1},
number = {1},
pages = {1},
pmid = {42006912},
issn = {3059-328X},
abstract = {Domestic cats (Felis catus) are understudied regarding how commercial diets impact their gut microbiomes. Here, we reanalyzed the 16S rRNA gene (V4) amplicon sequencing Kittybiome dataset, using new tools and techniques. Results demonstrated significant microbial composition differences between cats eating commercial dry kibble diets and those eating canned wet food. Kibble-fed cats showed enriched Prevotella, Bifidobacterium, and Megamonas amplicon sequencing variants (ASVs), linked to carbohydrate metabolism and metabolic disease.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Olanzapine and peripheral metabolic dysregulation: organ-resolved mechanisms, risk, and MASLD-aligned care pathways.
Frontiers in pharmacology, 16:1729264.
This review examines how olanzapine drives metabolic injury beyond the brain and why an organ-resolved perspective is needed. We synthesize clinical signals of early weight gain, insulin resistance, dyslipidemia, and steatotic liver disease, and integrate translational evidence across liver, adipose tissue, skeletal muscle, pancreatic β-cells, and the gut-liver axis. Mechanistic strands include disordered hepatic lipid handling, suppression of brown-fat thermogenesis, β-cell endoplasmic-reticulum stress with impaired secretion, and skeletal-muscle insulin-signaling defects with altered epigenetic programs that blunt glucose disposal. We summarize modifiers of risk across life stage, treatment exposure, genetic variation, smoking status, and pregnancy, and distill a pragmatic pathway that prioritizes early reassessment, MASLD-aligned liver evaluation, targeted lifestyle treatment, metformin for early deterioration, and GLP-1 receptor agonists when required. We advance the view that weight-independent extra-cerebral mechanisms are central to olanzapine's metabolic liability and that psychiatric practice should adopt metabolic frameworks used in hepatology and endocrinology. We propose an agenda for organ-specific human phenotyping and exposure-aware designs that integrate therapeutic drug monitoring with microbiome, metabolomics, and bile-acid profiling, alongside comparative trials that test stepped algorithms within psychiatric care. This perspective outlines a path to preserve antipsychotic efficacy while reducing preventable systemic metabolic harm.
Additional Links: PMID-42007333
PubMed:
Citation:
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@article {pmid42007333,
year = {2025},
author = {Weng, S and Lin, J and Chai, D},
title = {Olanzapine and peripheral metabolic dysregulation: organ-resolved mechanisms, risk, and MASLD-aligned care pathways.},
journal = {Frontiers in pharmacology},
volume = {16},
number = {},
pages = {1729264},
pmid = {42007333},
issn = {1663-9812},
abstract = {This review examines how olanzapine drives metabolic injury beyond the brain and why an organ-resolved perspective is needed. We synthesize clinical signals of early weight gain, insulin resistance, dyslipidemia, and steatotic liver disease, and integrate translational evidence across liver, adipose tissue, skeletal muscle, pancreatic β-cells, and the gut-liver axis. Mechanistic strands include disordered hepatic lipid handling, suppression of brown-fat thermogenesis, β-cell endoplasmic-reticulum stress with impaired secretion, and skeletal-muscle insulin-signaling defects with altered epigenetic programs that blunt glucose disposal. We summarize modifiers of risk across life stage, treatment exposure, genetic variation, smoking status, and pregnancy, and distill a pragmatic pathway that prioritizes early reassessment, MASLD-aligned liver evaluation, targeted lifestyle treatment, metformin for early deterioration, and GLP-1 receptor agonists when required. We advance the view that weight-independent extra-cerebral mechanisms are central to olanzapine's metabolic liability and that psychiatric practice should adopt metabolic frameworks used in hepatology and endocrinology. We propose an agenda for organ-specific human phenotyping and exposure-aware designs that integrate therapeutic drug monitoring with microbiome, metabolomics, and bile-acid profiling, alongside comparative trials that test stepped algorithms within psychiatric care. This perspective outlines a path to preserve antipsychotic efficacy while reducing preventable systemic metabolic harm.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
An overview of the role of the gut microbiota in rheumatoid arthritis.
Microbiome research reports, 5(1):3.
Rheumatoid arthritis (RA) is a chronic autoimmune disease preceded by a prolonged preclinical phase marked by the emergence of autoantibodies and mucosal immune dysregulation. Evidence from human studies and animal models consistently demonstrates that gut microbiota dysbiosis contributes to this transition, particularly through impaired intestinal barrier function, activation of pro-inflammatory pathways, and molecular mimicry. Specific taxa - including Prevotella copri, Collinsella aerofaciens, and reductions in butyrate-producing bacteria - have been linked to heightened systemic inflammation, increased T helper 17 responses, and the generation of RA-associated autoantibodies. Current research also indicates that anti-rheumatic medications such as methotrexate, sulfasalazine, and minocycline produce measurable shifts in gut microbial composition, suggesting that microbiota-drug interactions may influence treatment response. Therapeutic approaches aimed at modifying gut ecology - including dietary interventions, prebiotics, probiotics, and fecal microbiota transplantation - show early potential in restoring microbial balance, improving intestinal barrier integrity, and reducing inflammatory markers, although evidence in the preclinical RA stage remains limited. Additionally, emerging data highlight the importance of intestinal autophagy and microRNA networks in regulating epithelial integrity and systemic immune activation. Taken together, the literature supports a mechanistic link between gut dysbiosis and the onset of RA. It points to microbiota-targeted strategies as promising avenues for delaying or preventing disease progression. Future studies should prioritize longitudinal analyses and interventional trials focusing specifically on individuals at risk for RA.
Additional Links: PMID-42007373
PubMed:
Citation:
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@article {pmid42007373,
year = {2026},
author = {Poznyak, AV and Vatlin, AA and Pavshintsev, VV and Mitkin, NA and Maltseva, ON and Utkina, AS and Orekhov, AN},
title = {An overview of the role of the gut microbiota in rheumatoid arthritis.},
journal = {Microbiome research reports},
volume = {5},
number = {1},
pages = {3},
pmid = {42007373},
issn = {2771-5965},
abstract = {Rheumatoid arthritis (RA) is a chronic autoimmune disease preceded by a prolonged preclinical phase marked by the emergence of autoantibodies and mucosal immune dysregulation. Evidence from human studies and animal models consistently demonstrates that gut microbiota dysbiosis contributes to this transition, particularly through impaired intestinal barrier function, activation of pro-inflammatory pathways, and molecular mimicry. Specific taxa - including Prevotella copri, Collinsella aerofaciens, and reductions in butyrate-producing bacteria - have been linked to heightened systemic inflammation, increased T helper 17 responses, and the generation of RA-associated autoantibodies. Current research also indicates that anti-rheumatic medications such as methotrexate, sulfasalazine, and minocycline produce measurable shifts in gut microbial composition, suggesting that microbiota-drug interactions may influence treatment response. Therapeutic approaches aimed at modifying gut ecology - including dietary interventions, prebiotics, probiotics, and fecal microbiota transplantation - show early potential in restoring microbial balance, improving intestinal barrier integrity, and reducing inflammatory markers, although evidence in the preclinical RA stage remains limited. Additionally, emerging data highlight the importance of intestinal autophagy and microRNA networks in regulating epithelial integrity and systemic immune activation. Taken together, the literature supports a mechanistic link between gut dysbiosis and the onset of RA. It points to microbiota-targeted strategies as promising avenues for delaying or preventing disease progression. Future studies should prioritize longitudinal analyses and interventional trials focusing specifically on individuals at risk for RA.},
}
RevDate: 2026-04-20
CmpDate: 2026-04-20
A responder-informed gut microbial consortium enhances anti-PD-1 efficacy in a mouse cancer model.
Microbiome research reports, 5(1):2.
Aim: Immune checkpoint inhibitors (ICIs), particularly anti-programmed cell death protein 1 (PD-1) therapy, have improved cancer treatment outcomes, yet durable benefit is achieved in only a subset of patients. Growing evidence implicates the gut microbiome as a modulator of ICI responsiveness, but defined and experimentally validated microbial strategies remain limited. This study aimed to identify responder-associated gut microbes and to evaluate a defined bacterial consortium for enhancing PD-1 blockade efficacy. Methods: Publicly available shotgun metagenomic datasets from anti-PD-1-treated cancer patients were re-analyzed to compare gut microbiome profiles between responders and non-responders. Bacterial taxa reproducibly enriched in responders were selected based on consistency across analytical criteria and cultivability and assembled into a four-strain consortium (UJ-04). The immune-adjuvant potential of UJ-04, alone or combined with anti-PD-1 therapy, was evaluated in a B16-F10 melanoma mouse model, with tumor growth and immune responses assessed by flow cytometry. Results: Metagenomic re-analysis identified four commensal bacterial taxa consistently enriched in responder patients, forming the defined UJ-04 consortium. While UJ-04 alone showed minimal antitumor activity, combination treatment with anti-PD-1 significantly enhanced tumor growth inhibition compared with anti-PD-1 monotherapy. This effect was accompanied by increased intratumoral CD8[+] T cells and natural killer cells, with concordant immune trends in peripheral compartments. Conclusion: A responder-informed, defined microbial consortium functionally translates clinical microbiome associations into in vivo validation and enhances PD-1 blockade efficacy by modulating host antitumor immunity. These findings support defined bacterial consortia as microbiome-based immunomodulatory adjuncts for immunotherapy.
Additional Links: PMID-42007374
PubMed:
Citation:
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@article {pmid42007374,
year = {2026},
author = {Jeong, UJ and Ali, M and Park, YJ and You, JS and Yoon, SS},
title = {A responder-informed gut microbial consortium enhances anti-PD-1 efficacy in a mouse cancer model.},
journal = {Microbiome research reports},
volume = {5},
number = {1},
pages = {2},
pmid = {42007374},
issn = {2771-5965},
abstract = {Aim: Immune checkpoint inhibitors (ICIs), particularly anti-programmed cell death protein 1 (PD-1) therapy, have improved cancer treatment outcomes, yet durable benefit is achieved in only a subset of patients. Growing evidence implicates the gut microbiome as a modulator of ICI responsiveness, but defined and experimentally validated microbial strategies remain limited. This study aimed to identify responder-associated gut microbes and to evaluate a defined bacterial consortium for enhancing PD-1 blockade efficacy. Methods: Publicly available shotgun metagenomic datasets from anti-PD-1-treated cancer patients were re-analyzed to compare gut microbiome profiles between responders and non-responders. Bacterial taxa reproducibly enriched in responders were selected based on consistency across analytical criteria and cultivability and assembled into a four-strain consortium (UJ-04). The immune-adjuvant potential of UJ-04, alone or combined with anti-PD-1 therapy, was evaluated in a B16-F10 melanoma mouse model, with tumor growth and immune responses assessed by flow cytometry. Results: Metagenomic re-analysis identified four commensal bacterial taxa consistently enriched in responder patients, forming the defined UJ-04 consortium. While UJ-04 alone showed minimal antitumor activity, combination treatment with anti-PD-1 significantly enhanced tumor growth inhibition compared with anti-PD-1 monotherapy. This effect was accompanied by increased intratumoral CD8[+] T cells and natural killer cells, with concordant immune trends in peripheral compartments. Conclusion: A responder-informed, defined microbial consortium functionally translates clinical microbiome associations into in vivo validation and enhances PD-1 blockade efficacy by modulating host antitumor immunity. These findings support defined bacterial consortia as microbiome-based immunomodulatory adjuncts for immunotherapy.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Predicting Dietary Impact on Multiple Sclerosis-Related Symptoms With the Gut Microbiome: A Pilot Study Using Unsupervised Machine Learning.
Brain and behavior, 16(4):e71394.
BACKGROUND: Multiple sclerosis (MS) is a neurodegenerative disease where dietary intervention has emerged as a potential adjunct treatment. Recently, the modified Paleolithic elimination (MPE) diet, also known as the Wahls diet, and the low-saturated fat (LSF) diet, also known as the Swank diet, were linked to reduced fatigue and improved quality of life (QoL) in the WAVES study (NCT02914964). However, how diet impacts these outcomes remains unclear. As diet impacts gut microbiota, we investigated whether the baseline gut microbiota can predict response to diet in people with MS (pwMS).
METHODS: We performed fecal 16s rRNA sequencing to profile the microbiome changes associated with pwMS receiving the MPE (n = 11) and LSF diet (n = 12). Next, we utilized topic modeling, a machine learning technique, to determine whether baseline microbiome features predicted diet response in the combined MPE + LSF dietary cohort (n = 23).
RESULTS: Specific genera significantly differed over time on both diets. On the MPE diet, Hungateiclostridiaceae, Ruminiclostridium, and Shuttleworthia decreased, while Coriobacteriaceae Collinsella decreased on LSF. Predictive machine-learning analysis associated a baseline microbiome enriched with Akkermansia, Bacteroides, and Barnesiella with fatigue response in the combined MPE + LSF cohort. For a non-response in Mental QoL improvement in the combined MPE + LSF cohort, our analysis associated an enrichment of Faecalibacterium and Alistipes at the start of the diet.
DISCUSSION: Utilizing topic modeling, this pilot study identified baseline microbiota communities linked to improvements in fatigue and Mental QoL in pwMS on dietary intervention. These findings highlight the microbiota's role in dietary response and the potential for personalized nutrition. Given the small cohort and exploratory design, the results are hypothesis-generating and require validation in larger mechanistic studies.
Additional Links: PMID-42007545
PubMed:
Citation:
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@article {pmid42007545,
year = {2026},
author = {Meza, LA and Fitzjerrells, RL and Shemirani, F and Titcomb, TJ and Rubenstein, LM and Eyck, PT and Snetselaar, LG and Shahi, SK and Wahls, TL and Mangalam, AK},
title = {Predicting Dietary Impact on Multiple Sclerosis-Related Symptoms With the Gut Microbiome: A Pilot Study Using Unsupervised Machine Learning.},
journal = {Brain and behavior},
volume = {16},
number = {4},
pages = {e71394},
pmid = {42007545},
issn = {2162-3279},
support = {1RO1AI137075//NIAID/NIH/ ; 1I01CX002212//US Department of Veteran Affairs/ ; 1F31DE033564-01//NIDCR/NIH/ ; NIEHS/NIH P30 ES005605//University of Iowa Environmental Health Sciences Research Center/ ; UM1TR004403//National Center for Advancing Translational Sciences of the NIH/ ; 1506-04312//National Multiple Sclerosis Society/ ; //P. Heppelmann and M. Wacek Fund/ ; //the Carver Trust Pilot Grant/ ; //Center for Biocatalysis and Bioprocessing/ ; //University of Iowa institutional funds/ ; //Carter Chapman Shreve Family Foundation/ ; //Carter Chapman Shreve Fellowship Fund/ ; //Helen Harris Fund/ ; //University of Iowa College of Public Health Preventive Intervention Center/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Pilot Projects ; Male ; *Multiple Sclerosis/diet therapy/microbiology ; Female ; Adult ; Middle Aged ; *Unsupervised Machine Learning ; Feces/microbiology ; Quality of Life ; *Diet, Paleolithic ; *Diet ; RNA, Ribosomal, 16S ; },
abstract = {BACKGROUND: Multiple sclerosis (MS) is a neurodegenerative disease where dietary intervention has emerged as a potential adjunct treatment. Recently, the modified Paleolithic elimination (MPE) diet, also known as the Wahls diet, and the low-saturated fat (LSF) diet, also known as the Swank diet, were linked to reduced fatigue and improved quality of life (QoL) in the WAVES study (NCT02914964). However, how diet impacts these outcomes remains unclear. As diet impacts gut microbiota, we investigated whether the baseline gut microbiota can predict response to diet in people with MS (pwMS).
