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RJR: Recommended Bibliography 04 Apr 2026 at 01:55 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2026-04-01
The phylum Fusobacteriota is associated with CRC-specific mortality: Results from the Translational Research Program in Cancer Differences across Populations.
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology pii:780784 [Epub ahead of print].
BACKGROUND: The microbiome is an important component of the tumor microenvironment implicated in colorectal cancer (CRC). However, its relationship with CRC-specific mortality remains unclear.
METHODS: We included 581 participants with CRC (167 African American, 176 Alaska Native, 118 Hispanic, 120 non-Hispanic White) from the Translational Research Program in Cancer Differences across Populations (TRPCDP). We sequenced the V4 region of the 16S rRNA bacterial gene using DNA extracted from formalin-fixed paraffin embedded tumors. 204 participants died of CRC and 377 did not die of CRC. Participants who died of CRC were matched to participants who did not die of CRC during follow-up by age, sex, tumor site, tumor stage, year of diagnosis, and population group. Logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs) for associations between bacterial presence with CRC-specific mortality, adjusting for matching factors and tissue macrodissection status.
RESULTS: Individuals who died from CRC were 1.71 times as likely to have bacteria from the Fusobacteriota phylum present in their tumors (OR=1.71, 95% CI: 1.19-2.47). Associations with Fusobacteriota were strongest among African American participants (OR=2.36, 95% CI: 1.14-4.99) compared to other populations, however this different was not statistically significant (OR range = 1.05-1.38, Pinteraction = 0.697). Candidate pathways of pyruvate fermentation to acetate and lactate II and peptidoglycan biosynthesis I were associated with higher odds of CRC death.
CONCLUSIONS: Fusobacteriota was significantly associated with CRC-specific mortality with noted differences across populations.
IMPACT: This finding highlights the tumor microbiome as a candidate for further investigation into CRC outcome disparities.
Additional Links: PMID-41920180
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PubMed:
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@article {pmid41920180,
year = {2026},
author = {Thomas, CE and Loroña, NC and LaBrie, SD and Curtis, KR and Yin, H and Ma, N and Randolph, TW and Qu, C and Huyghe, JR and Thomas, S and Hsu, L and Koehne, AL and Nayemi, S and Ammar, H and Kahsai, OJ and Redwood, D and Li, CI and Li, L and Peters, U and Figueiredo, JC and Thomas, TK and Phipps, AI and Hullar, MAJ},
title = {The phylum Fusobacteriota is associated with CRC-specific mortality: Results from the Translational Research Program in Cancer Differences across Populations.},
journal = {Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology},
volume = {},
number = {},
pages = {},
doi = {10.1158/1055-9965.EPI-25-1580},
pmid = {41920180},
issn = {1538-7755},
abstract = {BACKGROUND: The microbiome is an important component of the tumor microenvironment implicated in colorectal cancer (CRC). However, its relationship with CRC-specific mortality remains unclear.
METHODS: We included 581 participants with CRC (167 African American, 176 Alaska Native, 118 Hispanic, 120 non-Hispanic White) from the Translational Research Program in Cancer Differences across Populations (TRPCDP). We sequenced the V4 region of the 16S rRNA bacterial gene using DNA extracted from formalin-fixed paraffin embedded tumors. 204 participants died of CRC and 377 did not die of CRC. Participants who died of CRC were matched to participants who did not die of CRC during follow-up by age, sex, tumor site, tumor stage, year of diagnosis, and population group. Logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs) for associations between bacterial presence with CRC-specific mortality, adjusting for matching factors and tissue macrodissection status.
RESULTS: Individuals who died from CRC were 1.71 times as likely to have bacteria from the Fusobacteriota phylum present in their tumors (OR=1.71, 95% CI: 1.19-2.47). Associations with Fusobacteriota were strongest among African American participants (OR=2.36, 95% CI: 1.14-4.99) compared to other populations, however this different was not statistically significant (OR range = 1.05-1.38, Pinteraction = 0.697). Candidate pathways of pyruvate fermentation to acetate and lactate II and peptidoglycan biosynthesis I were associated with higher odds of CRC death.
CONCLUSIONS: Fusobacteriota was significantly associated with CRC-specific mortality with noted differences across populations.
IMPACT: This finding highlights the tumor microbiome as a candidate for further investigation into CRC outcome disparities.},
}
RevDate: 2026-04-01
Intake of Fiber From Different Food Sources and Type 2 Diabetes Risk: An Integrated Analysis of Epidemiological and Multiomic Data.
Diabetes care pii:164656 [Epub ahead of print].
OBJECTIVE: To examine the association between fiber from various food sources and type 2 diabetes (T2D) risk, as well as the molecular profiles involved.
RESEARCH DESIGN AND METHODS: Using data from three large prospective U.S. cohorts comprising 195,222 participants observed for up to 34 years, we evaluated the association between fiber from various food sources and T2D risk. We also assessed the association between fiber intake, plasma metabolic biomarkers, and a metabolomic profile indicative of T2D risk. Additionally, we examined gut microbial features related to fiber intake and the T2D metabolomic profile.
RESULTS: During follow-up, we documented 18,369 incident T2D cases. Higher intakes of total fiber (hazard ratio [HR] comparing extreme quintiles 0.88; 95% CI 0.82, 0.94), cereal fiber (HR 0.77; 95% CI 0.73, 0.82), and fruit fiber (HR 0.82; 95% CI 0.78, 0.87) were each associated with a lower T2D risk. Greater intakes of total fiber, cereal fiber, and fruit fiber, but not vegetable fiber, were linked to more favorable plasma profiles of insulinemic, lipid, and inflammatory biomarkers and a metabolomic profile indicative of a lower T2D risk. We also identified multiple gut microbial species, such as Faecalibacterium prausnitzii, Ruminococcus lactaris, and Gemmiger formicilis, along with relevant butyric acid-producing enzymes, all of which were associated with higher fruit fiber intake and a metabolomic profile indicating a lower likelihood of T2D development.
CONCLUSIONS: Higher intakes of total, cereal, and fruit fiber are associated with a lower risk of T2D and a more favorable metabolic profile, with the gut microbiome potentially contributing to the beneficial association of fruit fiber.
Additional Links: PMID-41920710
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PubMed:
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@article {pmid41920710,
year = {2026},
author = {Wan, Y and Alessa, HB and Guasch-Ferré, M and Tobias, DK and Lee, KH and Manson, JE and Willett, WC and Sun, Q and Hu, FB},
title = {Intake of Fiber From Different Food Sources and Type 2 Diabetes Risk: An Integrated Analysis of Epidemiological and Multiomic Data.},
journal = {Diabetes care},
volume = {},
number = {},
pages = {},
doi = {10.2337/dc25-2957},
pmid = {41920710},
issn = {1935-5548},
support = {/NH/NIH HHS/United States ; //Novo Nordisk Foundation/ ; },
abstract = {OBJECTIVE: To examine the association between fiber from various food sources and type 2 diabetes (T2D) risk, as well as the molecular profiles involved.
RESEARCH DESIGN AND METHODS: Using data from three large prospective U.S. cohorts comprising 195,222 participants observed for up to 34 years, we evaluated the association between fiber from various food sources and T2D risk. We also assessed the association between fiber intake, plasma metabolic biomarkers, and a metabolomic profile indicative of T2D risk. Additionally, we examined gut microbial features related to fiber intake and the T2D metabolomic profile.
RESULTS: During follow-up, we documented 18,369 incident T2D cases. Higher intakes of total fiber (hazard ratio [HR] comparing extreme quintiles 0.88; 95% CI 0.82, 0.94), cereal fiber (HR 0.77; 95% CI 0.73, 0.82), and fruit fiber (HR 0.82; 95% CI 0.78, 0.87) were each associated with a lower T2D risk. Greater intakes of total fiber, cereal fiber, and fruit fiber, but not vegetable fiber, were linked to more favorable plasma profiles of insulinemic, lipid, and inflammatory biomarkers and a metabolomic profile indicative of a lower T2D risk. We also identified multiple gut microbial species, such as Faecalibacterium prausnitzii, Ruminococcus lactaris, and Gemmiger formicilis, along with relevant butyric acid-producing enzymes, all of which were associated with higher fruit fiber intake and a metabolomic profile indicating a lower likelihood of T2D development.
CONCLUSIONS: Higher intakes of total, cereal, and fruit fiber are associated with a lower risk of T2D and a more favorable metabolic profile, with the gut microbiome potentially contributing to the beneficial association of fruit fiber.},
}
RevDate: 2026-04-01
Metabolism by ex vivo cultures of human stool increases the activity of coumarin, a widespread antioxidant from herbal supplements.
Cell reports, 45(4):117199 pii:S2211-1247(26)00277-9 [Epub ahead of print].
Host and microbiome metabolism of bioactive compounds can alter their efficacy. Herbal supplements contain many bioactive compounds, but their metabolism by gut microbes and the effects on efficacy remain poorly understood. To gain clarity, we investigate coumarin, an antioxidant in food, cosmetics, and supplements and a scaffold for diverse bioactive compounds. In this study, we characterize coumarin metabolism by the human gut microbiome, which produces 3,4-dihydrocoumarin and melilotic acid. We characterize this pathway in the culturable microbiota from 9 stool donors with liquid chromatography-tandem mass spectrometry (LC-MS/MS) metabolomics and microbiome profiling. We discover that 17 microbiome species metabolize coumarin and that the E. coli gene nemA is necessary for coumarin reduction. In antioxidant assays, melilotic acid is more potent than coumarin, suggesting that this pathway may impact bioactivity, with possible contributions to supplement efficacy. Further characterization may provide insights on the metabolic fate of coumarins and contributions of the microbiome to their efficacy.
Additional Links: PMID-41920740
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PubMed:
Citation:
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@article {pmid41920740,
year = {2026},
author = {Mingolelli, G and Subedi, P and Bonitatibus, S and Johnson, JJ and Henke, M},
title = {Metabolism by ex vivo cultures of human stool increases the activity of coumarin, a widespread antioxidant from herbal supplements.},
journal = {Cell reports},
volume = {45},
number = {4},
pages = {117199},
doi = {10.1016/j.celrep.2026.117199},
pmid = {41920740},
issn = {2211-1247},
abstract = {Host and microbiome metabolism of bioactive compounds can alter their efficacy. Herbal supplements contain many bioactive compounds, but their metabolism by gut microbes and the effects on efficacy remain poorly understood. To gain clarity, we investigate coumarin, an antioxidant in food, cosmetics, and supplements and a scaffold for diverse bioactive compounds. In this study, we characterize coumarin metabolism by the human gut microbiome, which produces 3,4-dihydrocoumarin and melilotic acid. We characterize this pathway in the culturable microbiota from 9 stool donors with liquid chromatography-tandem mass spectrometry (LC-MS/MS) metabolomics and microbiome profiling. We discover that 17 microbiome species metabolize coumarin and that the E. coli gene nemA is necessary for coumarin reduction. In antioxidant assays, melilotic acid is more potent than coumarin, suggesting that this pathway may impact bioactivity, with possible contributions to supplement efficacy. Further characterization may provide insights on the metabolic fate of coumarins and contributions of the microbiome to their efficacy.},
}
RevDate: 2026-04-01
Human Milk Oligosaccharides Support Coordinated Microbiome and Immune Development and Function in Infancy.
Annals of nutrition & metabolism pii:000549867 [Epub ahead of print].
BACKGROUND: Human milk contains functional ingredients that shape the microbiome and immune development of infants. Human milk oligosaccharides (HMOs) are among the largest and most diverse components of human milk. Their heterogeneity enables unique structure-function relationships that contribute to their physiological effects. This narrative review will focus on how HMOs directly and indirectly protect the infant from pathogens and educate the immune system.
SUMMARY: Preclinical research, observational studies, and intervention trials demonstrate that HMOs provide multilayer modulation of host defense and immune development. HMOs are soluble glycans that are acetylated, sialylated, or fucosylated, which mediate their interactions with viruses and bacteria to reduce infectivity. Additionally, HMOs enhance pathogen exclusion by promoting intestinal cell maturation, mucin production, and barrier function. Moreover, HMOs directly interact with immune cells through binding to carbohydrate recognition domains. HMOs promote the growth of beneficial bacteria, particularly Bifidobacterium longum subspecies infantis, which is also immunomodulatory. Lastly, HMOs are fermented to short-chain fatty acids, which lower the pH of the intestinal lumen, providing further antimicrobial defense.
KEY MESSAGES: Breastfed infants have a reduced risk of infectious disease compared to non-breastfed infants, attributable in part to the high concentration and structural diversity of HMOs. Clinical trials using formulas supplemented with synthetic human-identical milk oligosaccharides (HiMOs) have demonstrated benefits to adaptive and innate immunity, reduced infections, increased bifidobacteria, and reduced pathogenic bacteria. These benefits are amplified in formulas containing higher concentrations and greater varieties of HiMOs. However, the clinical benefit of routinely supplementing term infant formulae with HiMOs remains unsettled due to variability across existing clinical trials. Further research in healthy infants focused on short- and long-term immune outcomes is needed.
Additional Links: PMID-41920780
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PubMed:
Citation:
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@article {pmid41920780,
year = {2026},
author = {Donovan, SM},
title = {Human Milk Oligosaccharides Support Coordinated Microbiome and Immune Development and Function in Infancy.},
journal = {Annals of nutrition & metabolism},
volume = {},
number = {},
pages = {1-15},
doi = {10.1159/000549867},
pmid = {41920780},
issn = {1421-9697},
abstract = {BACKGROUND: Human milk contains functional ingredients that shape the microbiome and immune development of infants. Human milk oligosaccharides (HMOs) are among the largest and most diverse components of human milk. Their heterogeneity enables unique structure-function relationships that contribute to their physiological effects. This narrative review will focus on how HMOs directly and indirectly protect the infant from pathogens and educate the immune system.
SUMMARY: Preclinical research, observational studies, and intervention trials demonstrate that HMOs provide multilayer modulation of host defense and immune development. HMOs are soluble glycans that are acetylated, sialylated, or fucosylated, which mediate their interactions with viruses and bacteria to reduce infectivity. Additionally, HMOs enhance pathogen exclusion by promoting intestinal cell maturation, mucin production, and barrier function. Moreover, HMOs directly interact with immune cells through binding to carbohydrate recognition domains. HMOs promote the growth of beneficial bacteria, particularly Bifidobacterium longum subspecies infantis, which is also immunomodulatory. Lastly, HMOs are fermented to short-chain fatty acids, which lower the pH of the intestinal lumen, providing further antimicrobial defense.
KEY MESSAGES: Breastfed infants have a reduced risk of infectious disease compared to non-breastfed infants, attributable in part to the high concentration and structural diversity of HMOs. Clinical trials using formulas supplemented with synthetic human-identical milk oligosaccharides (HiMOs) have demonstrated benefits to adaptive and innate immunity, reduced infections, increased bifidobacteria, and reduced pathogenic bacteria. These benefits are amplified in formulas containing higher concentrations and greater varieties of HiMOs. However, the clinical benefit of routinely supplementing term infant formulae with HiMOs remains unsettled due to variability across existing clinical trials. Further research in healthy infants focused on short- and long-term immune outcomes is needed.},
}
RevDate: 2026-04-01
Multidimensional scaling informed by F-statistic: Visualizing grouped microbiome data with inference.
PLoS computational biology, 22(4):e1014102 pii:PCOMPBIOL-D-25-00623 [Epub ahead of print].
Multidimensional scaling (MDS) is a widely used dimensionality reduction technique in microbial ecology data analysis that captures the multivariate structure of the data while preserving pairwise distances between samples. While improvements in MDS have enhanced the ability to reveal group-specific data patterns, these MDS-based methods require prior assumptions for inference, limiting their application in general microbiome analysis. In this study, we introduce a new MDS-based ordination method, "F-informed MDS," which configures the data distribution based on the F-statistic, the ratio of dispersion between groups sharing common and different characteristics. Using semisynthetic datasets, we demonstrate that the proposed method is robust to hyperparameter selection while maintaining statistical significance throughout the ordination process. Various quality metrics for evaluating dimensionality reduction confirm that F-informed MDS is comparable to state-of-the-art methods in preserving both local and global data structures. Its application to a diatom-associated bacterial community suggests the role of this new method in interpreting the community's response to the host. Our approach offers a well-founded refinement of MDS that aligns with statistical test results, which can be beneficial for broader multidimensional data analyses in microbiology and ecology. This new visualization tool can be incorporated into standard microbiome data analyses.
Additional Links: PMID-41920852
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PubMed:
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@article {pmid41920852,
year = {2026},
author = {Kim, H and Kim, S and Kimbrel, JA and Morris, MM and Mayali, X and Buie, CR},
title = {Multidimensional scaling informed by F-statistic: Visualizing grouped microbiome data with inference.},
journal = {PLoS computational biology},
volume = {22},
number = {4},
pages = {e1014102},
doi = {10.1371/journal.pcbi.1014102},
pmid = {41920852},
issn = {1553-7358},
abstract = {Multidimensional scaling (MDS) is a widely used dimensionality reduction technique in microbial ecology data analysis that captures the multivariate structure of the data while preserving pairwise distances between samples. While improvements in MDS have enhanced the ability to reveal group-specific data patterns, these MDS-based methods require prior assumptions for inference, limiting their application in general microbiome analysis. In this study, we introduce a new MDS-based ordination method, "F-informed MDS," which configures the data distribution based on the F-statistic, the ratio of dispersion between groups sharing common and different characteristics. Using semisynthetic datasets, we demonstrate that the proposed method is robust to hyperparameter selection while maintaining statistical significance throughout the ordination process. Various quality metrics for evaluating dimensionality reduction confirm that F-informed MDS is comparable to state-of-the-art methods in preserving both local and global data structures. Its application to a diatom-associated bacterial community suggests the role of this new method in interpreting the community's response to the host. Our approach offers a well-founded refinement of MDS that aligns with statistical test results, which can be beneficial for broader multidimensional data analyses in microbiology and ecology. This new visualization tool can be incorporated into standard microbiome data analyses.},
}
RevDate: 2026-04-01
Investigating the Link between the Intestinal Microbiome and Th17/Treg Dysregulation in Hashimoto's Thyroiditis, and the Therapeutic Potential of Vitamin D.
Journal of the American Nutrition Association [Epub ahead of print].
Objective:Autoimmune disease (AD) has become a leading cause of illness in the twenty-first century, with autoimmune thyroid disease at the forefront of these conditions. Hashimoto's thyroiditis (HT) shares many features with other ADs, including associations with gastrointestinal symptoms linked to intestinal dysbiosis (ID). However, the pathogenesis of HT remains incompletely understood, particularly the role of specific T cell lymphocyte activity. The primary objective of this review was to investigate links between ID and HT pathogenesis, focusing on the relationship between a specific cluster of differentiation 4 (CD4) T cell subsets including T helper 17 (Th17) and regulatory T cells (Treg). A secondary aim was to explore whether vitamin D supplementation may serve as a viable intervention in managing HT, given existing research demonstrating links between Vitamin D status, HT pathogenesis and ID. Methods:A systematic literature search was conducted in PubMed using predefined inclusion/exclusion criteria across three tranches. A search of the review literature pertaining to thyroid autoimmunity, HT and the intestinal microbiome identified 21 papers for inclusion. A mechanistic literature search covering animal, in vitro and human studies on HT, autoimmunity, ID, intestinal microbiota, intestinal permeability (IP) and Th17 yielded 43 papers. A final search of human studies examining vitamin D status or supplementation in relation to ID, IP, Th17 and interleukin (IL)-17 identified 45 relevant papers. Accepted studies were critically appraised and synthesized in a narrative analysis.Results:Evidence across the included studies suggests an association between ID and pathogenesis of HT. Increased IP and alterations in Th17/Treg balance emerged as key contributing mechanisms. Vitamin D status was also associated with immune modulation, particularly involving Th17 activity, and was strongly linked to both ID and HT pathogenesis.Conclusions:ID may play a contributory role in HT pathogenesis through immune modulation involving CD4+ T cell subsets. Vitamin D supplementation demonstrates potential as an adjunctive strategy; however, further targeted human studies are required to clarify causality and therapeutic efficacy.
Additional Links: PMID-41920977
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PubMed:
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@article {pmid41920977,
year = {2026},
author = {Flower, S and Gruvstad Melén, A and Seidler, K},
title = {Investigating the Link between the Intestinal Microbiome and Th17/Treg Dysregulation in Hashimoto's Thyroiditis, and the Therapeutic Potential of Vitamin D.},
journal = {Journal of the American Nutrition Association},
volume = {},
number = {},
pages = {1-19},
doi = {10.1080/27697061.2026.2644894},
pmid = {41920977},
issn = {2769-707X},
abstract = {Objective:Autoimmune disease (AD) has become a leading cause of illness in the twenty-first century, with autoimmune thyroid disease at the forefront of these conditions. Hashimoto's thyroiditis (HT) shares many features with other ADs, including associations with gastrointestinal symptoms linked to intestinal dysbiosis (ID). However, the pathogenesis of HT remains incompletely understood, particularly the role of specific T cell lymphocyte activity. The primary objective of this review was to investigate links between ID and HT pathogenesis, focusing on the relationship between a specific cluster of differentiation 4 (CD4) T cell subsets including T helper 17 (Th17) and regulatory T cells (Treg). A secondary aim was to explore whether vitamin D supplementation may serve as a viable intervention in managing HT, given existing research demonstrating links between Vitamin D status, HT pathogenesis and ID. Methods:A systematic literature search was conducted in PubMed using predefined inclusion/exclusion criteria across three tranches. A search of the review literature pertaining to thyroid autoimmunity, HT and the intestinal microbiome identified 21 papers for inclusion. A mechanistic literature search covering animal, in vitro and human studies on HT, autoimmunity, ID, intestinal microbiota, intestinal permeability (IP) and Th17 yielded 43 papers. A final search of human studies examining vitamin D status or supplementation in relation to ID, IP, Th17 and interleukin (IL)-17 identified 45 relevant papers. Accepted studies were critically appraised and synthesized in a narrative analysis.Results:Evidence across the included studies suggests an association between ID and pathogenesis of HT. Increased IP and alterations in Th17/Treg balance emerged as key contributing mechanisms. Vitamin D status was also associated with immune modulation, particularly involving Th17 activity, and was strongly linked to both ID and HT pathogenesis.Conclusions:ID may play a contributory role in HT pathogenesis through immune modulation involving CD4+ T cell subsets. Vitamin D supplementation demonstrates potential as an adjunctive strategy; however, further targeted human studies are required to clarify causality and therapeutic efficacy.},
}
RevDate: 2026-04-01
Biomarker-guided immunotherapy in gastric cancer: current insights and future perspectives.
Cancer treatment reviews, 145:103124 pii:S0305-7372(26)00038-1 [Epub ahead of print].
Gastric and gastroesophageal junction adenocarcinoma (GC) is a biologically challenging malignancy associated with suboptimal clinical outcomes due to limited effective treatment options. The recent incorporation of immune checkpoint inhibitors (ICIs) into therapeutic algorithms has improved the clinical prospects of subsets of GC patients. However, responses to anti-PD-1/PD-L1 agents remain highly heterogeneous, with only some patients deriving long-term benefits. This variability highlights the importance of identifying optimal biomarkers to enhance patient selection, thereby enabling tailored immunotherapy strategies. Whereas microsatellite instability has demonstrated a potent capacity for predicting immunotherapy benefits in GC, other predictive biomarkers, such as PD-L1 expression, remain suboptimal. Advances in gene expression and epigenetic profiling, liquid biopsy approaches, gut microbiome characterization, and artificial intelligence-driven multimodal algorithms applied to multi-omics or digital pathology are key drivers for the comprehensive characterization of the GC tumour microenvironment (TME), which could be used for better treatment selection. Similarly, elucidating the complex tumour-immune interplay with these technologies will be crucial for the success of novel immunotherapeutic approaches under clinical development, by evaluating alternative immune pathways alone or in combination with current actionable targets of GC. The current review aims to give an overview of the current immunotherapeutic landscape in GC, evaluate standard-of-care and emerging biomarkers of immunotherapy response, and discuss the translational potential of incorporating multi-omic and AI-derived biomarkers into biomarker-enriched clinical decision-making frameworks.
Additional Links: PMID-41921305
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PubMed:
Citation:
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@article {pmid41921305,
year = {2026},
author = {Teixidó Mulet, M and Veas Rodriguez, J and Terán, E and Piñol, M and Vilardell, F and Iglesias, M and Hierro, C and Calvo, M and Matias-Guiu, X and Salud, A and Tabernero, J and Montal, R},
title = {Biomarker-guided immunotherapy in gastric cancer: current insights and future perspectives.},
journal = {Cancer treatment reviews},
volume = {145},
number = {},
pages = {103124},
doi = {10.1016/j.ctrv.2026.103124},
pmid = {41921305},
issn = {1532-1967},
abstract = {Gastric and gastroesophageal junction adenocarcinoma (GC) is a biologically challenging malignancy associated with suboptimal clinical outcomes due to limited effective treatment options. The recent incorporation of immune checkpoint inhibitors (ICIs) into therapeutic algorithms has improved the clinical prospects of subsets of GC patients. However, responses to anti-PD-1/PD-L1 agents remain highly heterogeneous, with only some patients deriving long-term benefits. This variability highlights the importance of identifying optimal biomarkers to enhance patient selection, thereby enabling tailored immunotherapy strategies. Whereas microsatellite instability has demonstrated a potent capacity for predicting immunotherapy benefits in GC, other predictive biomarkers, such as PD-L1 expression, remain suboptimal. Advances in gene expression and epigenetic profiling, liquid biopsy approaches, gut microbiome characterization, and artificial intelligence-driven multimodal algorithms applied to multi-omics or digital pathology are key drivers for the comprehensive characterization of the GC tumour microenvironment (TME), which could be used for better treatment selection. Similarly, elucidating the complex tumour-immune interplay with these technologies will be crucial for the success of novel immunotherapeutic approaches under clinical development, by evaluating alternative immune pathways alone or in combination with current actionable targets of GC. The current review aims to give an overview of the current immunotherapeutic landscape in GC, evaluate standard-of-care and emerging biomarkers of immunotherapy response, and discuss the translational potential of incorporating multi-omic and AI-derived biomarkers into biomarker-enriched clinical decision-making frameworks.},
}
RevDate: 2026-04-01
Deciphering pharmaceutical resistance in sulfur-driven autotrophic denitrification: an integrated multi-omics artificial intelligence-driven structural biology approach.
Water research, 298:125834 pii:S0043-1354(26)00516-6 [Epub ahead of print].
Sulfur-driven autotrophic denitrification (SdAD) is a promising low-carbon technology for nitrogen removal; however, its stability and adaptive mechanisms under pharmaceutical stress remain poorly understood. In this study, ibuprofen (IBU) was used as a representative pharmaceutical to investigate the response of an SdAD system. Throughout the 210-day operational period, the system demonstrated exceptional functional robustness, maintaining high sulfide (97.46 ± 3.18%) and inorganic nitrogen (99.17 ± 4.34%) removal efficiencies across IBU concentrations ranging from environmentally relevant levels to elevated shock loads (100-2000 μg/L). Underpinning this macroscopic stability, community-level analyses revealed that instead of succumbing to inhibition, the SdAD microbiome actively reorganized its composition and topological structure to accommodate the selective pressure. This adaptation was characterized by enhanced microbial diversity and stress-induced network modularity (particularly at 100-500 μg/L), alongside strengthened cooperative interactions between sulfur-oxidizing bacteria and denitrifiers. To unravel the specific molecular drivers of this resilience, we integrated AlphaFold-based structural modeling with machine learning-coupled molecular docking. This enabled us to resolve the three-dimensional structure of sulfide: quinone oxidoreductase (SQR) and perform the first structure-function analysis of SQR within an SdAD context under pharmaceutical stress, revealing that arginine residues serve as key interaction hotspots for IBU binding. Consistent with this binding mechanism, multi-omics data further corroborated a systemic adjustment involving the coordinated regulation of sulfur oxidation genes and the transcriptional upregulation of arginine biosynthesis pathways. Overall, these findings shed light on how the SdAD community mitigates pharmaceutical toxicity through a multi-tiered strategy involving ecological network reorganization and metabolic compensation. Methodologically, this work highlights the value of integrating artificial intelligence-driven structural biology with multi-omics analyses to decode the mechanisms of contaminant resistance in biological wastewater treatment systems.
Additional Links: PMID-41921320
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PubMed:
Citation:
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@article {pmid41921320,
year = {2026},
author = {Huang, DQ and Zhou, S and Jia, Y and Yan, Y and Lu, H},
title = {Deciphering pharmaceutical resistance in sulfur-driven autotrophic denitrification: an integrated multi-omics artificial intelligence-driven structural biology approach.},
journal = {Water research},
volume = {298},
number = {},
pages = {125834},
doi = {10.1016/j.watres.2026.125834},
pmid = {41921320},
issn = {1879-2448},
abstract = {Sulfur-driven autotrophic denitrification (SdAD) is a promising low-carbon technology for nitrogen removal; however, its stability and adaptive mechanisms under pharmaceutical stress remain poorly understood. In this study, ibuprofen (IBU) was used as a representative pharmaceutical to investigate the response of an SdAD system. Throughout the 210-day operational period, the system demonstrated exceptional functional robustness, maintaining high sulfide (97.46 ± 3.18%) and inorganic nitrogen (99.17 ± 4.34%) removal efficiencies across IBU concentrations ranging from environmentally relevant levels to elevated shock loads (100-2000 μg/L). Underpinning this macroscopic stability, community-level analyses revealed that instead of succumbing to inhibition, the SdAD microbiome actively reorganized its composition and topological structure to accommodate the selective pressure. This adaptation was characterized by enhanced microbial diversity and stress-induced network modularity (particularly at 100-500 μg/L), alongside strengthened cooperative interactions between sulfur-oxidizing bacteria and denitrifiers. To unravel the specific molecular drivers of this resilience, we integrated AlphaFold-based structural modeling with machine learning-coupled molecular docking. This enabled us to resolve the three-dimensional structure of sulfide: quinone oxidoreductase (SQR) and perform the first structure-function analysis of SQR within an SdAD context under pharmaceutical stress, revealing that arginine residues serve as key interaction hotspots for IBU binding. Consistent with this binding mechanism, multi-omics data further corroborated a systemic adjustment involving the coordinated regulation of sulfur oxidation genes and the transcriptional upregulation of arginine biosynthesis pathways. Overall, these findings shed light on how the SdAD community mitigates pharmaceutical toxicity through a multi-tiered strategy involving ecological network reorganization and metabolic compensation. Methodologically, this work highlights the value of integrating artificial intelligence-driven structural biology with multi-omics analyses to decode the mechanisms of contaminant resistance in biological wastewater treatment systems.},
}
RevDate: 2026-04-01
Gene-centric analysis of Raskinella chloraquaticus reveals a functionally conserved taxonomic group in global drinking water distribution systems.
Water research, 298:125784 pii:S0043-1354(26)00466-5 [Epub ahead of print].
A recent metagenomic survey of drinking water systems revealed that a highly prevalent and dominant uncultured bacterial genus (Raskinella) was represented globally by a single species (Raskinella chloraquaticus). R. chloraquaticus comprises of two sub-species groups, Lineages 1 and 2, the former representing a globally prevalent genomovar. The objective of this study was to perform comparative analysis of the gene content of R. chloraquaticus to characterize the gene-level diversity and determine factors shaping the diversity of this species. Pangenome analysis revealed that R. chloraquaticus possesses a core set of genes that constitute a major portion (87.74%) of the known gene content of the genome. Furthermore, most of the gene diversity of R. chloraquaticus is associated with Lineage 2 organisms, which consists of at least four distinct genomovars. Lineage 1 organisms consist of a higher proportion of identical genes than would have been expected if changes primarily occurred through random mutations and thus is potentially indicative of recombination. In contrast, Lineage 2 organisms appear to have emerged through random mutations and display stronger geographic preference. These results indicate that homologous recombination and geographic isolation likely shape the genetic repertoire of R. chloraquaticus. Further, the high level of gene conservation in R. chloraquaticus may be reflective of highly selective environment in drinking water systems. Thus, R. chloraquaticus may represent a model organism to probe selective pressures shaping the drinking water microbiome.
Additional Links: PMID-41921321
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@article {pmid41921321,
year = {2026},
author = {Sudarshan, AS and Konstantinidis, KT and Pinto, AJ},
title = {Gene-centric analysis of Raskinella chloraquaticus reveals a functionally conserved taxonomic group in global drinking water distribution systems.},
journal = {Water research},
volume = {298},
number = {},
pages = {125784},
doi = {10.1016/j.watres.2026.125784},
pmid = {41921321},
issn = {1879-2448},
abstract = {A recent metagenomic survey of drinking water systems revealed that a highly prevalent and dominant uncultured bacterial genus (Raskinella) was represented globally by a single species (Raskinella chloraquaticus). R. chloraquaticus comprises of two sub-species groups, Lineages 1 and 2, the former representing a globally prevalent genomovar. The objective of this study was to perform comparative analysis of the gene content of R. chloraquaticus to characterize the gene-level diversity and determine factors shaping the diversity of this species. Pangenome analysis revealed that R. chloraquaticus possesses a core set of genes that constitute a major portion (87.74%) of the known gene content of the genome. Furthermore, most of the gene diversity of R. chloraquaticus is associated with Lineage 2 organisms, which consists of at least four distinct genomovars. Lineage 1 organisms consist of a higher proportion of identical genes than would have been expected if changes primarily occurred through random mutations and thus is potentially indicative of recombination. In contrast, Lineage 2 organisms appear to have emerged through random mutations and display stronger geographic preference. These results indicate that homologous recombination and geographic isolation likely shape the genetic repertoire of R. chloraquaticus. Further, the high level of gene conservation in R. chloraquaticus may be reflective of highly selective environment in drinking water systems. Thus, R. chloraquaticus may represent a model organism to probe selective pressures shaping the drinking water microbiome.},
}
RevDate: 2026-04-01
Feasibility of Low-Biomass Exhaled Breath Microbiome Sequencing Using a PDC-Sampler in Febrile and Healthy Individuals.
Journal of breath research [Epub ahead of print].
Exhaled breath is a noninvasive and repeatable biological matrix offering new opportunities for respiratory microbiome analysis, yet its extremely low microbial biomass limits current high-throughput applications. Building on our previously developed phase-change drywall cyclone sampler (PDC-sampler), which integrates condensational growth with dry-wall cyclone separation, we established a validated workflow for efficient aerosol collection and multi-omics sequencing of exhaled breath. Using this platform, exhaled breath from 15 febrile patients and 6 healthy volunteers was analyzed via shotgun metagenomic and 16S rRNA sequencing to assess microbial composition, diversity, and functional features. The PDC-sampler significantly increased microbial DNA yield, enabling stable detection of bacterial taxa dominated by Pseudomonadota, Bacillota, Bacteroidota, and Actinomycetota. Functional annotations and diversity metrics revealed distinct microbial and metabolic patterns between individuals, confirming the platform's analytical sensitivity and biological representativeness. This work experimentally validates the feasibility of exhaled breath microbiome sequencing using the PDC-sampler, providing a practical and generalizable framework for noninvasive respiratory microecology studies and future diagnostic applications.
Additional Links: PMID-41921531
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@article {pmid41921531,
year = {2026},
author = {Li, W and Lv, M and Cheng, M and Han, Y and Yu, H and Huang, Y and Meng, D and Xu, X and Sun, L and Lu, Z and Liu, QL},
title = {Feasibility of Low-Biomass Exhaled Breath Microbiome Sequencing Using a PDC-Sampler in Febrile and Healthy Individuals.},
journal = {Journal of breath research},
volume = {},
number = {},
pages = {},
doi = {10.1088/1752-7163/ae5a51},
pmid = {41921531},
issn = {1752-7163},
abstract = {Exhaled breath is a noninvasive and repeatable biological matrix offering new opportunities for respiratory microbiome analysis, yet its extremely low microbial biomass limits current high-throughput applications. Building on our previously developed phase-change drywall cyclone sampler (PDC-sampler), which integrates condensational growth with dry-wall cyclone separation, we established a validated workflow for efficient aerosol collection and multi-omics sequencing of exhaled breath. Using this platform, exhaled breath from 15 febrile patients and 6 healthy volunteers was analyzed via shotgun metagenomic and 16S rRNA sequencing to assess microbial composition, diversity, and functional features. The PDC-sampler significantly increased microbial DNA yield, enabling stable detection of bacterial taxa dominated by Pseudomonadota, Bacillota, Bacteroidota, and Actinomycetota. Functional annotations and diversity metrics revealed distinct microbial and metabolic patterns between individuals, confirming the platform's analytical sensitivity and biological representativeness. This work experimentally validates the feasibility of exhaled breath microbiome sequencing using the PDC-sampler, providing a practical and generalizable framework for noninvasive respiratory microecology studies and future diagnostic applications.},
}
RevDate: 2026-04-01
Colonization of Salmonella Newport and Microbiome Analyses of Bulb Onions Grown in Artificially Contaminated Soil at Lab-Scale Under a Controlled Environment.
Journal of food protection pii:S0362-028X(26)00074-8 [Epub ahead of print].
INTRODUCTION: Several multistate Salmonella outbreaks in the United States have been linked to bulb onions. In this study we investigated the extent of Salmonella colonization on bulb onions grown in contaminated soil.
PURPOSE: The study evaluated the colonization potential and microbial community dynamics of Salmonella Newport on bulb onions grown in artificially spiked soil.
METHODS: Red bulb onions were grown from seed, and resultant seedlings were transplanted into pots containing soil. Soil surface was spiked with S. Newport at transplant and again two weeks before harvest. Three inoculum levels [10[2] (low), 10[4](medium), 10[6] (high) CFU per 200 g soil] of Salmonella Newport were investigated in triplicate, with three unspiked controls. Three independent trials were conducted using two different soil types. Microbiome analyses were performed on the bulb onions and soil from the high inoculum group in Trial 1 (field topsoil) at 0 h, 1 h, and 24 h pre-enrichment. Results Salmonella was detected in one high-inoculum bulb onion in Trial 1 (field topsoil) and in all high-inoculum onions in Trials 2 and 3 (Miracle-Gro soil). Among the medium inoculum groups, all onions in Trial 2, one in Trial 3, and none in Trial 1 were positive for Salmonella. No onions in the low inoculum group were Salmonella-positive. Microbiome analysis of control and Salmonella-spiked high inoculum field topsoil samples and associated bulb onions revealed that bacterial community composition remained stable at 0 h and 1 h pre-enrichment but underwent notable shifts after 24 h. Bacterial diversity decreased following 24 h of pre-enrichment, with increased dominance of Proteobacteria and Firmicutes. However, Salmonella spiking had minimal or no effect on microbiome dynamics. Significance These findings provide insights into the colonization capability of Salmonella Newport on bulb onions in different soil types and associated microbial community shifts after 24h pre-enrichment.
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@article {pmid41921618,
year = {2026},
author = {Khajanchi, BK and Grocholl, J and Alam, M and Hasan, NA and Wang, H and Hughes, S},
title = {Colonization of Salmonella Newport and Microbiome Analyses of Bulb Onions Grown in Artificially Contaminated Soil at Lab-Scale Under a Controlled Environment.},
journal = {Journal of food protection},
volume = {},
number = {},
pages = {100769},
doi = {10.1016/j.jfp.2026.100769},
pmid = {41921618},
issn = {1944-9097},
abstract = {INTRODUCTION: Several multistate Salmonella outbreaks in the United States have been linked to bulb onions. In this study we investigated the extent of Salmonella colonization on bulb onions grown in contaminated soil.
PURPOSE: The study evaluated the colonization potential and microbial community dynamics of Salmonella Newport on bulb onions grown in artificially spiked soil.
METHODS: Red bulb onions were grown from seed, and resultant seedlings were transplanted into pots containing soil. Soil surface was spiked with S. Newport at transplant and again two weeks before harvest. Three inoculum levels [10[2] (low), 10[4](medium), 10[6] (high) CFU per 200 g soil] of Salmonella Newport were investigated in triplicate, with three unspiked controls. Three independent trials were conducted using two different soil types. Microbiome analyses were performed on the bulb onions and soil from the high inoculum group in Trial 1 (field topsoil) at 0 h, 1 h, and 24 h pre-enrichment. Results Salmonella was detected in one high-inoculum bulb onion in Trial 1 (field topsoil) and in all high-inoculum onions in Trials 2 and 3 (Miracle-Gro soil). Among the medium inoculum groups, all onions in Trial 2, one in Trial 3, and none in Trial 1 were positive for Salmonella. No onions in the low inoculum group were Salmonella-positive. Microbiome analysis of control and Salmonella-spiked high inoculum field topsoil samples and associated bulb onions revealed that bacterial community composition remained stable at 0 h and 1 h pre-enrichment but underwent notable shifts after 24 h. Bacterial diversity decreased following 24 h of pre-enrichment, with increased dominance of Proteobacteria and Firmicutes. However, Salmonella spiking had minimal or no effect on microbiome dynamics. Significance These findings provide insights into the colonization capability of Salmonella Newport on bulb onions in different soil types and associated microbial community shifts after 24h pre-enrichment.},
}
RevDate: 2026-04-03
The oral-gut microbiome axis in diabetes mellitus: a systematic review and emerging clinical perspectives.
Diabetes research and clinical practice, 235:113232 pii:S0168-8227(26)00151-8 [Epub ahead of print].
Emerging evidence suggests that diabetes mellitus (DM) is not only a metabolic disorder but also a mucosal disease shaped by microbial interactions across body niches. This review synthesizes current evidence on the oral-gut microbiome axis in DM, focusing on microbial transmission, functional overlap, and clinical relevance. A systematic search of six databases identified studies profiling paired oral and gut microbiomes in individuals with diabetes. Across included studies, consistent findings demonstrate concurrent dysbiosis in both niches. Notably, oral-associated taxa such as Streptococcus, Prevotella, Fusobacterium, and Porphyromonas were detected in the gut, suggesting ectopic colonization and inter-niche microbial transmission. Functional analyses revealed shared disruptions in key metabolic pathways, including short-chain fatty acid production and glycine betaine metabolism, with downstream effects on inflammation and insulin resistance. These microbial alterations correlated with established clinical markers such as HbA1c, fasting glucose, and inflammatory indices. Emerging machine-learning models integrating oral and gut microbiota demonstrated promising diagnostic performance (AUC > 0.83). Collectively, these findings support a potential bidirectional oral-gut axis associated with metabolic dysregulation in DM. Despite limitations including cross-sectional design and heterogeneity, this axis represents a novel target for biomarker development and therapeutic intervention. Future longitudinal and interventional studies are required to determine causal relationships and clinical utility.
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@article {pmid41921761,
year = {2026},
author = {Nee, GW and Agrawal, K and Dalan, R and Kasahara, K and Xiang Darren, LY and Ali, Y and Wong, S},
title = {The oral-gut microbiome axis in diabetes mellitus: a systematic review and emerging clinical perspectives.},
journal = {Diabetes research and clinical practice},
volume = {235},
number = {},
pages = {113232},
doi = {10.1016/j.diabres.2026.113232},
pmid = {41921761},
issn = {1872-8227},
abstract = {Emerging evidence suggests that diabetes mellitus (DM) is not only a metabolic disorder but also a mucosal disease shaped by microbial interactions across body niches. This review synthesizes current evidence on the oral-gut microbiome axis in DM, focusing on microbial transmission, functional overlap, and clinical relevance. A systematic search of six databases identified studies profiling paired oral and gut microbiomes in individuals with diabetes. Across included studies, consistent findings demonstrate concurrent dysbiosis in both niches. Notably, oral-associated taxa such as Streptococcus, Prevotella, Fusobacterium, and Porphyromonas were detected in the gut, suggesting ectopic colonization and inter-niche microbial transmission. Functional analyses revealed shared disruptions in key metabolic pathways, including short-chain fatty acid production and glycine betaine metabolism, with downstream effects on inflammation and insulin resistance. These microbial alterations correlated with established clinical markers such as HbA1c, fasting glucose, and inflammatory indices. Emerging machine-learning models integrating oral and gut microbiota demonstrated promising diagnostic performance (AUC > 0.83). Collectively, these findings support a potential bidirectional oral-gut axis associated with metabolic dysregulation in DM. Despite limitations including cross-sectional design and heterogeneity, this axis represents a novel target for biomarker development and therapeutic intervention. Future longitudinal and interventional studies are required to determine causal relationships and clinical utility.},
}
RevDate: 2026-04-01
The microbiome and eating disorders: a new framework at the interface of interoception and reward.
Neuroscience pii:S0306-4522(26)00242-3 [Epub ahead of print].
Accumulating evidence suggests that the gut microbiome can modulate brain and behaviour including those relevant to eating behaviours and reward signalling through the dynamic communication pathways of the microbiota-gut-brain-axis. Emerging evidence links altered gut microbial composition to disordered eating patterns, implicating the gut microbiome as a possible mechanism underlying eating disorders, as well as a potential therapeutic target for these conditions. In this review, we synthesise evidence across preclinical and clinical research to propose an integrated framework wherein the gut microbiome, interoception and reward circuits may interact to shape disordered eating behaviours. We firstly explore how microbial signals modulate homeostatic and reward feeding systems via vagal afferents, neurotransmitter modulation and immune-neural pathways, and how these signals converge in brain regions implicated in reward systems and interoception. Particular attention is given to how these interactions may occur in under- and over-eating phenotypes of disordered eating. The therapeutic potential of microbiota-targeted interventions to modulate eating disorder-induced dysregulations in interoception and reward signalling is discussed. Combined evidence suggests a paradigm shift in the etiological considerations of eating disorders is warranted taking into account dysregulations of gut microbiota and its effects on reward processing and interoceptive signalling. Specifically, we propose that EDs are underpinned by dysregulations of gut microbiota, reward processing and interoceptive signalling, rather than neurobehaviour alone. The novel, integrated, and transdiagnostic framework posited in this review could represent a conceptual shift in the aetiological understanding of eating disorders with the potential to derive new neurobiological targets for intervention.
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@article {pmid41921818,
year = {2026},
author = {Ziade, I and McDermott, MM and O'Riordan, KJ and Cryan, JF and Schneider, E},
title = {The microbiome and eating disorders: a new framework at the interface of interoception and reward.},
journal = {Neuroscience},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.neuroscience.2026.03.050},
pmid = {41921818},
issn = {1873-7544},
abstract = {Accumulating evidence suggests that the gut microbiome can modulate brain and behaviour including those relevant to eating behaviours and reward signalling through the dynamic communication pathways of the microbiota-gut-brain-axis. Emerging evidence links altered gut microbial composition to disordered eating patterns, implicating the gut microbiome as a possible mechanism underlying eating disorders, as well as a potential therapeutic target for these conditions. In this review, we synthesise evidence across preclinical and clinical research to propose an integrated framework wherein the gut microbiome, interoception and reward circuits may interact to shape disordered eating behaviours. We firstly explore how microbial signals modulate homeostatic and reward feeding systems via vagal afferents, neurotransmitter modulation and immune-neural pathways, and how these signals converge in brain regions implicated in reward systems and interoception. Particular attention is given to how these interactions may occur in under- and over-eating phenotypes of disordered eating. The therapeutic potential of microbiota-targeted interventions to modulate eating disorder-induced dysregulations in interoception and reward signalling is discussed. Combined evidence suggests a paradigm shift in the etiological considerations of eating disorders is warranted taking into account dysregulations of gut microbiota and its effects on reward processing and interoceptive signalling. Specifically, we propose that EDs are underpinned by dysregulations of gut microbiota, reward processing and interoceptive signalling, rather than neurobehaviour alone. The novel, integrated, and transdiagnostic framework posited in this review could represent a conceptual shift in the aetiological understanding of eating disorders with the potential to derive new neurobiological targets for intervention.},
}
RevDate: 2026-04-03
Virulence and antimicrobial resistance profiling of Klebsiella pneumoniae isolated from foxes in northern China.
Microbial pathogenesis, 215:108476 pii:S0882-4010(26)00202-0 [Epub ahead of print].
Klebsiella pneumoniae is a significant opportunistic pathogen in animal farming. To investigate the occurrence of K. pneumoniae and associated antimicrobial resistance risk in foxes, this study collected 350 fecal samples from foxes across five northern Chinese provinces. A total of 163 K. pneumoniae isolates were recovered (isolation rate: 46.57%), and all isolates were classified as multidrug-resistant (MDR). All isolates were resistant to azithromycin and sulfisoxazole, with high resistance to enrofloxacin (98.16%), ciprofloxacin (87.12%), and tetracycline (70.55%). Resistance to tigecycline and polymyxin B was lower. Notably, all isolates were susceptible to meropenem. Antimicrobial resistance gene (ARG) analysis revealed high carriage rates of tet(E), aac(3)-IIa, and qnrS, alongside the colistin resistance genes mcr-1 and mcr-8. Whole-genome sequencing of 66 isolates revealed substantial genetic diversity: 45 sequence types (STs) were identified among 64 typeable isolates, with ST35 and ST603 being the most common (5/64, 7.81% each), and lineages previously reported in human clinical settings (e.g., ST307 and ST15) were also detected; however, no direct cross-host transmission was evaluated in this study. Capsular types KL22 (10/64, 15.63%) was the most common. Metagenomic analysis further showed that the fox gut microbiome harbored diverse ARGs, with 29 ARGs detected in both K. pneumoniae isolates and fox gut resistome datasets (descriptive overlap). Among these, 20 genes (e.g., blaCTX-M-55 and aac(3)-IIa) were located on predicted plasmids or transposons, suggesting potential mobility rather than confirmed transfer. Conjugation assays provided limited proof-of-concept evidence for plasmid-mediated transfer of tet(A) and tet(E). Collectively, these findings suggest that farmed foxes may serve as potential reservoirs of MDR K. pneumoniae and transferable resistance determinants, supporting the need for continued surveillance and prudent antibiotic use within a One Health framework.
Additional Links: PMID-41921920
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@article {pmid41921920,
year = {2026},
author = {Yang, MT and Qin, Y and Xu, C and Leng, X and Li, XM and Hou, QY and Sun, YZ and Zhao, Q and Liu, S and Tang, LY and Ma, H and Chen, BN and Zhang, XX and Li, ZY and Ni, HB},
title = {Virulence and antimicrobial resistance profiling of Klebsiella pneumoniae isolated from foxes in northern China.},
journal = {Microbial pathogenesis},
volume = {215},
number = {},
pages = {108476},
doi = {10.1016/j.micpath.2026.108476},
pmid = {41921920},
issn = {1096-1208},
abstract = {Klebsiella pneumoniae is a significant opportunistic pathogen in animal farming. To investigate the occurrence of K. pneumoniae and associated antimicrobial resistance risk in foxes, this study collected 350 fecal samples from foxes across five northern Chinese provinces. A total of 163 K. pneumoniae isolates were recovered (isolation rate: 46.57%), and all isolates were classified as multidrug-resistant (MDR). All isolates were resistant to azithromycin and sulfisoxazole, with high resistance to enrofloxacin (98.16%), ciprofloxacin (87.12%), and tetracycline (70.55%). Resistance to tigecycline and polymyxin B was lower. Notably, all isolates were susceptible to meropenem. Antimicrobial resistance gene (ARG) analysis revealed high carriage rates of tet(E), aac(3)-IIa, and qnrS, alongside the colistin resistance genes mcr-1 and mcr-8. Whole-genome sequencing of 66 isolates revealed substantial genetic diversity: 45 sequence types (STs) were identified among 64 typeable isolates, with ST35 and ST603 being the most common (5/64, 7.81% each), and lineages previously reported in human clinical settings (e.g., ST307 and ST15) were also detected; however, no direct cross-host transmission was evaluated in this study. Capsular types KL22 (10/64, 15.63%) was the most common. Metagenomic analysis further showed that the fox gut microbiome harbored diverse ARGs, with 29 ARGs detected in both K. pneumoniae isolates and fox gut resistome datasets (descriptive overlap). Among these, 20 genes (e.g., blaCTX-M-55 and aac(3)-IIa) were located on predicted plasmids or transposons, suggesting potential mobility rather than confirmed transfer. Conjugation assays provided limited proof-of-concept evidence for plasmid-mediated transfer of tet(A) and tet(E). Collectively, these findings suggest that farmed foxes may serve as potential reservoirs of MDR K. pneumoniae and transferable resistance determinants, supporting the need for continued surveillance and prudent antibiotic use within a One Health framework.},
}
RevDate: 2026-04-01
Aspirin reprograms platelet signaling and the intrahepatic microbiome to suppress RyR2-driven inflammation and fibrosis in preclinical chronic liver disease.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 198:119296 pii:S0753-3322(26)00329-X [Epub ahead of print].
Platelet deactivation by aspirin possibly helps in regression of liver fibrosis, though the mechanisms are unclear. We administered aspirin in a murine model of liver fibrosis and studied molecular signatures associated with fibrosis regression; both in vivo (murine model/ patients) and in vitro. Increase in intrahepatic PF4, p-selectin, PDGFR-β levels (platelet activation) correlated with increase in liver fibrosis (p < 0.05, r[2]>0.3). Aspirin reduced the number and activation of intrahepatic platelets, inflammation and fibrosis (p < 0.05). Platelet deactivation using aspirin in murine model increased autophagy, glutathione, energy metabolism and decreased arachidonic acid and butanoate metabolism (p < 0.05). Aspirin modulated liver microenvironment and showed decrease in intrahepatic immune cell activation (blood transcription module) which correlated with histidine and tryptophan metabolism (r2 > 0.5, p < 0.05). The intrahepatic microbiome post-aspirin showed increased abundance of Firmicutes (Ruminococcaceae, Lachnospiraceae, and Clostridiaceae) and improved functionality (p < 0.05). Aspirin caused decreased expression of Ryanodine-receptor-2 (RyR2), Arginase-1 and Kynurenine-3-monooxygenase, which correlate with reduction in α-SMA and degree of hepatic fibrosis (r2 > 0.75; p < 0.05). In addition, pan specific blocking of RyR2 by carvedilol/flecainide markedly inhibited HSC activation and proliferation in-vitro by reducing Ca[2+] overload, ER/mitochondrial stress (p < 0.05). Further, RyR2 blockade in HSCs reduced its activation by activated platelet secretome or TGFβ1 (p < 0.05). CONCLUSIONS: Platelet deactivation using aspirin regresses hepatic fibrosis by decreasing intrahepatic platelet accumulation/activation, inflammation and modulation of intrahepatic microbiome. Induction of RyR2 is critical for fibrosis development and pharmacological inhibition of RyR2 could ameliorate liver fibrosis.
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@article {pmid41922110,
year = {2026},
author = {Bhat, A and Chaudhary, S and Kumari, A and Sharma, S and Sarin, SK and Maras, JS},
title = {Aspirin reprograms platelet signaling and the intrahepatic microbiome to suppress RyR2-driven inflammation and fibrosis in preclinical chronic liver disease.},
journal = {Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie},
volume = {198},
number = {},
pages = {119296},
doi = {10.1016/j.biopha.2026.119296},
pmid = {41922110},
issn = {1950-6007},
abstract = {Platelet deactivation by aspirin possibly helps in regression of liver fibrosis, though the mechanisms are unclear. We administered aspirin in a murine model of liver fibrosis and studied molecular signatures associated with fibrosis regression; both in vivo (murine model/ patients) and in vitro. Increase in intrahepatic PF4, p-selectin, PDGFR-β levels (platelet activation) correlated with increase in liver fibrosis (p < 0.05, r[2]>0.3). Aspirin reduced the number and activation of intrahepatic platelets, inflammation and fibrosis (p < 0.05). Platelet deactivation using aspirin in murine model increased autophagy, glutathione, energy metabolism and decreased arachidonic acid and butanoate metabolism (p < 0.05). Aspirin modulated liver microenvironment and showed decrease in intrahepatic immune cell activation (blood transcription module) which correlated with histidine and tryptophan metabolism (r2 > 0.5, p < 0.05). The intrahepatic microbiome post-aspirin showed increased abundance of Firmicutes (Ruminococcaceae, Lachnospiraceae, and Clostridiaceae) and improved functionality (p < 0.05). Aspirin caused decreased expression of Ryanodine-receptor-2 (RyR2), Arginase-1 and Kynurenine-3-monooxygenase, which correlate with reduction in α-SMA and degree of hepatic fibrosis (r2 > 0.75; p < 0.05). In addition, pan specific blocking of RyR2 by carvedilol/flecainide markedly inhibited HSC activation and proliferation in-vitro by reducing Ca[2+] overload, ER/mitochondrial stress (p < 0.05). Further, RyR2 blockade in HSCs reduced its activation by activated platelet secretome or TGFβ1 (p < 0.05). CONCLUSIONS: Platelet deactivation using aspirin regresses hepatic fibrosis by decreasing intrahepatic platelet accumulation/activation, inflammation and modulation of intrahepatic microbiome. Induction of RyR2 is critical for fibrosis development and pharmacological inhibition of RyR2 could ameliorate liver fibrosis.},
}
RevDate: 2026-04-01
CmpDate: 2026-04-01
Rhizosphere Microbiome as an Underexplored Resource for Agroecosystem Sustainability: Insights From the Carrot Root Zone.
Environmental microbiology reports, 18(2):e70325.
Rhizosphere microbiome is critical for nutrient turnover, pathogen suppression, and stress modulation, forming the basis of microbial products relevant to agriculture. However, microbial communities associated with carrot root zone remain relatively underexplored, with limited studies focused beyond descriptive surveys. Here, we synthesise existing information on the structural, functional, and ecological dynamics of the carrot rhizomicrobiome, highlighting its emerging yet underdeveloped mechanistic profiling. Existing literature indicates that carrot-associated microbes may play a role in nutrient mobilisation, growth promotion, and antagonism. The early proof-of-concept works demonstrate that the microbes may gain potential applications in biofertilizers, biostimulants, and biocontrol agents. While these functions are strongly influenced by soil properties, genotype, and management, only a few carrot-specific isolates/consortia have been multi-environmentally validated. The limited progress partly reflects the overall underrepresentation of vegetables in microbiome-based studies, compared to other major crops. We explored the key characteristics, economic, and agricultural significance of the carrot rhizosphere, highlighting its richness with beneficial microorganisms. Among the gaps identified are inadequate functional-level and field trial, and insufficient multi-omics integration, which currently limit biotechnological translation. Addressing these gaps through targeted isolation, mechanistic functional and field validation could position carrot rhizosphere microbiome as a valuable yet underexplored resource for enhancing agroecosystem sustainability.