METHODS: We performed fecal 16s rRNA sequencing to profile the microbiome changes associated with pwMS receiving the MPE (n = 11) and LSF diet (n = 12). Next, we utilized topic modeling, a machine learning technique, to determine whether baseline microbiome features predicted diet response in the combined MPE + LSF dietary cohort (n = 23).
RESULTS: Specific genera significantly differed over time on both diets. On the MPE diet, Hungateiclostridiaceae, Ruminiclostridium, and Shuttleworthia decreased, while Coriobacteriaceae Collinsella decreased on LSF. Predictive machine-learning analysis associated a baseline microbiome enriched with Akkermansia, Bacteroides, and Barnesiella with fatigue response in the combined MPE + LSF cohort. For a non-response in Mental QoL improvement in the combined MPE + LSF cohort, our analysis associated an enrichment of Faecalibacterium and Alistipes at the start of the diet.
DISCUSSION: Utilizing topic modeling, this pilot study identified baseline microbiota communities linked to improvements in fatigue and Mental QoL in pwMS on dietary intervention. These findings highlight the microbiota's role in dietary response and the potential for personalized nutrition. Given the small cohort and exploratory design, the results are hypothesis-generating and require validation in larger mechanistic studies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology
Pilot Projects
Male
*Multiple Sclerosis/diet therapy/microbiology
Female
Adult
Middle Aged
*Unsupervised Machine Learning
Feces/microbiology
Quality of Life
*Diet, Paleolithic
*Diet
RNA, Ribosomal, 16S
RevDate: 2026-04-21
Pseudoalteromonas is a symbiont of marine invertebrates that exhibits broad patterns of phylosymbiosis.
The ISME journal pii:8659212 [Epub ahead of print].
Despite growing insights into the composition of marine invertebrate microbiomes, our understanding of their ecological and evolutionary patterns remains poor, owing to limited sampling depth and low-resolution datasets. Previous studies have provided conflicting results that both confirm and deny the existence of phylosymbiosis between marine invertebrates and marine bacteria. Here, we investigated potential animal-microbe symbioses in Pseudoalteromonas, a bacterial genus consistently identified as a core microbiome taxon in diverse invertebrates. Using a pangenomic analysis of 236 free-living and invertebrate-associated bacterial strains (including two new nematode-associated isolates generated in this study), we confirm that Pseudoalteromonas is a symbiont with substantial evidence of phylosymbiosis across at least three marine invertebrate phyla (e.g., Nematoda, Mollusca, and Cnidaria). Patterns of symbiosis were consistent irrespective of geography (including in Antarctica), with FISH images from nematodes indicating that bacterial symbionts form biofilms in the mouth and esophagus and are sometimes present in female nematode ovaries exhibiting stunted development. The evolutionary history of Pseudoalteromonas is marked by substantial host-switching and lifestyle transitions, and host-associated genomes suggest that these bacteria are facultative symbionts involved in nutritional symbioses. In marine environments, we hypothesize that horizontally acquired symbionts may have co-evolved with invertebrates, using host mucus as a physical niche and food source, while providing their animal hosts with Vitamin B, amino acids, and bioavailable carbon compounds in return.
Additional Links: PMID-42007585
Publisher:
PubMed:
Citation:
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@article {pmid42007585,
year = {2026},
author = {De Santiago, A and Barnes, S and Pereira, TJ and Marcellino-Barros, M and Durden, L and Han, MK and Thrash, JC and Bik, HM},
title = {Pseudoalteromonas is a symbiont of marine invertebrates that exhibits broad patterns of phylosymbiosis.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag091},
pmid = {42007585},
issn = {1751-7370},
abstract = {Despite growing insights into the composition of marine invertebrate microbiomes, our understanding of their ecological and evolutionary patterns remains poor, owing to limited sampling depth and low-resolution datasets. Previous studies have provided conflicting results that both confirm and deny the existence of phylosymbiosis between marine invertebrates and marine bacteria. Here, we investigated potential animal-microbe symbioses in Pseudoalteromonas, a bacterial genus consistently identified as a core microbiome taxon in diverse invertebrates. Using a pangenomic analysis of 236 free-living and invertebrate-associated bacterial strains (including two new nematode-associated isolates generated in this study), we confirm that Pseudoalteromonas is a symbiont with substantial evidence of phylosymbiosis across at least three marine invertebrate phyla (e.g., Nematoda, Mollusca, and Cnidaria). Patterns of symbiosis were consistent irrespective of geography (including in Antarctica), with FISH images from nematodes indicating that bacterial symbionts form biofilms in the mouth and esophagus and are sometimes present in female nematode ovaries exhibiting stunted development. The evolutionary history of Pseudoalteromonas is marked by substantial host-switching and lifestyle transitions, and host-associated genomes suggest that these bacteria are facultative symbionts involved in nutritional symbioses. In marine environments, we hypothesize that horizontally acquired symbionts may have co-evolved with invertebrates, using host mucus as a physical niche and food source, while providing their animal hosts with Vitamin B, amino acids, and bioavailable carbon compounds in return.},
}
RevDate: 2026-04-21
A Synthetic Community from Campeiostachys nutans Rhizosphere in the Qinghai-Tibet Plateau Endow Alfalfa with the Ability to Resist Drought and Cold.
Journal of agricultural and food chemistry [Epub ahead of print].
Campeiostachys nutans, widely distributed in the Qinghai-Tibet Plateau, possesses notable stress tolerance, yet the exploration of its functional rhizosphere microbes remains limited. In this study, we characterized bacterial variations across rhizosphere surrounding soil, rhizosphere, and endosphere compartments from five grassland types, isolated core strains, and established a synthetic community (SynCom). Results revealed that under PEG-induced drought, SynCom significantly altered alfalfa responses by scavenging reactive oxygen species (ROS), modulating immune gene expression, and synthesizing glutamate metabolites. Additionally, SynCom inoculation conferred cold resistance to alfalfa by enhancing photosynthetic activity, boosting antioxidant enzymes, and producing osmotic adjustment compounds like trehalose. This investigation underscores the capacity of core rhizosphere taxa to enhance stress tolerance, offering novel perspectives for developing microbial inoculants to improve crop productivity under drought and cold stress.
Additional Links: PMID-42007648
Publisher:
PubMed:
Citation:
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@article {pmid42007648,
year = {2026},
author = {Xu, S and Cao, Z and Ma, K and Song, J and Miao, Y and Li, Q and Song, D and Fu, J and Yang, P},
title = {A Synthetic Community from Campeiostachys nutans Rhizosphere in the Qinghai-Tibet Plateau Endow Alfalfa with the Ability to Resist Drought and Cold.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c14225},
pmid = {42007648},
issn = {1520-5118},
abstract = {Campeiostachys nutans, widely distributed in the Qinghai-Tibet Plateau, possesses notable stress tolerance, yet the exploration of its functional rhizosphere microbes remains limited. In this study, we characterized bacterial variations across rhizosphere surrounding soil, rhizosphere, and endosphere compartments from five grassland types, isolated core strains, and established a synthetic community (SynCom). Results revealed that under PEG-induced drought, SynCom significantly altered alfalfa responses by scavenging reactive oxygen species (ROS), modulating immune gene expression, and synthesizing glutamate metabolites. Additionally, SynCom inoculation conferred cold resistance to alfalfa by enhancing photosynthetic activity, boosting antioxidant enzymes, and producing osmotic adjustment compounds like trehalose. This investigation underscores the capacity of core rhizosphere taxa to enhance stress tolerance, offering novel perspectives for developing microbial inoculants to improve crop productivity under drought and cold stress.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Mapping the Research Landscape and Evolutionary Trends of the Oral Microbiome in Periodontitis.
APMIS : acta pathologica, microbiologica, et immunologica Scandinavica, 134(4):e70209.
The conceptual transition from the "Red Complex" paradigm to the "Ecological Plaque Hypothesis" has fundamentally reshaped the understanding of periodontitis, but a quantitative mapping of this intellectual evolution and its emerging research frontiers remains limited. This study systematically characterized the global research landscape and evolutionary trends of the oral microbiome in periodontitis from 2000 to 2025. English-language articles published between 2000 and 17 November 2025 were retrieved from the Web of Science Core Collection and Scopus databases. After deduplication, bibliometric analyses were performed on 2827 unique publications to evaluate spatiotemporal distributions, collaboration patterns, thematic evolution, and citation bursts. The results revealed exponential growth in publications, particularly after 2020, with the United States and China leading global contributions. Thematic evolution analyses demonstrated a clear shift from single-pathogen-focused research, exemplified by Porphyromonas gingivalis, toward ecological frameworks emphasizing dysbiosis and microbial community structure. Recent citation bursts highlighted growing attention to broader microbial taxa, inflammatory mediators, clinically relevant periodontal indicators, microbiome-based therapeutic strategies, and methodological standardization. Overall, research on the oral microbiome in periodontitis has evolved toward a host-microbiome systems biology framework, with future studies likely to emphasize functional multi-omics integration, AI-assisted diagnostics, and precision interventions targeting oral-systemic health links.
Additional Links: PMID-42007708
Publisher:
PubMed:
Citation:
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@article {pmid42007708,
year = {2026},
author = {Wang, X and Ma, Y and Yang, Y and Dong, Q},
title = {Mapping the Research Landscape and Evolutionary Trends of the Oral Microbiome in Periodontitis.},
journal = {APMIS : acta pathologica, microbiologica, et immunologica Scandinavica},
volume = {134},
number = {4},
pages = {e70209},
doi = {10.1111/apm.70209},
pmid = {42007708},
issn = {1600-0463},
mesh = {Humans ; *Periodontitis/microbiology ; *Microbiota ; *Mouth/microbiology ; Dysbiosis/microbiology ; Bibliometrics ; },
abstract = {The conceptual transition from the "Red Complex" paradigm to the "Ecological Plaque Hypothesis" has fundamentally reshaped the understanding of periodontitis, but a quantitative mapping of this intellectual evolution and its emerging research frontiers remains limited. This study systematically characterized the global research landscape and evolutionary trends of the oral microbiome in periodontitis from 2000 to 2025. English-language articles published between 2000 and 17 November 2025 were retrieved from the Web of Science Core Collection and Scopus databases. After deduplication, bibliometric analyses were performed on 2827 unique publications to evaluate spatiotemporal distributions, collaboration patterns, thematic evolution, and citation bursts. The results revealed exponential growth in publications, particularly after 2020, with the United States and China leading global contributions. Thematic evolution analyses demonstrated a clear shift from single-pathogen-focused research, exemplified by Porphyromonas gingivalis, toward ecological frameworks emphasizing dysbiosis and microbial community structure. Recent citation bursts highlighted growing attention to broader microbial taxa, inflammatory mediators, clinically relevant periodontal indicators, microbiome-based therapeutic strategies, and methodological standardization. Overall, research on the oral microbiome in periodontitis has evolved toward a host-microbiome systems biology framework, with future studies likely to emphasize functional multi-omics integration, AI-assisted diagnostics, and precision interventions targeting oral-systemic health links.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Periodontitis/microbiology
*Microbiota
*Mouth/microbiology
Dysbiosis/microbiology
Bibliometrics
RevDate: 2026-04-20
A synthetic microbial community for soybean biofertilization designed via chlorophyll-based iterative selection.
Applied and environmental microbiology [Epub ahead of print].
Improving the effectiveness of microbial inoculants for soybean is essential to enhance biological nitrogen fixation and reduce fertilizer dependence; however, inoculated Bradyrhizobium strains frequently display inconsistent field performance. Inoculation is usually carried out with single-strain formulations, overlooking the possible influence of the native soil microbiota on nodulation success. This limitation may be addressed by formulating inoculants with consortia that include selected members of the soil microbiota. To this end, a synthetic microbial community (SynCom) was developed through a host-mediated microbiome engineering approach guided by leaf chlorophyll content as a rapid, non-destructive plant trait. The experiment was initiated by inoculating soybean plants with a consortium of 9 Bradyrhizobium spp. and 14 non-rhizobial soil isolates. Across eight consecutive selection rounds under gnotobiotic conditions, rhizosphere communities associated with superior plant performance were pooled and propagated. Recurrent selection induced significant shifts in community composition, consistently favoring Bradyrhizobium diazoefficiens as the dominant nodulating member and enriching taxa from Pseudomonadales, Burkholderiales, and Sphingomonadales. Sequencing-based profiling and network analysis suggested the emergence of a cohesive and functionally enriched community, with increased potential for nitrogen transformations and organic matter turnover. When evaluated in non-sterile soil, the SynCom derived from the sixth selection round increased nodule number and biomass relative to an uninoculated control and a commercial inoculant strain. These results suggest that plant-guided selection can steer rhizosphere community assembly toward beneficial configurations and support the development of improved soybean bioinoculants.IMPORTANCESoybean [Glycine max (L.) Merr.] is a major global crop characterized by high seed protein content, which demands elevated nitrogen assimilation. To meet this demand, the crop can utilize atmospheric nitrogen through the process of biological nitrogen fixation in symbiosis with Bradyrhizobium bacteria, thus mitigating soil nitrogen depletion. Although Bradyrhizobium-based inoculants are applied at sowing, their interplay with other members of the rhizosphere microbiota remains poorly understood. It is well documented that plants and rhizosphere microbiota interact to shape plant growth and soil productivity. Therefore, this work evaluated the inoculation of soybean with a synthetic microbial consortium as a strategy to develop new-generation inoculants. These bioinputs are designed to harness plant-soil-microbe interactions to improve soybean productivity while preserving soil properties.