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@article {pmid41922261,
year = {2026},
author = {Adebayo, AA and Babalola, OO},
title = {Rhizosphere Microbiome as an Underexplored Resource for Agroecosystem Sustainability: Insights From the Carrot Root Zone.},
journal = {Environmental microbiology reports},
volume = {18},
number = {2},
pages = {e70325},
pmid = {41922261},
issn = {1758-2229},
support = {CRP/ZAF22-93//International Centre for Genetic Engineering and Biotechnology/ ; },
mesh = {*Daucus carota/microbiology/growth & development ; *Rhizosphere ; *Plant Roots/microbiology ; *Microbiota ; *Soil Microbiology ; Agriculture ; Bacteria/classification/genetics/isolation & purification/metabolism ; },
abstract = {Rhizosphere microbiome is critical for nutrient turnover, pathogen suppression, and stress modulation, forming the basis of microbial products relevant to agriculture. However, microbial communities associated with carrot root zone remain relatively underexplored, with limited studies focused beyond descriptive surveys. Here, we synthesise existing information on the structural, functional, and ecological dynamics of the carrot rhizomicrobiome, highlighting its emerging yet underdeveloped mechanistic profiling. Existing literature indicates that carrot-associated microbes may play a role in nutrient mobilisation, growth promotion, and antagonism. The early proof-of-concept works demonstrate that the microbes may gain potential applications in biofertilizers, biostimulants, and biocontrol agents. While these functions are strongly influenced by soil properties, genotype, and management, only a few carrot-specific isolates/consortia have been multi-environmentally validated. The limited progress partly reflects the overall underrepresentation of vegetables in microbiome-based studies, compared to other major crops. We explored the key characteristics, economic, and agricultural significance of the carrot rhizosphere, highlighting its richness with beneficial microorganisms. Among the gaps identified are inadequate functional-level and field trial, and insufficient multi-omics integration, which currently limit biotechnological translation. Addressing these gaps through targeted isolation, mechanistic functional and field validation could position carrot rhizosphere microbiome as a valuable yet underexplored resource for enhancing agroecosystem sustainability.},
}
MeSH Terms:
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*Daucus carota/microbiology/growth & development
*Rhizosphere
*Plant Roots/microbiology
*Microbiota
*Soil Microbiology
Agriculture
Bacteria/classification/genetics/isolation & purification/metabolism
RevDate: 2026-04-01
Hypoalbuminemia and reduced sputum microbiome diversity associated with antibiotic treatment failure in nursing and healthcare-associated pneumonia.
Drug discoveries & therapeutics [Epub ahead of print].
Nursing and healthcare-associated pneumonia (NHCAP) pose significant challenges in older populations, yet factors predicting antibiotic treatment failure remain elusive. This exploratory secondary analysis of a multicenter phase IV trial aimed to identify the clinical and microbiome predictors of treatment failure in patients with NHCAP treated with lascufloxacin. Among the 56 evaluable patients (median age 86 years; cured n = 44, not cured n = 12), paired sputum and tongue samples were analyzed using 16S ribosomal RNA gene clone library sequencing. Alpha diversity was assessed using the Shannon index, Simpson index, observed richness, and Pielou's evenness, whereas beta diversity was calculated using Bray-Curtis dissimilarity and visualized by principal coordinate analysis. Serum albumin was significantly lower in not cured patients (3.0 vs. 3.5 g/dL, p = 0.0497) and emerged as the strongest predictor of treatment failure in univariate logistic regression (odds ratio 0.18, 95% confidence interval 0.05-0.73, p = 0.016). Sputum Pielou's evenness showed a comparable predictive ability (odds ratio 0.010, p = 0.047). The overall microbiome community composition did not differ according to the outcome. Notably, patients with hypoalbuminemia (< 2.85 g/dL) exhibited significantly reduced sputum alpha diversity (Shannon p = 0.034, Simpson p = 0.025, Pielou's evenness p = 0.010). A simple risk stratification combining hypoalbuminemia and denture use identified a high-risk subgroup with markedly elevated treatment failure rates (75.0% vs. 12.5%, p = 0.001). These findings suggest an interconnected pathophysiology linking nutritional status and respiratory microbiome stability in patients with NHCAP. Nutritional status and oral health may be modifiable targets for improving treatment outcomes in high-risk patients.
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@article {pmid41922263,
year = {2026},
author = {Hosogaya, N and Fukui, S and Takazono, T and Fukushima, K and Morio, R and Irifune, S and Morimoto, S and Nakada, N and Yoshida, M and Takeda, K and Ide, S and Iwanaga, N and Nemoto, K and Izumikawa, K and Yatera, K and Yanagihara, K and Mukae, H},
title = {Hypoalbuminemia and reduced sputum microbiome diversity associated with antibiotic treatment failure in nursing and healthcare-associated pneumonia.},
journal = {Drug discoveries & therapeutics},
volume = {},
number = {},
pages = {},
doi = {10.5582/ddt.2026.01005},
pmid = {41922263},
issn = {1881-784X},
abstract = {Nursing and healthcare-associated pneumonia (NHCAP) pose significant challenges in older populations, yet factors predicting antibiotic treatment failure remain elusive. This exploratory secondary analysis of a multicenter phase IV trial aimed to identify the clinical and microbiome predictors of treatment failure in patients with NHCAP treated with lascufloxacin. Among the 56 evaluable patients (median age 86 years; cured n = 44, not cured n = 12), paired sputum and tongue samples were analyzed using 16S ribosomal RNA gene clone library sequencing. Alpha diversity was assessed using the Shannon index, Simpson index, observed richness, and Pielou's evenness, whereas beta diversity was calculated using Bray-Curtis dissimilarity and visualized by principal coordinate analysis. Serum albumin was significantly lower in not cured patients (3.0 vs. 3.5 g/dL, p = 0.0497) and emerged as the strongest predictor of treatment failure in univariate logistic regression (odds ratio 0.18, 95% confidence interval 0.05-0.73, p = 0.016). Sputum Pielou's evenness showed a comparable predictive ability (odds ratio 0.010, p = 0.047). The overall microbiome community composition did not differ according to the outcome. Notably, patients with hypoalbuminemia (< 2.85 g/dL) exhibited significantly reduced sputum alpha diversity (Shannon p = 0.034, Simpson p = 0.025, Pielou's evenness p = 0.010). A simple risk stratification combining hypoalbuminemia and denture use identified a high-risk subgroup with markedly elevated treatment failure rates (75.0% vs. 12.5%, p = 0.001). These findings suggest an interconnected pathophysiology linking nutritional status and respiratory microbiome stability in patients with NHCAP. Nutritional status and oral health may be modifiable targets for improving treatment outcomes in high-risk patients.},
}
RevDate: 2026-04-01
Characterizing the Microbiome and Prevalence of Wolbachia in Culex pipiens Complex and Culex restuans Mosquitoes in the Midwest United States.
Microbial ecology pii:10.1007/s00248-026-02750-1 [Epub ahead of print].
Additional Links: PMID-41922553
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@article {pmid41922553,
year = {2026},
author = {Cloud, RE and Irwin, P and Muturi, EJ and Cáceres, CE},
title = {Characterizing the Microbiome and Prevalence of Wolbachia in Culex pipiens Complex and Culex restuans Mosquitoes in the Midwest United States.},
journal = {Microbial ecology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00248-026-02750-1},
pmid = {41922553},
issn = {1432-184X},
support = {DEB - 1754115//National Science Foundation/ ; DEB - 1754115//National Science Foundation/ ; DBI - 2022049//Genomics and Eco-evolution of Multi-scale Symbioses Institute/ ; },
}
RevDate: 2026-04-01
Patient-derived intestinal organoids as a model for site-specific mucosal bacterial interactions in paediatric inflammatory bowel disease.
Scientific reports pii:10.1038/s41598-026-46184-8 [Epub ahead of print].
Inflammatory bowel disease (IBD) is secondary to an abnormal immune response to the microbiota. To study this, models of host-microbe interactions that represent mucosal bacterial communities and inter-patient diversity are required. Human intestinal organoids (HIOs) are an established model to investigate epithelial responses. Here, we describe a technique of culturing bacteria directly from the sites of inflammation in IBD, while simultaneously sampling host tissue. We generated HIOs from a cohort of newly diagnosed paediatric IBD patients, without confounding treatments or comorbidities, and explored their response to site-specific bacteria. A unique biobank of matched HIOs and cultured mucosa-attached bacteria was established from 27 paediatric patients. Transcriptional profiling revealed differential gene expression between control and IBD-derived organoids. We used microinjection to introduce bacteria to the apical surface of the epithelium, to determine the effect of bacteria on host epithelial cells. We measured survival and growth of bacteria within the HIOs and tested several related bacterial isolates for their impact on the epithelium. An isolate from a control patient stimulated inflammatory signalling pathways but this was not observed in response to a closely related isolate originating from an IBD patient. This study demonstrates the feasibility of isolating bacteria and generating organoids from the same biopsy tissue, to explore personalised host-microbe interactions. The microinjections, while labour-intensive, demonstrate that closely related bacteria can induce very different epithelial responses, with downstream implications for immune response. This highlights the importance of understanding host-microbe interactions in a strain- and site-specific manner and developing techniques for personalised microbiome-based therapeutics.
Additional Links: PMID-41922622
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@article {pmid41922622,
year = {2026},
author = {Chan, E and Chan, WH and Kerr, G and Archer, SK and Jardé, T and Engel, RM and Gould, JA and Amarasinghe, SL and Rutten, EL and D'Adamo, GL and Gulliver, EL and Gearing, LJ and Forster, SC and Giles, EM and Abud, HE},
title = {Patient-derived intestinal organoids as a model for site-specific mucosal bacterial interactions in paediatric inflammatory bowel disease.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-46184-8},
pmid = {41922622},
issn = {2045-2322},
support = {1188689//National Health and Medical Research Council of Australia/ ; 1188689//National Health and Medical Research Council of Australia/ ; },
abstract = {Inflammatory bowel disease (IBD) is secondary to an abnormal immune response to the microbiota. To study this, models of host-microbe interactions that represent mucosal bacterial communities and inter-patient diversity are required. Human intestinal organoids (HIOs) are an established model to investigate epithelial responses. Here, we describe a technique of culturing bacteria directly from the sites of inflammation in IBD, while simultaneously sampling host tissue. We generated HIOs from a cohort of newly diagnosed paediatric IBD patients, without confounding treatments or comorbidities, and explored their response to site-specific bacteria. A unique biobank of matched HIOs and cultured mucosa-attached bacteria was established from 27 paediatric patients. Transcriptional profiling revealed differential gene expression between control and IBD-derived organoids. We used microinjection to introduce bacteria to the apical surface of the epithelium, to determine the effect of bacteria on host epithelial cells. We measured survival and growth of bacteria within the HIOs and tested several related bacterial isolates for their impact on the epithelium. An isolate from a control patient stimulated inflammatory signalling pathways but this was not observed in response to a closely related isolate originating from an IBD patient. This study demonstrates the feasibility of isolating bacteria and generating organoids from the same biopsy tissue, to explore personalised host-microbe interactions. The microinjections, while labour-intensive, demonstrate that closely related bacteria can induce very different epithelial responses, with downstream implications for immune response. This highlights the importance of understanding host-microbe interactions in a strain- and site-specific manner and developing techniques for personalised microbiome-based therapeutics.},
}
RevDate: 2026-04-01
CmpDate: 2026-04-01
Toward microbiome-assisted remediation: Vanadium-titanium magnetite mining reshapes cropland soil chemistry and rhizosphere microbiomes.
Crop health, 4(1):.
Vanadium-titanium magnetite (VTM) mining can modify cropland soils and root-associated microbiomes with implications for crop health. However, how crop rhizosphere microbiomes reorganize under VTM-derived stress-particularly when bacteria and fungi are considered together-remains poorly understood. In the Hongge district (Panzhihua, China), we sampled bulk soils and rhizospheres of lettuce, rapeseed, and pea from croplands within the VTM mining influence zone (mining-impacted fields) and paired croplands outside the zone (reference fields). We measured soil chemistry and profiled bacterial and fungal communities using 16S rRNA and ITS amplicon sequencing, respectively. Mining-impacted soils generally showed a VTM geochemical imprint, neutral-alkaline pH, and reduced plant-available P and K. Bray-Curtis-based ordinations indicated a clear separation between mining-impacted and reference rhizospheres, and taxonomic profiles suggested host-dependent reassembly of both bacterial and fungal communities. Putative functional profiling suggested a shift toward stress-accommodation processes, and fungal guild assignments tended to tilt toward saprotrophic/endophytic categories. Mantel analyses identified pH as one of the strongest correlates of community turnover, whereas structural equation modeling was consistent with nutrient availability (available N/P/K composite) explaining a substantial portion of the VTM effect; the composite total-metal-load axis (Fe/V/Ti/Zn) showed limited explanatory power, especially for fungi. Together, these field-based, two-kingdom signals link VTM-altered soil chemistry to rhizosphere restructuring in edible crops and provide actionable indicators for crop health management.
Additional Links: PMID-41922662
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@article {pmid41922662,
year = {2026},
author = {Liu, B and Huang, X and Chang, C and Wan, X and Liu, M and Li, R and Li, J and Li, Q and Tao, Y},
title = {Toward microbiome-assisted remediation: Vanadium-titanium magnetite mining reshapes cropland soil chemistry and rhizosphere microbiomes.},
journal = {Crop health},
volume = {4},
number = {1},
pages = {},
pmid = {41922662},
issn = {2948-1945},
support = {2024NSFSC1202//Natural Science Foundation of Sichuan Province/ ; 25FTZLCL0012//Open Projects of the Sichuan Provincial Key Laboratory for Critical Strategic Materials of Vanadium and Titanium/ ; TYNSYS-2023-Z-03//Open Projects of the Sichuan Provincial University Key Laboratory for Solar Energy Technology Integration and Application Promotion/ ; Z3785//the start-up funds provided by Chengdu University/ ; },
abstract = {Vanadium-titanium magnetite (VTM) mining can modify cropland soils and root-associated microbiomes with implications for crop health. However, how crop rhizosphere microbiomes reorganize under VTM-derived stress-particularly when bacteria and fungi are considered together-remains poorly understood. In the Hongge district (Panzhihua, China), we sampled bulk soils and rhizospheres of lettuce, rapeseed, and pea from croplands within the VTM mining influence zone (mining-impacted fields) and paired croplands outside the zone (reference fields). We measured soil chemistry and profiled bacterial and fungal communities using 16S rRNA and ITS amplicon sequencing, respectively. Mining-impacted soils generally showed a VTM geochemical imprint, neutral-alkaline pH, and reduced plant-available P and K. Bray-Curtis-based ordinations indicated a clear separation between mining-impacted and reference rhizospheres, and taxonomic profiles suggested host-dependent reassembly of both bacterial and fungal communities. Putative functional profiling suggested a shift toward stress-accommodation processes, and fungal guild assignments tended to tilt toward saprotrophic/endophytic categories. Mantel analyses identified pH as one of the strongest correlates of community turnover, whereas structural equation modeling was consistent with nutrient availability (available N/P/K composite) explaining a substantial portion of the VTM effect; the composite total-metal-load axis (Fe/V/Ti/Zn) showed limited explanatory power, especially for fungi. Together, these field-based, two-kingdom signals link VTM-altered soil chemistry to rhizosphere restructuring in edible crops and provide actionable indicators for crop health management.},
}
RevDate: 2026-04-01
Pathophysiology of colitis-associated colorectal cancer.
Nature reviews. Gastroenterology & hepatology [Epub ahead of print].
Colitis-associated colorectal cancer (caCRC) is a subset of lower gastrointestinal tract malignancies that occurs in patients with inflammatory bowel disease (IBD), such as ulcerative colitis and Crohn's disease. The global prevalence of IBD is increasing, putting more individuals at risk of developing caCRC. The pathophysiological mechanisms that underlie the initiation and growth of caCRC remain to be fully elucidated. Nevertheless, studies have provided novel insights into the pathophysiology of caCRC, underscoring the distinguishing characteristics of caCRC compared with sporadic forms of CRC. In this Review, we describe the key mechanisms that drive caCRC. Starting from a clinical perspective and highlighting key features of the tumour epithelium, we discuss typical caCRC-related characteristics among subtypes of CRC, with a particular focus on the role of stromal cells in the tumour microenvironment. In addition, we review the contributions of immune cells to tumour control versus tumour promotion, and how signals from the gut microbiome might influence tumour development in caCRC. We also discuss various aspects of the pathophysiological heterogeneity of caCRC. Finally, we outline potential implications for therapy, and how these findings could be translated into future strategies of personalized medicine targeting caCRC.
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@article {pmid41922722,
year = {2026},
author = {Neufert, C and Neurath, MF},
title = {Pathophysiology of colitis-associated colorectal cancer.},
journal = {Nature reviews. Gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
pmid = {41922722},
issn = {1759-5053},
abstract = {Colitis-associated colorectal cancer (caCRC) is a subset of lower gastrointestinal tract malignancies that occurs in patients with inflammatory bowel disease (IBD), such as ulcerative colitis and Crohn's disease. The global prevalence of IBD is increasing, putting more individuals at risk of developing caCRC. The pathophysiological mechanisms that underlie the initiation and growth of caCRC remain to be fully elucidated. Nevertheless, studies have provided novel insights into the pathophysiology of caCRC, underscoring the distinguishing characteristics of caCRC compared with sporadic forms of CRC. In this Review, we describe the key mechanisms that drive caCRC. Starting from a clinical perspective and highlighting key features of the tumour epithelium, we discuss typical caCRC-related characteristics among subtypes of CRC, with a particular focus on the role of stromal cells in the tumour microenvironment. In addition, we review the contributions of immune cells to tumour control versus tumour promotion, and how signals from the gut microbiome might influence tumour development in caCRC. We also discuss various aspects of the pathophysiological heterogeneity of caCRC. Finally, we outline potential implications for therapy, and how these findings could be translated into future strategies of personalized medicine targeting caCRC.},
}
RevDate: 2026-04-01
Development of gut microbiota composition in captive Asian elephants: a year-long analysis.
Scientific reports pii:10.1038/s41598-026-46586-8 [Epub ahead of print].
The establishment of gut microbiota is vital for the health and development of elephant calves, especially during their first year of life. This study investigates the transformation of the gut microbiome in captive Asian elephant calves, focusing the influence of maternal milk and subsequent dietary transitions on microbial colonization. A single meconium was collected at birth, followed by monthly fresh fecal samples during the first year. Mothers' fecal samples were also collected when calves reached three months of age. Gut microbiota profiling was conducted using 16 S rRNA gene sequencing. Meconium exhibited a diverse microbiota with moderate richness at birth. Richness subsequently declined in the monthly fecal samples, reaching its lowest point by three months of age. Firmicutes, Actinobacteriota, and Bacteroidota were the dominant bacterial phyla throughout the first year. A major shift was observed around 7 to 8 months of age with emergence of the archaeal genus Methanobrevibacter from phylum Euryarchaeota, which subsequently declined by 11 to 12 months. By this age, the calf microbial community had become more similar to that of adult elephants; however, species richness and diversity remained lower, indicating that microbial maturation was still ongoing. These findings advance our understanding of gut microbiota development in elephant calves and underscore the critical role of dietary management in promoting gut health and survival, providing essential data for captive conservation and management strategies.
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@article {pmid41922727,
year = {2026},
author = {Klinhom, S and Kunasol, C and Sriwichaiin, S and Kerdphoo, S and Chattipakorn, N and Chattipakorn, SC and Thitaram, C},
title = {Development of gut microbiota composition in captive Asian elephants: a year-long analysis.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-46586-8},
pmid = {41922727},
issn = {2045-2322},
support = {59/2565//The CMU Presidential Scholarship and Chiang Mai University/ ; N42A660301//The Distinguished Research Professor Grant from the National Research Council of Thailand/ ; RSA6280095//Thailand Research Fund/ ; },
abstract = {The establishment of gut microbiota is vital for the health and development of elephant calves, especially during their first year of life. This study investigates the transformation of the gut microbiome in captive Asian elephant calves, focusing the influence of maternal milk and subsequent dietary transitions on microbial colonization. A single meconium was collected at birth, followed by monthly fresh fecal samples during the first year. Mothers' fecal samples were also collected when calves reached three months of age. Gut microbiota profiling was conducted using 16 S rRNA gene sequencing. Meconium exhibited a diverse microbiota with moderate richness at birth. Richness subsequently declined in the monthly fecal samples, reaching its lowest point by three months of age. Firmicutes, Actinobacteriota, and Bacteroidota were the dominant bacterial phyla throughout the first year. A major shift was observed around 7 to 8 months of age with emergence of the archaeal genus Methanobrevibacter from phylum Euryarchaeota, which subsequently declined by 11 to 12 months. By this age, the calf microbial community had become more similar to that of adult elephants; however, species richness and diversity remained lower, indicating that microbial maturation was still ongoing. These findings advance our understanding of gut microbiota development in elephant calves and underscore the critical role of dietary management in promoting gut health and survival, providing essential data for captive conservation and management strategies.},
}
RevDate: 2026-04-01
Forensic analysis of environmental and skin microbiome differences in college dormitories based on 16 S rRNA.
International journal of legal medicine [Epub ahead of print].
Additional Links: PMID-41922879
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@article {pmid41922879,
year = {2026},
author = {Dou, S and Shen, J and Wang, C and Ma, G and Fu, G and Fu, L and Cong, B and Li, S},
title = {Forensic analysis of environmental and skin microbiome differences in college dormitories based on 16 S rRNA.},
journal = {International journal of legal medicine},
volume = {},
number = {},
pages = {},
pmid = {41922879},
issn = {1437-1596},
support = {82572154//National Natural Science Foundation of China/ ; 30705010060//HeBei Medical University Postdoctoral Fund/ ; },
}
RevDate: 2026-04-02
Porphyromonas gingivalis induces intestinal inflammation through gingipain-dependent gut microbiome dysbiosis.
Microbiome pii:10.1186/s40168-026-02389-7 [Epub ahead of print].
BACKGROUND: Porphyromonas gingivalis (Pg), a key pathogen in periodontitis, is implicated in various systemic diseases such as pancreatic cancer and Alzheimer's disease. However, as a periodontal pathogen that can directly enter the lower gastrointestinal tract via saliva, its potential impact on the gut microbiome, intestinal inflammation, and its underlying mechanisms remains largely elusive.
RESULTS: Here, we observed that oral administration of Pg exacerbates intestinal inflammation in mice by inducing gut microbiome dysbiosis, increasing Th17 cells and the release of pro-inflammatory cytokines. Inhibition of Th17 activity with GSK805 or an anti-IL-17A blocking antibody mitigated this inflammatory response, highlighting the mediating role of Th17 cells. Gingipains, the virulence factors of Pg, played a crucial role in this process. Sequential knockout of gingipain genes revealed a gradual reduction in inflammatory phenotypes, with statistically significant alleviation observed when all three gingipain genes were deleted. Co-housing experiments showed that gut microbiota remodeling effectively protected against Th17-driven inflammatory response. Furthermore, immunization with inactivated Pg effectively prevented gut microbiome dysbiosis and Th17 cell-mediated inflammation.
CONCLUSION: Our findings suggest that Pg may exacerbate intestinal inflammation, potentially via its gingipain virulence proteases, which are linked to gut microbiota dysbiosis and enhanced Th17-mediated immune responses. These results suggest that gingipains could be promising targets for further investigation in Pg-associated intestinal disorders. Video Abstract.
Additional Links: PMID-41923122
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PubMed:
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@article {pmid41923122,
year = {2026},
author = {Li, M and Cui, J and Qu, R and Liu, R and Sun, Y and Li, P and Liu, J and Low, A and Huang, X and Gan, F and Xu, ZZ},
title = {Porphyromonas gingivalis induces intestinal inflammation through gingipain-dependent gut microbiome dysbiosis.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02389-7},
pmid = {41923122},
issn = {2049-2618},
support = {2025AHGXZK40069//Natural Science Foundation of Education Department of Anhui Province/ ; },
abstract = {BACKGROUND: Porphyromonas gingivalis (Pg), a key pathogen in periodontitis, is implicated in various systemic diseases such as pancreatic cancer and Alzheimer's disease. However, as a periodontal pathogen that can directly enter the lower gastrointestinal tract via saliva, its potential impact on the gut microbiome, intestinal inflammation, and its underlying mechanisms remains largely elusive.
RESULTS: Here, we observed that oral administration of Pg exacerbates intestinal inflammation in mice by inducing gut microbiome dysbiosis, increasing Th17 cells and the release of pro-inflammatory cytokines. Inhibition of Th17 activity with GSK805 or an anti-IL-17A blocking antibody mitigated this inflammatory response, highlighting the mediating role of Th17 cells. Gingipains, the virulence factors of Pg, played a crucial role in this process. Sequential knockout of gingipain genes revealed a gradual reduction in inflammatory phenotypes, with statistically significant alleviation observed when all three gingipain genes were deleted. Co-housing experiments showed that gut microbiota remodeling effectively protected against Th17-driven inflammatory response. Furthermore, immunization with inactivated Pg effectively prevented gut microbiome dysbiosis and Th17 cell-mediated inflammation.
CONCLUSION: Our findings suggest that Pg may exacerbate intestinal inflammation, potentially via its gingipain virulence proteases, which are linked to gut microbiota dysbiosis and enhanced Th17-mediated immune responses. These results suggest that gingipains could be promising targets for further investigation in Pg-associated intestinal disorders. Video Abstract.},
}
RevDate: 2026-04-02
Associations between phloem microbiota and metabolomes in three North American ash species (Fraxinus spp.) susceptible to emerald ash borer (Agrilus planipennis).
Environmental microbiome pii:10.1186/s40793-026-00884-w [Epub ahead of print].
BACKGROUND: Microorganisms play crucial roles in the survival and fitness of their plant and insects hosts, including invasive species. The emerald ash borer (Agrilus planipennis, Fairmaire; EAB) is an invasive insect from Asia. It represents a significant threat to North American forest ecosystems, causing widespread mortality in susceptible native ash (Fraxinus) species. While previous studies have shown differences in specific plant defense metabolites between susceptible North American ash species and their more resistant Asian counterparts, widely targeted metabolite profiles and their interactions with phloem microbiota in response to EAB infestation has thus far received little attention. This study aimed to profile microbial communities associated with ash phloem and EAB larval guts and their relationship to ash phloem metabolites in three native susceptible North American ash species: F. pennsylvanica (green ash), F. nigra (black ash) and F. americana (white ash).
RESULTS: Using metabarcoding to characterize the microbial communities associated with the larval gut and host tree phloem and widely targeted metabolomics to establish the first global metabolomic profile of phloem in these ash species, we examined interspecies differences in profiles and associations of ash phloem microbiota and metabolites in relation to EAB infestation. Multivariate analysis revealed that fungal communities were distinct in all ash species, while F. pennsylvanica (green ash) harbored bacterial communities distinct from black ash. Only black ash showed a phloem profile significantly associated with EAB attack symptoms and had the largest number of differentially abundant bacterial taxa. In contrast, larval gut bacterial communities from green ash were distinct from those in other ash species. Green ash displayed a distinct global metabolite profile from the other two species and had the highest number of differentially regulated metabolites, while black ash had the least. Green and white ash shared a strong upregulation of terpenoid compounds, several of which were among compounds significantly associated with microbial communities in green ash phloem or the EAB larval gut.
CONCLUSIONS: Our results provide the first comparative analysis of phloem-associated microbial communities and metabolomes across three susceptible North American ash species and their response to EAB. We found that microbiota and metabolites in green ash showed a distinct response to EAB infestation from the other ash species and we identified specific metabolites exhibiting significant correlations with microbial communities in ash phloem or the EAB larval gut. These findings contribute novel insights into interspecies variability in host-associated microbial communities and metabolomes and their response to an invasive insect.
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@article {pmid41923148,
year = {2026},
author = {Mogouong Tambue, J and Yager, C and Bushley, KE},
title = {Associations between phloem microbiota and metabolomes in three North American ash species (Fraxinus spp.) susceptible to emerald ash borer (Agrilus planipennis).},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-026-00884-w},
pmid = {41923148},
issn = {2524-6372},
support = {DEB 2030036//National Science Foundation/ ; },
abstract = {BACKGROUND: Microorganisms play crucial roles in the survival and fitness of their plant and insects hosts, including invasive species. The emerald ash borer (Agrilus planipennis, Fairmaire; EAB) is an invasive insect from Asia. It represents a significant threat to North American forest ecosystems, causing widespread mortality in susceptible native ash (Fraxinus) species. While previous studies have shown differences in specific plant defense metabolites between susceptible North American ash species and their more resistant Asian counterparts, widely targeted metabolite profiles and their interactions with phloem microbiota in response to EAB infestation has thus far received little attention. This study aimed to profile microbial communities associated with ash phloem and EAB larval guts and their relationship to ash phloem metabolites in three native susceptible North American ash species: F. pennsylvanica (green ash), F. nigra (black ash) and F. americana (white ash).
RESULTS: Using metabarcoding to characterize the microbial communities associated with the larval gut and host tree phloem and widely targeted metabolomics to establish the first global metabolomic profile of phloem in these ash species, we examined interspecies differences in profiles and associations of ash phloem microbiota and metabolites in relation to EAB infestation. Multivariate analysis revealed that fungal communities were distinct in all ash species, while F. pennsylvanica (green ash) harbored bacterial communities distinct from black ash. Only black ash showed a phloem profile significantly associated with EAB attack symptoms and had the largest number of differentially abundant bacterial taxa. In contrast, larval gut bacterial communities from green ash were distinct from those in other ash species. Green ash displayed a distinct global metabolite profile from the other two species and had the highest number of differentially regulated metabolites, while black ash had the least. Green and white ash shared a strong upregulation of terpenoid compounds, several of which were among compounds significantly associated with microbial communities in green ash phloem or the EAB larval gut.
CONCLUSIONS: Our results provide the first comparative analysis of phloem-associated microbial communities and metabolomes across three susceptible North American ash species and their response to EAB. We found that microbiota and metabolites in green ash showed a distinct response to EAB infestation from the other ash species and we identified specific metabolites exhibiting significant correlations with microbial communities in ash phloem or the EAB larval gut. These findings contribute novel insights into interspecies variability in host-associated microbial communities and metabolomes and their response to an invasive insect.},
}
RevDate: 2026-04-02
Phenotypic resistance profiles and resistome variations between endophytic and epiphytic bacteria in apple fruits.
Environmental microbiome pii:10.1186/s40793-026-00880-0 [Epub ahead of print].
BACKGROUND: In recent years, there has been increasing concerns about antibiotic resistance. Although studies have investigated resistance in food-associated bacteria, fresh produce microbes remain underexplored as potential hub of resistance genes capable for horizontal transfer to human via consumption. To this end, we tested the antibiotic resistance profiles of bacterial isolates recovered from Golden Reinders and Mandy apple cultivars. We aimed to investigate the effects of orchard-cultivar combinations and microbial lifestyle on the antibiotic resistance profiles. The apples (Golden Reinders and Mandy) were sampled from four separate orchards (EEL-Lleida, Esterri, Fruits-de-Ponent and Gotarta) in Spain. We used combination of culture-dependent and whole genome sequencing approaches to analyse the antibiotic resistance profiles.
RESULTS: A total of 516 bacterial isolates were screened for susceptibility against seven different classes of antibiotics. Results showed that 272 isolates were resistant to at least one antibiotic. From those, 203 were epiphytes and 95 classified as endophytes (isolated from surface-sterilized apple peels), whereas 26 isolates were shared between the groups. The resistance profiles varied across the antibiotics, with over 50% of the isolates exhibiting resistance to tetracycline, quinolones and cephalosporins. In contrast, none of the isolates showed resistance to imipenem. Whole genome sequencing (WGS) was performed on 18 isolates, however, only 10 genomes passed quality-control thresholds and were included in subsequent resistome analyses. We found ARGs encoding resistance to 14 main antibiotic classes, with the majority of the confirmed resistances attributed to multidrug resistance (MDR). Only few target-specific ARGs were annotated, including (Rif)iri (rifampicin), lnu(A) (lincomycin) and FosD (Fosfomycin). Pantoea agglomerans possessed higher number of ARGs, while Staphylococcus arlettae exhibited notable prevalence of plasmid-encoded ARGs.
CONCLUSION: Overall, the study highlights the prevalence of antibiotic resistance in apple microbiomes. The presence of multidrug-resistance (MDR) genes further underscores the persistent threat of 'antibiotic resistance', underlining the necessity for deeper insight into antibiotic resistance within food chain.
Additional Links: PMID-41923164
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@article {pmid41923164,
year = {2026},
author = {Kiplimo, D and Sánchez, AM and Ramakrishnan, DK and Wicaksono, WA and Mwirichia, R and Teixidó, N and Berg, G and Abdelfattah, A},
title = {Phenotypic resistance profiles and resistome variations between endophytic and epiphytic bacteria in apple fruits.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-026-00880-0},
pmid = {41923164},
issn = {2524-6372},
support = {PID2020-117607RR-I00 (ENVIRONAPPLE)//University of Lleida and IRTA predoctoral UdL-IRTA Sponsored Fellowship 2021, Spanish 'Agencia Estatal de Investigación' (AEI), European Regional Development Fund (ERDF), 2021 SGR 01477 grant and the CERCA Programme from the 'Generalitat de Catalunya'/ ; },
abstract = {BACKGROUND: In recent years, there has been increasing concerns about antibiotic resistance. Although studies have investigated resistance in food-associated bacteria, fresh produce microbes remain underexplored as potential hub of resistance genes capable for horizontal transfer to human via consumption. To this end, we tested the antibiotic resistance profiles of bacterial isolates recovered from Golden Reinders and Mandy apple cultivars. We aimed to investigate the effects of orchard-cultivar combinations and microbial lifestyle on the antibiotic resistance profiles. The apples (Golden Reinders and Mandy) were sampled from four separate orchards (EEL-Lleida, Esterri, Fruits-de-Ponent and Gotarta) in Spain. We used combination of culture-dependent and whole genome sequencing approaches to analyse the antibiotic resistance profiles.
RESULTS: A total of 516 bacterial isolates were screened for susceptibility against seven different classes of antibiotics. Results showed that 272 isolates were resistant to at least one antibiotic. From those, 203 were epiphytes and 95 classified as endophytes (isolated from surface-sterilized apple peels), whereas 26 isolates were shared between the groups. The resistance profiles varied across the antibiotics, with over 50% of the isolates exhibiting resistance to tetracycline, quinolones and cephalosporins. In contrast, none of the isolates showed resistance to imipenem. Whole genome sequencing (WGS) was performed on 18 isolates, however, only 10 genomes passed quality-control thresholds and were included in subsequent resistome analyses. We found ARGs encoding resistance to 14 main antibiotic classes, with the majority of the confirmed resistances attributed to multidrug resistance (MDR). Only few target-specific ARGs were annotated, including (Rif)iri (rifampicin), lnu(A) (lincomycin) and FosD (Fosfomycin). Pantoea agglomerans possessed higher number of ARGs, while Staphylococcus arlettae exhibited notable prevalence of plasmid-encoded ARGs.
CONCLUSION: Overall, the study highlights the prevalence of antibiotic resistance in apple microbiomes. The presence of multidrug-resistance (MDR) genes further underscores the persistent threat of 'antibiotic resistance', underlining the necessity for deeper insight into antibiotic resistance within food chain.},
}
RevDate: 2026-04-02
Coral color morphs exhibit distinct microbial and proteomic profiles linked to stress and immune mechanisms in a changing ocean.
Microbiome pii:10.1186/s40168-026-02391-z [Epub ahead of print].
BACKGROUND: Coral phenotypic plasticity facilitates acclimation and adaptation to environmental variability. Coral species often display a variety of color morphs, yet key biological and ecological implications of such phenotypic variation remain underexplored. Here, we present the first proteomic and untargeted lipidomic and metabolomic survey to explore the biological characteristics and potential ecological significance of different color morphs (pink and brown) of healthy Pocillopora verrucosa sampled along a latitudinal gradient.
RESULTS: Our multi-omic approach elucidated distinct mechanisms associated with these dominant color morphs. We discovered bacterial indicators specific to each morph: putative pathogens such as Salmonella, Escherichia-Shigella, and carotenoid-producing Gemmatimonas were notably associated with the pink morph, whereas the brown morph was associated with potentially beneficial bacteria, such as Lysobacter, Acinetobacter, and Endozoicomonas. Despite these microbiome differences, the lipidome and metabolome of P. verrucosa were surprisingly homogeneous across colors and locations, suggesting similar metabolic performances during summer conditions. Key polar and apolar lipid classes, such as fatty acids, glycerophosphocholines, and retinoids, were prevalent. Notably, our proteomic analysis revealed morph-specific expressions, with pink morphs exhibiting enhanced levels of GFP-like proteins, Ankyrin, and the enzyme pullulanase, suggesting novel putative protective roles. In contrast, the brown morphs showed a higher abundance of heat shock proteins, indicating putative differential stress response capabilities.
CONCLUSION: This comprehensive study provides the first proteomic survey of P. verrucosa and identifies key physiological pathways and trade-offs linked to color morphs, which can further contribute to enhancing our understanding of coral resilience in the face of climate change.
SIGNIFICANCE STATEMENT: Understanding the phenotypic plasticity of corals is crucial for uncovering mechanisms of resilience in warming oceans, yet the biological significance of coral color morphs still needs to be explored. Using an innovative multi-omic approach (proteomics, lipidomics, and metabolomics), we provide the first comprehensive analysis of differences between pink and brown morphs of Pocillopora verrucosa. Our data reveal key taxa, potentially pathogenic or beneficial, associated with each morph, and suggest different strategies for each color morph to cope with heat stress, either expressing proteins involved in UV protection and heterotrophic activity or enhanced levels of heat stress resilience and DNA repair. These findings offer insights into the phenotypic plasticity of coral color morphs and their differential responses to climate change. Video Abstract.
Additional Links: PMID-41923171
Publisher:
PubMed:
Citation:
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@article {pmid41923171,
year = {2026},
author = {Delgadillo-Ordoñez, N and Schwarzenberg, A and Zhang, H and Beenham, L and Bensaddek, D and Raimundo, I and Terraneo, T and Benzoni, F and Peixoto, RS},
title = {Coral color morphs exhibit distinct microbial and proteomic profiles linked to stress and immune mechanisms in a changing ocean.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02391-z},
pmid = {41923171},
issn = {2049-2618},
abstract = {BACKGROUND: Coral phenotypic plasticity facilitates acclimation and adaptation to environmental variability. Coral species often display a variety of color morphs, yet key biological and ecological implications of such phenotypic variation remain underexplored. Here, we present the first proteomic and untargeted lipidomic and metabolomic survey to explore the biological characteristics and potential ecological significance of different color morphs (pink and brown) of healthy Pocillopora verrucosa sampled along a latitudinal gradient.
RESULTS: Our multi-omic approach elucidated distinct mechanisms associated with these dominant color morphs. We discovered bacterial indicators specific to each morph: putative pathogens such as Salmonella, Escherichia-Shigella, and carotenoid-producing Gemmatimonas were notably associated with the pink morph, whereas the brown morph was associated with potentially beneficial bacteria, such as Lysobacter, Acinetobacter, and Endozoicomonas. Despite these microbiome differences, the lipidome and metabolome of P. verrucosa were surprisingly homogeneous across colors and locations, suggesting similar metabolic performances during summer conditions. Key polar and apolar lipid classes, such as fatty acids, glycerophosphocholines, and retinoids, were prevalent. Notably, our proteomic analysis revealed morph-specific expressions, with pink morphs exhibiting enhanced levels of GFP-like proteins, Ankyrin, and the enzyme pullulanase, suggesting novel putative protective roles. In contrast, the brown morphs showed a higher abundance of heat shock proteins, indicating putative differential stress response capabilities.
CONCLUSION: This comprehensive study provides the first proteomic survey of P. verrucosa and identifies key physiological pathways and trade-offs linked to color morphs, which can further contribute to enhancing our understanding of coral resilience in the face of climate change.
SIGNIFICANCE STATEMENT: Understanding the phenotypic plasticity of corals is crucial for uncovering mechanisms of resilience in warming oceans, yet the biological significance of coral color morphs still needs to be explored. Using an innovative multi-omic approach (proteomics, lipidomics, and metabolomics), we provide the first comprehensive analysis of differences between pink and brown morphs of Pocillopora verrucosa. Our data reveal key taxa, potentially pathogenic or beneficial, associated with each morph, and suggest different strategies for each color morph to cope with heat stress, either expressing proteins involved in UV protection and heterotrophic activity or enhanced levels of heat stress resilience and DNA repair. These findings offer insights into the phenotypic plasticity of coral color morphs and their differential responses to climate change. Video Abstract.},
}
RevDate: 2026-04-02
EXPRESS: Oral administration of Enterococcus lactis strain SF68 speeds the recovery of amoxicillin-clavulanate-induced dysbiosis in cats.
Journal of feline medicine and surgery [Epub ahead of print].
OBJECTIVES: In a previous study, Torres-Henderson et al. (2017), the probiotic Enterococcus lactis strain SF68 was clinically shown to lessen amoxicillin-clavulanate associated diarrhea. The cause or mechanism as to why this clinical benefit occurred, however, was unknown. The cause or mechanism as to why this clinical benefit occurred, however, was not apparent in that study. Since the completion of that work, a new feline dysbiosis index (DI) has been developed and new information concerning the microbiome and bile acid metabolism has been published. The objective of this study was to assess changes in the feline DI and fecal bile acid metabolism to explain how this probiotic lessened amoxicillin-clavulanate-associated diarrhea.
METHODS: Prospective, randomized, placebo-controlled, double-blinded study. 27 healthy, young, adult, purpose-bred cats were used for a previous study. Cats were randomized into the probiotic (13 cats) or placebo (14 cats) group. Each cat received amoxicillin-clavulanate for 7 days at a standard dose and either the probiotic or placebo for 14 days. Fecal samples from all cats were obtained at baseline, day 7 and day 14. All samples were frozen at -80°C until assessed. Targeted qPCR assays were then used to determine the fecal feline DI and unconjugated fecal bile acid concentrations were measured at each time point.
RESULTS: An antibiotic-induced shift in fecal microbiota and unconjugated bile acids was observed, with the probiotic group showing normalization of the feline DI and increased secondary bile acids on Day 14 compared to the placebo group (P = 0.0322).
CONCLUSIONS AND RELEVANCE: The probiotic E. lactis strain SF68 lessened amoxicillin-clavulanate-associated clinical signs of disease at least in part from the positive effects on the selected microbiota and bile acid metabolism. These findings support supplementing this probiotic to cats that have a clinical need for amoxicillin-clavulanate treatment.
Additional Links: PMID-41923274
Publisher:
PubMed:
Citation:
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@article {pmid41923274,
year = {2026},
author = {Slaughter, M and Sung, CH and Suchodolski, JS and Pilla, R and Torres, C and Lappin, MR},
title = {EXPRESS: Oral administration of Enterococcus lactis strain SF68 speeds the recovery of amoxicillin-clavulanate-induced dysbiosis in cats.},
journal = {Journal of feline medicine and surgery},
volume = {},
number = {},
pages = {1098612X261441923},
doi = {10.1177/1098612X261441923},
pmid = {41923274},
issn = {1532-2750},
abstract = {OBJECTIVES: In a previous study, Torres-Henderson et al. (2017), the probiotic Enterococcus lactis strain SF68 was clinically shown to lessen amoxicillin-clavulanate associated diarrhea. The cause or mechanism as to why this clinical benefit occurred, however, was unknown. The cause or mechanism as to why this clinical benefit occurred, however, was not apparent in that study. Since the completion of that work, a new feline dysbiosis index (DI) has been developed and new information concerning the microbiome and bile acid metabolism has been published. The objective of this study was to assess changes in the feline DI and fecal bile acid metabolism to explain how this probiotic lessened amoxicillin-clavulanate-associated diarrhea.
METHODS: Prospective, randomized, placebo-controlled, double-blinded study. 27 healthy, young, adult, purpose-bred cats were used for a previous study. Cats were randomized into the probiotic (13 cats) or placebo (14 cats) group. Each cat received amoxicillin-clavulanate for 7 days at a standard dose and either the probiotic or placebo for 14 days. Fecal samples from all cats were obtained at baseline, day 7 and day 14. All samples were frozen at -80°C until assessed. Targeted qPCR assays were then used to determine the fecal feline DI and unconjugated fecal bile acid concentrations were measured at each time point.
RESULTS: An antibiotic-induced shift in fecal microbiota and unconjugated bile acids was observed, with the probiotic group showing normalization of the feline DI and increased secondary bile acids on Day 14 compared to the placebo group (P = 0.0322).
CONCLUSIONS AND RELEVANCE: The probiotic E. lactis strain SF68 lessened amoxicillin-clavulanate-associated clinical signs of disease at least in part from the positive effects on the selected microbiota and bile acid metabolism. These findings support supplementing this probiotic to cats that have a clinical need for amoxicillin-clavulanate treatment.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Network Pharmacology Combined With Gut Microbiome and Serum Metabolomics Reveals the Therapeutic Mechanisms of Hydroxysafflor Yellow A in Diabetic Kidney Disease.
Journal of diabetes research, 2026(1):e2131566.
Diabetic kidney disease (DKD) is a severe complication of diabetes, primarily driven by chronic inflammation, oxidative stress, and gut microbiota dysbiosis. Hydroxysafflor yellow A (HSY), a bioactive compound derived from Carthamus tinctorius L., demonstrates promising renoprotective effects. However, its mechanisms, especially through modulation of the gut-kidney axis, remain poorly understood. This study employed a combination of network pharmacology, a high-fat diet/streptozotocin-induced type 2 diabetic mouse model, 16S rRNA sequencing, and serum metabolomics to explore the therapeutic mechanisms of HSY. Renal function, oxidative stress, inflammation, and gut microbiota composition were evaluated. HSY significantly alleviated renal injury by reducing blood glucose, creatinine, and urea nitrogen levels (p < 0.05), while enhancing renal antioxidant enzyme activity (GSH, SOD, CAT). Inflammatory markers (TNF-α, IL-1β) and AGE-RAGE signaling were suppressed. Analysis of the gut microbiota revealed that HSY enriched SCFA-producing genera (e.g., Lactobacillus, Alloprevotella) and decreased the abundance of Schaedlerella. Serum metabolomics further indicated that HSY modulated riboflavin metabolism, linoleic acid metabolism, and steroid hormone biosynthesis, thereby linking microbial metabolites to renal protection. Spearman correlation analysis revealed strong associations between specific gut microbiota (e.g., Prevotella) and serum metabolites (e.g., eicosapentaenoic acid). HSY mitigates DKD by targeting AGE-RAGE-mediated inflammation, oxidative stress, and gut microbiota dysbiosis while correcting metabolic disturbances. This study offers a novel multi-omics approach to understanding HSY's renoprotective effects, highlighting its potential as a therapeutic agent for DKD.
Additional Links: PMID-41923440
PubMed:
Citation:
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@article {pmid41923440,
year = {2026},
author = {Wang, P and Liu, X and Sun, W and Dong, X and Tan, J and Chen, M and He, J and Ali, A and Wu, L and Shao, K},
title = {Network Pharmacology Combined With Gut Microbiome and Serum Metabolomics Reveals the Therapeutic Mechanisms of Hydroxysafflor Yellow A in Diabetic Kidney Disease.},
journal = {Journal of diabetes research},
volume = {2026},
number = {1},
pages = {e2131566},
pmid = {41923440},
issn = {2314-6753},
support = {SH2023073//Zhenjiang Science and Technology Innovation Fund (Key R&D Program-Social Development) Project/ ; YK2024116//Scientific Research Project of Yancheng Municipal Health Commission/ ; MS2022126//Project of Jiangsu Provincial Science and Technology Development Plan for Traditional Chinese Medicine/ ; },
mesh = {*Gastrointestinal Microbiome/drug effects ; Animals ; *Diabetic Nephropathies/drug therapy/metabolism/blood/microbiology ; Metabolomics ; *Chalcone/analogs & derivatives/pharmacology/therapeutic use ; *Quinones/pharmacology/therapeutic use ; Male ; Mice ; Oxidative Stress/drug effects ; *Network Pharmacology ; Kidney/drug effects/metabolism ; *Diabetes Mellitus, Experimental/drug therapy/metabolism/complications ; Mice, Inbred C57BL ; },
abstract = {Diabetic kidney disease (DKD) is a severe complication of diabetes, primarily driven by chronic inflammation, oxidative stress, and gut microbiota dysbiosis. Hydroxysafflor yellow A (HSY), a bioactive compound derived from Carthamus tinctorius L., demonstrates promising renoprotective effects. However, its mechanisms, especially through modulation of the gut-kidney axis, remain poorly understood. This study employed a combination of network pharmacology, a high-fat diet/streptozotocin-induced type 2 diabetic mouse model, 16S rRNA sequencing, and serum metabolomics to explore the therapeutic mechanisms of HSY. Renal function, oxidative stress, inflammation, and gut microbiota composition were evaluated. HSY significantly alleviated renal injury by reducing blood glucose, creatinine, and urea nitrogen levels (p < 0.05), while enhancing renal antioxidant enzyme activity (GSH, SOD, CAT). Inflammatory markers (TNF-α, IL-1β) and AGE-RAGE signaling were suppressed. Analysis of the gut microbiota revealed that HSY enriched SCFA-producing genera (e.g., Lactobacillus, Alloprevotella) and decreased the abundance of Schaedlerella. Serum metabolomics further indicated that HSY modulated riboflavin metabolism, linoleic acid metabolism, and steroid hormone biosynthesis, thereby linking microbial metabolites to renal protection. Spearman correlation analysis revealed strong associations between specific gut microbiota (e.g., Prevotella) and serum metabolites (e.g., eicosapentaenoic acid). HSY mitigates DKD by targeting AGE-RAGE-mediated inflammation, oxidative stress, and gut microbiota dysbiosis while correcting metabolic disturbances. This study offers a novel multi-omics approach to understanding HSY's renoprotective effects, highlighting its potential as a therapeutic agent for DKD.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Gastrointestinal Microbiome/drug effects
Animals
*Diabetic Nephropathies/drug therapy/metabolism/blood/microbiology
Metabolomics
*Chalcone/analogs & derivatives/pharmacology/therapeutic use
*Quinones/pharmacology/therapeutic use
Male
Mice
Oxidative Stress/drug effects
*Network Pharmacology
Kidney/drug effects/metabolism
*Diabetes Mellitus, Experimental/drug therapy/metabolism/complications
Mice, Inbred C57BL
RevDate: 2026-04-02
CmpDate: 2026-04-02
Comparative Amplicon and Shotgun Metagenome Profiling of Soil Microbial Communities in Kauri Forests Affected by Phytophthora agathidicida.
Environmental microbiology reports, 18(2):e70324.
Soil-borne pathogens can influence microbial communities and ecosystem function, making it important to understand their broader ecological impacts. We investigated interactions between Phytophthora agathidicida (the causal agent of kauri tree dieback) and soil microbial communities, while also comparing detection and community-profiling methods. Soils from 60 kauri trees across three sites in the Waitākere Ranges, New Zealand, were analysed using loop-mediated isothermal amplification (LAMP) for pathogen detection, and 16S rRNA gene/ITS gene amplicon sequencing alongside shotgun metagenomics for community characterisation. LAMP detected P. agathidicida in 39/60 samples, while shotgun sequencing detected Phytophthora-associated DNA at low abundance across all samples. Microbial community structure and functional potential showed weak association with pathogen presence, though differential abundance testing identified several genera enriched in pathogen-detected soils, including taxa previously linked to disease suppression. Amplicon and shotgun profiles indicated broadly comparable patterns at higher taxonomic and functional levels, while differences between approaches emerged primarily at finer taxonomic resolution. Importantly, functional predictions from PICRUSt2 closely matched shotgun-derived profiles at broader scales, indicating its suitability as a cost-effective tool for broad-scale monitoring. These findings suggest limited direct pathogen effects on microbial communities and highlight how integrating molecular approaches provides complementary insights into soil microbiome-pathogen interactions.
Additional Links: PMID-41923466
PubMed:
Citation:
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@article {pmid41923466,
year = {2026},
author = {King, Z and Buckley, HL and Lear, G and Seale, B and Lee, KC and Schwendenmann, L and Lacap-Bugler, DC},
title = {Comparative Amplicon and Shotgun Metagenome Profiling of Soil Microbial Communities in Kauri Forests Affected by Phytophthora agathidicida.},
journal = {Environmental microbiology reports},
volume = {18},
number = {2},
pages = {e70324},
pmid = {41923466},
issn = {1758-2229},
support = {C09X1817//New Zealand's Biological Heritage/ ; //Ministry of Business, Innovation and Employment/ ; },
mesh = {*Phytophthora/genetics/isolation & purification ; *Soil Microbiology ; New Zealand ; RNA, Ribosomal, 16S/genetics ; *Metagenome ; Forests ; *Microbiota ; Plant Diseases/microbiology/parasitology ; Metagenomics ; Bacteria/classification/genetics/isolation & purification ; Nucleic Acid Amplification Techniques ; Phylogeny ; },
abstract = {Soil-borne pathogens can influence microbial communities and ecosystem function, making it important to understand their broader ecological impacts. We investigated interactions between Phytophthora agathidicida (the causal agent of kauri tree dieback) and soil microbial communities, while also comparing detection and community-profiling methods. Soils from 60 kauri trees across three sites in the Waitākere Ranges, New Zealand, were analysed using loop-mediated isothermal amplification (LAMP) for pathogen detection, and 16S rRNA gene/ITS gene amplicon sequencing alongside shotgun metagenomics for community characterisation. LAMP detected P. agathidicida in 39/60 samples, while shotgun sequencing detected Phytophthora-associated DNA at low abundance across all samples. Microbial community structure and functional potential showed weak association with pathogen presence, though differential abundance testing identified several genera enriched in pathogen-detected soils, including taxa previously linked to disease suppression. Amplicon and shotgun profiles indicated broadly comparable patterns at higher taxonomic and functional levels, while differences between approaches emerged primarily at finer taxonomic resolution. Importantly, functional predictions from PICRUSt2 closely matched shotgun-derived profiles at broader scales, indicating its suitability as a cost-effective tool for broad-scale monitoring. These findings suggest limited direct pathogen effects on microbial communities and highlight how integrating molecular approaches provides complementary insights into soil microbiome-pathogen interactions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Phytophthora/genetics/isolation & purification
*Soil Microbiology
New Zealand
RNA, Ribosomal, 16S/genetics
*Metagenome
Forests
*Microbiota
Plant Diseases/microbiology/parasitology
Metagenomics
Bacteria/classification/genetics/isolation & purification
Nucleic Acid Amplification Techniques
Phylogeny
RevDate: 2026-04-02
CmpDate: 2026-04-02
Gut Microbiota and Dyslipidemia in Type 2 Diabetes: A Pilot Study of 16S rRNA Profiles and Predicted Functional Shifts.
Journal of diabetes research, 2026(1):e9317962.
Hyperlipidemia is a major, modifiable driver of global cardiovascular risk. The intestinal microbiota, comprising bacteria, archaea, fungi, and viruses, modulates lipid metabolism through bile acid transformation, energy harvest, and inflammatory signaling. This study profiled the gut microbiota of 15 adults with type 2 diabetes mellitus (T2DM) and explored associations with fasting lipid measures using 16S rRNA gene sequencing (V3-V4 region) on the Illumina MiSeq platform and PICRUSt2 functional prediction. Overall α-diversity was reduced, and community composition was dominated by Firmicutes and Actinobacteria with relative depletion of Bacteroidetes. At lower taxonomic ranks, enrichment of Prevotella copri, Collinsella spp., Ruminococcus spp., and selected Bifidobacterium spp. was observed, alongside depletion of short-chain fatty acid (SCFA)-linked taxa, including Akkermansia muciniphila, Lactobacillus plantarum, and members of the Bacteroides and Parabacteroides lineages. Exploratory within-cohort trends indicated that higher triglycerides (TGs) and lower HDL-C tended to co-occur with increased Collinsella and clostridial signals and reduced SCFA-associated taxa. Predicted Kyoto Encyclopedia of Genes and Genomes (KEGG) ortholog functions suggested shifts in lipid, carbohydrate, and secondary bile acid metabolism, consistent with a metabolically activated and proinflammatory intestinal milieu. In this single-arm cohort of adults with T2DM, a low-diversity, Firmicutes/Actinobacteria-weighted microbiome with depletion of SCFA-linked taxa paralleled an atherogenic lipid profile, supporting an association between gut microbial dysbiosis and lipid abnormalities in adults with T2DM. These findings suggest the potential of microbiota-informed adjuncts, including dietary fermentable fiber, targeted probiotics and next-generation biotherapeutics, and bile-acid-modulating strategies as supportive approaches to lipid management in T2DM. This was a pilot, single-arm, exploratory study without a nondiabetic control group, and findings should be interpreted as hypothesis-generating. Nevertheless, the cross-sectional design, small sample size, and 16S-based taxonomic resolution limit causal interpretation. Larger, longitudinal studies integrating shotgun metagenomics and metabolomics are needed to confirm these associations, validate biomarkers, and elucidate mechanistic pathways that could guide precision interventions for diabetic dyslipidemia.