Additional Links: PMID-42007760
Publisher:
PubMed:
Citation:
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@article {pmid42007760,
year = {2026},
author = {Brignoli, D and Colla, D and Frickel-Critto, E and Castells, CB and Pérez-Giménez, J and Lodeiro, AR},
title = {A synthetic microbial community for soybean biofertilization designed via chlorophyll-based iterative selection.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0254825},
doi = {10.1128/aem.02548-25},
pmid = {42007760},
issn = {1098-5336},
abstract = {Improving the effectiveness of microbial inoculants for soybean is essential to enhance biological nitrogen fixation and reduce fertilizer dependence; however, inoculated Bradyrhizobium strains frequently display inconsistent field performance. Inoculation is usually carried out with single-strain formulations, overlooking the possible influence of the native soil microbiota on nodulation success. This limitation may be addressed by formulating inoculants with consortia that include selected members of the soil microbiota. To this end, a synthetic microbial community (SynCom) was developed through a host-mediated microbiome engineering approach guided by leaf chlorophyll content as a rapid, non-destructive plant trait. The experiment was initiated by inoculating soybean plants with a consortium of 9 Bradyrhizobium spp. and 14 non-rhizobial soil isolates. Across eight consecutive selection rounds under gnotobiotic conditions, rhizosphere communities associated with superior plant performance were pooled and propagated. Recurrent selection induced significant shifts in community composition, consistently favoring Bradyrhizobium diazoefficiens as the dominant nodulating member and enriching taxa from Pseudomonadales, Burkholderiales, and Sphingomonadales. Sequencing-based profiling and network analysis suggested the emergence of a cohesive and functionally enriched community, with increased potential for nitrogen transformations and organic matter turnover. When evaluated in non-sterile soil, the SynCom derived from the sixth selection round increased nodule number and biomass relative to an uninoculated control and a commercial inoculant strain. These results suggest that plant-guided selection can steer rhizosphere community assembly toward beneficial configurations and support the development of improved soybean bioinoculants.IMPORTANCESoybean [Glycine max (L.) Merr.] is a major global crop characterized by high seed protein content, which demands elevated nitrogen assimilation. To meet this demand, the crop can utilize atmospheric nitrogen through the process of biological nitrogen fixation in symbiosis with Bradyrhizobium bacteria, thus mitigating soil nitrogen depletion. Although Bradyrhizobium-based inoculants are applied at sowing, their interplay with other members of the rhizosphere microbiota remains poorly understood. It is well documented that plants and rhizosphere microbiota interact to shape plant growth and soil productivity. Therefore, this work evaluated the inoculation of soybean with a synthetic microbial consortium as a strategy to develop new-generation inoculants. These bioinputs are designed to harness plant-soil-microbe interactions to improve soybean productivity while preserving soil properties.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Distinct early-life gut microbiota patterns across SGA, AGA, and LGA infants.
European journal of pediatrics, 185(5):.
UNLABELLED: Birthweight-for-gestational-age influences neonatal physiology and health, yet its role in shaping early gut microbiome development remains insufficiently defined. Small-for-gestational-age (SGA), appropriate-for-gestational-age (AGA), and large-for-gestational-age (LGA) infants may exhibit distinct microbial maturation patterns that could influence later metabolic and developmental outcomes. We conducted a prospective cohort study and enrolled 50 late-preterm and term infants and classified them into SGA (n=18), AGA (n=20), and LGA (n=12). Serial fecal samples were collected at four postnatal time windows (0-14 and 15-80 days). 16S rRNA gene sequencing using Oxford Nanopore MinION characterized microbial composition, diversity, and community networks. Bioinformatic analyses included alpha- and beta-diversity metrics, co-occurrence network analysis, and functional pathway inference using PICRUSt2 mapped to the MetaCyc database. Clinical variables, including feeding pattern and antibiotic exposure, were assessed. Gut microbiome development differed according to birthweight categories. Microbial diversity increased with postnatal age, with SGA infants showing distinct community structures over time. Firmicutes predominated across all groups, while specific taxa exhibited group-specific patterns, including enrichment of Streptococcus spp. in LGA infants and Klebsiella spp. in SGA infants. Co-occurrence network analysis revealed a stable gut microbiota in LGA infants.
CONCLUSION: Birthweight-for-gestational-age status was associated with distinct trajectories of early gut microbial maturation. SGA infants exhibited delayed microbial stabilization and fragmented interaction networks, whereas LGA infants demonstrated relatively early establishment of stable, Streptococcus-enriched communities. These growth-specific microbial patterns may reflect differences in early metabolic programming and highlight the potential importance of tailored microbiome-targeted strategies to optimize neonatal development.
WHAT IS KNOWN: • Abnormal fetal growth is associated with increased neonatal morbidity and long-term metabolic risk. • Early-life gut microbiota play an important role in immune and metabolic development.
WHAT IS NEW: • This longitudinal study demonstrates growth-specific trajectories of early gut microbial maturation among SGA, AGA, and LGA infants born at ≥35-week gestation. • SGA infants exhibit delayed microbial stabilization and fragmented microbial interaction networks, whereas LGA infants show relatively earlier establishment of stable microbial communities.
Additional Links: PMID-42008183
PubMed:
Citation:
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@article {pmid42008183,
year = {2026},
author = {Hwang, JK and Lim, SM and Kwak, MJ and Kim, SH and Kang, Y and Mustafa, G and Tanpure, RS and Jeon, BH and Hoh, JK and Park, HK},
title = {Distinct early-life gut microbiota patterns across SGA, AGA, and LGA infants.},
journal = {European journal of pediatrics},
volume = {185},
number = {5},
pages = {},
pmid = {42008183},
issn = {1432-1076},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Infant, Newborn ; Prospective Studies ; Female ; Male ; *Infant, Small for Gestational Age/growth & development ; Infant ; *Birth Weight ; Feces/microbiology ; Gestational Age ; RNA, Ribosomal, 16S ; Infant, Large for Gestational Age ; },
abstract = {UNLABELLED: Birthweight-for-gestational-age influences neonatal physiology and health, yet its role in shaping early gut microbiome development remains insufficiently defined. Small-for-gestational-age (SGA), appropriate-for-gestational-age (AGA), and large-for-gestational-age (LGA) infants may exhibit distinct microbial maturation patterns that could influence later metabolic and developmental outcomes. We conducted a prospective cohort study and enrolled 50 late-preterm and term infants and classified them into SGA (n=18), AGA (n=20), and LGA (n=12). Serial fecal samples were collected at four postnatal time windows (0-14 and 15-80 days). 16S rRNA gene sequencing using Oxford Nanopore MinION characterized microbial composition, diversity, and community networks. Bioinformatic analyses included alpha- and beta-diversity metrics, co-occurrence network analysis, and functional pathway inference using PICRUSt2 mapped to the MetaCyc database. Clinical variables, including feeding pattern and antibiotic exposure, were assessed. Gut microbiome development differed according to birthweight categories. Microbial diversity increased with postnatal age, with SGA infants showing distinct community structures over time. Firmicutes predominated across all groups, while specific taxa exhibited group-specific patterns, including enrichment of Streptococcus spp. in LGA infants and Klebsiella spp. in SGA infants. Co-occurrence network analysis revealed a stable gut microbiota in LGA infants.
CONCLUSION: Birthweight-for-gestational-age status was associated with distinct trajectories of early gut microbial maturation. SGA infants exhibited delayed microbial stabilization and fragmented interaction networks, whereas LGA infants demonstrated relatively early establishment of stable, Streptococcus-enriched communities. These growth-specific microbial patterns may reflect differences in early metabolic programming and highlight the potential importance of tailored microbiome-targeted strategies to optimize neonatal development.
WHAT IS KNOWN: • Abnormal fetal growth is associated with increased neonatal morbidity and long-term metabolic risk. • Early-life gut microbiota play an important role in immune and metabolic development.
WHAT IS NEW: • This longitudinal study demonstrates growth-specific trajectories of early gut microbial maturation among SGA, AGA, and LGA infants born at ≥35-week gestation. • SGA infants exhibit delayed microbial stabilization and fragmented microbial interaction networks, whereas LGA infants show relatively earlier establishment of stable microbial communities.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology
Infant, Newborn
Prospective Studies
Female
Male
*Infant, Small for Gestational Age/growth & development
Infant
*Birth Weight
Feces/microbiology
Gestational Age
RNA, Ribosomal, 16S
Infant, Large for Gestational Age
RevDate: 2026-04-21
Sympathetic denervation alters pulmonary microbiota diversity and composition in mice.
International microbiology : the official journal of the Spanish Society for Microbiology [Epub ahead of print].
Additional Links: PMID-42008215
PubMed:
Citation:
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@article {pmid42008215,
year = {2026},
author = {Zhang, J and Yang, X and Xie, L and Liu, Q and Zhang, X},
title = {Sympathetic denervation alters pulmonary microbiota diversity and composition in mice.},
journal = {International microbiology : the official journal of the Spanish Society for Microbiology},
volume = {},
number = {},
pages = {},
pmid = {42008215},
issn = {1618-1905},
support = {SBGJ202103001//Health Commission of Henan Province/ ; },
}
RevDate: 2026-04-21
Fecal Microbiota Transplant and Multidrug-Resistant Organism Decolonization in Gastrointestinal Disease: A Randomized Clinical Trial.
JAMA internal medicine [Epub ahead of print].
IMPORTANCE: Gut colonization by multidrug-resistant organisms (MDROs) is a risk factor for infection with these pathogens. There are no approved therapeutic interventions to combat it.
OBJECTIVE: To assess the efficacy of fecal microbiota transplant (FMT) in causing MDRO decolonization and decreasing antimicrobial resistance (AMR) genes and its impact on gut microbiome, virome, and mycobiome composition in patients with gastrointestinal (GI) diseases.
This randomized, double-blind, sham-controlled clinical trial was conducted in a gastroenterology ward and intensive care unit at a tertiary care center in India. Participants were patients with GI diseases with persistent MDRO colonization. Patient recruitment occurred from July 2022 to June 2024, with follow-up completed in July 2024. Data were analyzed from October 1, 2024, to April 25, 2025.
INTERVENTION: FMT via colonoscopy or sham intervention (sigmoidoscopy with saline injection).
MAIN OUTCOMES AND MEASURES: Co-primary outcomes were MDRO decolonization rate and decrease in antimicrobial resistance genes (AMR) at 4 weeks after the intervention. Secondary outcomes included changes in stool microbiome (16S ribosomal RNA amplicon sequencing), virome (viruslike particles shotgun sequencing), and mycobiome (ITS2 sequencing); incidence of MDRO infections; and adverse events within 4 weeks.
RESULTS: Of 114 randomized patients (mean [SD] age, 40.6 [12.5] years; 80 [70.2%] male; 52 patients [45.6%] with pancreatitis; 43 patients [37.7%] with cirrhosis; 19 patients [16.7%] with other GI disorders), 58 received FMT and 56 received the sham intervention. Most patients were colonized with carbapenem-resistant Enterobacteriaceae or extended-spectrum β-lactamase-producing Enterobacteriaceae at baseline (55 patients [94.8%] in the FMT group and 56 patients [100%] in the sham group). Five patients (2 in the FMT group, 3 in the sham group) were lost to follow-up. Intention-to-treat analysis showed no significant differences in MDRO decolonization (18 patients [31.0%] in the FMT group vs 17 patients [30.4%] in the sham group; absolute difference, 0.6% [95% CI, -16.2% to 17.6%]; P = .94) or AMR genes (median [IQR], 2.5 [1.2 to 3.0] genes in the FMT group vs 2.0 [1.0 to 3.0] genes in the sham group; P = .68), with comparable adverse events. Among 71 patients who underwent 16S ribosomal RNA gene sequencing at 4 to 6 weeks after the intervention, enrichment of bacteria capable of producing short-chain fatty acids was observed in the FMT group. These microbial alterations were not observed in the sham group. However, viral diversity remained unchanged after FMT. Mycobiome analysis revealed that FMT induced only modest, transient alterations in the gut mycobiome.
CONCLUSIONS AND RELEVANCE: This randomized clinical trial found that while a single session of FMT did not significantly enhance MDRO decolonization or decrease AMR genes in patients with GI diseases, it modulated gut microbiome diversity and composition.
TRIAL REGISTRATION: Clinical Trials Registry-India Registration No. 2022/07/043847.
Additional Links: PMID-42008253
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Citation:
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@article {pmid42008253,
year = {2026},
author = {Narang, H and Talukdar, D and Kumar, B and Mathur, P and Ningombam, A and Singh, M and Bajaj, A and Markandey, M and Kalaivani, M and Verma, M and Kaur, M and Bakshi, S and Jana, P and Jamdhade, M and Bhardwaj, N and Puraswani, M and Ashita, and Ahmed, N and Goyal, MK and Mubbunu, M and Thomas, DM and Mundhra, S and Prasad, S and Garg, R and Gupta, A and Shalimar, and Gunjan, D and Mahapatra, SJ and Agarwal, S and Saraya, A and Garg, P and Makharia, G and Kedia, S and Das, B and Ahuja, V},
title = {Fecal Microbiota Transplant and Multidrug-Resistant Organism Decolonization in Gastrointestinal Disease: A Randomized Clinical Trial.},
journal = {JAMA internal medicine},
volume = {},
number = {},
pages = {},
pmid = {42008253},
issn = {2168-6114},
abstract = {IMPORTANCE: Gut colonization by multidrug-resistant organisms (MDROs) is a risk factor for infection with these pathogens. There are no approved therapeutic interventions to combat it.
OBJECTIVE: To assess the efficacy of fecal microbiota transplant (FMT) in causing MDRO decolonization and decreasing antimicrobial resistance (AMR) genes and its impact on gut microbiome, virome, and mycobiome composition in patients with gastrointestinal (GI) diseases.
This randomized, double-blind, sham-controlled clinical trial was conducted in a gastroenterology ward and intensive care unit at a tertiary care center in India. Participants were patients with GI diseases with persistent MDRO colonization. Patient recruitment occurred from July 2022 to June 2024, with follow-up completed in July 2024. Data were analyzed from October 1, 2024, to April 25, 2025.
INTERVENTION: FMT via colonoscopy or sham intervention (sigmoidoscopy with saline injection).
MAIN OUTCOMES AND MEASURES: Co-primary outcomes were MDRO decolonization rate and decrease in antimicrobial resistance genes (AMR) at 4 weeks after the intervention. Secondary outcomes included changes in stool microbiome (16S ribosomal RNA amplicon sequencing), virome (viruslike particles shotgun sequencing), and mycobiome (ITS2 sequencing); incidence of MDRO infections; and adverse events within 4 weeks.