Additional Links: PMID-41923582
PubMed:
Citation:
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@article {pmid41923582,
year = {2026},
author = {Menezes, GA and Sekar, P and Akhter, A and Tayade, KD and Fathima, S and Hussain, ZFZ and Nigam, A},
title = {Gut Microbiota and Dyslipidemia in Type 2 Diabetes: A Pilot Study of 16S rRNA Profiles and Predicted Functional Shifts.},
journal = {Journal of diabetes research},
volume = {2026},
number = {1},
pages = {e9317962},
pmid = {41923582},
issn = {2314-6753},
mesh = {Humans ; *Gastrointestinal Microbiome/genetics ; *Diabetes Mellitus, Type 2/microbiology/complications/blood ; Pilot Projects ; Middle Aged ; *Dyslipidemias/microbiology/blood ; Male ; *RNA, Ribosomal, 16S/genetics ; Female ; Aged ; Adult ; Bacteria/genetics/classification ; },
abstract = {Hyperlipidemia is a major, modifiable driver of global cardiovascular risk. The intestinal microbiota, comprising bacteria, archaea, fungi, and viruses, modulates lipid metabolism through bile acid transformation, energy harvest, and inflammatory signaling. This study profiled the gut microbiota of 15 adults with type 2 diabetes mellitus (T2DM) and explored associations with fasting lipid measures using 16S rRNA gene sequencing (V3-V4 region) on the Illumina MiSeq platform and PICRUSt2 functional prediction. Overall α-diversity was reduced, and community composition was dominated by Firmicutes and Actinobacteria with relative depletion of Bacteroidetes. At lower taxonomic ranks, enrichment of Prevotella copri, Collinsella spp., Ruminococcus spp., and selected Bifidobacterium spp. was observed, alongside depletion of short-chain fatty acid (SCFA)-linked taxa, including Akkermansia muciniphila, Lactobacillus plantarum, and members of the Bacteroides and Parabacteroides lineages. Exploratory within-cohort trends indicated that higher triglycerides (TGs) and lower HDL-C tended to co-occur with increased Collinsella and clostridial signals and reduced SCFA-associated taxa. Predicted Kyoto Encyclopedia of Genes and Genomes (KEGG) ortholog functions suggested shifts in lipid, carbohydrate, and secondary bile acid metabolism, consistent with a metabolically activated and proinflammatory intestinal milieu. In this single-arm cohort of adults with T2DM, a low-diversity, Firmicutes/Actinobacteria-weighted microbiome with depletion of SCFA-linked taxa paralleled an atherogenic lipid profile, supporting an association between gut microbial dysbiosis and lipid abnormalities in adults with T2DM. These findings suggest the potential of microbiota-informed adjuncts, including dietary fermentable fiber, targeted probiotics and next-generation biotherapeutics, and bile-acid-modulating strategies as supportive approaches to lipid management in T2DM. This was a pilot, single-arm, exploratory study without a nondiabetic control group, and findings should be interpreted as hypothesis-generating. Nevertheless, the cross-sectional design, small sample size, and 16S-based taxonomic resolution limit causal interpretation. Larger, longitudinal studies integrating shotgun metagenomics and metabolomics are needed to confirm these associations, validate biomarkers, and elucidate mechanistic pathways that could guide precision interventions for diabetic dyslipidemia.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/genetics
*Diabetes Mellitus, Type 2/microbiology/complications/blood
Pilot Projects
Middle Aged
*Dyslipidemias/microbiology/blood
Male
*RNA, Ribosomal, 16S/genetics
Female
Aged
Adult
Bacteria/genetics/classification
RevDate: 2026-04-02
CmpDate: 2026-04-02
Emerging synthetic biology-assisted technologies for overcoming antibiotic resistance: CRISPR-Cas, bacteriophage, microbiome, and metabolic engineering-based solutions.
Journal of microbiology (Seoul, Korea), 64(3):e2512002.
Antibiotic resistance has become a critical global health challenge due to the decreased efficacy of existing antibiotics and the emergence of multidrug-resistant pathogens. In particular, the rapid horizontal transfer of resistance genes and the diverse mechanisms by which bacteria acquire resistance have significantly undermined the effectiveness of conventional therapeutic strategies, revealing fundamental limitations in current infectious disease management. In this context, synthetic biology provides a promising framework to overcome the limitations of conventional antibiotics by integrating engineering principles with bioengineering approaches, thereby enabling precise and programmable control of biological processes. These synthetic biology-based approaches offer substantial potential for developing sustainable and highly specific antimicrobial strategies. This review comprehensively examines recent advances in synthetic biology-assisted antimicrobial strategies, including CRISPR-Cas systems, bacteriophage engineering, microbiome engineering, and metabolic engineering-driven antibiotic discovery. Collectively, these approaches represent a precision antimicrobial paradigm that enables selective targeting of resistant bacteria while preserving microbiome homeostasis. These strategies also provide new directions for limiting resistance dissemination and guiding the development of next-generation therapeutics.
Additional Links: PMID-41923586
Publisher:
PubMed:
Citation:
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@article {pmid41923586,
year = {2026},
author = {Oh, Y and Lee, H and Jang, S},
title = {Emerging synthetic biology-assisted technologies for overcoming antibiotic resistance: CRISPR-Cas, bacteriophage, microbiome, and metabolic engineering-based solutions.},
journal = {Journal of microbiology (Seoul, Korea)},
volume = {64},
number = {3},
pages = {e2512002},
doi = {10.71150/jm.2512002},
pmid = {41923586},
issn = {1976-3794},
support = {//National Research Foundation of Korea/ ; RS-2025-02214910//Ministry of Science and ICT/ ; //Incheon National University/ ; },
mesh = {*CRISPR-Cas Systems ; *Synthetic Biology/methods ; *Bacteriophages/genetics ; *Metabolic Engineering/methods ; *Anti-Bacterial Agents/pharmacology ; *Microbiota/genetics ; *Bacteria/drug effects/genetics ; Humans ; *Drug Resistance, Bacterial/genetics ; *Drug Resistance, Microbial/genetics ; },
abstract = {Antibiotic resistance has become a critical global health challenge due to the decreased efficacy of existing antibiotics and the emergence of multidrug-resistant pathogens. In particular, the rapid horizontal transfer of resistance genes and the diverse mechanisms by which bacteria acquire resistance have significantly undermined the effectiveness of conventional therapeutic strategies, revealing fundamental limitations in current infectious disease management. In this context, synthetic biology provides a promising framework to overcome the limitations of conventional antibiotics by integrating engineering principles with bioengineering approaches, thereby enabling precise and programmable control of biological processes. These synthetic biology-based approaches offer substantial potential for developing sustainable and highly specific antimicrobial strategies. This review comprehensively examines recent advances in synthetic biology-assisted antimicrobial strategies, including CRISPR-Cas systems, bacteriophage engineering, microbiome engineering, and metabolic engineering-driven antibiotic discovery. Collectively, these approaches represent a precision antimicrobial paradigm that enables selective targeting of resistant bacteria while preserving microbiome homeostasis. These strategies also provide new directions for limiting resistance dissemination and guiding the development of next-generation therapeutics.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*CRISPR-Cas Systems
*Synthetic Biology/methods
*Bacteriophages/genetics
*Metabolic Engineering/methods
*Anti-Bacterial Agents/pharmacology
*Microbiota/genetics
*Bacteria/drug effects/genetics
Humans
*Drug Resistance, Bacterial/genetics
*Drug Resistance, Microbial/genetics
RevDate: 2026-04-02
Tanshinones from Salvia miltiorrhiza alleviate ulcerative colitis via reprogramming the gut microbiota-metabolite axis.
Acta biochimica et biophysica Sinica [Epub ahead of print].
The anti-inflammatory properties of the traditional herb Salvia miltiorrhiza Bunge are well-established, yet its precise mechanism of action in ulcerative colitis (UC) remains unclear. Herein, we evaluate the therapeutic potential of four major tanshinones-tanshinone IIA (Tan IIA), miltirone, neocryptotanshinone, and dihydrotanshinone I-in a murine dextran sulfate sodium (DSS)-induced colitis model. Our results show that tanshinones effectively alleviate disease severity, suppress systemic and local inflammation, and restore intestinal barrier integrity. Integrated multi-omics analysis reveals that the therapeutic efficacy originates from a comprehensive reprogramming of the gut microbiota-metabolite axis. Specifically, tanshinones reverse colitis-associated dysbiosis and rectify metabolic disturbances in linoleic acid metabolism, bile acid biosynthesis, and amino acid utilization. Correlation network analysis identifies key functional modules linking beneficial microbes (e. g., Akkermansia) to anti-inflammatory lipid mediators and associating pathobionts (e . g., Desulfovibrio) with disrupted bile acid metabolism. Notably, supplementation with Akkermansia muciniphila synergizes with Tan IIA to amplify barrier restoration and metabolic normalization. Our findings establish that tanshinones ameliorate UC through microbiota-driven metabolic reprogramming, wherein the restructured microbial community actively shapes a therapeutic metabolic output. This work elucidates a metabolite-mediated mechanism of action and positions tanshinones as promising microbiome-targeting therapeutics for inflammatory bowel disease.
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@article {pmid41923590,
year = {2026},
author = {Liu, Z and Hui, C and Zhang, G and Yang, H and Wang, Y and Shi, Y and Wang, C and Liu, Y and Gao, X and Wen, Y},
title = {Tanshinones from Salvia miltiorrhiza alleviate ulcerative colitis via reprogramming the gut microbiota-metabolite axis.},
journal = {Acta biochimica et biophysica Sinica},
volume = {},
number = {},
pages = {},
doi = {10.3724/abbs.2026054},
pmid = {41923590},
issn = {1745-7270},
abstract = {The anti-inflammatory properties of the traditional herb Salvia miltiorrhiza Bunge are well-established, yet its precise mechanism of action in ulcerative colitis (UC) remains unclear. Herein, we evaluate the therapeutic potential of four major tanshinones-tanshinone IIA (Tan IIA), miltirone, neocryptotanshinone, and dihydrotanshinone I-in a murine dextran sulfate sodium (DSS)-induced colitis model. Our results show that tanshinones effectively alleviate disease severity, suppress systemic and local inflammation, and restore intestinal barrier integrity. Integrated multi-omics analysis reveals that the therapeutic efficacy originates from a comprehensive reprogramming of the gut microbiota-metabolite axis. Specifically, tanshinones reverse colitis-associated dysbiosis and rectify metabolic disturbances in linoleic acid metabolism, bile acid biosynthesis, and amino acid utilization. Correlation network analysis identifies key functional modules linking beneficial microbes (e. g., Akkermansia) to anti-inflammatory lipid mediators and associating pathobionts (e . g., Desulfovibrio) with disrupted bile acid metabolism. Notably, supplementation with Akkermansia muciniphila synergizes with Tan IIA to amplify barrier restoration and metabolic normalization. Our findings establish that tanshinones ameliorate UC through microbiota-driven metabolic reprogramming, wherein the restructured microbial community actively shapes a therapeutic metabolic output. This work elucidates a metabolite-mediated mechanism of action and positions tanshinones as promising microbiome-targeting therapeutics for inflammatory bowel disease.},
}
RevDate: 2026-04-02
Soil microbial diversity associates with lower prevalence of human bacterial pathogens across global soils.
Cell host & microbe pii:S1931-3128(26)00119-8 [Epub ahead of print].
Soil-inhabiting pathogens threaten human health, but their biogeography and associations with soil biodiversity remain poorly understood. Here, we present global patterns of dominant human bacterial pathogens by integrating 1,602 soil metagenomes from 59 countries across continents. We show that dominant human pathogens are more prevalent (i.e., relative abundance) in wet (tropical and temperate) ecosystems and are particularly abundant in cropland soils. We find a global negative association between soil microbiome diversity and pathogen prevalence. We further reveal a significant and positive correlation between the abundance of dominant human pathogens and both disease virulence and global patterns of mortality associated with infectious diseases. Many dominant pathogens are likely to increase their proportion under global change scenarios. Our work provides a global atlas of dominant soil-inhabiting human pathogens and reveals their biogeography and ecology. These findings can guide the development of effective surveillance and risk management strategies to reduce outbreaks and pandemics.
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@article {pmid41923636,
year = {2026},
author = {Xiong, C and Delgado-Baquerizo, M and Liang, J and Wang, J and Yan, Z and Jensen, SO and Gao, M and Sáez-Sandino, T and Guirado, E and Muñoz-Rojas, M and Román, R and Maestre, FT and Singh, BK},
title = {Soil microbial diversity associates with lower prevalence of human bacterial pathogens across global soils.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.03.011},
pmid = {41923636},
issn = {1934-6069},
abstract = {Soil-inhabiting pathogens threaten human health, but their biogeography and associations with soil biodiversity remain poorly understood. Here, we present global patterns of dominant human bacterial pathogens by integrating 1,602 soil metagenomes from 59 countries across continents. We show that dominant human pathogens are more prevalent (i.e., relative abundance) in wet (tropical and temperate) ecosystems and are particularly abundant in cropland soils. We find a global negative association between soil microbiome diversity and pathogen prevalence. We further reveal a significant and positive correlation between the abundance of dominant human pathogens and both disease virulence and global patterns of mortality associated with infectious diseases. Many dominant pathogens are likely to increase their proportion under global change scenarios. Our work provides a global atlas of dominant soil-inhabiting human pathogens and reveals their biogeography and ecology. These findings can guide the development of effective surveillance and risk management strategies to reduce outbreaks and pandemics.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Clostridioides difficile Colonization and Infection in Pediatric Oncology and Stem Cell Transplant Patients.
Open forum infectious diseases, 13(4):ofag149.
BACKGROUND: Pediatric oncology and hematopoietic stem cell transplant (HSCT) patients have elevated risk for Clostridioides difficile infection (CDI), which can prolong hospitalization and delay chemotherapy. Colonization is an important prelude to symptomatic CDI. We sought to characterize colonization status in these patients.
METHODS: We retrospectively studied 276 stools longitudinally collected over 34 months from 32 HSCT and 12 oncology patients treated at a single tertiary center. Specimens were cultured for C difficile and compared by whole genome sequencing. The fecal microbiome was characterized by 16S rRNA gene sequencing.
RESULTS: Baseline cultures were positive in 16 (50%) HSCT patients and 2 (12%) oncology. On subsequent samples, 64% of patients who were initially negative acquired colonization: 8 of 15 (53%) HSCT and 8 of 10 (80%) oncology. Nine clonal strains and 25 multilocus sequence types were identified by whole genome sequencing, with 4 clones found in both cohorts. Nine patients had different strains at different time points. Seven clonal strains were found in multiple patients. Seven (15.9%) patients had symptomatic CDI. C difficile-positive stools had greater microbial diversity than negative stools in both the oncology cohort (Simpson diversity index, 0.07; 95% CI, .01-.14; P = .03) and the HSCT cohort (0.15; 95% CI, .07-.24; P < .001).
CONCLUSIONS: C difficile acquisition and colonization are common in pediatric oncology and HSCT patients. The high prevalence of clonally related strains in multiple patients suggests that asymptomatic patients may be important reservoirs of this pathogen and lead to symptomatic CDI in some patients. Gut microbial composition may influence the risk of colonization.
Additional Links: PMID-41923890
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@article {pmid41923890,
year = {2026},
author = {Willis, DN and Dubberke, ER and Hayashi, RJ and Tarr, PI and Haslam, DB and Hink, T and Luo, J and Tao, Y and Padhye, A and Hall, EM and Storch, GA},
title = {Clostridioides difficile Colonization and Infection in Pediatric Oncology and Stem Cell Transplant Patients.},
journal = {Open forum infectious diseases},
volume = {13},
number = {4},
pages = {ofag149},
pmid = {41923890},
issn = {2328-8957},
abstract = {BACKGROUND: Pediatric oncology and hematopoietic stem cell transplant (HSCT) patients have elevated risk for Clostridioides difficile infection (CDI), which can prolong hospitalization and delay chemotherapy. Colonization is an important prelude to symptomatic CDI. We sought to characterize colonization status in these patients.
METHODS: We retrospectively studied 276 stools longitudinally collected over 34 months from 32 HSCT and 12 oncology patients treated at a single tertiary center. Specimens were cultured for C difficile and compared by whole genome sequencing. The fecal microbiome was characterized by 16S rRNA gene sequencing.
RESULTS: Baseline cultures were positive in 16 (50%) HSCT patients and 2 (12%) oncology. On subsequent samples, 64% of patients who were initially negative acquired colonization: 8 of 15 (53%) HSCT and 8 of 10 (80%) oncology. Nine clonal strains and 25 multilocus sequence types were identified by whole genome sequencing, with 4 clones found in both cohorts. Nine patients had different strains at different time points. Seven clonal strains were found in multiple patients. Seven (15.9%) patients had symptomatic CDI. C difficile-positive stools had greater microbial diversity than negative stools in both the oncology cohort (Simpson diversity index, 0.07; 95% CI, .01-.14; P = .03) and the HSCT cohort (0.15; 95% CI, .07-.24; P < .001).
CONCLUSIONS: C difficile acquisition and colonization are common in pediatric oncology and HSCT patients. The high prevalence of clonally related strains in multiple patients suggests that asymptomatic patients may be important reservoirs of this pathogen and lead to symptomatic CDI in some patients. Gut microbial composition may influence the risk of colonization.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
The microbiome: regulating anti-tumor immunity.
Frontiers in immunology, 17:1781872.
Microorganisms distributed throughout the human body have always been a complex ecosystem that has long coexisted with other organisms. They are involved in essential key links, such as nutrient absorption, energy regulation, metabolism, toxin clearance, and immune regulation. With a deeper understanding of the microbiome, many studies have shown that the microbiome is also actively involved in the occurrence and development of tumors. The core mechanism of dysregulated microorganisms and their derivatives in the treatment response and toxicity management of tumors is the regulation of the immune function. This article explores the evolution of the microbiome and its impact on the immune function during tumor progression, and focuses on analyzing cutting-edge treatment strategies targeting the microbiome, as well as future research directions and challenges in clinical translation.
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@article {pmid41924284,
year = {2026},
author = {Tao, YL and Wu, XX and Wang, JR and Liu, M and Liu, YN and Lian, YQ and Liang, ZY and Zhu, SF},
title = {The microbiome: regulating anti-tumor immunity.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1781872},
pmid = {41924284},
issn = {1664-3224},
mesh = {Humans ; *Neoplasms/immunology/microbiology/therapy ; Animals ; *Microbiota/immunology ; *Gastrointestinal Microbiome/immunology ; Tumor Microenvironment/immunology ; },
abstract = {Microorganisms distributed throughout the human body have always been a complex ecosystem that has long coexisted with other organisms. They are involved in essential key links, such as nutrient absorption, energy regulation, metabolism, toxin clearance, and immune regulation. With a deeper understanding of the microbiome, many studies have shown that the microbiome is also actively involved in the occurrence and development of tumors. The core mechanism of dysregulated microorganisms and their derivatives in the treatment response and toxicity management of tumors is the regulation of the immune function. This article explores the evolution of the microbiome and its impact on the immune function during tumor progression, and focuses on analyzing cutting-edge treatment strategies targeting the microbiome, as well as future research directions and challenges in clinical translation.},
}
MeSH Terms:
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Humans
*Neoplasms/immunology/microbiology/therapy
Animals
*Microbiota/immunology
*Gastrointestinal Microbiome/immunology
Tumor Microenvironment/immunology
RevDate: 2026-04-02
CmpDate: 2026-04-02
The gut microbiota and sleep in infants: a focus on diurnal rhythmicity patterns.
Gut microbes reports, 3(1):2649096.
Emerging evidence supports a bidirectional relationship between the gut microbiome and sleep, which is partly mediated by the microbiota‒gut‒brain axis. Infancy is a critical window for the establishment of both the gut microbiome and sleep regulation, which we hypothesize to be linked across both short (diurnal) and long (monthly) time scales. In this longitudinal study, we investigated associations between gut microbiota development and sleep patterns in 20 infants at 2, 4, and 6 months of age (n = 163 samples). Infants were continuously monitored across 48-h sampling periods. The gut microbiota profiles were characterized using 16S rRNA gene sequencing; gut melatonin concentrations were measured; sleep data were collected via wearable actimetry, 24-h parent-reported sleep diaries, and the Brief Infant Sleep Questionnaire; and parenting style and behavioral development were assessed. In some infants, bacterial diversity followed diurnal rhythmic patterns. While bacterial rhythmicity was not significantly associated with sleep rhythmicity, infants with higher microbial alpha diversity showed more robust sleep patterns. Infant age emerged as the strongest predictor of gut microbial diversity and melatonin levels. Our findings suggest that gut microbial establishment may support the maturation of sleep‒wake rhythms in early infancy. Further research is needed to elucidate mechanistic roles of the gut microbiome in sleep development.
Additional Links: PMID-41924305
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@article {pmid41924305,
year = {2026},
author = {Kerff, F and Mühlematter, C and Adamov, A and Fast, D and Plüss, S and Zimmermann, P and Kurth, S and Bokulich, NA},
title = {The gut microbiota and sleep in infants: a focus on diurnal rhythmicity patterns.},
journal = {Gut microbes reports},
volume = {3},
number = {1},
pages = {2649096},
pmid = {41924305},
issn = {2993-3935},
abstract = {Emerging evidence supports a bidirectional relationship between the gut microbiome and sleep, which is partly mediated by the microbiota‒gut‒brain axis. Infancy is a critical window for the establishment of both the gut microbiome and sleep regulation, which we hypothesize to be linked across both short (diurnal) and long (monthly) time scales. In this longitudinal study, we investigated associations between gut microbiota development and sleep patterns in 20 infants at 2, 4, and 6 months of age (n = 163 samples). Infants were continuously monitored across 48-h sampling periods. The gut microbiota profiles were characterized using 16S rRNA gene sequencing; gut melatonin concentrations were measured; sleep data were collected via wearable actimetry, 24-h parent-reported sleep diaries, and the Brief Infant Sleep Questionnaire; and parenting style and behavioral development were assessed. In some infants, bacterial diversity followed diurnal rhythmic patterns. While bacterial rhythmicity was not significantly associated with sleep rhythmicity, infants with higher microbial alpha diversity showed more robust sleep patterns. Infant age emerged as the strongest predictor of gut microbial diversity and melatonin levels. Our findings suggest that gut microbial establishment may support the maturation of sleep‒wake rhythms in early infancy. Further research is needed to elucidate mechanistic roles of the gut microbiome in sleep development.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Oleoylethanolamide supplementation enriches Akkermansia muciniphila and modulates intestinal barrier function in adults with obesity: A randomized, double-blind, placebo-controlled trial.
Gut microbes reports, 3(1):2622259.
Targeted modulation of the gut microbiome represents a promising nutritional strategy to support metabolic and intestinal health in overweight and obese adults. Oleoylethanolamide (OEA) is an endogenous lipid mediator that regulates satiety, lipid metabolism, and inflammation, but its effects on the human microbiome are not well defined. In this randomized, double-blind, placebo-controlled trial, 57 adults with obesity (BMI 30-40 kg/m[2]) received either 300 mg of TRPTI, providing 250 mg/day of OEA (n = 28), or placebo (n = 29) for 12 weeks. Outcomes included shotgun metagenomics, microbiome profiling, intestinal barrier and inflammatory biomarkers, and safety measures. OEA was safe and well-tolerated with no adverse changes in clinical biomarkers. Although overall microbial diversity remained stable, OEA induced selective, health-relevant compositional shifts. Notably, Faecalibacterium prausnitzii and Akkermansia muciniphila were enriched. These changes coincided with functional host benefits, including increased occludin at Week 12 and interleukin-2 at Week 6, while reducing interleukin-1β, consistent with improved epithelial barrier dynamics and reduced inflammation. Functional pathway analysis suggested enhanced microbial metabolic and redox capacity. These findings indicate OEA supplementation selectively enriches beneficial gut bacteria - particularly A. muciniphila, while improving gut barrier biomarkers and immune function without disrupting microbiome stability. These findings position OEA as a safe, targeted microbiome-modulating ingredient with potential applications for supporting gut and metabolic health.
Additional Links: PMID-41924306
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@article {pmid41924306,
year = {2026},
author = {Batacan, R and Rao, A and Bajagai, YS and Stanley, D and Briskey, D},
title = {Oleoylethanolamide supplementation enriches Akkermansia muciniphila and modulates intestinal barrier function in adults with obesity: A randomized, double-blind, placebo-controlled trial.},
journal = {Gut microbes reports},
volume = {3},
number = {1},
pages = {2622259},
pmid = {41924306},
issn = {2993-3935},
abstract = {Targeted modulation of the gut microbiome represents a promising nutritional strategy to support metabolic and intestinal health in overweight and obese adults. Oleoylethanolamide (OEA) is an endogenous lipid mediator that regulates satiety, lipid metabolism, and inflammation, but its effects on the human microbiome are not well defined. In this randomized, double-blind, placebo-controlled trial, 57 adults with obesity (BMI 30-40 kg/m[2]) received either 300 mg of TRPTI, providing 250 mg/day of OEA (n = 28), or placebo (n = 29) for 12 weeks. Outcomes included shotgun metagenomics, microbiome profiling, intestinal barrier and inflammatory biomarkers, and safety measures. OEA was safe and well-tolerated with no adverse changes in clinical biomarkers. Although overall microbial diversity remained stable, OEA induced selective, health-relevant compositional shifts. Notably, Faecalibacterium prausnitzii and Akkermansia muciniphila were enriched. These changes coincided with functional host benefits, including increased occludin at Week 12 and interleukin-2 at Week 6, while reducing interleukin-1β, consistent with improved epithelial barrier dynamics and reduced inflammation. Functional pathway analysis suggested enhanced microbial metabolic and redox capacity. These findings indicate OEA supplementation selectively enriches beneficial gut bacteria - particularly A. muciniphila, while improving gut barrier biomarkers and immune function without disrupting microbiome stability. These findings position OEA as a safe, targeted microbiome-modulating ingredient with potential applications for supporting gut and metabolic health.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Cafeteria diet exposure, and not weight gain propensity, impacts gut microbiota of rats - a within laboratory meta-analysis.
Gut microbes reports, 3(1):2649442.
Preclinical studies have implicated the microbiota in body weight control, but its translation to humans remains uncertain, partly owing to methodological variability in assessing the relationship between diet-induced obesity and microbiota composition. We performed an internal meta-analysis to determine whether the propensity for diet-induced obesity, defined by relative weight gain due to a high-fat, high-sugar "cafeteria" diet, is associated with changes in microbiota composition. We collated fecal microbiome data from 12 studies using our validated model of diet-induced obesity (208 male and 74 female Sprague-Dawley rats; 3.5-13 weeks of chow (control) or cafeteria diet) and determined whether the alpha diversity and composition of the gut microbiota differed between obese-prone and obese-resistant rats. We found consistent effects of cafeteria diet exposure on the microbiota, with marked changes in overall composition, and reduced microbial richness and evenness. Furthermore, specific obesity-associated microbial genera, such as Bacteroides and Blautia, were enriched by the cafeteria diet. Critically, alpha diversity measures and the gut microbiota composition did not differ between obese-prone and obese-resistant rats in either diet group. Our findings suggest that while the microbiota is substantially altered by cafeteria diet intake, these changes appear unrelated to individual susceptibility to weight gain, highlighting the role of additional host factors in modulating diet-induced obesity.
Additional Links: PMID-41924307
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@article {pmid41924307,
year = {2026},
author = {Bhagavata Srinivasan, SP and Kendig, MD and Hasebe, K and Kaakoush, NO and Morris, MJ and Leigh, SJ},
title = {Cafeteria diet exposure, and not weight gain propensity, impacts gut microbiota of rats - a within laboratory meta-analysis.},
journal = {Gut microbes reports},
volume = {3},
number = {1},
pages = {2649442},
pmid = {41924307},
issn = {2993-3935},
abstract = {Preclinical studies have implicated the microbiota in body weight control, but its translation to humans remains uncertain, partly owing to methodological variability in assessing the relationship between diet-induced obesity and microbiota composition. We performed an internal meta-analysis to determine whether the propensity for diet-induced obesity, defined by relative weight gain due to a high-fat, high-sugar "cafeteria" diet, is associated with changes in microbiota composition. We collated fecal microbiome data from 12 studies using our validated model of diet-induced obesity (208 male and 74 female Sprague-Dawley rats; 3.5-13 weeks of chow (control) or cafeteria diet) and determined whether the alpha diversity and composition of the gut microbiota differed between obese-prone and obese-resistant rats. We found consistent effects of cafeteria diet exposure on the microbiota, with marked changes in overall composition, and reduced microbial richness and evenness. Furthermore, specific obesity-associated microbial genera, such as Bacteroides and Blautia, were enriched by the cafeteria diet. Critically, alpha diversity measures and the gut microbiota composition did not differ between obese-prone and obese-resistant rats in either diet group. Our findings suggest that while the microbiota is substantially altered by cafeteria diet intake, these changes appear unrelated to individual susceptibility to weight gain, highlighting the role of additional host factors in modulating diet-induced obesity.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Systems analysis of the HPV-microbiome-biofilm triad.
Frontiers in cellular and infection microbiology, 16:1767224.
BACKGROUND: Human papillomavirus (HPV) remains the leading cause of cervical cancer worldwide, however, its pathogenesis cannot be sufficiently explained by viral factors alone. Accumulating evidence highlights the critical role of cervicovaginal microbiome composition and biofilm formation in shaping viral persistence, epithelial barrier disruption and carcinogenic progression.
METHODS: This systems-based integrative synthesis analyzed peer-reviewed literature published between January 2000 and July 2025, retrieved from PubMed and Google Scholar with additional records identified through backward citation screening. The collected data were synthesized to construct a conceptual model of the HPV-microbiome-biofilm triad and to evaluate its clinical and biological implications.
RESULTS: The analysis indicates that depletion of Lactobacillus-dominated communities and expansion of anaerobic taxa, particularly Gardnerella vaginalis, are associated with biofilm development, chronic inflammation and immune modulation. These interrelated processes form self-reinforcing feedback loops that promote HPV persistence and reduce therapeutic efficacy. Microbiome dysbiosis and biofilm formation were further linked to impaired epithelial integrity, altered cytokine signaling pathways and clinically relevant phenotypes including immune escape, metabolic shifts and treatment non-responsiveness.
DISCUSSION: This systems perspective challenges reductionist pathogen-centered models and emphasizes the importance of integrating microbiome profiling and biofilm dynamics into cervical cancer risk stratification and therapeutic strategies. The coupled interactions between microbial communities, host immunity and viral persistence underscore the cervicovaginal ecosystem as an active regulator of disease progression rather than a passive bystander. Incorporating ecosystem-based parameters into clinical decision-making may enhance prognostic assessment and improve treatment outcomes, particularly in low- and middle-income countries where high HPV prevalence coincides with increased microbiome vulnerability.
https://www.crd.york.ac.uk/PROSPERO/, identifier CRD420251208178.