RESULTS: Of 114 randomized patients (mean [SD] age, 40.6 [12.5] years; 80 [70.2%] male; 52 patients [45.6%] with pancreatitis; 43 patients [37.7%] with cirrhosis; 19 patients [16.7%] with other GI disorders), 58 received FMT and 56 received the sham intervention. Most patients were colonized with carbapenem-resistant Enterobacteriaceae or extended-spectrum β-lactamase-producing Enterobacteriaceae at baseline (55 patients [94.8%] in the FMT group and 56 patients [100%] in the sham group). Five patients (2 in the FMT group, 3 in the sham group) were lost to follow-up. Intention-to-treat analysis showed no significant differences in MDRO decolonization (18 patients [31.0%] in the FMT group vs 17 patients [30.4%] in the sham group; absolute difference, 0.6% [95% CI, -16.2% to 17.6%]; P = .94) or AMR genes (median [IQR], 2.5 [1.2 to 3.0] genes in the FMT group vs 2.0 [1.0 to 3.0] genes in the sham group; P = .68), with comparable adverse events. Among 71 patients who underwent 16S ribosomal RNA gene sequencing at 4 to 6 weeks after the intervention, enrichment of bacteria capable of producing short-chain fatty acids was observed in the FMT group. These microbial alterations were not observed in the sham group. However, viral diversity remained unchanged after FMT. Mycobiome analysis revealed that FMT induced only modest, transient alterations in the gut mycobiome.
CONCLUSIONS AND RELEVANCE: This randomized clinical trial found that while a single session of FMT did not significantly enhance MDRO decolonization or decrease AMR genes in patients with GI diseases, it modulated gut microbiome diversity and composition.
TRIAL REGISTRATION: Clinical Trials Registry-India Registration No. 2022/07/043847.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Gut site and sex-specific enrichment of bacterial taxa and predicted metabolic pathways in wild American black bear (Ursus americanus).
PloS one, 21(4):e0345317.
American black bears' (Ursus americanus) omnivorous feeding strategy, simple gut morphology, and rapid transit time prevent regulation of the gut microbiome (GMB). We analyzed stable isotopes and 16S rRNA sequences from 48 wild bears to assess the impacts of diet, age, gut site, and sex on GMB composition and PICRUSt2-predicted functional pathways. While alpha and beta diversity did not differ, we identified bacterial taxa and predicted pathways enriched based on gut site and sex. Enterococcus, Incertae, Papillibacter, and Shuttleworthia were enriched in jejunum samples (linear discriminant analysis effect size ≥ 3.5, p = 0.0374); and 6 genera drove colonic Bray-Curtis distances (SIMPER): Weisella (p = 0.0099), Anaeroplasma (p = 0.0495), Megamonas (p = 0.0099), Cellulosilyticum (p = 0.0495), Escherichia-Shigella (p = 0.0396) and Ochrobactrum (p = 0.0297). EdgeR identified isoflavonoid biosynthesis (p-adj = 0.001) and isoterpenoid biosynthesis (p-adj = 0.006) enriched in the colon, and SNARE interaction in vesicular transport (p-adj = 0.000) and secondary bile acid synthesis (p-adj = 0.005) enriched in females. Our findings provide nuanced insights to specific taxa and putative metabolic pathways that reflect sex and gut site differences in black bears, with important implications for understanding bear physiology and informing wildlife management.
Additional Links: PMID-42008544
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Citation:
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@article {pmid42008544,
year = {2026},
author = {McKenney, EA and De Jesus, E and Hatfield, T and Hayes, D and Holder, K and Ivarsson, C and Morais, N and Payne, H and Simpson, K and Staal, AM and Thompson, H and Hildreth, R and Olfenbuttel, C and Lafferty, DJR},
title = {Gut site and sex-specific enrichment of bacterial taxa and predicted metabolic pathways in wild American black bear (Ursus americanus).},
journal = {PloS one},
volume = {21},
number = {4},
pages = {e0345317},
pmid = {42008544},
issn = {1932-6203},
mesh = {Animals ; *Ursidae/microbiology/metabolism ; *Gastrointestinal Microbiome ; Female ; Male ; *Bacteria/genetics/classification ; RNA, Ribosomal, 16S/genetics ; *Metabolic Networks and Pathways ; Sex Factors ; Animals, Wild/microbiology ; },
abstract = {American black bears' (Ursus americanus) omnivorous feeding strategy, simple gut morphology, and rapid transit time prevent regulation of the gut microbiome (GMB). We analyzed stable isotopes and 16S rRNA sequences from 48 wild bears to assess the impacts of diet, age, gut site, and sex on GMB composition and PICRUSt2-predicted functional pathways. While alpha and beta diversity did not differ, we identified bacterial taxa and predicted pathways enriched based on gut site and sex. Enterococcus, Incertae, Papillibacter, and Shuttleworthia were enriched in jejunum samples (linear discriminant analysis effect size ≥ 3.5, p = 0.0374); and 6 genera drove colonic Bray-Curtis distances (SIMPER): Weisella (p = 0.0099), Anaeroplasma (p = 0.0495), Megamonas (p = 0.0099), Cellulosilyticum (p = 0.0495), Escherichia-Shigella (p = 0.0396) and Ochrobactrum (p = 0.0297). EdgeR identified isoflavonoid biosynthesis (p-adj = 0.001) and isoterpenoid biosynthesis (p-adj = 0.006) enriched in the colon, and SNARE interaction in vesicular transport (p-adj = 0.000) and secondary bile acid synthesis (p-adj = 0.005) enriched in females. Our findings provide nuanced insights to specific taxa and putative metabolic pathways that reflect sex and gut site differences in black bears, with important implications for understanding bear physiology and informing wildlife management.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Ursidae/microbiology/metabolism
*Gastrointestinal Microbiome
Female
Male
*Bacteria/genetics/classification
RNA, Ribosomal, 16S/genetics
*Metabolic Networks and Pathways
Sex Factors
Animals, Wild/microbiology
RevDate: 2026-04-20
Domestic travel as a driver for the dissemination of mcr-1 in healthy travelers in China: a prospective, genomic epidemiological and gut microbiome study.
Antimicrobial agents and chemotherapy [Epub ahead of print].
The global spread of plasmid-mediated colistin resistance gene mcr-1 poses a significant threat to public health. Although international travel is a known driver of antimicrobial resistance, the role of domestic travel in high-prevalence settings remains unclear. We conducted a prospective cohort study of 81 healthy volunteers traveling in China (June-September 2022). Fecal samples collected before and after travel were screened for mcr-1-positive Escherichia coli (MCRPEC). Antimicrobial resistance genes (ARGs), virulence factors (VFs), plasmid replicons, and gut microbial dynamics were investigated using whole-genome sequencing and 16S rRNA sequencing. Risk factors were analyzed using logistic regression analysis. Of the 81 participants who were negative for mcr-1 at baseline, 12 (14.8%) acquired mcr-1 after travel. Acquisition was associated with residence near poultry farms (odds ratio [OR] = 5.9, P = 0.04) and diarrhea during travel (OR = 11.22, P = 0.027). MCRPEC exhibited marked genetic diversity comprising 10 sequence types and the carriage of additional 23 ARGs and nine adherence-associated VFs. mcr-1 was located on IncI2, IncX4, IncHI2, or IncP plasmids, with 91.7% (n = 11) transferable in conjugation assays. Gut microbiome analysis showed increased α-diversity, but a stable community structure, indicating colonization without major disruption. Our study demonstrated that domestic travel in China substantially contributes to the dissemination of mcr-1. Poultry exposure and gastrointestinal disturbances are key risk factors. Genetic diversity, plasmid transferability, and co-carriage of resistance and virulence determinants highlight the risk of onward spread. Antimicrobial resistance surveillance should extend beyond international travel and incorporate domestic mobility within a "One Health" framework.
Additional Links: PMID-42008653
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PubMed:
Citation:
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@article {pmid42008653,
year = {2026},
author = {Wu, M and Chen, Y and Su, M and Wu, H and Luo, L and Ao, X and Zhao, C and Shui, J and Wen, S and Lin, J and Pu, J and Zeng, J and Jiang, Y and Ng, H and Zhang, Z and Hu, M and Huang, B and Xu, L and Chen, C and Shen, C},
title = {Domestic travel as a driver for the dissemination of mcr-1 in healthy travelers in China: a prospective, genomic epidemiological and gut microbiome study.},
journal = {Antimicrobial agents and chemotherapy},
volume = {},
number = {},
pages = {e0174625},
doi = {10.1128/aac.01746-25},
pmid = {42008653},
issn = {1098-6596},
abstract = {The global spread of plasmid-mediated colistin resistance gene mcr-1 poses a significant threat to public health. Although international travel is a known driver of antimicrobial resistance, the role of domestic travel in high-prevalence settings remains unclear. We conducted a prospective cohort study of 81 healthy volunteers traveling in China (June-September 2022). Fecal samples collected before and after travel were screened for mcr-1-positive Escherichia coli (MCRPEC). Antimicrobial resistance genes (ARGs), virulence factors (VFs), plasmid replicons, and gut microbial dynamics were investigated using whole-genome sequencing and 16S rRNA sequencing. Risk factors were analyzed using logistic regression analysis. Of the 81 participants who were negative for mcr-1 at baseline, 12 (14.8%) acquired mcr-1 after travel. Acquisition was associated with residence near poultry farms (odds ratio [OR] = 5.9, P = 0.04) and diarrhea during travel (OR = 11.22, P = 0.027). MCRPEC exhibited marked genetic diversity comprising 10 sequence types and the carriage of additional 23 ARGs and nine adherence-associated VFs. mcr-1 was located on IncI2, IncX4, IncHI2, or IncP plasmids, with 91.7% (n = 11) transferable in conjugation assays. Gut microbiome analysis showed increased α-diversity, but a stable community structure, indicating colonization without major disruption. Our study demonstrated that domestic travel in China substantially contributes to the dissemination of mcr-1. Poultry exposure and gastrointestinal disturbances are key risk factors. Genetic diversity, plasmid transferability, and co-carriage of resistance and virulence determinants highlight the risk of onward spread. Antimicrobial resistance surveillance should extend beyond international travel and incorporate domestic mobility within a "One Health" framework.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Connecting habitats, boosting disease resistance: Spatial connectivity enhances amphibian microbiome defenses against fungal pathogen.
Proceedings of the National Academy of Sciences of the United States of America, 123(17):e2520745123.
Disruption of habitat connectivity alters host movement patterns and pathogen exposure in wildlife. Changes in exposure dynamics have led to increased research interest in host-associated microbial communities (i.e., microbiomes), particularly in how repeated encounters with pathogens may drive microbial filtering processes that favor the assembly of pathogen-inhibiting microbiomes, a concept known as the adaptive microbiome principle. Understanding how habitat connectivity and pathogen exposure shape adaptive microbiomes remains a key frontier in disease ecology. For widely distributed waterborne pathogens such as the amphibian chytrid fungus Batrachochytrium dendrobatidis (Bd), sustained host exposure in contiguous terrestrial-aquatic habitats may promote selection of microbiomes with enhanced antifungal properties. In contrast, under conditions of high habitat split, where key habitats such as forests and water bodies are spatially disconnected, limited exposure to Bd during the pre-tbreeding and overwintering seasons may hinder the selection of Bd-inhibitory microbiomes that are critical for host protection during the subsequent breeding season, when pathogen exposure in water bodies is at its peak. Our results demonstrate that habitat split may limit recruitment of putative Bd-inhibitory skin bacteria, while Bd loads increase with habitat split for certain amphibian species. Results from Joint Species Distribution Models also indicate that habitat split is a key driver of reduced skin bacterial diversity, even after accounting for biotic and abiotic metrics. Our study provides evidence that spatial connectivity among natural habitats is essential for maintaining multiple levels of biodiversity, from host species to their associated functional microbiomes, highlighting a critical link between environmental disturbance, microbial defenses, and disease dynamics.
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PubMed:
Citation:
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@article {pmid42008677,
year = {2026},
author = {Medina, D and Martins, RA and Prist, PR and Buttimer, S and Neely, WJ and Schuck, LK and Greenspan, SE and Lyra, ML and Kearns, PJ and Woodhams, DC and Bletz, MC and São-Pedro, VA and Haddad, CFB and Becker, CG},
title = {Connecting habitats, boosting disease resistance: Spatial connectivity enhances amphibian microbiome defenses against fungal pathogen.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {17},
pages = {e2520745123},
doi = {10.1073/pnas.2520745123},
pmid = {42008677},
issn = {1091-6490},
support = {IOS-1947681 DEB-2227340 DEB-2413542 BII-2120084//NSF (NSF)/ ; 2021/10639-5//Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)/ ; IOS-1845634 and BII 2120084//NSF (NSF)/ ; },
mesh = {Animals ; *Batrachochytrium/pathogenicity ; *Microbiota ; *Ecosystem ; *Amphibians/microbiology ; *Disease Resistance ; *Mycoses/microbiology/veterinary ; Host-Pathogen Interactions ; Chytridiomycota ; },
abstract = {Disruption of habitat connectivity alters host movement patterns and pathogen exposure in wildlife. Changes in exposure dynamics have led to increased research interest in host-associated microbial communities (i.e., microbiomes), particularly in how repeated encounters with pathogens may drive microbial filtering processes that favor the assembly of pathogen-inhibiting microbiomes, a concept known as the adaptive microbiome principle. Understanding how habitat connectivity and pathogen exposure shape adaptive microbiomes remains a key frontier in disease ecology. For widely distributed waterborne pathogens such as the amphibian chytrid fungus Batrachochytrium dendrobatidis (Bd), sustained host exposure in contiguous terrestrial-aquatic habitats may promote selection of microbiomes with enhanced antifungal properties. In contrast, under conditions of high habitat split, where key habitats such as forests and water bodies are spatially disconnected, limited exposure to Bd during the pre-tbreeding and overwintering seasons may hinder the selection of Bd-inhibitory microbiomes that are critical for host protection during the subsequent breeding season, when pathogen exposure in water bodies is at its peak. Our results demonstrate that habitat split may limit recruitment of putative Bd-inhibitory skin bacteria, while Bd loads increase with habitat split for certain amphibian species. Results from Joint Species Distribution Models also indicate that habitat split is a key driver of reduced skin bacterial diversity, even after accounting for biotic and abiotic metrics. Our study provides evidence that spatial connectivity among natural habitats is essential for maintaining multiple levels of biodiversity, from host species to their associated functional microbiomes, highlighting a critical link between environmental disturbance, microbial defenses, and disease dynamics.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Batrachochytrium/pathogenicity
*Microbiota
*Ecosystem
*Amphibians/microbiology
*Disease Resistance
*Mycoses/microbiology/veterinary
Host-Pathogen Interactions
Chytridiomycota
RevDate: 2026-04-20
CmpDate: 2026-04-21
Cancer epigenetics: unraveling etiology and mechanisms to advance prevention.
Journal of the National Cancer Institute. Monographs, 2026(72):44-58.
The increased understanding of epigenetics has significantly advanced our understanding of cancer development, especially regarding environmental, occupational, and lifestyle exposures. Unlike genetic mutations, epigenetic changes may be reversible, making them critical mediators and promising targets for cancer prevention and control. This review synthesizes two decades of transformative research by the International Agency for Research on Cancer (IARC), which positioned the epigenome as a central focus in cancer epidemiology and mechanistic research among the 10 Key Characteristics (KCs) of carcinogens by the IARC Monographs program. From foundational in vitro and animal studies to large-scale population-based research, IARC researchers contributed to unraveling epigenetic mechanisms of carcinogenesis and identifying epigenetic biomarkers of exposures and cancer risk. We highlight progress in epigenetic biomarker development, mechanistic epigenomics, toxico-epigenomics, and the interplay between diet, microbiome, and epigenome. As IARC marks its 60th anniversary, this review underscores the growing role of epigenetics in guiding global cancer prevention efforts and public health strategies.
Additional Links: PMID-42008732
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PubMed:
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@article {pmid42008732,
year = {2026},
author = {Herceg, Z and Ghantous, A and Gheit, T and Rahman Talukdar, F and Matar, C and Chung, F and Korenjak, M and Zavadil, J and Ribeiro Pinto, LF and Fry, RC and Khoueiry, R},
title = {Cancer epigenetics: unraveling etiology and mechanisms to advance prevention.},
journal = {Journal of the National Cancer Institute. Monographs},
volume = {2026},
number = {72},
pages = {44-58},
doi = {10.1093/jncimonographs/lgaf044},
pmid = {42008732},
issn = {1745-6614},
mesh = {Humans ; *Neoplasms/prevention & control/genetics/etiology/epidemiology ; *Epigenesis, Genetic ; *Epigenomics/methods ; Animals ; Biomarkers, Tumor/genetics ; },
abstract = {The increased understanding of epigenetics has significantly advanced our understanding of cancer development, especially regarding environmental, occupational, and lifestyle exposures. Unlike genetic mutations, epigenetic changes may be reversible, making them critical mediators and promising targets for cancer prevention and control. This review synthesizes two decades of transformative research by the International Agency for Research on Cancer (IARC), which positioned the epigenome as a central focus in cancer epidemiology and mechanistic research among the 10 Key Characteristics (KCs) of carcinogens by the IARC Monographs program. From foundational in vitro and animal studies to large-scale population-based research, IARC researchers contributed to unraveling epigenetic mechanisms of carcinogenesis and identifying epigenetic biomarkers of exposures and cancer risk. We highlight progress in epigenetic biomarker development, mechanistic epigenomics, toxico-epigenomics, and the interplay between diet, microbiome, and epigenome. As IARC marks its 60th anniversary, this review underscores the growing role of epigenetics in guiding global cancer prevention efforts and public health strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Neoplasms/prevention & control/genetics/etiology/epidemiology
*Epigenesis, Genetic
*Epigenomics/methods
Animals
Biomarkers, Tumor/genetics
RevDate: 2026-04-21
CmpDate: 2026-04-21
Intrahepatic cholestasis of pregnancy in Chile: Analysis of epidemiological change and a microbiological hypothesis.
Medwave, 26(3):e3161.
Intrahepatic cholestasis of pregnancy is a gestational pathology with an unusual epidemiological and pathophysiological behavior that remains partially unexplained. Its current global incidence ranges from 0.1% to 2%. However, in Chile, the incidence reached up to 15% in the 1970s, with a marked decrease over subsequent decades, being nowadays about 1 to 2%. The reasons for this historical change are not fully understood. A literature-based analysis was conducted, focusing on clinical, microbiological, and epidemiological studies on intrahepatic cholestasis and other hepatobiliary diseases. The aim of this was to explore existing evidence and to propose a microbiological hypothesis that could help explain the epidemiological transition observed in Chile. Notably, the temporal reduction in incidence paralleled a nationwide decline in biliary disease and typhoid fever. We hypothesize that the eradication or significant reduction of certain pathogens, such as Typhi, may have contributed to the normalization of intrahepatic cholestasis of pregnancy rates in Chile.
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@article {pmid42008798,
year = {2026},
author = {Contreras Vidal, C and Carvajal Cabrera, J},
title = {Intrahepatic cholestasis of pregnancy in Chile: Analysis of epidemiological change and a microbiological hypothesis.},
journal = {Medwave},
volume = {26},
number = {3},
pages = {e3161},
doi = {10.5867/medwave.2026.03.3161},
pmid = {42008798},
issn = {0717-6384},
mesh = {Humans ; Pregnancy ; Chile/epidemiology ; *Cholestasis, Intrahepatic/epidemiology/microbiology ; Female ; *Pregnancy Complications/epidemiology/microbiology ; Incidence ; Typhoid Fever/epidemiology ; Pregnancy Complications, Infectious/epidemiology/microbiology ; },
abstract = {Intrahepatic cholestasis of pregnancy is a gestational pathology with an unusual epidemiological and pathophysiological behavior that remains partially unexplained. Its current global incidence ranges from 0.1% to 2%. However, in Chile, the incidence reached up to 15% in the 1970s, with a marked decrease over subsequent decades, being nowadays about 1 to 2%. The reasons for this historical change are not fully understood. A literature-based analysis was conducted, focusing on clinical, microbiological, and epidemiological studies on intrahepatic cholestasis and other hepatobiliary diseases. The aim of this was to explore existing evidence and to propose a microbiological hypothesis that could help explain the epidemiological transition observed in Chile. Notably, the temporal reduction in incidence paralleled a nationwide decline in biliary disease and typhoid fever. We hypothesize that the eradication or significant reduction of certain pathogens, such as Typhi, may have contributed to the normalization of intrahepatic cholestasis of pregnancy rates in Chile.},
}
MeSH Terms:
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hide MeSH Terms
Humans
Pregnancy
Chile/epidemiology
*Cholestasis, Intrahepatic/epidemiology/microbiology
Female
*Pregnancy Complications/epidemiology/microbiology
Incidence
Typhoid Fever/epidemiology
Pregnancy Complications, Infectious/epidemiology/microbiology
RevDate: 2026-04-20
Advancing precision medicine in pancreatic cancer using novel biomarkers and clinical targets.
Molecular aspects of medicine, 109:101476 pii:S0098-2997(26)00032-4 [Epub ahead of print].
Precision-guided therapy is imperative in the battle against pancreatic ductal adenocarcinoma (PDAC), one of the most lethal solid malignancies with limited improvements in survival despite advances in molecular profiling and systemic therapy. While oncogenic drivers such as KRAS, TP53, CDKN2A, and SMAD4 are nearly ubiquitous, their translation into effective targeted therapies has been constrained by profound tumor heterogeneity, a therapy-resistant tumor microenvironment (TME), and a paucity of predictive biomarkers. In parallel, clinical outcomes are increasingly shaped by extrinsic modifiers, including metabolic disease, chronic inflammation, and microbiome dysregulation, which remain under-integrated into current treatment paradigms. Recent progress in precision oncology has enabled regulatory approval of biomarker-defined therapies for select PDAC subsets, including immune checkpoint inhibitors for mismatch repair-deficient tumors, PARP inhibitors for BRCA1/2-mutant disease, and combination cytotoxic regimens such as NALIRIFOX in the metastatic setting. However, these advances benefit only a minority of patients, underscoring the urgent need for improved patient stratification and rational combination strategies. Emerging clinical and translational studies highlight the promise of integrating multi-omic profiling, liquid biopsies, functional precision models (organoids and patient-derived xenografts), and artificial intelligence-driven analytics to uncover actionable vulnerabilities, monitor response, and guide adaptive trial design. In this review, we critically evaluate the clinical relevance of molecular, metabolic, and microenvironmental determinants of PDAC progression and therapeutic resistance. We focus on translational bottlenecks that have limited clinical success to date and highlight biomarker-driven strategies, ongoing clinical trials, and emerging technologies poised to shift treatment from uniform algorithms toward biologically informed, patient-specific therapeutic approaches in pancreatic cancer.
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PubMed:
Citation:
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@article {pmid42008879,
year = {2026},
author = {Murthy, D and Seyhan, AA and den Hollander, P and Lu, S and Kuburich, NA and Gould, C and Karam, AA and Sun, K and Schupp, PG and Safran, H and Kurzrock, R and El-Deiry, W and Mani, SA},
title = {Advancing precision medicine in pancreatic cancer using novel biomarkers and clinical targets.},
journal = {Molecular aspects of medicine},
volume = {109},
number = {},
pages = {101476},
doi = {10.1016/j.mam.2026.101476},
pmid = {42008879},
issn = {1872-9452},
abstract = {Precision-guided therapy is imperative in the battle against pancreatic ductal adenocarcinoma (PDAC), one of the most lethal solid malignancies with limited improvements in survival despite advances in molecular profiling and systemic therapy. While oncogenic drivers such as KRAS, TP53, CDKN2A, and SMAD4 are nearly ubiquitous, their translation into effective targeted therapies has been constrained by profound tumor heterogeneity, a therapy-resistant tumor microenvironment (TME), and a paucity of predictive biomarkers. In parallel, clinical outcomes are increasingly shaped by extrinsic modifiers, including metabolic disease, chronic inflammation, and microbiome dysregulation, which remain under-integrated into current treatment paradigms. Recent progress in precision oncology has enabled regulatory approval of biomarker-defined therapies for select PDAC subsets, including immune checkpoint inhibitors for mismatch repair-deficient tumors, PARP inhibitors for BRCA1/2-mutant disease, and combination cytotoxic regimens such as NALIRIFOX in the metastatic setting. However, these advances benefit only a minority of patients, underscoring the urgent need for improved patient stratification and rational combination strategies. Emerging clinical and translational studies highlight the promise of integrating multi-omic profiling, liquid biopsies, functional precision models (organoids and patient-derived xenografts), and artificial intelligence-driven analytics to uncover actionable vulnerabilities, monitor response, and guide adaptive trial design. In this review, we critically evaluate the clinical relevance of molecular, metabolic, and microenvironmental determinants of PDAC progression and therapeutic resistance. We focus on translational bottlenecks that have limited clinical success to date and highlight biomarker-driven strategies, ongoing clinical trials, and emerging technologies poised to shift treatment from uniform algorithms toward biologically informed, patient-specific therapeutic approaches in pancreatic cancer.},
}
RevDate: 2026-04-20
Chronic Inflammation in Virus-suppressed People Living with Human Immunodeficiency Virus Infection: A Microbiology-oriented Perspective on Gut Barrier Failure, Microbial Translocation, and Immune Activation.
Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy pii:S1341-321X(26)00070-X [Epub ahead of print].
Potent antiretroviral therapy (ART) has transformed human immunodeficiency virus (HIV) infection into a chronic manageable condition; however, many people living with HIV (PLWH) exhibit persistent immune activation and inflammation despite long-term virological suppression. Residual inflammation is strongly associated with an increased risk of cardiovascular disease, chronic kidney disease, metabolic dysfunction-associated steatotic liver disease, cancer, and neurocognitive impairment. This review summarizes the current evidence on the microbiology-oriented mechanisms that sustain this state. We first outline a multifactorial network in which incomplete repair of intestinal mucosal damage, dysbiosis, reduced short-chain fatty acid production, and disturbed bile acid metabolism generate a patchy "leaky gut." Continuous translocation of bacterial lipopolysaccharide, fungal β-D-glucan, and other microbial products activates monocyte-macrophage and portal-liver inflammatory circuits. These inputs interact with intermittent HIV antigen expression from latent reservoirs, inflammatory cell death, chronic coinfections, lymphoid tissue fibrosis, mitochondrial dysfunction, and traditional lifestyle-related risk factors. Together, they establish a self-reinforcing gut-liver-immune axis that maintains low-grade inflammation and a procoagulant milieu under viral suppression. We then link these mechanisms to organ-specific complications and review the intervention data, focusing on early ART initiation, statin therapy, and cotrimoxazole prophylaxis as a proof-of-concept that modifying inflammatory and mucosal pressures can improve outcomes. Finally, we highlight research priorities and argue that the effective prevention of long-term complications in virally suppressed PLWH requires combination strategies targeting multiple nodes of this network, with particular attention to gut barrier repair and microbiome modulation.
Additional Links: PMID-42009106
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@article {pmid42009106,
year = {2026},
author = {Yoshino, Y and Kimura, Y and Ito, F},
title = {Chronic Inflammation in Virus-suppressed People Living with Human Immunodeficiency Virus Infection: A Microbiology-oriented Perspective on Gut Barrier Failure, Microbial Translocation, and Immune Activation.},
journal = {Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy},
volume = {},
number = {},
pages = {102972},
doi = {10.1016/j.jiac.2026.102972},
pmid = {42009106},
issn = {1437-7780},
abstract = {Potent antiretroviral therapy (ART) has transformed human immunodeficiency virus (HIV) infection into a chronic manageable condition; however, many people living with HIV (PLWH) exhibit persistent immune activation and inflammation despite long-term virological suppression. Residual inflammation is strongly associated with an increased risk of cardiovascular disease, chronic kidney disease, metabolic dysfunction-associated steatotic liver disease, cancer, and neurocognitive impairment. This review summarizes the current evidence on the microbiology-oriented mechanisms that sustain this state. We first outline a multifactorial network in which incomplete repair of intestinal mucosal damage, dysbiosis, reduced short-chain fatty acid production, and disturbed bile acid metabolism generate a patchy "leaky gut." Continuous translocation of bacterial lipopolysaccharide, fungal β-D-glucan, and other microbial products activates monocyte-macrophage and portal-liver inflammatory circuits. These inputs interact with intermittent HIV antigen expression from latent reservoirs, inflammatory cell death, chronic coinfections, lymphoid tissue fibrosis, mitochondrial dysfunction, and traditional lifestyle-related risk factors. Together, they establish a self-reinforcing gut-liver-immune axis that maintains low-grade inflammation and a procoagulant milieu under viral suppression. We then link these mechanisms to organ-specific complications and review the intervention data, focusing on early ART initiation, statin therapy, and cotrimoxazole prophylaxis as a proof-of-concept that modifying inflammatory and mucosal pressures can improve outcomes. Finally, we highlight research priorities and argue that the effective prevention of long-term complications in virally suppressed PLWH requires combination strategies targeting multiple nodes of this network, with particular attention to gut barrier repair and microbiome modulation.},
}
RevDate: 2026-04-20
Emerging biomarkers for early detection of colorectal cancer.
Clinica chimica acta; international journal of clinical chemistry pii:S0009-8981(26)00195-6 [Epub ahead of print].