Additional Links: PMID-41924422
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@article {pmid41924422,
year = {2026},
author = {Nazarova, V and Kamzayeva, N and Ukybassova, T and Kozhakhmetov, S and Kushugulova, A},
title = {Systems analysis of the HPV-microbiome-biofilm triad.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1767224},
pmid = {41924422},
issn = {2235-2988},
mesh = {*Biofilms/growth & development ; Humans ; *Microbiota ; Female ; *Papillomavirus Infections/microbiology/virology/immunology ; Dysbiosis/microbiology ; *Papillomaviridae/physiology ; Vagina/microbiology/virology ; Uterine Cervical Neoplasms/virology/microbiology ; },
abstract = {BACKGROUND: Human papillomavirus (HPV) remains the leading cause of cervical cancer worldwide, however, its pathogenesis cannot be sufficiently explained by viral factors alone. Accumulating evidence highlights the critical role of cervicovaginal microbiome composition and biofilm formation in shaping viral persistence, epithelial barrier disruption and carcinogenic progression.
METHODS: This systems-based integrative synthesis analyzed peer-reviewed literature published between January 2000 and July 2025, retrieved from PubMed and Google Scholar with additional records identified through backward citation screening. The collected data were synthesized to construct a conceptual model of the HPV-microbiome-biofilm triad and to evaluate its clinical and biological implications.
RESULTS: The analysis indicates that depletion of Lactobacillus-dominated communities and expansion of anaerobic taxa, particularly Gardnerella vaginalis, are associated with biofilm development, chronic inflammation and immune modulation. These interrelated processes form self-reinforcing feedback loops that promote HPV persistence and reduce therapeutic efficacy. Microbiome dysbiosis and biofilm formation were further linked to impaired epithelial integrity, altered cytokine signaling pathways and clinically relevant phenotypes including immune escape, metabolic shifts and treatment non-responsiveness.
DISCUSSION: This systems perspective challenges reductionist pathogen-centered models and emphasizes the importance of integrating microbiome profiling and biofilm dynamics into cervical cancer risk stratification and therapeutic strategies. The coupled interactions between microbial communities, host immunity and viral persistence underscore the cervicovaginal ecosystem as an active regulator of disease progression rather than a passive bystander. Incorporating ecosystem-based parameters into clinical decision-making may enhance prognostic assessment and improve treatment outcomes, particularly in low- and middle-income countries where high HPV prevalence coincides with increased microbiome vulnerability.
https://www.crd.york.ac.uk/PROSPERO/, identifier CRD420251208178.},
}
MeSH Terms:
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*Biofilms/growth & development
Humans
*Microbiota
Female
*Papillomavirus Infections/microbiology/virology/immunology
Dysbiosis/microbiology
*Papillomaviridae/physiology
Vagina/microbiology/virology
Uterine Cervical Neoplasms/virology/microbiology
RevDate: 2026-04-02
CmpDate: 2026-04-02
Jinzhi and fecal microbiota transplantation: a comparative review of historical and modern microbial therapeutics.
Frontiers in microbiology, 17:1700764.
Since its formal introduction in 1958, fecal microbiota transplantation (FMT) has gained prominence. However, challenges remain in standardizing protocols and optimizing efficacy. This review provides a systematic comparison between the historical practice of Jinzhi and modern FMT, focusing on their preparation methodologies. We hypothesize that specific, underexplored features of Jinzhi preparation could inform and refine current FMT practices. Specifically, we propose that the utilization of adolescent donors, underground low-temperature fermentation, and the careful consideration of seasonal timing, all integral to Jinzhi's traditional protocol, may offer novel insights and testable hypotheses for enhancing microbial diversity, functionality, and therapeutic stability in FMT. By bridging this ancient wisdom with modern microbiome science, we aim to outline a novel and actionable framework for developing the next generation of microbiota-based therapeutics, urging future research to empirically test these historically inspired hypotheses.
Additional Links: PMID-41924474
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@article {pmid41924474,
year = {2026},
author = {Li, M and Dai, L and Yang, Y and Chen, S and Ma, J and Feng, P},
title = {Jinzhi and fecal microbiota transplantation: a comparative review of historical and modern microbial therapeutics.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1700764},
pmid = {41924474},
issn = {1664-302X},
abstract = {Since its formal introduction in 1958, fecal microbiota transplantation (FMT) has gained prominence. However, challenges remain in standardizing protocols and optimizing efficacy. This review provides a systematic comparison between the historical practice of Jinzhi and modern FMT, focusing on their preparation methodologies. We hypothesize that specific, underexplored features of Jinzhi preparation could inform and refine current FMT practices. Specifically, we propose that the utilization of adolescent donors, underground low-temperature fermentation, and the careful consideration of seasonal timing, all integral to Jinzhi's traditional protocol, may offer novel insights and testable hypotheses for enhancing microbial diversity, functionality, and therapeutic stability in FMT. By bridging this ancient wisdom with modern microbiome science, we aim to outline a novel and actionable framework for developing the next generation of microbiota-based therapeutics, urging future research to empirically test these historically inspired hypotheses.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Multi-omics insights into triticale silage as a sustainable alternative to corn silage in heifer diets.
Frontiers in microbiology, 17:1761287.
BACKGROUND: Intensive ruminant production systems rely heavily on corn silage (CS) as a primary forage source; however, its resource-intensive cultivation and environmental constraints necessitate the development of sustainable alternatives.
METHODS: In a 90-day feeding trial, 24 growing heifers were assigned to diets in which CS was replaced by triticale silage (TS) at 0, 25, 50%, or 100% (DM basis). Growth performance, rumen fermentation, ruminal fatty acid (FA) profiles, and integrated rumen microbiome-metabolome interactions were evaluated.
RESULTS: A 25% substitution (TS25) as the optimal level, maintaining growth performance comparable to the control while achieving the lowest feed cost of gain. TS25 improved rumen fermentation (lower A: P and high total VFA), promoted more efficient nitrogen utilization (higher MCP with lower ammonia N), and enriched functionally relevant bacteria associated with fiber degradation and fermentation (e.g., Ruminococcus, Prevotella, and Rikenellaceae_RC9_gut_group). Consistently, TS inclusion shifted ruminal lipid metabolism, increasing UFA proportions and elevating PUFA (TS25 and TS50 increased PUFA by 15.2 and 23.7% vs. control), alongside metabolomic signals indicating upregulation of linoleic acid metabolism and aromatic amino acid biosynthesis pathways. In contrast, TS substitution ≥50% reduced DMI and ADG, impairing feed utilization.
CONCLUSION: Partial replacement of CS with TS at 25% provides a practical, data-supported strategy to improve economic efficiency while maintaining productivity and promoting favorable rumen microbial-metabolic features. This feeding approach may be applicable in water-limited or double-cropping regions, where TS can enhance forage system sustainability without compromising heifer growth.
Additional Links: PMID-41924483
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@article {pmid41924483,
year = {2026},
author = {Niu, Y and Wang, C and Kuang, Y and Ma, X and Nan, S and Zhang, P and Lu, Q and Qi, Y and Nie, C and Wu, Y and Zhang, W},
title = {Multi-omics insights into triticale silage as a sustainable alternative to corn silage in heifer diets.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1761287},
pmid = {41924483},
issn = {1664-302X},
abstract = {BACKGROUND: Intensive ruminant production systems rely heavily on corn silage (CS) as a primary forage source; however, its resource-intensive cultivation and environmental constraints necessitate the development of sustainable alternatives.
METHODS: In a 90-day feeding trial, 24 growing heifers were assigned to diets in which CS was replaced by triticale silage (TS) at 0, 25, 50%, or 100% (DM basis). Growth performance, rumen fermentation, ruminal fatty acid (FA) profiles, and integrated rumen microbiome-metabolome interactions were evaluated.
RESULTS: A 25% substitution (TS25) as the optimal level, maintaining growth performance comparable to the control while achieving the lowest feed cost of gain. TS25 improved rumen fermentation (lower A: P and high total VFA), promoted more efficient nitrogen utilization (higher MCP with lower ammonia N), and enriched functionally relevant bacteria associated with fiber degradation and fermentation (e.g., Ruminococcus, Prevotella, and Rikenellaceae_RC9_gut_group). Consistently, TS inclusion shifted ruminal lipid metabolism, increasing UFA proportions and elevating PUFA (TS25 and TS50 increased PUFA by 15.2 and 23.7% vs. control), alongside metabolomic signals indicating upregulation of linoleic acid metabolism and aromatic amino acid biosynthesis pathways. In contrast, TS substitution ≥50% reduced DMI and ADG, impairing feed utilization.
CONCLUSION: Partial replacement of CS with TS at 25% provides a practical, data-supported strategy to improve economic efficiency while maintaining productivity and promoting favorable rumen microbial-metabolic features. This feeding approach may be applicable in water-limited or double-cropping regions, where TS can enhance forage system sustainability without compromising heifer growth.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Editorial: Role of endophytic/symbiotic fungi in plant growth promotion and disease suppression.
Frontiers in fungal biology, 7:1820241.
Additional Links: PMID-41924563
PubMed:
Citation:
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@article {pmid41924563,
year = {2026},
author = {Santoyo, G and Kumar, A and Orozco-Mosqueda, MDC and de Oliveira Mendes, G},
title = {Editorial: Role of endophytic/symbiotic fungi in plant growth promotion and disease suppression.},
journal = {Frontiers in fungal biology},
volume = {7},
number = {},
pages = {1820241},
pmid = {41924563},
issn = {2673-6128},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Vaginal microbial community state types fail to predict IVF outcomes, whereas Ureaplasma parvum and Lactobacillus iners are negative predictors of implantation, clinical pregnancy, and live birth.
Human reproduction open, 2026(2):hoag018.
STUDY QUESTION: Are previously proposed vaginal microbial community state types (CSTs) valid predictors of IVF success, or do alternative microbial signatures provide stronger associations?
SUMMARY ANSWER: Previously proposed CSTs as predictors of implantation, clinical pregnancy, and live birth were not confirmed, while an interaction between Ureaplasma parvum and Lactobacillus iners emerged as a strong negative predictor.
WHAT IS KNOWN ALREADY: Infertility affects 17% of the global population. Only one-third of treatment cycles of assisted reproductive technologies result in embryo implantation, and even fewer lead to clinical pregnancy or live births. While early findings have spurred the development of microbiome-based tests for success prediction, evidence on supporting their reliability remains inconclusive.
STUDY DESIGN SIZE DURATION: This prospective, single-centre study aimed to validate existing, and identify better, microbial predictors of infertility treatment outcomes. A cohort of 266 infertile female patients (age 18-45 years) undergoing a frozen-thawed embryo transfer cycle in an anovulatory regimen (i.e. a cycle with transfer of an embryo following a previous oocyte retrieval, fertilization, and freezing of embryos) was recruited for the study within a timeframe from May 2017 to March 2019.
The female, infertile patients, aged 18-45 years, were undergoing routine care. Vaginal swabs were taken prior to embryo transfer and subjected to DNA isolation for 16S-based microbiota analysis. Extended demographic and treatment data were recorded. Clinical outcomes were defined as: (i) implantation, confirmed by a positive hCG test, (ii) clinical pregnancy, and (iii) live birth (defined as the birth of a viable infant). Sequencing data were processed in mothur following established pipelines, and microbial composition (taxonomy) as well as microbial diversity (dissimilarity analyses) were determined using the open-source software R. A prediction model for implantation success was built using binary logistic regression based on abundance of putatively predictive microbial taxa.
This study suggests that vaginal microbial CSTs, alpha-diversity, and the ratio of dominant Lactobacillus species do not correlate in statistical terms or in a clinically meaningful manner with implantation and clinical pregnancy (as a surrogate for endometrial receptivity) or with live birth (as a surrogate for ongoing pregnancy viability). However, Ureaplasma parvum and Lactobacillus iners abundances were identified as negative predictors of embryo implantation, clinical pregnancy, and live birth. A subset of women colonized by these taxa experienced drastically reduced embryo implantation and completely failed to achieve clinical pregnancy or give birth to live offspring, suggesting a potential role of these organisms in implantation failure and reproductive outcome, independent of other influencing factors such as age, oestradiol levels, endometrial thickness etc.
LARGE SCALE DATA: The raw sequencing data used for this manuscript are publicly available at the European Nucleotide Archive under accession number PRJEB107113.
This study is a single-centre study warranting further validation cohorts. Given the variable nature of the vaginal microbiota, sample sizes need to be enlarged for better refinement of the analyses. Further, the underlying mechanistical basis of our findings is yet elusive and clinical translation has yet to be established.
While this novel association warrants confirmation, the results caution against reliance on previously suggested CSTs as predictors, and highlight the need for refined, reproducible microbiome-based diagnostics in reproductive medicine.
Financial support was received from the University of Lübeck and the German Center of Infection Research. M.L., A.M., I.P., M.D., and J.R. declare no conflicts of interest. S.G. discloses personal fees from Organon outside the submitted work. T.K.E. discloses honoraria from Ferring; travel support from Ferring, Merck, Theramex, and Gedeon-Richter; and receipt of equipment/materials/laboratory analyses (to institution) from Arthrex, Besins, Merck, and Abbott outside the submitted work. N.H. discloses personal fees from Gedeon Richter, Ferring, and Merck. G.G. reports that his institution received grants or contracts from Besins, Merck, Abbott, Ferring, and Theramex. He has received personal consulting fees, support for travel fees and meeting attendance, and honoraria for lectures or educational events from Organon, Ferring, Merck, Gedeon-Richter, Theramex, Abbott, ReproNovo, Igyxos, OxoLife, Philipps, ReprodWissen, PregLem, Guerbet, Roche, IBSA, and Besins. He also received support for travel and meeting attendance from Merck, Organon, Ferring, Theramex, Gedeon-Richter, and Abbott. Additionally, he holds unpaid leadership positions as a member of the ESHRE Working Group on RIF, the ESHRE Working Group on clinical KPI, and the ESHRE guideline development group on ovarian stimulation. A.S.-M. reports consulting fees and speaker's fees from Merck, Theramex, and Gedeon-Richter as well as travel support from Merck, Theramex, Gedeon-Richter, IBSA, Ferring, and MSD.
Additional Links: PMID-41924635
PubMed:
Citation:
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@article {pmid41924635,
year = {2026},
author = {Graspeuntner, S and Lupatsii, M and Hamala, N and Masuch, A and Depenbusch, M and Pfeffer, I and Schultze-Mosgau, A and Eggersmann, TK and Rupp, J and Griesinger, G},
title = {Vaginal microbial community state types fail to predict IVF outcomes, whereas Ureaplasma parvum and Lactobacillus iners are negative predictors of implantation, clinical pregnancy, and live birth.},
journal = {Human reproduction open},
volume = {2026},
number = {2},
pages = {hoag018},
pmid = {41924635},
issn = {2399-3529},
abstract = {STUDY QUESTION: Are previously proposed vaginal microbial community state types (CSTs) valid predictors of IVF success, or do alternative microbial signatures provide stronger associations?
SUMMARY ANSWER: Previously proposed CSTs as predictors of implantation, clinical pregnancy, and live birth were not confirmed, while an interaction between Ureaplasma parvum and Lactobacillus iners emerged as a strong negative predictor.
WHAT IS KNOWN ALREADY: Infertility affects 17% of the global population. Only one-third of treatment cycles of assisted reproductive technologies result in embryo implantation, and even fewer lead to clinical pregnancy or live births. While early findings have spurred the development of microbiome-based tests for success prediction, evidence on supporting their reliability remains inconclusive.
STUDY DESIGN SIZE DURATION: This prospective, single-centre study aimed to validate existing, and identify better, microbial predictors of infertility treatment outcomes. A cohort of 266 infertile female patients (age 18-45 years) undergoing a frozen-thawed embryo transfer cycle in an anovulatory regimen (i.e. a cycle with transfer of an embryo following a previous oocyte retrieval, fertilization, and freezing of embryos) was recruited for the study within a timeframe from May 2017 to March 2019.
The female, infertile patients, aged 18-45 years, were undergoing routine care. Vaginal swabs were taken prior to embryo transfer and subjected to DNA isolation for 16S-based microbiota analysis. Extended demographic and treatment data were recorded. Clinical outcomes were defined as: (i) implantation, confirmed by a positive hCG test, (ii) clinical pregnancy, and (iii) live birth (defined as the birth of a viable infant). Sequencing data were processed in mothur following established pipelines, and microbial composition (taxonomy) as well as microbial diversity (dissimilarity analyses) were determined using the open-source software R. A prediction model for implantation success was built using binary logistic regression based on abundance of putatively predictive microbial taxa.
This study suggests that vaginal microbial CSTs, alpha-diversity, and the ratio of dominant Lactobacillus species do not correlate in statistical terms or in a clinically meaningful manner with implantation and clinical pregnancy (as a surrogate for endometrial receptivity) or with live birth (as a surrogate for ongoing pregnancy viability). However, Ureaplasma parvum and Lactobacillus iners abundances were identified as negative predictors of embryo implantation, clinical pregnancy, and live birth. A subset of women colonized by these taxa experienced drastically reduced embryo implantation and completely failed to achieve clinical pregnancy or give birth to live offspring, suggesting a potential role of these organisms in implantation failure and reproductive outcome, independent of other influencing factors such as age, oestradiol levels, endometrial thickness etc.
LARGE SCALE DATA: The raw sequencing data used for this manuscript are publicly available at the European Nucleotide Archive under accession number PRJEB107113.
This study is a single-centre study warranting further validation cohorts. Given the variable nature of the vaginal microbiota, sample sizes need to be enlarged for better refinement of the analyses. Further, the underlying mechanistical basis of our findings is yet elusive and clinical translation has yet to be established.
While this novel association warrants confirmation, the results caution against reliance on previously suggested CSTs as predictors, and highlight the need for refined, reproducible microbiome-based diagnostics in reproductive medicine.
Financial support was received from the University of Lübeck and the German Center of Infection Research. M.L., A.M., I.P., M.D., and J.R. declare no conflicts of interest. S.G. discloses personal fees from Organon outside the submitted work. T.K.E. discloses honoraria from Ferring; travel support from Ferring, Merck, Theramex, and Gedeon-Richter; and receipt of equipment/materials/laboratory analyses (to institution) from Arthrex, Besins, Merck, and Abbott outside the submitted work. N.H. discloses personal fees from Gedeon Richter, Ferring, and Merck. G.G. reports that his institution received grants or contracts from Besins, Merck, Abbott, Ferring, and Theramex. He has received personal consulting fees, support for travel fees and meeting attendance, and honoraria for lectures or educational events from Organon, Ferring, Merck, Gedeon-Richter, Theramex, Abbott, ReproNovo, Igyxos, OxoLife, Philipps, ReprodWissen, PregLem, Guerbet, Roche, IBSA, and Besins. He also received support for travel and meeting attendance from Merck, Organon, Ferring, Theramex, Gedeon-Richter, and Abbott. Additionally, he holds unpaid leadership positions as a member of the ESHRE Working Group on RIF, the ESHRE Working Group on clinical KPI, and the ESHRE guideline development group on ovarian stimulation. A.S.-M. reports consulting fees and speaker's fees from Merck, Theramex, and Gedeon-Richter as well as travel support from Merck, Theramex, Gedeon-Richter, IBSA, Ferring, and MSD.},
}
RevDate: 2026-04-02
Response of the mTOR signaling pathway to the reproductive dysfunction of dysbiosis-induced male mice.
Reproductive biology, 26(2):101213 pii:S1642-431X(26)00035-5 [Epub ahead of print].
The mammalian target of rapamycin (mTOR) signaling pathway plays a key role in coordinating several cellular activities in response to environmental signals, thereby influencing metabolism and reproduction. This study aimed to determine the role of mTOR signaling pathway in testicular dysfunction caused by intestinal microbiome imbalance. An antibiotic mixture containing ampicillin, neomycin sulfate, vancomycin, and metronidazole was administered orally to mice for four weeks, and subsequently serum, and tissues were obtained following sacrifice. Glucose, cholesterol, and sex hormone levels were measured in the serum, and real-time PCR was performed using extracts of the ileum and testis to determine the expression of genes associated with pro-inflammatory cytokines, mTOR signals and testosterone synthesis. The levels of glucose and sex hormones in the serum of antibiotic-induced dysbiosis (WD) mice were significantly decreased, while the cholesterol levels were elevated (p < 0.05). The mRNA expression of IL-1β, IL-6 and TNF-α significantly increased in the testis of the WD group (p < 0.05 & p < 0.01), while testosterone synthesis, such as the expression of 3β-HSD and P450scc decreased (p < 0.05). Immunofluorescence revealed the localization of mTOR in the mid-piece and tail of the epididymal spermatozoa. The mRNA expression of mTOR signaling pathway, including Mtor, Raptor, p53, PI3K, Akt1, P70s6k, and Rheb, was significantly upregulated in the testis of the WD group (p < 0.05). Consequently, antibiotic-induced dysbiosis in male mice led to increased secretion of pro-inflammatory cytokines in the testis, decreased serum sex hormone levels, and impaired sperm quality, all of which could be associated with altered regulation of the mTOR signaling pathway.
Additional Links: PMID-41924822
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PubMed:
Citation:
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@article {pmid41924822,
year = {2026},
author = {Gamage, MAGNDMA and Dissanayake, WMN and Yi, YJ},
title = {Response of the mTOR signaling pathway to the reproductive dysfunction of dysbiosis-induced male mice.},
journal = {Reproductive biology},
volume = {26},
number = {2},
pages = {101213},
doi = {10.1016/j.repbio.2026.101213},
pmid = {41924822},
issn = {2300-732X},
abstract = {The mammalian target of rapamycin (mTOR) signaling pathway plays a key role in coordinating several cellular activities in response to environmental signals, thereby influencing metabolism and reproduction. This study aimed to determine the role of mTOR signaling pathway in testicular dysfunction caused by intestinal microbiome imbalance. An antibiotic mixture containing ampicillin, neomycin sulfate, vancomycin, and metronidazole was administered orally to mice for four weeks, and subsequently serum, and tissues were obtained following sacrifice. Glucose, cholesterol, and sex hormone levels were measured in the serum, and real-time PCR was performed using extracts of the ileum and testis to determine the expression of genes associated with pro-inflammatory cytokines, mTOR signals and testosterone synthesis. The levels of glucose and sex hormones in the serum of antibiotic-induced dysbiosis (WD) mice were significantly decreased, while the cholesterol levels were elevated (p < 0.05). The mRNA expression of IL-1β, IL-6 and TNF-α significantly increased in the testis of the WD group (p < 0.05 & p < 0.01), while testosterone synthesis, such as the expression of 3β-HSD and P450scc decreased (p < 0.05). Immunofluorescence revealed the localization of mTOR in the mid-piece and tail of the epididymal spermatozoa. The mRNA expression of mTOR signaling pathway, including Mtor, Raptor, p53, PI3K, Akt1, P70s6k, and Rheb, was significantly upregulated in the testis of the WD group (p < 0.05). Consequently, antibiotic-induced dysbiosis in male mice led to increased secretion of pro-inflammatory cytokines in the testis, decreased serum sex hormone levels, and impaired sperm quality, all of which could be associated with altered regulation of the mTOR signaling pathway.},
}
RevDate: 2026-04-03
Caenorhabditis elegans fed native gut microbiota have altered bioenergetic pathway utilization impacting mitochondrial function and susceptibility to pollutants.
Environmental science. Processes & impacts [Epub ahead of print].
The gut microbiome can influence host health by facilitating digestion, immune function, and xenobiotic metabolism. Microbial metabolites can influence mitochondrial function by shifting bioenergetic pathways, potentially altering sensitivity to mitochondrial toxicants. However, mechanisms through which the gut microbiota can alter mitochondrial function and susceptibility to mitochondrial toxicity are not well characterized. We used the model organism Caenorhabditis elegans and the microbiome kit CeMbio, a characterized collection of native gut commensals, to explore the interactions between gut microbiota, mitochondrial function, and chemical susceptibility. C. elegans grown on selected bacterial strains had varying levels of steady-state whole-body ATP, with an ∼3 fold difference between the highest and lowest strains, as well as 2- and 3-fold changes in antioxidant and mitochondrial unfolded protein gene induction. Further, C. elegans grown on selected bacterial strains showed differential sensitivity to short-term exposure to chemicals that inhibit mitochondrial electron transport chain Complexes I, II, and V, and fatty acid oxidation. To test mechanistically how microbiome-mediated sensitivities could result in chemical susceptibility, we carried out follow-up experiments using the Complex I inhibitor rotenone. We found that C. elegans grown on BIGb0170 (Sphingobacterium multivorum) had much higher lethality after 24- and 48-hour exposures than when grown on MYb10 (Acinetobacter guillouiae), MYb11 (Pseudomonas lurida), and OP50 (Escherichia coli) strains. Metabolomic analysis revealed that C. elegans grown on BIGb0170 had lower amounts of triglycerides and acylcarnitines. ATP levels were partially rescued by supplementing BIGb0170 with pyruvate. This work suggests that BIGb0170 can impact mitochondrial function through changes in metabolite abundance, which can increase sensitivity to the Complex I inhibitor rotenone.
Additional Links: PMID-41925161
PubMed:
Citation:
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@article {pmid41925161,
year = {2026},
author = {Bergemann, CM and Jameson, LE and Kenny-Ganzert, IW and Huayta, J and Castellano-Escuder, P and Sarkar, A and Ilkayeva, OR and Sherwood, DR and Hirschey, MD and Meyer, JN},
title = {Caenorhabditis elegans fed native gut microbiota have altered bioenergetic pathway utilization impacting mitochondrial function and susceptibility to pollutants.},
journal = {Environmental science. Processes & impacts},
volume = {},
number = {},
pages = {},
pmid = {41925161},
issn = {2050-7895},
support = {P42 ES010356/ES/NIEHS NIH HHS/United States ; R01 ES034270/ES/NIEHS NIH HHS/United States ; R35 GM118049/GM/NIGMS NIH HHS/United States ; T32 ES021432/ES/NIEHS NIH HHS/United States ; },
abstract = {The gut microbiome can influence host health by facilitating digestion, immune function, and xenobiotic metabolism. Microbial metabolites can influence mitochondrial function by shifting bioenergetic pathways, potentially altering sensitivity to mitochondrial toxicants. However, mechanisms through which the gut microbiota can alter mitochondrial function and susceptibility to mitochondrial toxicity are not well characterized. We used the model organism Caenorhabditis elegans and the microbiome kit CeMbio, a characterized collection of native gut commensals, to explore the interactions between gut microbiota, mitochondrial function, and chemical susceptibility. C. elegans grown on selected bacterial strains had varying levels of steady-state whole-body ATP, with an ∼3 fold difference between the highest and lowest strains, as well as 2- and 3-fold changes in antioxidant and mitochondrial unfolded protein gene induction. Further, C. elegans grown on selected bacterial strains showed differential sensitivity to short-term exposure to chemicals that inhibit mitochondrial electron transport chain Complexes I, II, and V, and fatty acid oxidation. To test mechanistically how microbiome-mediated sensitivities could result in chemical susceptibility, we carried out follow-up experiments using the Complex I inhibitor rotenone. We found that C. elegans grown on BIGb0170 (Sphingobacterium multivorum) had much higher lethality after 24- and 48-hour exposures than when grown on MYb10 (Acinetobacter guillouiae), MYb11 (Pseudomonas lurida), and OP50 (Escherichia coli) strains. Metabolomic analysis revealed that C. elegans grown on BIGb0170 had lower amounts of triglycerides and acylcarnitines. ATP levels were partially rescued by supplementing BIGb0170 with pyruvate. This work suggests that BIGb0170 can impact mitochondrial function through changes in metabolite abundance, which can increase sensitivity to the Complex I inhibitor rotenone.},
}
RevDate: 2026-04-02
Phage-display immunoprecipitation sequencing reveals distinct antibody signatures against bacterial flagellins associated with treatment response in Crohn's disease.
Clinical and translational gastroenterology pii:01720094-990000000-00569 [Epub ahead of print].
OBJECTIVES: Enhanced immune response against bacterial flagellins among patients with Crohn's disease (CD) is associated with aggressive disease course. However, its association with response to biologic treatment is unknown. We aimed to assess whether treatment response among patients with CD is associated with antibody reaction to bacterial flagellins and related microbial alterations.
METHODS: Thirty-nine patients with active CD (Harvey-Bradshaw Index [HBI]>4 or fecal calprotectin [FCP]>150μg/g) commencing biologic treatment were included. Serum and stool samples were collected at baseline and during treatment at weeks 14, 22 and 52. Serum samples were analyzed using high-throughput phage-display immunoprecipitation sequencing (PhIP-Seq) and fecal samples by DNA shotgun metagenomic sequencing.
RESULTS: Using PhIP-Seq analysis, only the anti-flagellin antibodies library showed consistently attenuated antibody responses against bacterial flagellins in patients achieving remission (HBI≤4 and FCP≤150) versus non-remission at all time points (p<0.05). Of the 55 anti-flagellin antibodies analyzed, 15 showed consistent >1.5-fold over-representation in non-remission samples, with high conservation of amino-acid sequences and targeting of Clostridiales, Lachnospiraceae, or Roseburia species. Remission was associated with increased abundance of flagellin-target taxa including Roseburia intestinalis and decreased Ruminococcus_B gnavus and pathways involved in cellular oxidative stress, while non-remission showed increased Bacteroides species and pathways involved in 5-aminoimidazole ribonucleotide and semi-essential amino acids biosynthesis (q<0.05).
CONCLUSIONS: PhIP-Seq revealed that biologic treatment response in patients with CD associates with consistently decreased antibody responses against specific bacterial flagellins with conserved sequences. These findings identify potential biomarkers and therapeutic targets for improving treatment outcomes.
Additional Links: PMID-41925202
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PubMed:
Citation:
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@article {pmid41925202,
year = {2026},
author = {Leibovitzh, H and Krongauz, D and Schlesinger, Y and Cohen, NA and Hirsch, A and Ron, Y and Thurm, T and Godneva, A and Weinberger, A and Segal, E and Maharshak, N},
title = {Phage-display immunoprecipitation sequencing reveals distinct antibody signatures against bacterial flagellins associated with treatment response in Crohn's disease.},
journal = {Clinical and translational gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.14309/ctg.0000000000001030},
pmid = {41925202},
issn = {2155-384X},
abstract = {OBJECTIVES: Enhanced immune response against bacterial flagellins among patients with Crohn's disease (CD) is associated with aggressive disease course. However, its association with response to biologic treatment is unknown. We aimed to assess whether treatment response among patients with CD is associated with antibody reaction to bacterial flagellins and related microbial alterations.
METHODS: Thirty-nine patients with active CD (Harvey-Bradshaw Index [HBI]>4 or fecal calprotectin [FCP]>150μg/g) commencing biologic treatment were included. Serum and stool samples were collected at baseline and during treatment at weeks 14, 22 and 52. Serum samples were analyzed using high-throughput phage-display immunoprecipitation sequencing (PhIP-Seq) and fecal samples by DNA shotgun metagenomic sequencing.
RESULTS: Using PhIP-Seq analysis, only the anti-flagellin antibodies library showed consistently attenuated antibody responses against bacterial flagellins in patients achieving remission (HBI≤4 and FCP≤150) versus non-remission at all time points (p<0.05). Of the 55 anti-flagellin antibodies analyzed, 15 showed consistent >1.5-fold over-representation in non-remission samples, with high conservation of amino-acid sequences and targeting of Clostridiales, Lachnospiraceae, or Roseburia species. Remission was associated with increased abundance of flagellin-target taxa including Roseburia intestinalis and decreased Ruminococcus_B gnavus and pathways involved in cellular oxidative stress, while non-remission showed increased Bacteroides species and pathways involved in 5-aminoimidazole ribonucleotide and semi-essential amino acids biosynthesis (q<0.05).
CONCLUSIONS: PhIP-Seq revealed that biologic treatment response in patients with CD associates with consistently decreased antibody responses against specific bacterial flagellins with conserved sequences. These findings identify potential biomarkers and therapeutic targets for improving treatment outcomes.},
}
RevDate: 2026-04-02
Microoxic conditions promote Escherichia-associated cellulase expression in the giant panda gut.
The ISME journal pii:8572364 [Epub ahead of print].
Giant pandas possess a carnivore-like gastrointestinal tract yet subsist on bamboo, and their gut communities contain few canonical cellulolytic taxa. We investigated how fiber processing proceeds in this setting by building a species-resolved reference and linking community features to cellular transcriptional profiles and isolate phenotypes. Using culturomics and PacBio HiFi metagenomics, we assembled a species-resolved reference catalog for the panda gut microbiome (Pbac v2; 466 species-level genomes). Community profiling across 142 samples resolved three enterotypes dominated by Escherichia coli (ET-Ecoli), Clostridium SGBP116 (ET-Clos), and Streptococcus alactolyticus (ET-StreA), with ET-Ecoli enriched for tricarboxylic-acid and respiratory-chain modules and showing higher abundance of an endo-β-1,4-glucanase marker. Droplet-based microbial single-cell RNA-seq from four samples (16 659 cells) assigned a substantial share of cellulase-associated transcripts (GH1/GH3/GH5/GH9) in situ to Escherichia and revealed within-species heterogeneity: E. coli subpopulations segregated into respiration-enriched versus three-carbon/anaerobic-like programs, with cellulase/LPMO-linked transcripts concentrated in the former. Guided by these associations, panda-derived E. coli isolates assayed under defined atmospheres showed oxygen-dependent cellulolytic readouts in vitro. Although in vivo oxygen levels were not measured, the convergence of species-resolved community signatures, single-cell attribution and isolate phenotypes indicates that E. coli can contribute to cellulose processing under microoxic conditions in this cohort. The Pbac v2 resource and the integrated workflow (culturomics + HiFi metagenomes, multi-omics, microbial scRNA-seq) provide a template for species-level assignment of microbiome functions in hosts with unconventional diet-physiology combinations.
Additional Links: PMID-41925227
Publisher:
PubMed:
Citation:
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@article {pmid41925227,
year = {2026},
author = {Deng, F and Han, Y and Peng, Y and Xu, Z and Yang, J and He, J and Li, D and Dong, G and Zhang, P and Jiang, H and Chai, J and Wang, C and Zhao, J and Li, Y},
title = {Microoxic conditions promote Escherichia-associated cellulase expression in the giant panda gut.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag068},
pmid = {41925227},
issn = {1751-7370},
abstract = {Giant pandas possess a carnivore-like gastrointestinal tract yet subsist on bamboo, and their gut communities contain few canonical cellulolytic taxa. We investigated how fiber processing proceeds in this setting by building a species-resolved reference and linking community features to cellular transcriptional profiles and isolate phenotypes. Using culturomics and PacBio HiFi metagenomics, we assembled a species-resolved reference catalog for the panda gut microbiome (Pbac v2; 466 species-level genomes). Community profiling across 142 samples resolved three enterotypes dominated by Escherichia coli (ET-Ecoli), Clostridium SGBP116 (ET-Clos), and Streptococcus alactolyticus (ET-StreA), with ET-Ecoli enriched for tricarboxylic-acid and respiratory-chain modules and showing higher abundance of an endo-β-1,4-glucanase marker. Droplet-based microbial single-cell RNA-seq from four samples (16 659 cells) assigned a substantial share of cellulase-associated transcripts (GH1/GH3/GH5/GH9) in situ to Escherichia and revealed within-species heterogeneity: E. coli subpopulations segregated into respiration-enriched versus three-carbon/anaerobic-like programs, with cellulase/LPMO-linked transcripts concentrated in the former. Guided by these associations, panda-derived E. coli isolates assayed under defined atmospheres showed oxygen-dependent cellulolytic readouts in vitro. Although in vivo oxygen levels were not measured, the convergence of species-resolved community signatures, single-cell attribution and isolate phenotypes indicates that E. coli can contribute to cellulose processing under microoxic conditions in this cohort. The Pbac v2 resource and the integrated workflow (culturomics + HiFi metagenomes, multi-omics, microbial scRNA-seq) provide a template for species-level assignment of microbiome functions in hosts with unconventional diet-physiology combinations.},
}
RevDate: 2026-04-02
Harnessing the lung microbiome for precision management of fibrotic lung disease.
Trends in molecular medicine pii:S1471-4914(26)00032-8 [Epub ahead of print].
Interstitial lung diseases, particularly idiopathic pulmonary fibrosis (IPF), have dismal prognoses, with a median survival of 3-5 years, owing to a lack of early biomarkers or effective treatments. This review highlights the lung microbiome as a key biological factor in IPF pathogenesis and a promising therapeutic target. Elevated burdens of pathogenic bacteria, including Streptococcus and Staphylococcus, in bronchoalveolar lavage fluid correlate with accelerated progression and higher mortality. These bacteria release toxins and activate Th17-driven inflammation, providing mechanistic links to alveolar injury and fibrosis. Host genetics and systemic factors, including oral-gut-lung interactions, further shape disease progression. Although antibiotic trials have been unsuccessful, embracing the microbiome as an active participant in IPF may open unprecedented opportunities for personalized interventions.
Additional Links: PMID-41925420
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PubMed:
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@article {pmid41925420,
year = {2026},
author = {Leroy, S and Roméo, B and Belaid, A and Brest, P and Marquette, CH and Vouret-Craviari, V and Hofman, V and Hofman, P and Mograbi, B},
title = {Harnessing the lung microbiome for precision management of fibrotic lung disease.},
journal = {Trends in molecular medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.molmed.2026.02.002},
pmid = {41925420},
issn = {1471-499X},
abstract = {Interstitial lung diseases, particularly idiopathic pulmonary fibrosis (IPF), have dismal prognoses, with a median survival of 3-5 years, owing to a lack of early biomarkers or effective treatments. This review highlights the lung microbiome as a key biological factor in IPF pathogenesis and a promising therapeutic target. Elevated burdens of pathogenic bacteria, including Streptococcus and Staphylococcus, in bronchoalveolar lavage fluid correlate with accelerated progression and higher mortality. These bacteria release toxins and activate Th17-driven inflammation, providing mechanistic links to alveolar injury and fibrosis. Host genetics and systemic factors, including oral-gut-lung interactions, further shape disease progression. Although antibiotic trials have been unsuccessful, embracing the microbiome as an active participant in IPF may open unprecedented opportunities for personalized interventions.},
}
RevDate: 2026-04-02
The rhizosphere microbiome as a decentralized immune system.
Trends in microbiology pii:S0966-842X(26)00065-X [Epub ahead of print].
Plant immunity should be reconsidered beyond the boundaries of the plant genome. We propose that the rhizosphere microbiome may function analogously to a decentralized immune system, contributing adaptive defenselike properties and memory effects. In this forum article, we discuss how this perspective reframes immunity as an emergent property of plant-microbiome interactions, shifting the focus from a solitary host toward an integrated holobiont.
Additional Links: PMID-41925447
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@article {pmid41925447,
year = {2026},
author = {Araujo, ASF and Pereira, APA and de Medeiros, EV and Mendes, LW},
title = {The rhizosphere microbiome as a decentralized immune system.},
journal = {Trends in microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tim.2026.03.006},
pmid = {41925447},
issn = {1878-4380},
abstract = {Plant immunity should be reconsidered beyond the boundaries of the plant genome. We propose that the rhizosphere microbiome may function analogously to a decentralized immune system, contributing adaptive defenselike properties and memory effects. In this forum article, we discuss how this perspective reframes immunity as an emergent property of plant-microbiome interactions, shifting the focus from a solitary host toward an integrated holobiont.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
The Gut Microbiome in Amyotrophic Lateral Sclerosis: Emerging Mechanisms and Therapeutic Potential.
Molecular neurobiology, 63(1):.
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder marked by progressive loss of motor neurons and a median survival of 2 to 3 years after symptom onset. Despite advances in genetics, particularly the identification of mutations in C9ORF72, SOD1, and TDP 43, substantial variability in disease onset and progression remains unexplained. Mounting evidence points to the gut microbiome as a potential modifier of ALS biology. Microbial communities within the intestine influence systemic and central immune responses, energy metabolism, and the bioavailability of nutrients and therapeutic agents. Animal studies reveal that dysbiosis contributes to intestinal barrier dysfunction, immune activation, and altered metabolite production, while supplementation with beneficial metabolites such as butyrate or nicotinamide can delay disease progression and extend survival. Human studies, though inconsistent in their findings, consistently identify microbial imbalances and loss of diversity in subsets of patients. The gut-brain axis provides a plausible framework for these effects, as microbial products can signal through endocrine, neural, and immune pathways to influence central nervous system function. Beyond motor decline, microbiota alterations may also contribute to non-motor symptoms such as depression, anxiety, and gastrointestinal dysfunction, further shaping quality of life. While methodological variability complicates interpretation, integration of microbiome research with host genomics and metabolomics offers a path toward precision medicine. Targeting microbial composition and function may ultimately represent a novel therapeutic approach capable of modifying both disease biology and patient outcomes in ALS.
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@article {pmid41925964,
year = {2026},
author = {Oriquat, G and H, M and Maharana, L and Dhyani, A and Al-Hasnaawei, S and Singh-Chauhan, A and Arora, V and Sharma, J and Sadeghi-Samarjan, R},
title = {The Gut Microbiome in Amyotrophic Lateral Sclerosis: Emerging Mechanisms and Therapeutic Potential.},
journal = {Molecular neurobiology},
volume = {63},
number = {1},
pages = {},
pmid = {41925964},
issn = {1559-1182},
mesh = {*Amyotrophic Lateral Sclerosis/microbiology/therapy ; Humans ; *Gastrointestinal Microbiome/physiology ; Animals ; Dysbiosis ; },
abstract = {Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder marked by progressive loss of motor neurons and a median survival of 2 to 3 years after symptom onset. Despite advances in genetics, particularly the identification of mutations in C9ORF72, SOD1, and TDP 43, substantial variability in disease onset and progression remains unexplained. Mounting evidence points to the gut microbiome as a potential modifier of ALS biology. Microbial communities within the intestine influence systemic and central immune responses, energy metabolism, and the bioavailability of nutrients and therapeutic agents. Animal studies reveal that dysbiosis contributes to intestinal barrier dysfunction, immune activation, and altered metabolite production, while supplementation with beneficial metabolites such as butyrate or nicotinamide can delay disease progression and extend survival. Human studies, though inconsistent in their findings, consistently identify microbial imbalances and loss of diversity in subsets of patients. The gut-brain axis provides a plausible framework for these effects, as microbial products can signal through endocrine, neural, and immune pathways to influence central nervous system function. Beyond motor decline, microbiota alterations may also contribute to non-motor symptoms such as depression, anxiety, and gastrointestinal dysfunction, further shaping quality of life. While methodological variability complicates interpretation, integration of microbiome research with host genomics and metabolomics offers a path toward precision medicine. Targeting microbial composition and function may ultimately represent a novel therapeutic approach capable of modifying both disease biology and patient outcomes in ALS.},
}
MeSH Terms:
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*Amyotrophic Lateral Sclerosis/microbiology/therapy
Humans
*Gastrointestinal Microbiome/physiology
Animals
Dysbiosis
RevDate: 2026-04-02
Integrative Dermatology for Longevity: The Synergy of Topical and Internal Approaches.
Dermatology and therapy [Epub ahead of print].
Skin aging reflects both intrinsic biological decline and extrinsic influences collectively known as the skin exposome, including ultraviolet (UV) radiation, air pollution, psychosocial stress, fatigue, sleep disruption, and suboptimal lifestyle behaviors. These factors contribute to cumulative molecular and structural damage, positioning the skin as both a visible marker of whole-body aging and a target for longevity strategies. This review examines the validity of an integrative "In and Out" approach, combining topical treatments, such as retinoids, peptides, antioxidants, and exosome-based formulations, with internal nutraceuticals including NAD[+] precursors, collagen peptides, polyphenols, and microbiome modulators. By targeting key hallmarks of aging, oxidative stress, inflammation, and epigenetic changes, this dual-modality model has the potential to promote skin regeneration, enhance aesthetic and functional outcomes, and contribute to broader health span optimization. Emerging tools such as skin aging clocks, biomarker-driven personalization, and artificial intelligence (AI)-guided interventions further strengthen this paradigm, establishing a scientifically grounded, preventive, and personalized framework that redefines the role of dermatology in the context of longevity. Personalized strategies that integrate diagnostic tools, lifestyle coaching, and tracking technologies allow for adaptive, dynamic strategies both internally and externally.
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@article {pmid41926038,
year = {2026},
author = {Haykal, D and Flament, F and Balooch, G and Mora, P and Kovylkina, N and Calixto, LS and Mercurio, DG and Sachdev, M and Sundaram, H},
title = {Integrative Dermatology for Longevity: The Synergy of Topical and Internal Approaches.},
journal = {Dermatology and therapy},
volume = {},
number = {},
pages = {},
pmid = {41926038},
issn = {2193-8210},
abstract = {Skin aging reflects both intrinsic biological decline and extrinsic influences collectively known as the skin exposome, including ultraviolet (UV) radiation, air pollution, psychosocial stress, fatigue, sleep disruption, and suboptimal lifestyle behaviors. These factors contribute to cumulative molecular and structural damage, positioning the skin as both a visible marker of whole-body aging and a target for longevity strategies. This review examines the validity of an integrative "In and Out" approach, combining topical treatments, such as retinoids, peptides, antioxidants, and exosome-based formulations, with internal nutraceuticals including NAD[+] precursors, collagen peptides, polyphenols, and microbiome modulators. By targeting key hallmarks of aging, oxidative stress, inflammation, and epigenetic changes, this dual-modality model has the potential to promote skin regeneration, enhance aesthetic and functional outcomes, and contribute to broader health span optimization. Emerging tools such as skin aging clocks, biomarker-driven personalization, and artificial intelligence (AI)-guided interventions further strengthen this paradigm, establishing a scientifically grounded, preventive, and personalized framework that redefines the role of dermatology in the context of longevity. Personalized strategies that integrate diagnostic tools, lifestyle coaching, and tracking technologies allow for adaptive, dynamic strategies both internally and externally.},
}
RevDate: 2026-04-02
The Maternal Brain in Context: Systemic Physiological Changes Across Pregnancy.
Annual review of neuroscience [Epub ahead of print].
During pregnancy, the maternal body undergoes profound, coordinated physiological adaptations to support the developing fetus, including major shifts in immune regulation and dramatic changes in the vascular system. Accompanying these peripheral adaptations, recent longitudinal studies in humans point to significant remodeling of the nervous system, occurring in lockstep with increases in gonadal hormone production. To understand the neural adaptations tied to pregnancy and the postpartum period, a holistic approach is essential-one that accounts for changes across multiple peripheral systems. In this review, we consider the impact of the endocrine, cardiovascular, microbiome, and immune systems on the maternal brain. By adopting this integrative approach, we aim to better understand the biological pathways that shape the maternal brain during normative pregnancies and those marked by adverse events.
Additional Links: PMID-41926198
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@article {pmid41926198,
year = {2026},
author = {Grotzinger, H and Martínez-García, M and Miller, EC and Stelzer, IA and Collado, MC and Jacobs, EG},
title = {The Maternal Brain in Context: Systemic Physiological Changes Across Pregnancy.},
journal = {Annual review of neuroscience},
volume = {},
number = {},
pages = {},
doi = {10.1146/annurev-neuro-102124-043515},
pmid = {41926198},
issn = {1545-4126},
abstract = {During pregnancy, the maternal body undergoes profound, coordinated physiological adaptations to support the developing fetus, including major shifts in immune regulation and dramatic changes in the vascular system. Accompanying these peripheral adaptations, recent longitudinal studies in humans point to significant remodeling of the nervous system, occurring in lockstep with increases in gonadal hormone production. To understand the neural adaptations tied to pregnancy and the postpartum period, a holistic approach is essential-one that accounts for changes across multiple peripheral systems. In this review, we consider the impact of the endocrine, cardiovascular, microbiome, and immune systems on the maternal brain. By adopting this integrative approach, we aim to better understand the biological pathways that shape the maternal brain during normative pregnancies and those marked by adverse events.},
}
RevDate: 2026-04-02
CmpDate: 2026-04-02
Analysis of the Impact of Preterm Premature Rupture of Membranes (PPROM) on Maternal and Infant Outcomes and Countermeasures.
International journal of women's health, 18:534571.
OBJECTIVE: This study aimed to analyze the risk factors for Preterm Premature Rupture of Membranes (PPROM) and evaluate the impact of the timing of antibiotic administration on maternal and neonatal outcomes.
METHODS: A retrospective cohort study was conducted involving 480 pregnant women (240 with PPROM and 240 without PPROM) hospitalized between January 2021 and December 2022. Maternal data, genital microbiome profiles, and pregnancy outcomes were collected and compared. Within the PPROM group, patients were subdivided into an Early Treatment group (received intravenous cefuroxime sodium within 12 hours of membrane rupture, n=120) and a Late Treatment group (received antibiotics after 12 hours, n=120). Statistical analyses were performed using SPSS 22.0.
RESULTS: Genital infections (73.8% vs 20.4%, p<0.001) and gestational diabetes mellitus (GDM; 53.3% vs 22.9%, p<0.001) were significantly more prevalent in the PPROM group and were identified as independent risk factors (Genital infections: OR=3.895; GDM: OR=11.166). The PPROM group had worse outcomes, including a higher cesarean section rate (39.2% vs 25.8%, p=0.002) and higher incidences of neonatal asphyxia (4.2% vs 0.4%, p=0.006) and sepsis (2.5% vs 0%, p=0.040). Compared to the Late Treatment group, the Early Treatment group demonstrated significantly lower rates of intrauterine infection (1.67% vs 7.50%, p<0.05), cesarean section (30.0% vs 48.3%, p<0.05), neonatal asphyxia (0.83% vs 7.50%, p<0.01), and neonatal sepsis (0% vs 5.00%, p<0.05).
CONCLUSION: Genital tract infections and GDM are significant risk factors for PPROM. Early administration of antibiotics within 12 hours of membrane rupture is associated with substantially improved maternal and neonatal outcomes, underscoring its critical importance in clinical management.
Additional Links: PMID-41926522
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@article {pmid41926522,
year = {2026},
author = {Chen, Y and Zhou, D and Tu, Y and Wang, Y},
title = {Analysis of the Impact of Preterm Premature Rupture of Membranes (PPROM) on Maternal and Infant Outcomes and Countermeasures.},
journal = {International journal of women's health},
volume = {18},
number = {},
pages = {534571},
pmid = {41926522},
issn = {1179-1411},
abstract = {OBJECTIVE: This study aimed to analyze the risk factors for Preterm Premature Rupture of Membranes (PPROM) and evaluate the impact of the timing of antibiotic administration on maternal and neonatal outcomes.
METHODS: A retrospective cohort study was conducted involving 480 pregnant women (240 with PPROM and 240 without PPROM) hospitalized between January 2021 and December 2022. Maternal data, genital microbiome profiles, and pregnancy outcomes were collected and compared. Within the PPROM group, patients were subdivided into an Early Treatment group (received intravenous cefuroxime sodium within 12 hours of membrane rupture, n=120) and a Late Treatment group (received antibiotics after 12 hours, n=120). Statistical analyses were performed using SPSS 22.0.
RESULTS: Genital infections (73.8% vs 20.4%, p<0.001) and gestational diabetes mellitus (GDM; 53.3% vs 22.9%, p<0.001) were significantly more prevalent in the PPROM group and were identified as independent risk factors (Genital infections: OR=3.895; GDM: OR=11.166). The PPROM group had worse outcomes, including a higher cesarean section rate (39.2% vs 25.8%, p=0.002) and higher incidences of neonatal asphyxia (4.2% vs 0.4%, p=0.006) and sepsis (2.5% vs 0%, p=0.040). Compared to the Late Treatment group, the Early Treatment group demonstrated significantly lower rates of intrauterine infection (1.67% vs 7.50%, p<0.05), cesarean section (30.0% vs 48.3%, p<0.05), neonatal asphyxia (0.83% vs 7.50%, p<0.01), and neonatal sepsis (0% vs 5.00%, p<0.05).
CONCLUSION: Genital tract infections and GDM are significant risk factors for PPROM. Early administration of antibiotics within 12 hours of membrane rupture is associated with substantially improved maternal and neonatal outcomes, underscoring its critical importance in clinical management.},
}
RevDate: 2026-04-02
Maternal Preconception Antibiotic Exposure Disrupts Microbial Succession: A Transgenerational Risk for Offspring Gut Mucosal Immaturity and Colitis Susceptibility.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
The early-life microbiome plays a pivotal role in host development and lifelong health. Maternal factors are increasingly recognized as crucial in shaping offspring microbiome. However, how maternal preconception perturbations affects offspring health remain unclear. Thus, we combined animal and clinical data to elucidate whether preconception microbial perturbations disrupt microbial succession and increase offspring susceptibility to colitis. In animals, preconception antibiotic exposure induced long-lasting disruptions in offspring microbial ecology, through enhanced maternal-offspring microbial transmission, altered microbial developmental trajectories, and increased selective pressures during microbial community assembly. Ultimately, these alterations resulted in persistent gut mucosal immaturity and heightened susceptibility to colitis in adulthood. Complementary clinical studies revealed concordant alterations in gut microbiome and metabolome of children with inflammatory bowel disease (IBD) and their seemingly healthy mothers, characterized by pro-inflammatory taxa and metabolites. Notably, mothers of IBD children reported significantly higher antibiotic exposure than controls, which was also associated with enhanced maternal-offspring microbial transmission and increased selective pressures during microbial community assembly. Our findings reveal a potential intergenerational mechanism in which preconception perturbations are associated with disrupted microbial succession, transgenerational propagation of gut mucosal immaturity, and susceptibility to colitis. These results underscore the importance of judicious antibiotic use during the often-overlooked preconception period.
Additional Links: PMID-41926667
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@article {pmid41926667,
year = {2026},
author = {Chen, Y and Duan, R and Zhang, C and Li, G and Ji, X and Zhang, Q and Pei, F and Wang, K and Duan, L},
title = {Maternal Preconception Antibiotic Exposure Disrupts Microbial Succession: A Transgenerational Risk for Offspring Gut Mucosal Immaturity and Colitis Susceptibility.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e16931},
doi = {10.1002/advs.202516931},
pmid = {41926667},
issn = {2198-3844},
support = {2021YFA1301300//National Key R&D Program of China/ ; 82470578//National Natural Science Foundation of China/ ; 7254451//Beijing Natural Science Foundation/ ; },
abstract = {The early-life microbiome plays a pivotal role in host development and lifelong health. Maternal factors are increasingly recognized as crucial in shaping offspring microbiome. However, how maternal preconception perturbations affects offspring health remain unclear. Thus, we combined animal and clinical data to elucidate whether preconception microbial perturbations disrupt microbial succession and increase offspring susceptibility to colitis. In animals, preconception antibiotic exposure induced long-lasting disruptions in offspring microbial ecology, through enhanced maternal-offspring microbial transmission, altered microbial developmental trajectories, and increased selective pressures during microbial community assembly. Ultimately, these alterations resulted in persistent gut mucosal immaturity and heightened susceptibility to colitis in adulthood. Complementary clinical studies revealed concordant alterations in gut microbiome and metabolome of children with inflammatory bowel disease (IBD) and their seemingly healthy mothers, characterized by pro-inflammatory taxa and metabolites. Notably, mothers of IBD children reported significantly higher antibiotic exposure than controls, which was also associated with enhanced maternal-offspring microbial transmission and increased selective pressures during microbial community assembly. Our findings reveal a potential intergenerational mechanism in which preconception perturbations are associated with disrupted microbial succession, transgenerational propagation of gut mucosal immaturity, and susceptibility to colitis. These results underscore the importance of judicious antibiotic use during the often-overlooked preconception period.},
}
RevDate: 2026-04-02
Immune Checkpoint Inhibitors and Immunomodulators for Cancer Immunotherapy: Insights Into Resistance and Therapeutic Strategies.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
Cancer immunotherapy has redefined cancer treatment. However, the molecular and cellular basis of immune evasion and therapeutic resistance remains incompletely understood. Early immune checkpoint inhibitors have delivered significant clinical benefit, but their efficacy and durability remain limited in many patients. These limitations have driven the exploration of next-generation immune checkpoints and additional regulatory pathways that shape tumor-immune interactions. Recent advances have broadened the immune checkpoint landscape and revealed new targets. These targets operate within interconnected networks shaped by tumor-intrinsic alterations, microenvironmental cues, the microbiome, and neuroimmune crosstalk. The application of emerging technologies has enabled high-resolution dissection of immune-tumor dynamics, providing a technological foundation for improving clinical outcomes through precise patient stratification and intervention. Furthermore, distinct regulated cell deaths, including apoptosis, ferroptosis, pyroptosis, necroptosis, and alkaliptosis, are increasingly recognized as critical modulators of antitumor immunity. Harnessing these mechanisms offers a rational path toward designing targeted and controllable therapeutic strategies that enhance the efficacy and durability of cancer immunotherapy.
Additional Links: PMID-41926670
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@article {pmid41926670,
year = {2026},
author = {Chen, F and Yu, Y and Cai, X and Lin, J and Liang, R and Kang, R and Tang, D and Liu, J},
title = {Immune Checkpoint Inhibitors and Immunomodulators for Cancer Immunotherapy: Insights Into Resistance and Therapeutic Strategies.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e21355},
doi = {10.1002/advs.202521355},
pmid = {41926670},
issn = {2198-3844},
support = {32500653//National Natural Science Foundation of China/ ; 20261A031076//Guangzhou Health Science and Technology Young Talents Cultivation Program/ ; 2025M782596//China Postdoctoral Science Foundation/ ; GZC20251317//Postdoctoral Fellowship Program of China Postdoctoral Science Foundation/ ; 2024A03J0895//Guangzhou Municipal Science and Technology Bureau/ ; },
abstract = {Cancer immunotherapy has redefined cancer treatment. However, the molecular and cellular basis of immune evasion and therapeutic resistance remains incompletely understood. Early immune checkpoint inhibitors have delivered significant clinical benefit, but their efficacy and durability remain limited in many patients. These limitations have driven the exploration of next-generation immune checkpoints and additional regulatory pathways that shape tumor-immune interactions. Recent advances have broadened the immune checkpoint landscape and revealed new targets. These targets operate within interconnected networks shaped by tumor-intrinsic alterations, microenvironmental cues, the microbiome, and neuroimmune crosstalk. The application of emerging technologies has enabled high-resolution dissection of immune-tumor dynamics, providing a technological foundation for improving clinical outcomes through precise patient stratification and intervention. Furthermore, distinct regulated cell deaths, including apoptosis, ferroptosis, pyroptosis, necroptosis, and alkaliptosis, are increasingly recognized as critical modulators of antitumor immunity. Harnessing these mechanisms offers a rational path toward designing targeted and controllable therapeutic strategies that enhance the efficacy and durability of cancer immunotherapy.},
}
RevDate: 2026-04-02
Humic acid supplementation modulates ruminal and fecal microbial communities in lamb.