The worldwide impact of colorectal cancer (CRC) as a primary cause of cancer-related morbidity and mortality demonstrates the urgent need for better early detection methods and personalized treatment approaches. While colonoscopy and fecal tests have contributed to reduced mortality rates from CRC, they encounter important limitations stemming from their invasive procedures and insufficient sensitivity plus patient adherence issues. Consequently, the latest progress in molecular biology and omics technologies has enabled researchers to identify new biomarkers which present effective solutions for early detection and risk assessment while monitoring treatment efficacy. Therefore, this review explores new developments in CRC biomarker research through the lens of emerging liquid biopsy methods like circulating tumor DNA (ctDNA) and microRNAs (miRNAs) as well as genomic, epigenomic, gut microbiome, metabolomic, and proteomic markers. The usage of biomarker-based methods demonstrates transformative potential for CRC treatment by boosting survival rates and lessening global impact through precision medicine development in oncology.
Additional Links: PMID-42009160
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PubMed:
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@article {pmid42009160,
year = {2026},
author = {Qannita, RA and Zenati, RA and Abuhelwa, AY and Alqudah, MAY and Aleidi, SM and El-Huneidi, W and Abu-Gharbieh, E and AlShareef, ZM and Alzoubi, KH and Bustanji, Y and Semreen, MH},
title = {Emerging biomarkers for early detection of colorectal cancer.},
journal = {Clinica chimica acta; international journal of clinical chemistry},
volume = {},
number = {},
pages = {121013},
doi = {10.1016/j.cca.2026.121013},
pmid = {42009160},
issn = {1873-3492},
abstract = {The worldwide impact of colorectal cancer (CRC) as a primary cause of cancer-related morbidity and mortality demonstrates the urgent need for better early detection methods and personalized treatment approaches. While colonoscopy and fecal tests have contributed to reduced mortality rates from CRC, they encounter important limitations stemming from their invasive procedures and insufficient sensitivity plus patient adherence issues. Consequently, the latest progress in molecular biology and omics technologies has enabled researchers to identify new biomarkers which present effective solutions for early detection and risk assessment while monitoring treatment efficacy. Therefore, this review explores new developments in CRC biomarker research through the lens of emerging liquid biopsy methods like circulating tumor DNA (ctDNA) and microRNAs (miRNAs) as well as genomic, epigenomic, gut microbiome, metabolomic, and proteomic markers. The usage of biomarker-based methods demonstrates transformative potential for CRC treatment by boosting survival rates and lessening global impact through precision medicine development in oncology.},
}
RevDate: 2026-04-20
CmpDate: 2026-04-20
Community Turnover and Connectivity at Two Study Sites in the North and Wadden Seas: Dynamics From Hours to Seasons.
Environmental microbiology, 28(4):e70310.
Microbial communities underpin ecosystem processes and biogeochemical cycles in marine ecosystems, yet their spatial and temporal dynamics at hourly scales remain poorly understood. We surveyed two stations from the North Sea (NS) and Wadden Sea (WS), generating six high-frequency time-series datasets across depths and seasons, complemented by sediment cores. Across seasons, the sites in the NS and the WS harbored distinct microbial communities shaped by contrasts in salinity, temperature, and potentially the quantity and lability of organic matter. Connectivity between communities was limited but favoured by known seasonal hydrographic exchanges. Despite taxonomic contrasts between sites, functional turnover remained low, with communities harbouring similar metabolic potential but being adapted to local conditions, suggesting potential functional redundancy. At hourly scales, community turnover was weaker and largely driven by vertical and horizontal mixing between water masses, occasional resuspension from sediments, or a summer bloom from a copiotroph. These shifts were transient and did not disrupt the coupling between taxonomic and functional composition. However, their immediate effects on ecosystem processes, such as organic matter remineralisation and nutrient recycling remain unclear. Continued high-resolution microbiome monitoring, paired with biogeochemical flux measurements, is needed to better predict climate-driven changes in coastal ecosystem functioning.
Additional Links: PMID-42009250
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PubMed:
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@article {pmid42009250,
year = {2026},
author = {Ramond, P and de Groot, T and Niemann, H and Engelmann, JC},
title = {Community Turnover and Connectivity at Two Study Sites in the North and Wadden Seas: Dynamics From Hours to Seasons.},
journal = {Environmental microbiology},
volume = {28},
number = {4},
pages = {e70310},
doi = {10.1111/1462-2920.70310},
pmid = {42009250},
issn = {1462-2920},
support = {ERC-CoG-772923/ERC_/European Research Council/International ; //Wise NWO/ ; },
mesh = {Seasons ; *Microbiota ; *Seawater/microbiology ; *Geologic Sediments/microbiology ; North Sea ; Ecosystem ; *Bacteria/classification/genetics/isolation & purification ; Temperature ; Salinity ; Oceans and Seas ; },
abstract = {Microbial communities underpin ecosystem processes and biogeochemical cycles in marine ecosystems, yet their spatial and temporal dynamics at hourly scales remain poorly understood. We surveyed two stations from the North Sea (NS) and Wadden Sea (WS), generating six high-frequency time-series datasets across depths and seasons, complemented by sediment cores. Across seasons, the sites in the NS and the WS harbored distinct microbial communities shaped by contrasts in salinity, temperature, and potentially the quantity and lability of organic matter. Connectivity between communities was limited but favoured by known seasonal hydrographic exchanges. Despite taxonomic contrasts between sites, functional turnover remained low, with communities harbouring similar metabolic potential but being adapted to local conditions, suggesting potential functional redundancy. At hourly scales, community turnover was weaker and largely driven by vertical and horizontal mixing between water masses, occasional resuspension from sediments, or a summer bloom from a copiotroph. These shifts were transient and did not disrupt the coupling between taxonomic and functional composition. However, their immediate effects on ecosystem processes, such as organic matter remineralisation and nutrient recycling remain unclear. Continued high-resolution microbiome monitoring, paired with biogeochemical flux measurements, is needed to better predict climate-driven changes in coastal ecosystem functioning.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Seasons
*Microbiota
*Seawater/microbiology
*Geologic Sediments/microbiology
North Sea
Ecosystem
*Bacteria/classification/genetics/isolation & purification
Temperature
Salinity
Oceans and Seas
RevDate: 2026-04-21
CmpDate: 2026-04-21
Post-Heatwave Coral Health Coincides With Host-Specific Symbiodiniaceae-Bacteria Consortia.
Environmental microbiology, 28(4):e70306.
Coral reefs are facing unprecedented damage due to climate-driven marine heatwaves (MHWs). While coral response to elevated temperatures is inextricably linked to coral-associated microalgae (Symbiodiniaceae) and bacteria, the role of algal-bacterial interactions in affecting coral resilience to thermal stress remains obscure. Here we show coral health indicated by distinct compositions of Symbiodiniaceae-bacteria consortia in two coral species, the massive Porites lutea and the laminar Duncanopsammia peltata, upon exposure to an unusual MHW. P. lutea exhibited thermal resilience by maintaining an obligate partnership with the heat-tolerant Cladocopium C15 under both healthy and bleached states, alongside conservative bacterial community changes between the two states driven primarily by deterministic processes; whereas D. peltata associated with the heat-sensitive Cladocopium C1 in bleached state but the heat-tolerant Durusdinium D1/D4 in healthy state, with stochastically driven, more liberal bacterial community changes between the two states. This distinction between P. lutea and D. peltata in their Symbiodiniaceae-bacteria consortia reflects a specialist/generalist strategy in partner selection given the status of coral health, underscoring an evolutionary trade-off between high-fidelity symbioses for persistence under chronic stress and rapid microbiome turnover for transient bleaching resilience. Broadly, the host-specific, coordinated Symbiodiniaceae-bacteria community differentiation following MHWs, may inform future coral conservation and restoration practises in an era of escalating climate change.
Additional Links: PMID-42009295
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PubMed:
Citation:
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@article {pmid42009295,
year = {2026},
author = {Zhang, H and Zheng, X and Wang, Q and Zhou, X and Cai, L and Zhan, L and Huang, D and Shi, T},
title = {Post-Heatwave Coral Health Coincides With Host-Specific Symbiodiniaceae-Bacteria Consortia.},
journal = {Environmental microbiology},
volume = {28},
number = {4},
pages = {e70306},
doi = {10.1111/1462-2920.70306},
pmid = {42009295},
issn = {1462-2920},
support = {2022YFC3102003//National Key Research and Development Program of China/ ; 2020YFA0607602//National Key Research and Development Program of China/ ; 2020017//Scientific Research Foundation of the Third Institute of Oceanography, Ministry of Natural Resources of China/ ; 2019017//Scientific Research Foundation of the Third Institute of Oceanography, Ministry of Natural Resources of China/ ; 42376110//National Natural Science Foundation of China/ ; 41876119//National Natural Science Foundation of China/ ; //global Ocean Negative Carbon Emission (ONCE) program/ ; 2023J06043//Science Fund for Distinguished Young Scholars of Fujian Province/ ; },
mesh = {Animals ; *Anthozoa/microbiology/physiology ; Symbiosis ; Coral Reefs ; *Hot Temperature ; *Bacteria/classification/genetics/isolation & purification ; *Dinoflagellida/physiology ; *Microbial Consortia ; Microbiota ; },
abstract = {Coral reefs are facing unprecedented damage due to climate-driven marine heatwaves (MHWs). While coral response to elevated temperatures is inextricably linked to coral-associated microalgae (Symbiodiniaceae) and bacteria, the role of algal-bacterial interactions in affecting coral resilience to thermal stress remains obscure. Here we show coral health indicated by distinct compositions of Symbiodiniaceae-bacteria consortia in two coral species, the massive Porites lutea and the laminar Duncanopsammia peltata, upon exposure to an unusual MHW. P. lutea exhibited thermal resilience by maintaining an obligate partnership with the heat-tolerant Cladocopium C15 under both healthy and bleached states, alongside conservative bacterial community changes between the two states driven primarily by deterministic processes; whereas D. peltata associated with the heat-sensitive Cladocopium C1 in bleached state but the heat-tolerant Durusdinium D1/D4 in healthy state, with stochastically driven, more liberal bacterial community changes between the two states. This distinction between P. lutea and D. peltata in their Symbiodiniaceae-bacteria consortia reflects a specialist/generalist strategy in partner selection given the status of coral health, underscoring an evolutionary trade-off between high-fidelity symbioses for persistence under chronic stress and rapid microbiome turnover for transient bleaching resilience. Broadly, the host-specific, coordinated Symbiodiniaceae-bacteria community differentiation following MHWs, may inform future coral conservation and restoration practises in an era of escalating climate change.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Anthozoa/microbiology/physiology
Symbiosis
Coral Reefs
*Hot Temperature
*Bacteria/classification/genetics/isolation & purification
*Dinoflagellida/physiology
*Microbial Consortia
Microbiota
RevDate: 2026-04-21
CmpDate: 2026-04-21
Protocol for a pilot feasibility randomised controlled trial of fecal microbiota transplantation for adolescent anorexia nervosa.
BMJ open, 16(4):e109115 pii:bmjopen-2025-109115.
INTRODUCTION: Despite its serious impact, anorexia nervosa (AN) remains one of the least understood mental illnesses, with significant gaps in effective treatment options. No medications have been deemed effective and only 50% of individuals respond to conventional psychotherapies. Gastrointestinal (GI) bacteria have been found to be altered in individuals with AN. While, Fecal microbiota transplantation (FMT) has shown potential for alleviating anxiety and depression, its effects remain understudied for individuals with AN. This study aims to determine whether oral capsular FMT is acceptable to adolescents with AN and results in clinical improvement in weight and/or psychological symptoms.
METHODS: This study will randomise 20 adolescents with AN, ages 12-17 years, to receive either FMT or placebo capsules. These 20 youth, as well as an additional 10 youth who decline trial enrolment, will participate in qualitative interviews. We will track recruitment rates and collect psychological and biological measures (blood, stool, urine and saliva) at multiple timepoints to assess how gut microbiota and their metabolites may influence the symptoms of AN. Interviews with participants and caregivers will explore their experiences and views on FMT as a treatment approach.
ETHICS AND DISSEMINATION: This study has received ethics approval by the Hamilton Integrated Research Ethics Board (#17493) and investigational drug approval by Health Canada (Dossier ID: c292423). Informed consent will be obtained by research staff from all participants. Findings will be disseminated through academic conferences, clinical forums and partnerships with advocacy organisations to reach clinicians, researchers and individuals with lived experience.
TRIAL REGISTRATION NUMBER: NCT06593366.
Additional Links: PMID-42009386
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PubMed:
Citation:
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@article {pmid42009386,
year = {2026},
author = {Couturier, J and Kenner, E and Nicula, M and Chowdhury, F and Surette, M and Pai, N},
title = {Protocol for a pilot feasibility randomised controlled trial of fecal microbiota transplantation for adolescent anorexia nervosa.},
journal = {BMJ open},
volume = {16},
number = {4},
pages = {e109115},
doi = {10.1136/bmjopen-2025-109115},
pmid = {42009386},
issn = {2044-6055},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; Adolescent ; *Anorexia Nervosa/therapy/psychology ; Pilot Projects ; Feasibility Studies ; Child ; Female ; Male ; Randomized Controlled Trials as Topic ; Gastrointestinal Microbiome ; },
abstract = {INTRODUCTION: Despite its serious impact, anorexia nervosa (AN) remains one of the least understood mental illnesses, with significant gaps in effective treatment options. No medications have been deemed effective and only 50% of individuals respond to conventional psychotherapies. Gastrointestinal (GI) bacteria have been found to be altered in individuals with AN. While, Fecal microbiota transplantation (FMT) has shown potential for alleviating anxiety and depression, its effects remain understudied for individuals with AN. This study aims to determine whether oral capsular FMT is acceptable to adolescents with AN and results in clinical improvement in weight and/or psychological symptoms.
METHODS: This study will randomise 20 adolescents with AN, ages 12-17 years, to receive either FMT or placebo capsules. These 20 youth, as well as an additional 10 youth who decline trial enrolment, will participate in qualitative interviews. We will track recruitment rates and collect psychological and biological measures (blood, stool, urine and saliva) at multiple timepoints to assess how gut microbiota and their metabolites may influence the symptoms of AN. Interviews with participants and caregivers will explore their experiences and views on FMT as a treatment approach.
ETHICS AND DISSEMINATION: This study has received ethics approval by the Hamilton Integrated Research Ethics Board (#17493) and investigational drug approval by Health Canada (Dossier ID: c292423). Informed consent will be obtained by research staff from all participants. Findings will be disseminated through academic conferences, clinical forums and partnerships with advocacy organisations to reach clinicians, researchers and individuals with lived experience.
TRIAL REGISTRATION NUMBER: NCT06593366.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Fecal Microbiota Transplantation/methods
Adolescent
*Anorexia Nervosa/therapy/psychology
Pilot Projects
Feasibility Studies
Child
Female
Male
Randomized Controlled Trials as Topic
Gastrointestinal Microbiome
RevDate: 2026-04-20
Microbiome modulating remedies for chronic diseases: a review of current interventions and future directions.
Inflammopharmacology [Epub ahead of print].
Additional Links: PMID-42009997
PubMed:
Citation:
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@article {pmid42009997,
year = {2026},
author = {Swain, MP and Mehta, CH and Padya, BS and Sharma, S and Velagacherla, V and Mitra, A and Mohanty, S and Mukherjee, T},
title = {Microbiome modulating remedies for chronic diseases: a review of current interventions and future directions.},
journal = {Inflammopharmacology},
volume = {},
number = {},
pages = {},
pmid = {42009997},
issn = {1568-5608},
}
RevDate: 2026-04-20
Microbiome signature of Parkinson's disease in healthy and genetically at-risk individuals.
Nature medicine [Epub ahead of print].
Parkinson's disease (PD) is a major cause of disability. GBA1 variants are the most common genetic risk factor for PD and increase the risk up to 30-fold. Why only approximately 20% of GBA1 variant carriers develop PD remains unknown. Here, by combining clinical and fecal metagenomics data from 271 patients with PD, from 43 carriers of GBA1 variants not manifesting PD symptoms (GBA-NMC) and from 150 healthy controls, and using an innovative microbiome analysis, combining differential abundance of species and coherence of differential abundance variation between the groups as assessed by Cliff's delta (δ), we show that the composition of a large component of the gut microbiome (approximately 25%) in GBA-NMC is intermediate between healthy controls and patients with PD. This component is strongly correlated with disease progression in patients and prodromal symptoms suggestive of future development of PD in both GBA-NMC and healthy individuals. We found microbiome alterations similar to those described here in three independent cohorts from the United States, Korea and Turkey, totaling 638 patients with PD and 319 healthy controls, and we conclude that gut microbiome alterations can identify both genetically and non-genetically at-risk individuals in the general population who may be progressing toward PD, thus serving as an early marker of disease development in the premanifest phase.
Additional Links: PMID-42010118
PubMed:
Citation:
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@article {pmid42010118,
year = {2026},
author = {Menozzi, E and Ren, Y and Geiger, M and Macnaughtan, J and Avenali, M and Toffoli, M and Gilles, M and Calabrese, R and Mitrotti, P and Gallo, L and Famechon, A and Del Pozo, SL and Mezabrovschi, R and Koletsi, S and Loefflad, N and Yalkic, S and Limbachiya, N and Clasen, F and Yildirim, S and Shoaie, S and Blottière, H and Morabito, C and David, A and Quinquis, B and Pons, N and Le Chatelier, E and Valzania, F and Cavallieri, F and Fioravanti, V and Toschi, G and Blandini, F and Almeida, M and Ehrlich, SD and Meslier, V and Schapira, AHV},
title = {Microbiome signature of Parkinson's disease in healthy and genetically at-risk individuals.},
journal = {Nature medicine},
volume = {},
number = {},
pages = {},
pmid = {42010118},
issn = {1546-170X},
support = {MR/T046007/1//EU Joint Programme - Neurodegenerative Disease Research (Programi i Përbashkët i BE-së për Kërkimet mbi Sëmundjet Neuro-degjeneruese)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; },
abstract = {Parkinson's disease (PD) is a major cause of disability. GBA1 variants are the most common genetic risk factor for PD and increase the risk up to 30-fold. Why only approximately 20% of GBA1 variant carriers develop PD remains unknown. Here, by combining clinical and fecal metagenomics data from 271 patients with PD, from 43 carriers of GBA1 variants not manifesting PD symptoms (GBA-NMC) and from 150 healthy controls, and using an innovative microbiome analysis, combining differential abundance of species and coherence of differential abundance variation between the groups as assessed by Cliff's delta (δ), we show that the composition of a large component of the gut microbiome (approximately 25%) in GBA-NMC is intermediate between healthy controls and patients with PD. This component is strongly correlated with disease progression in patients and prodromal symptoms suggestive of future development of PD in both GBA-NMC and healthy individuals. We found microbiome alterations similar to those described here in three independent cohorts from the United States, Korea and Turkey, totaling 638 patients with PD and 319 healthy controls, and we conclude that gut microbiome alterations can identify both genetically and non-genetically at-risk individuals in the general population who may be progressing toward PD, thus serving as an early marker of disease development in the premanifest phase.},
}
RevDate: 2026-04-20
Considerations for the design of impactful citizen-science projects in microbiome research.
Nature protocols [Epub ahead of print].
Citizen science offers a transformative approach to microbiome research. It allows the collection of rich, context-specific data from diverse sources, such as varying human populations and environments. Here, we describe guidelines that cover the design and implementation of community-engaged citizen-science projects focused on microbiome research. We outline essential research steps, beginning with defining the objectives and forming a transdisciplinary team, and continuing with community interaction, standardized self-sampling protocols, strategies for data processing, analysis and communication of results to community members and policymakers, as well as the implementation of robust data management practices that uphold participant privacy and data sovereignty. The guidelines highlight culturally-sensitive outreach strategies and capacity building in research teams and communities, emphasizing ethical considerations and tailored recruitment strategies. Community engagement may help reduce sampling bias but does not automatically ensure participant diversity: intentional inclusion strategies are essential. They cover culturally sensitive outreach, ethical considerations and tailored recruitment approaches that support inclusive participation and meaningful collaboration. These recommendations draw inspiration from a range of health and environment-related citizen-science projects in Belgium, Peru and Cameroon, and collaborative projects across the world. Specific examples highlight the importance of adapting methodologies to diverse cultural contexts and logistical constraints. While wet-laboratory sample processing and downstream analyses are detailed elsewhere, this Perspective focuses on the unique considerations and best practices needed for designing impactful cocreative citizen-science projects that combine scientific discovery with community, environmental health and well-being. It can serve as a blueprint for future citizen-science initiatives that aim to expand access to microbiome research, foster global collaboration and promote long-term research equity and environmental sustainability.
Additional Links: PMID-42010351
PubMed:
Citation:
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@article {pmid42010351,
year = {2026},
author = {Ahannach, S and Condori-Catachura, S and Dillen, J and Dricot, C and Gehrmann, T and Wittouck, S and Kenfack, JM and Van Beeck, W and De Boeck, I and Eilers, T and Ticlla, M and Santullo Latorre, A and Smets, W and Temmermans, J and Arconada Nuin, E and , and Van Puyvelde, S and Spacova, I and Verhoeven, V and Lebeer, S},
title = {Considerations for the design of impactful citizen-science projects in microbiome research.},
journal = {Nature protocols},
volume = {},
number = {},
pages = {},
pmid = {42010351},
issn = {1750-2799},
abstract = {Citizen science offers a transformative approach to microbiome research. It allows the collection of rich, context-specific data from diverse sources, such as varying human populations and environments. Here, we describe guidelines that cover the design and implementation of community-engaged citizen-science projects focused on microbiome research. We outline essential research steps, beginning with defining the objectives and forming a transdisciplinary team, and continuing with community interaction, standardized self-sampling protocols, strategies for data processing, analysis and communication of results to community members and policymakers, as well as the implementation of robust data management practices that uphold participant privacy and data sovereignty. The guidelines highlight culturally-sensitive outreach strategies and capacity building in research teams and communities, emphasizing ethical considerations and tailored recruitment strategies. Community engagement may help reduce sampling bias but does not automatically ensure participant diversity: intentional inclusion strategies are essential. They cover culturally sensitive outreach, ethical considerations and tailored recruitment approaches that support inclusive participation and meaningful collaboration. These recommendations draw inspiration from a range of health and environment-related citizen-science projects in Belgium, Peru and Cameroon, and collaborative projects across the world. Specific examples highlight the importance of adapting methodologies to diverse cultural contexts and logistical constraints. While wet-laboratory sample processing and downstream analyses are detailed elsewhere, this Perspective focuses on the unique considerations and best practices needed for designing impactful cocreative citizen-science projects that combine scientific discovery with community, environmental health and well-being. It can serve as a blueprint for future citizen-science initiatives that aim to expand access to microbiome research, foster global collaboration and promote long-term research equity and environmental sustainability.},
}
RevDate: 2026-04-20
Altered microbial cargo in fecal microbiome-derived outer membrane vesicles as novel biomarkers for vascular dementia.
BMC microbiology pii:10.1186/s12866-026-05040-5 [Epub ahead of print].
Additional Links: PMID-42010400
Publisher:
PubMed:
Citation:
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@article {pmid42010400,
year = {2026},
author = {Li, X and Wei, W and Wei, S and Xu, W and Mo, L and Wang, J and Zhu, H and Liu, Z and Jin, F},
title = {Altered microbial cargo in fecal microbiome-derived outer membrane vesicles as novel biomarkers for vascular dementia.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05040-5},
pmid = {42010400},
issn = {1471-2180},
support = {2022A21//the Doctoral Research Startup Project of Central People's Hospital of Zhanjiang/ ; 2022A10//the Doctoral Research Startup Project of Central People's Hospital of Zhanjiang/ ; 2022A14//the Doctoral Research Startup Project of Central People's Hospital of Zhanjiang/ ; 2022A22//the Doctoral Research Startup Project of Central People's Hospital of Zhanjiang/ ; 2021X091662//Weifang Municipal Health Commission Scientific Research Project/ ; 2022A1515010749//the Natural Science Foundation of Guangdong Province/ ; 2024B01238//Zhanjiang City Science and Technology Plan Project/ ; },
}
RevDate: 2026-04-21
Metagenomics reveals gut microbial differences and ecological adaptation in plateau zokor (Eospalax baileyi) populations.
BMC microbiology pii:10.1186/s12866-026-05069-6 [Epub ahead of print].
Additional Links: PMID-42010457
Publisher:
PubMed:
Citation:
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@article {pmid42010457,
year = {2026},
author = {Guo, J and Liang, C and Cairang, L and Si, L and Yan, J and Liu, D},
title = {Metagenomics reveals gut microbial differences and ecological adaptation in plateau zokor (Eospalax baileyi) populations.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05069-6},
pmid = {42010457},
issn = {1471-2180},
support = {LHZX-2023-02//Sanjiangyuan National Park Joint Grant from the Chinese Academy of Sciences and the People's Government of Qinghai Province/ ; },
}
RevDate: 2026-04-21
Trimethylamine-producing microbe Bacillus megaterium KCTC 3007 promotes antitumor immunity in endometrial cancer via type I interferon response pathways.
Microbiome pii:10.1186/s40168-026-02373-1 [Epub ahead of print].
BACKGROUND: Endometrial cancer (ECa) is one of the most common gynecologic malignancies, with limited therapeutic responses in metastatic or recurrent cases. The bacterial microbiota has emerged as a key modulator of carcinogenesis and antitumor immunity. However, the role of endometrial microbiota in ECa pathogenesis and prognosis remains poorly understood.
METHODS: We performed comprehensive multi-omics analysis integrating metatranscriptomics, transcriptomics, and targeted metabolomics from 60 ECa and 18 benign patients. RNA sequencing enabled simultaneous profiling of active tissue-resident microbiota and host gene expression. Serum metabolomics was conducted on all patients. Identified microbial-metabolite associations were validated through in vitro co-culture experiments using peripheral blood mononuclear cells (PBMCs), cancer cell lines, RNA sequencing, and live cell imaging.
RESULTS: ECa patients exhibited significantly altered microbial diversity and composition compared to benign controls. Through integrated multi-omics analysis, we identified Bacillus megaterium (BM) KCTC 3007 as a beneficial microbe associated with prolonged recurrence-free survival. In an exploratory analysis of ECa subtypes, Cupriavidus taiwanensis and Marinomonas primoryensis showed potential links to poor prognosis, although these observations warrant caution due to the limited size of certain subgroups. Tissue BM abundance positively correlated with serum trimethylamine N-oxide (TMAO) levels, particularly in postmenopausal women. In vitro experiments demonstrated that BM KCTC 3007 enhanced antitumor immunity by promoting interleukin and type I interferon expression, expanding CD8 + T cell populations, and increasing immune cell-tumor cell interactions. RNA sequencing revealed activation of interferon alpha response and immune cell proliferation pathways, with IFNAR1 identified as a key upstream regulator. TMAO treatment recapitulated these immune-activating effects, enhancing CD8 + T cell responses and preferentially inducing pyroptotic cancer cell death.
CONCLUSIONS: We provide the first evidence that tissue-resident BM KCTC 3007 promotes antitumor immunity in ECa through TMAO production and subsequent type I interferon-mediated immune activation. This integrated multi-omics approach establishes a complete microbe-metabolite-host mechanistic pathway and highlights the therapeutic potential of TMAO-producing probiotic strains for ECa treatment. Video Abstract.
Additional Links: PMID-42010642
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42010642,
year = {2026},
author = {Min, K and Kim, SI and Lee, M and Kim, Y and Jeong, C and Kim, S and Kim, SJ and Kim, H and Cho, B and Joo, Y and Park, H and Lee, M},
title = {Trimethylamine-producing microbe Bacillus megaterium KCTC 3007 promotes antitumor immunity in endometrial cancer via type I interferon response pathways.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02373-1},
pmid = {42010642},
issn = {2049-2618},
support = {grant of the MD-PhD/Medical Scientist Training Program//Korea Health Industry Development Institute/Republic of Korea ; KGCR-2022-01//Korean Gynecologic Cancer Research/ ; 2022R1A2C2008976 and RS-2023-00228315//Ministry of Science and ICT, Korean Government/ ; },
abstract = {BACKGROUND: Endometrial cancer (ECa) is one of the most common gynecologic malignancies, with limited therapeutic responses in metastatic or recurrent cases. The bacterial microbiota has emerged as a key modulator of carcinogenesis and antitumor immunity. However, the role of endometrial microbiota in ECa pathogenesis and prognosis remains poorly understood.
METHODS: We performed comprehensive multi-omics analysis integrating metatranscriptomics, transcriptomics, and targeted metabolomics from 60 ECa and 18 benign patients. RNA sequencing enabled simultaneous profiling of active tissue-resident microbiota and host gene expression. Serum metabolomics was conducted on all patients. Identified microbial-metabolite associations were validated through in vitro co-culture experiments using peripheral blood mononuclear cells (PBMCs), cancer cell lines, RNA sequencing, and live cell imaging.
RESULTS: ECa patients exhibited significantly altered microbial diversity and composition compared to benign controls. Through integrated multi-omics analysis, we identified Bacillus megaterium (BM) KCTC 3007 as a beneficial microbe associated with prolonged recurrence-free survival. In an exploratory analysis of ECa subtypes, Cupriavidus taiwanensis and Marinomonas primoryensis showed potential links to poor prognosis, although these observations warrant caution due to the limited size of certain subgroups. Tissue BM abundance positively correlated with serum trimethylamine N-oxide (TMAO) levels, particularly in postmenopausal women. In vitro experiments demonstrated that BM KCTC 3007 enhanced antitumor immunity by promoting interleukin and type I interferon expression, expanding CD8 + T cell populations, and increasing immune cell-tumor cell interactions. RNA sequencing revealed activation of interferon alpha response and immune cell proliferation pathways, with IFNAR1 identified as a key upstream regulator. TMAO treatment recapitulated these immune-activating effects, enhancing CD8 + T cell responses and preferentially inducing pyroptotic cancer cell death.
CONCLUSIONS: We provide the first evidence that tissue-resident BM KCTC 3007 promotes antitumor immunity in ECa through TMAO production and subsequent type I interferon-mediated immune activation. This integrated multi-omics approach establishes a complete microbe-metabolite-host mechanistic pathway and highlights the therapeutic potential of TMAO-producing probiotic strains for ECa treatment. Video Abstract.},
}
RevDate: 2026-04-21
A novel enterotype enriched with respiratory super-dominant pathobionts is associated with immunosuppression in pulmonary tuberculosis patients.
Journal of translational medicine pii:10.1186/s12967-026-08165-3 [Epub ahead of print].
BACKGROUND: Perturbations of the gut microbiota in pulmonary tuberculosis (PTB) patients, often antibiotic-induced, are frequently observed; however, the defining features of this dysbiosis and its relationship with clinical phenotypes remain insufficiently characterized.
METHODS: In this cross-sectional study, we collected fecal samples from 66 PTB patients and performed 16S rRNA gene (V3-V4) sequencing. Species-level taxonomic profiling was conducted using the Human Gut Microbiome Analysis Database (HGMAD). Enterotypes were constructed, and their associations with PTB were investigated. The predictive capacity of enterotype-specific microbial signatures (enterosignatures) for clinical phenotypes was assessed.
RESULTS: Taxonomic analysis revealed significantly reduced prevalence of high-abundance bacteria group in PTB patients (43.84%) compared to healthy controls (HC, 98.01%), indicating increased microbiota heterogeneity. Known pathogenic species, predominantly common respiratory opportunistic pathogens (e.g., Haemophilus parainfluenzae, Acinetobacter baumannii, Veillonella parvula), were more prevalent in the PTB cohort (21.37% vs. 11.49% in HC). Enterotype analysis revealed a distinct cluster, designated ETE (Enterobacterales-dominated enterotype), which was predominantly observed in PTB patients and differed from the conventional Prevotella-dominated enterotype (ETP) and Bacteroides-dominated enterotype (ETB), identified in HC. ETE was significantly enriched in taxa including Acinetobacter baumannii, Enterococcus, Veillonella, Pseudomonas, and Streptococcus, exhibited lower alpha diversity, and functional inference using PICRUSt2 suggested relative lower immune-related pathways. Clinically, ETE was associated with lower cellular immunity and a trend toward higher C-reactive protein (CRP) levels. A model based on ten super-dominant respiratory pathobionts enterosignatures effectively predicted key clinical phenotypes, with area under the curves (AUCs) of 0.83 for CD4[+] T-cell count, 0.74 for CD8[+] T-cell count, 0.74 for CD4[+]/CD8[+] ratio, 0.93 for CRP, 0.78 for CA125, and 0.70 for Mtb positivity. SHapley Additive exPlanation (SHAP) analysis identified Enterobacterales and Veillonella as key negative predictors for T-cell counts, while Streptococcus and Enterobacteriaceae were positive predictors for CRP. In the CA125 model, Veillonella acted as a positive predictor and Enterobacterales as a negative predictor.
CONCLUSION: This cross-sectional study identifies a distinct, PTB-associated enterotype (ETE) characterized by enrichment of respiratory pathobionts and associated with altered immune parameters in PTB patients. Enterosignatures derive from ETE represent exploratory biomarkers with promising predictive capacity for clinical outcomes, though their generalizability warrants validation in independent, prospective cohorts.
Additional Links: PMID-42010662
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42010662,
year = {2026},
author = {Yuan, T and Chen, J and Zheng, H and Pu, J and Li, L and Lu, S and Sun, Y and Lin, W and Yang, J and Xu, J},
title = {A novel enterotype enriched with respiratory super-dominant pathobionts is associated with immunosuppression in pulmonary tuberculosis patients.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-08165-3},
pmid = {42010662},
issn = {1479-5876},
abstract = {BACKGROUND: Perturbations of the gut microbiota in pulmonary tuberculosis (PTB) patients, often antibiotic-induced, are frequently observed; however, the defining features of this dysbiosis and its relationship with clinical phenotypes remain insufficiently characterized.
METHODS: In this cross-sectional study, we collected fecal samples from 66 PTB patients and performed 16S rRNA gene (V3-V4) sequencing. Species-level taxonomic profiling was conducted using the Human Gut Microbiome Analysis Database (HGMAD). Enterotypes were constructed, and their associations with PTB were investigated. The predictive capacity of enterotype-specific microbial signatures (enterosignatures) for clinical phenotypes was assessed.
RESULTS: Taxonomic analysis revealed significantly reduced prevalence of high-abundance bacteria group in PTB patients (43.84%) compared to healthy controls (HC, 98.01%), indicating increased microbiota heterogeneity. Known pathogenic species, predominantly common respiratory opportunistic pathogens (e.g., Haemophilus parainfluenzae, Acinetobacter baumannii, Veillonella parvula), were more prevalent in the PTB cohort (21.37% vs. 11.49% in HC). Enterotype analysis revealed a distinct cluster, designated ETE (Enterobacterales-dominated enterotype), which was predominantly observed in PTB patients and differed from the conventional Prevotella-dominated enterotype (ETP) and Bacteroides-dominated enterotype (ETB), identified in HC. ETE was significantly enriched in taxa including Acinetobacter baumannii, Enterococcus, Veillonella, Pseudomonas, and Streptococcus, exhibited lower alpha diversity, and functional inference using PICRUSt2 suggested relative lower immune-related pathways. Clinically, ETE was associated with lower cellular immunity and a trend toward higher C-reactive protein (CRP) levels. A model based on ten super-dominant respiratory pathobionts enterosignatures effectively predicted key clinical phenotypes, with area under the curves (AUCs) of 0.83 for CD4[+] T-cell count, 0.74 for CD8[+] T-cell count, 0.74 for CD4[+]/CD8[+] ratio, 0.93 for CRP, 0.78 for CA125, and 0.70 for Mtb positivity. SHapley Additive exPlanation (SHAP) analysis identified Enterobacterales and Veillonella as key negative predictors for T-cell counts, while Streptococcus and Enterobacteriaceae were positive predictors for CRP. In the CA125 model, Veillonella acted as a positive predictor and Enterobacterales as a negative predictor.
CONCLUSION: This cross-sectional study identifies a distinct, PTB-associated enterotype (ETE) characterized by enrichment of respiratory pathobionts and associated with altered immune parameters in PTB patients. Enterosignatures derive from ETE represent exploratory biomarkers with promising predictive capacity for clinical outcomes, though their generalizability warrants validation in independent, prospective cohorts.},
}
RevDate: 2026-04-21
Metabolome-driven rhizosphere microbiome assembly determining the health of medicinal herb (Angelica sinensis) against root rot.
Microbiome pii:10.1186/s40168-026-02393-x [Epub ahead of print].
BACKGROUND: The rhizosphere-associated microbiota plays a crucial role in plant responses to disease stress. Plant secondary metabolites are recognized as crucial mediators in the assembly of rhizosphere microbial communities, particularly by enhancing the colonization of beneficial microorganisms. Despite this recognized importance, a deeper understanding of how such metabolome-driven microbiome assembly specifically determines plant resistance against soil-borne diseases is still lacking.
RESULTS: Here, we focused on the widely planted medicinal plant Angelica sinensis and demonstrated that root rot-diseased rhizosphere soils (DRS) exhibited a higher relative abundance of Fusarium and a lower relative abundance of Streptomyces compared to healthy rhizosphere soils (HRS). Shotgun metagenomic sequencing revealed that metabolism-associated genes, particularly those related to steroid degradation, are significantly enriched in HRS samples. Subsequent genome and functional gene analysis of Streptomyces revealed that the steroid degradation-related genes are associated with rhizosphere colonization in hosts. Rhizosphere Streptomyces S15 directly antagonized Fusarium and enhanced the root resistance of A. sinensis. Comparative metabolomics showed that A. sinensis plants from HRS secreted more lipid and lipid-like molecules than those from DRS, especially sterol lipids and long-chain fatty acids, which promoted the growth of Streptomyces S15 isolates. Transcriptome analysis validated that the lipid hormones are essential for sporulation, biofilm formation, and streptomycin biosynthesis of S15 strain. Finally, exogenous application of synbiotics (lipid prebiotics and S15) to A. sinensis resulted in the enrichment of S15-homologous Streptomyces amplicon sequence variant (ASV), further establishing beneficial bacterial communities in Fusarium-stressed rhizospheres.
CONCLUSIONS: Our study proposes that A. sinensis recruits steroid-metabolizing Streptomyces species by exuding key lipid compounds (i.e., methyl jasmonate and brassinolide) to combat Fusarium root rot. This study provides novel insights into using functional synbiotics as a promising strategy for manipulating plant-microbiome interactions to promote sustainable agriculture. Video Abstract.
Additional Links: PMID-42010711
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42010711,
year = {2026},
author = {You, C and Zhang, W and Guan, Y and Liang, Q and Nong, C and Yang, T and Li, M and Banerjee, S and Zhou, X and Wang, X and Xu, Y and Shen, Q and Wei, Z},
title = {Metabolome-driven rhizosphere microbiome assembly determining the health of medicinal herb (Angelica sinensis) against root rot.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02393-x},
pmid = {42010711},
issn = {2049-2618},
support = {2022YFC3501501//National Key Research and Development Program of China/ ; KJYQ2025034, KJYQ2024039//Fundamental Research Funds for the Central Universities/ ; BK20240194//the Natural Science Foundation of Jiangsu Province/ ; },
abstract = {BACKGROUND: The rhizosphere-associated microbiota plays a crucial role in plant responses to disease stress. Plant secondary metabolites are recognized as crucial mediators in the assembly of rhizosphere microbial communities, particularly by enhancing the colonization of beneficial microorganisms. Despite this recognized importance, a deeper understanding of how such metabolome-driven microbiome assembly specifically determines plant resistance against soil-borne diseases is still lacking.
RESULTS: Here, we focused on the widely planted medicinal plant Angelica sinensis and demonstrated that root rot-diseased rhizosphere soils (DRS) exhibited a higher relative abundance of Fusarium and a lower relative abundance of Streptomyces compared to healthy rhizosphere soils (HRS). Shotgun metagenomic sequencing revealed that metabolism-associated genes, particularly those related to steroid degradation, are significantly enriched in HRS samples. Subsequent genome and functional gene analysis of Streptomyces revealed that the steroid degradation-related genes are associated with rhizosphere colonization in hosts. Rhizosphere Streptomyces S15 directly antagonized Fusarium and enhanced the root resistance of A. sinensis. Comparative metabolomics showed that A. sinensis plants from HRS secreted more lipid and lipid-like molecules than those from DRS, especially sterol lipids and long-chain fatty acids, which promoted the growth of Streptomyces S15 isolates. Transcriptome analysis validated that the lipid hormones are essential for sporulation, biofilm formation, and streptomycin biosynthesis of S15 strain. Finally, exogenous application of synbiotics (lipid prebiotics and S15) to A. sinensis resulted in the enrichment of S15-homologous Streptomyces amplicon sequence variant (ASV), further establishing beneficial bacterial communities in Fusarium-stressed rhizospheres.
CONCLUSIONS: Our study proposes that A. sinensis recruits steroid-metabolizing Streptomyces species by exuding key lipid compounds (i.e., methyl jasmonate and brassinolide) to combat Fusarium root rot. This study provides novel insights into using functional synbiotics as a promising strategy for manipulating plant-microbiome interactions to promote sustainable agriculture. Video Abstract.},
}
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ESP Quick Facts
ESP Origins
In the early 1990's, Robert Robbins was a faculty member at Johns Hopkins, where he directed the informatics core of GDB — the human gene-mapping database of the international human genome project. To share papers with colleagues around the world, he set up a small paper-sharing section on his personal web page. This small project evolved into The Electronic Scholarly Publishing Project.
ESP Support
In 1995, Robbins became the VP/IT of the Fred Hutchinson Cancer Research Center in Seattle, WA. Soon after arriving in Seattle, Robbins secured funding, through the ELSI component of the US Human Genome Project, to create the original ESP.ORG web site, with the formal goal of providing free, world-wide access to the literature of classical genetics.
ESP Rationale
Although the methods of molecular biology can seem almost magical to the uninitiated, the original techniques of classical genetics are readily appreciated by one and all: cross individuals that differ in some inherited trait, collect all of the progeny, score their attributes, and propose mechanisms to explain the patterns of inheritance observed.
ESP Goal
In reading the early works of classical genetics, one is drawn, almost inexorably, into ever more complex models, until molecular explanations begin to seem both necessary and natural. At that point, the tools for understanding genome research are at hand. Assisting readers reach this point was the original goal of The Electronic Scholarly Publishing Project.
ESP Usage
Usage of the site grew rapidly and has remained high. Faculty began to use the site for their assigned readings. Other on-line publishers, ranging from The New York Times to Nature referenced ESP materials in their own publications. Nobel laureates (e.g., Joshua Lederberg) regularly used the site and even wrote to suggest changes and improvements.
ESP Content
When the site began, no journals were making their early content available in digital format. As a result, ESP was obliged to digitize classic literature before it could be made available. For many important papers — such as Mendel's original paper or the first genetic map — ESP had to produce entirely new typeset versions of the works, if they were to be available in a high-quality format.
ESP Help
Early support from the DOE component of the Human Genome Project was critically important for getting the ESP project on a firm foundation. Since that funding ended (nearly 20 years ago), the project has been operated as a purely volunteer effort. Anyone wishing to assist in these efforts should send an email to Robbins.
ESP Plans
With the development of methods for adding typeset side notes to PDF files, the ESP project now plans to add annotated versions of some classical papers to its holdings. We also plan to add new reference and pedagogical material. We have already started providing regularly updated, comprehensive bibliographies to the ESP.ORG site.
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Dinosaur tail, complete with feathers, found preserved in amber.
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Mysterious fast radio burst (FRB) detected in the distant universe.
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Big Data: Buzzword or Big Deal?
Hacking the genome: Identifying anonymized human subjects using publicly available data.