Research in veterinary science, 205:106166 pii:S0034-5288(26)00119-0 [Epub ahead of print].
The gastrointestinal microbiome affects the health and productivity of animals. Modifying these traits with additives may enhance their effects, making it a relevant strategy. This study investigated the effects of humic acids (HA) on the ruminal and fecal microbiomes of lambs and its potential adherence to ruminal mucosa. Twenty weaned Hampshire Down crossbred lambs aged 102.1 ± 6.6 days with an average body weight of 24.2 ± 3.5 kg were randomly allocated into two groups. Control group was fed a basal diet without HA, and treatment group was fed a basal diet with commercial HA at a dose of 500 mg/kg BW/day for 56 days. At the end of the experiment, ruminal and fecal samples were analyzed using 16S rRNA gene sequencing, and ruminal mucosal tissue from the slaughtered lambs was evaluated using histology and scanning electron microscopy (SEM). The addition of HA to the feed of lambs increased the relative abundance of the genus Bifidobacterium and decreased the genus Lachnospiraceae CAG-127 in the ruminal microbiome of lambs. Furthermore, an increase in the relative abundance of the genera Acutalibacteraceae UBA5905 and Lachnospiraceae VUNI01, along with a reduction in the order Campylobacterales and the genus Acutalibacteraceae CAG-180 was observed in the fecal microbiome. HA was not found in the ruminal mucosa of lambs, as determined by histology or SEM. HA supplementation modulated the ruminal and fecal microbiomes of lambs by reducing harmful and increasing beneficial bacteria, highlighting its potential as a functional feed additive to support ovine gut health.
Additional Links: PMID-41926812
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@article {pmid41926812,
year = {2026},
author = {Santana, DAD and Rolinski, F and Trombetta, LG and Göhringer, RMD and Lipinski, LC and Weber, SH and Sotomaior, CS and Ollhoff, RD},
title = {Humic acid supplementation modulates ruminal and fecal microbial communities in lamb.},
journal = {Research in veterinary science},
volume = {205},
number = {},
pages = {106166},
doi = {10.1016/j.rvsc.2026.106166},
pmid = {41926812},
issn = {1532-2661},
abstract = {The gastrointestinal microbiome affects the health and productivity of animals. Modifying these traits with additives may enhance their effects, making it a relevant strategy. This study investigated the effects of humic acids (HA) on the ruminal and fecal microbiomes of lambs and its potential adherence to ruminal mucosa. Twenty weaned Hampshire Down crossbred lambs aged 102.1 ± 6.6 days with an average body weight of 24.2 ± 3.5 kg were randomly allocated into two groups. Control group was fed a basal diet without HA, and treatment group was fed a basal diet with commercial HA at a dose of 500 mg/kg BW/day for 56 days. At the end of the experiment, ruminal and fecal samples were analyzed using 16S rRNA gene sequencing, and ruminal mucosal tissue from the slaughtered lambs was evaluated using histology and scanning electron microscopy (SEM). The addition of HA to the feed of lambs increased the relative abundance of the genus Bifidobacterium and decreased the genus Lachnospiraceae CAG-127 in the ruminal microbiome of lambs. Furthermore, an increase in the relative abundance of the genera Acutalibacteraceae UBA5905 and Lachnospiraceae VUNI01, along with a reduction in the order Campylobacterales and the genus Acutalibacteraceae CAG-180 was observed in the fecal microbiome. HA was not found in the ruminal mucosa of lambs, as determined by histology or SEM. HA supplementation modulated the ruminal and fecal microbiomes of lambs by reducing harmful and increasing beneficial bacteria, highlighting its potential as a functional feed additive to support ovine gut health.},
}
RevDate: 2026-04-02
Microbial community dynamics and functional potential in response to organic micropollutants in river sediments.
Marine pollution bulletin, 229:119679 pii:S0025-326X(26)00466-2 [Epub ahead of print].
Freshwater river sediments are increasingly exposed to complex mixtures of anthropogenic contaminants, yet the ecological repercussions on indigenous microbial communities -the main drivers of biogeochemical cycling- remain poorly understood. Previous investigations have focused primarily on contaminant occurrence, with no integrated assessment linking sediment contamination to microbial community structure and function. The objective of this study is to characterize the microbiome of the Upper Litani River Basin and to determine how chronic inputs of pharmaceuticals and aromatic hydrocarbons influence taxonomic composition, diversity, and predicted metabolic functions. 54 sediment samples were collected across nine locations during consecutive wet and dry seasons. Target organic micropollutants were quantified in the river sediments using validated analytical methods, and spatiotemporal patterns in microbial composition and metabolic functional potential were determined using amplicon sequencing. Across all samples, 45 phyla were identified, with Pseudomonadota, Bacillota, and Actinomycetota consistently being the dominant taxa. At the genus level, microbial communities were dominated by Acinetobacter, Exiguobacterium, Proteiniclasticum, Planococcus, and Clostridium sensu stricto. Variations in microbial community structure were correlated with the occurrence and concentrations of specific organic micropollutants detected in the sediments, namely with the pharmaceuticals ibuprofen, clomipramine and atenolol, as well as the hydrocarbons o-xylene and toluene. Functional predictions revealed a microbiome highly oriented toward chemoheterotrophic metabolism, underscoring the community's response to persistent organic enrichment. Collectively, these results demonstrate that pollutant concentrations and chemical profiles act as a major ecological force that shapes sediment microbial community dynamics and metabolic function in impacted freshwater ecosystems.
Additional Links: PMID-41926825
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PubMed:
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@article {pmid41926825,
year = {2026},
author = {Ali Ahmad, F and Salam, DA},
title = {Microbial community dynamics and functional potential in response to organic micropollutants in river sediments.},
journal = {Marine pollution bulletin},
volume = {229},
number = {},
pages = {119679},
doi = {10.1016/j.marpolbul.2026.119679},
pmid = {41926825},
issn = {1879-3363},
abstract = {Freshwater river sediments are increasingly exposed to complex mixtures of anthropogenic contaminants, yet the ecological repercussions on indigenous microbial communities -the main drivers of biogeochemical cycling- remain poorly understood. Previous investigations have focused primarily on contaminant occurrence, with no integrated assessment linking sediment contamination to microbial community structure and function. The objective of this study is to characterize the microbiome of the Upper Litani River Basin and to determine how chronic inputs of pharmaceuticals and aromatic hydrocarbons influence taxonomic composition, diversity, and predicted metabolic functions. 54 sediment samples were collected across nine locations during consecutive wet and dry seasons. Target organic micropollutants were quantified in the river sediments using validated analytical methods, and spatiotemporal patterns in microbial composition and metabolic functional potential were determined using amplicon sequencing. Across all samples, 45 phyla were identified, with Pseudomonadota, Bacillota, and Actinomycetota consistently being the dominant taxa. At the genus level, microbial communities were dominated by Acinetobacter, Exiguobacterium, Proteiniclasticum, Planococcus, and Clostridium sensu stricto. Variations in microbial community structure were correlated with the occurrence and concentrations of specific organic micropollutants detected in the sediments, namely with the pharmaceuticals ibuprofen, clomipramine and atenolol, as well as the hydrocarbons o-xylene and toluene. Functional predictions revealed a microbiome highly oriented toward chemoheterotrophic metabolism, underscoring the community's response to persistent organic enrichment. Collectively, these results demonstrate that pollutant concentrations and chemical profiles act as a major ecological force that shapes sediment microbial community dynamics and metabolic function in impacted freshwater ecosystems.},
}
RevDate: 2026-04-02
The vaginal microbiome and HIV acquisition risk.
The lancet. HIV pii:S2352-3018(26)00032-9 [Epub ahead of print].
Non-optimal vaginal bacteriomes, vulvovaginal candidiasis, and sexually transmitted infections have been associated with increased risk of HIV acquisition in multiple clinical studies. However, there are still major gaps in our understanding of the role of the vaginal microbiome in HIV acquisition risk and non-bacterial components of the vaginal microbiome are not well characterised. Additionally, the functional interactions between the vaginal microbiome and its host that can result in increased risk of HIV acquisition are not fully understood. Better vaginal microbiome diagnostics and therapeutics feasible for implementation in settings with insufficient financial, human, and infrastructural resources are needed, and the effects of vaginal microbiome interventions on HIV risk need to be clinically evaluated. Progress is being made towards effective interventions through advanced omics technologies and improved in-vitro models that more accurately represent the complexity of the female genital tract. However, continued research and investments are needed to address this important women's health issue.
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@article {pmid41926978,
year = {2026},
author = {Masson, L and Radzey, N and Abrahams, AG and Ngcapu, S and McKinnon, L and Jaspan, HB},
title = {The vaginal microbiome and HIV acquisition risk.},
journal = {The lancet. HIV},
volume = {},
number = {},
pages = {},
doi = {10.1016/S2352-3018(26)00032-9},
pmid = {41926978},
issn = {2352-3018},
abstract = {Non-optimal vaginal bacteriomes, vulvovaginal candidiasis, and sexually transmitted infections have been associated with increased risk of HIV acquisition in multiple clinical studies. However, there are still major gaps in our understanding of the role of the vaginal microbiome in HIV acquisition risk and non-bacterial components of the vaginal microbiome are not well characterised. Additionally, the functional interactions between the vaginal microbiome and its host that can result in increased risk of HIV acquisition are not fully understood. Better vaginal microbiome diagnostics and therapeutics feasible for implementation in settings with insufficient financial, human, and infrastructural resources are needed, and the effects of vaginal microbiome interventions on HIV risk need to be clinically evaluated. Progress is being made towards effective interventions through advanced omics technologies and improved in-vitro models that more accurately represent the complexity of the female genital tract. However, continued research and investments are needed to address this important women's health issue.},
}
RevDate: 2026-04-02
Increased gastrointestinal cancer risk in cystic fibrosis: Screening, prevention, and future directions.
Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society pii:S1569-1993(26)00092-5 [Epub ahead of print].
The marked improvement in life expectancy from advances in treatment for cystic fibrosis has focused attention on diseases of aging. Cystic fibrosis (CF) is associated with increased risk for digestive system malignancies, including colorectal cancer and pancreaticobiliary cancers. Although risk factors for gastrointestinal malignancy include solid organ transplant and older age, people with CF may present with cancer at a younger age than the general population. Potential mechanisms for increased digestive cancer susceptibility include the underlying genetic defect, dietary patterns, or alterations in the gut microbiome. The impact of cystic fibrosis transmembrane regulator modulator therapies on gastrointestinal cancer risk remains unclear. Our review summarizes the previously published consensus screening recommendations for colorectal cancer, which endorsed starting colonoscopy at age 30 in patients with history of transplant and at age 40 in patients without a transplant. Recent work evaluating the use of non invasive testing for colorectal cancer is reviewed. We propose screening practices for non-colorectal cancers based on the limited evidence to date. We discuss potential preventative approaches and conclude with future directions to improve our ability to address this growing problem. Future work should focus on a greater understanding of the underlying mechanisms of pathogenesis at a molecular level, clinical risk factors for gastrointestinal malignancies at a population level, and preventative strategies.
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@article {pmid41927358,
year = {2026},
author = {Cummings, LC and Freedman, SD},
title = {Increased gastrointestinal cancer risk in cystic fibrosis: Screening, prevention, and future directions.},
journal = {Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jcf.2026.03.024},
pmid = {41927358},
issn = {1873-5010},
abstract = {The marked improvement in life expectancy from advances in treatment for cystic fibrosis has focused attention on diseases of aging. Cystic fibrosis (CF) is associated with increased risk for digestive system malignancies, including colorectal cancer and pancreaticobiliary cancers. Although risk factors for gastrointestinal malignancy include solid organ transplant and older age, people with CF may present with cancer at a younger age than the general population. Potential mechanisms for increased digestive cancer susceptibility include the underlying genetic defect, dietary patterns, or alterations in the gut microbiome. The impact of cystic fibrosis transmembrane regulator modulator therapies on gastrointestinal cancer risk remains unclear. Our review summarizes the previously published consensus screening recommendations for colorectal cancer, which endorsed starting colonoscopy at age 30 in patients with history of transplant and at age 40 in patients without a transplant. Recent work evaluating the use of non invasive testing for colorectal cancer is reviewed. We propose screening practices for non-colorectal cancers based on the limited evidence to date. We discuss potential preventative approaches and conclude with future directions to improve our ability to address this growing problem. Future work should focus on a greater understanding of the underlying mechanisms of pathogenesis at a molecular level, clinical risk factors for gastrointestinal malignancies at a population level, and preventative strategies.},
}
RevDate: 2026-04-02
Letter to the Editor re: "Age-related changes in the urinary microbiome of healthy Japanese children".
Additional Links: PMID-41927378
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@article {pmid41927378,
year = {2026},
author = {Cai, Z and Han, C},
title = {Letter to the Editor re: "Age-related changes in the urinary microbiome of healthy Japanese children".},
journal = {Journal of pediatric urology},
volume = {},
number = {},
pages = {105884},
doi = {10.1016/j.jpurol.2026.105884},
pmid = {41927378},
issn = {1873-4898},
}
RevDate: 2026-04-01
Terracing influences soil microbial assembly in citrus orchards: stochastic processes dominate community dynamics in a karst sloping land.
BMC microbiology, 26(1):.
BACKGROUND: Terracing is a key soil conservation practice in karst citrus orchards, yet its long-term effects on rhizosphere microbial community assembly remain poorly understood, especially the relative influence of deterministic (e.g., environmental filtering) versus stochastic processes (e.g., dispersal limitation).
RESULTS: We investigated rhizosphere soil microbial communities along a terrace chronosequence (0–12 years) in the Lijiang River Basin using MiSeq sequencing and metabolomics, with null model analysis employed to assess community assembly processes. Terrace age did not significantly affect microbial α-diversity, but was associated with subtle changes in community composition: Proteobacteria, a copiotrophic group, decreased slightly, while Chloroflexi, an oligotrophic group, increased modestly. These shifts suggest a weak trend toward lower soil nutrient availability rather than a clear successional reorganization. Microbial diversity and structure were significantly correlated with soil stoichiometric ratios and available phosphorus (p < 0.05). Terracing also affected microbial network complexity and potential function. Potential functional profiling and metabolome data revealed that L-glutamine, a key nitrogen source, was negatively correlated with potential catabolic nitrate reduction (p < 0.05). This relationship was most pronounced at the Y5 phase (peak diversity/network complexity), suggesting accelerated L-glutamine utilization tightly coupled with enhanced potential for dissimilatory nitrate reduction to maximize nitrogen-use efficiency during the successional climax. Notably, stochastic processes explained over 96% of the microbial assembly. Bacterial communities were primarily driven by homogenizing dispersal, while fungal communities followed undominated processes.
CONCLUSION: The prominence of stochasticity in our results complements current understanding of agricultural microbiome assembly, particularly emphasizing its vital role in fragile karst environments. We propose that optimizing terrace rotation intervals (e.g., every 5-year) could be a practical strategy to enhance nitrogen-cycling efficiency and support sustainable nutrient management in karst citrus cultivation.
GRAPHICAL ABSTRACT: [Image: see text]
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-026-04811-4.
Additional Links: PMID-41742032
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@article {pmid41742032,
year = {2026},
author = {Zhang, J and Dai, Y and Mustafa, A and Li, L and Li, Y and Sun, T and Chen, M and Yang, H and Ma, J},
title = {Terracing influences soil microbial assembly in citrus orchards: stochastic processes dominate community dynamics in a karst sloping land.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {},
pmid = {41742032},
issn = {1471-2180},
support = {GUIKE AB22080071//Guangxi Key Research and Development Program/ ; AA20161002//Science and Technology Major Project of Guangxi/ ; },
abstract = {BACKGROUND: Terracing is a key soil conservation practice in karst citrus orchards, yet its long-term effects on rhizosphere microbial community assembly remain poorly understood, especially the relative influence of deterministic (e.g., environmental filtering) versus stochastic processes (e.g., dispersal limitation).
RESULTS: We investigated rhizosphere soil microbial communities along a terrace chronosequence (0–12 years) in the Lijiang River Basin using MiSeq sequencing and metabolomics, with null model analysis employed to assess community assembly processes. Terrace age did not significantly affect microbial α-diversity, but was associated with subtle changes in community composition: Proteobacteria, a copiotrophic group, decreased slightly, while Chloroflexi, an oligotrophic group, increased modestly. These shifts suggest a weak trend toward lower soil nutrient availability rather than a clear successional reorganization. Microbial diversity and structure were significantly correlated with soil stoichiometric ratios and available phosphorus (p < 0.05). Terracing also affected microbial network complexity and potential function. Potential functional profiling and metabolome data revealed that L-glutamine, a key nitrogen source, was negatively correlated with potential catabolic nitrate reduction (p < 0.05). This relationship was most pronounced at the Y5 phase (peak diversity/network complexity), suggesting accelerated L-glutamine utilization tightly coupled with enhanced potential for dissimilatory nitrate reduction to maximize nitrogen-use efficiency during the successional climax. Notably, stochastic processes explained over 96% of the microbial assembly. Bacterial communities were primarily driven by homogenizing dispersal, while fungal communities followed undominated processes.
CONCLUSION: The prominence of stochasticity in our results complements current understanding of agricultural microbiome assembly, particularly emphasizing its vital role in fragile karst environments. We propose that optimizing terrace rotation intervals (e.g., every 5-year) could be a practical strategy to enhance nitrogen-cycling efficiency and support sustainable nutrient management in karst citrus cultivation.
GRAPHICAL ABSTRACT: [Image: see text]
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-026-04811-4.},
}
RevDate: 2026-04-02
Functional potential of archaeal KEGG enzymes in the Moringa oleifera rhizosphere revealed by metagenomic analysis.
BMC genomics, 27(1):.
BACKGROUND: Archaea are a major domain of life that inhabit diverse and often extreme environments, contributing to biogeochemical cycles and participating in nutrient cycling within plant rhizospheric soils. This study applies metagenomic whole-genome shotgun sequencing to characterize the archaeal component of the rhizospheric microbiome associated with the wild plant species Moringa oleifera in Saudi Arabia.
RESULTS: Based on KEGG-annotated enzymes, Thaumarchaeota and Euryarchaeota emerged as the predominant archaeal phyla in the rhizosphere, with higher abundance than in bulk soil. The most abundant archaeal enzymes were assigned to metabolic pathways related to nitrogen and sulfur metabolism, carbon transformations, and responses to oxidative stress, indicating a putative contribution to nutrient turnover and stress-related functions. Network analysis further identified archaeal chemotaxis-related regulators and two-component sensor kinases linked to the root–soil interface. Key enzymes detected included urease, glutamine synthetase, thiosulfate sulfurtransferase, and catalase-peroxidase.
CONCLUSIONS: These findings suggest that archaeal communities form a distinct functional module within the M. oleifera rhizosphere, potentially influencing soil nutrient dynamics and plant performance. The chief limitation is reliance on DNA-based metagenomic data from a single site and time point, without multi-omics or detailed soil characterization, restricting temporal and ecological generalization. Nonetheless, the dataset provides a genome-scale view of archaeal functional potential and offers testable directions for future experimental and process-oriented studies.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12864-026-12700-3.
Additional Links: PMID-41749104
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@article {pmid41749104,
year = {2026},
author = {Baz, L},
title = {Functional potential of archaeal KEGG enzymes in the Moringa oleifera rhizosphere revealed by metagenomic analysis.},
journal = {BMC genomics},
volume = {27},
number = {1},
pages = {},
pmid = {41749104},
issn = {1471-2164},
abstract = {BACKGROUND: Archaea are a major domain of life that inhabit diverse and often extreme environments, contributing to biogeochemical cycles and participating in nutrient cycling within plant rhizospheric soils. This study applies metagenomic whole-genome shotgun sequencing to characterize the archaeal component of the rhizospheric microbiome associated with the wild plant species Moringa oleifera in Saudi Arabia.
RESULTS: Based on KEGG-annotated enzymes, Thaumarchaeota and Euryarchaeota emerged as the predominant archaeal phyla in the rhizosphere, with higher abundance than in bulk soil. The most abundant archaeal enzymes were assigned to metabolic pathways related to nitrogen and sulfur metabolism, carbon transformations, and responses to oxidative stress, indicating a putative contribution to nutrient turnover and stress-related functions. Network analysis further identified archaeal chemotaxis-related regulators and two-component sensor kinases linked to the root–soil interface. Key enzymes detected included urease, glutamine synthetase, thiosulfate sulfurtransferase, and catalase-peroxidase.
CONCLUSIONS: These findings suggest that archaeal communities form a distinct functional module within the M. oleifera rhizosphere, potentially influencing soil nutrient dynamics and plant performance. The chief limitation is reliance on DNA-based metagenomic data from a single site and time point, without multi-omics or detailed soil characterization, restricting temporal and ecological generalization. Nonetheless, the dataset provides a genome-scale view of archaeal functional potential and offers testable directions for future experimental and process-oriented studies.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12864-026-12700-3.},
}
RevDate: 2026-04-01
Characteristics of gut microbiota and metabolites in patients with metabolic dysfunction-associated steatotic liver disease and colorectal adenoma.
Scientific reports, 16(1):.
UNLABELLED: Metabolic dysfunction-associated steatotic liver disease (MASLD) has become one of the most prevalent chronic liver conditions worldwide, with its incidence steadily rising. However, the underlying mechanisms linking MASLD to colorectal adenoma remain unclear, and the role of gut microbiota and metabolites in this association requires further investigation. This study aims to characterise the gut microbiota and metabolites in patients with MASLD and colorectal adenoma. A cohort of 58 MASLD patients was enrolled and stratified into two groups based on colorectal adenoma status: the MASLD with colorectal adenoma group (M-CA group, n = 30) and the MASLD without colorectal adenoma group (M-NCA group, n = 28). The gut microbial ecosystem in the M-CA group showed significant dysregulation, evidenced by a decreased Gut Microbiome Health Index (GMHI) and significantly increased Microbiome Dysbiosis Index (MDI). Linear Discriminant Analysis Effect Size (LEfSe) identified 75 differentially abundant microbial taxa between groups, with Bacteroides vulgatus, Bacteroides ovatus, uncultured bacterium of norank genus of Muribaculaceae family, Muribaculaceae, and norank of Muribaculaceae family being significantly enriched in the M-CA group, representing potential microbial biomarkers for this cohort. Partial Least Squares Discriminant Analysis (PLS-DA) screened 116 differential metabolites. When combined with Random Forest (RF), Support Vector Machine (SVM) and Least Absolute Shrinkage and Selection Operator (LASSO) machine learning algorithms, 16 significantly identified biomarkers were discovered. The joint analysis of both omics revealed that variations in differential metabolite levels were associated with changes in specific microbiota abundances. Kyoto encyclopedia of genes and genomes (KEGG) functional prediction analysis indicated that the coordinated alterations in metabolites and microbiota may collectively influence multiple metabolic pathways, including lipid metabolism, xenobiotics biodegradation and metabolism, amino acid metabolism, carbohydrate metabolism, biosynthesis of other secondary metabolites and nucleotide metabolism. This study revealed that patients with MASLD and colorectal adenoma exhibited significant alterations in the gut microbiota composition and metabolic profile, indicating potential impacts on associated metabolic pathways. These findings provided novel insights and a foundation for future research into potential intervention strategies for this clinical complication.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-45782-w.
Additional Links: PMID-41896654
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Citation:
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@article {pmid41896654,
year = {2026},
author = {Li, Y and Fu, W and Xiang, Z and Zhao, M and Xie, X and Guo, W and Zhou, Y and Zheng, M and Yang, J},
title = {Characteristics of gut microbiota and metabolites in patients with metabolic dysfunction-associated steatotic liver disease and colorectal adenoma.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {41896654},
issn = {2045-2322},
support = {2021J0252//Scientific Research Fund Project of Yunnan Provincial Department of Education/ ; 2025J0270//Scientific Research Fund Project of Yunnan Provincial Department of Education/ ; 2024B010//Innovation Fund for Postgraduate Education of Kunming Medical University/ ; 202501AY070001-088//Science and Technology Plan Project of Yunnan Provincial Department of Science and Technology/ ; 82160106//National Natural Science Foundation of China/ ; },
abstract = {UNLABELLED: Metabolic dysfunction-associated steatotic liver disease (MASLD) has become one of the most prevalent chronic liver conditions worldwide, with its incidence steadily rising. However, the underlying mechanisms linking MASLD to colorectal adenoma remain unclear, and the role of gut microbiota and metabolites in this association requires further investigation. This study aims to characterise the gut microbiota and metabolites in patients with MASLD and colorectal adenoma. A cohort of 58 MASLD patients was enrolled and stratified into two groups based on colorectal adenoma status: the MASLD with colorectal adenoma group (M-CA group, n = 30) and the MASLD without colorectal adenoma group (M-NCA group, n = 28). The gut microbial ecosystem in the M-CA group showed significant dysregulation, evidenced by a decreased Gut Microbiome Health Index (GMHI) and significantly increased Microbiome Dysbiosis Index (MDI). Linear Discriminant Analysis Effect Size (LEfSe) identified 75 differentially abundant microbial taxa between groups, with Bacteroides vulgatus, Bacteroides ovatus, uncultured bacterium of norank genus of Muribaculaceae family, Muribaculaceae, and norank of Muribaculaceae family being significantly enriched in the M-CA group, representing potential microbial biomarkers for this cohort. Partial Least Squares Discriminant Analysis (PLS-DA) screened 116 differential metabolites. When combined with Random Forest (RF), Support Vector Machine (SVM) and Least Absolute Shrinkage and Selection Operator (LASSO) machine learning algorithms, 16 significantly identified biomarkers were discovered. The joint analysis of both omics revealed that variations in differential metabolite levels were associated with changes in specific microbiota abundances. Kyoto encyclopedia of genes and genomes (KEGG) functional prediction analysis indicated that the coordinated alterations in metabolites and microbiota may collectively influence multiple metabolic pathways, including lipid metabolism, xenobiotics biodegradation and metabolism, amino acid metabolism, carbohydrate metabolism, biosynthesis of other secondary metabolites and nucleotide metabolism. This study revealed that patients with MASLD and colorectal adenoma exhibited significant alterations in the gut microbiota composition and metabolic profile, indicating potential impacts on associated metabolic pathways. These findings provided novel insights and a foundation for future research into potential intervention strategies for this clinical complication.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-45782-w.},
}
RevDate: 2026-03-31
CmpDate: 2026-03-31
Lentinula edodes Cultured Extract Intake at Puberty Mitigates Inflammatory Signals at the Mammary Glands by the Involvement of Epigenetic Mechanisms in BALB/c Mice.
The breast journal, 2026(1):e2122220.
Exposure to immune stress or lipopolysaccharide (LPS) during critical developmental stages like puberty may lead to gut microbiome dysbiosis and epigenetic dysregulation in mammary glands, affecting gene expression and potentially elevating breast cancer susceptibility in adulthood. Although LPS's adverse impacts on intestinal and brain functions are well-documented, its effects on mammary glands remain underexplored. Using an immunocompetent BALB/c mouse model, we administered an acute LPS dose (1.5 mg/kg body weight) during puberty. The study evaluated the long-term consequences of LPS exposure alone and combined with AHCC (Lentinula edodes cultured extract, 2 g/kg body weight/day) on DNA methylation patterns, cytokine profiles, and microRNA expression in mammary glands at 9 weeks of age. Analyses included DNA methylation sequencing, multiplex immunoassays, quantitative PCR, and image processing. Pubertal LPS exposure produced persistent molecular dysregulation in mammary glands, including differential DNA methylation (> 5% change vs. control; FDR-adjusted p < 0.05), elevated inflammatory mediators, and altered microRNA expression. Differentially methylated regions were enriched in regulatory features, with decreased methylation at transcription start sites, promoters, and 5' UTRs of genes implicated in mammary development and oncogenic signaling (including Vav3, Pdgfa, Pdgfc, Jag2, Hras, Ksr1, Il2rb, Il17b, and Il17rb) in the LPS group, whereas the AHCC + LPS group exhibited a shift toward hypermethylation at these loci (approximately 5%-10% decrease). Inflammatory profiling showed increased IL-17A/F (∼2-fold vs. control; p < 0.05), while microRNA analyses indicated reduced let-7a/c (∼30% vs. control; p < 0.05). Notably, miR-130a and miR-34a increased ∼1.5-fold across all treatment groups relative to control. Pubertal LPS exposure induces enduring epigenetic and inflammatory changes in mammary glands that may heighten breast cancer risk. AHCC's mitigating role indicates potential for dietary interventions to counteract these effects.
Additional Links: PMID-41915463
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@article {pmid41915463,
year = {2026},
author = {Yasavoli-Sharahi, H and Shahbazi, R and Alsadi, N and Sahebi, NB and Cuenin, C and Cahais, V and Chung, FF and Herceg, Z and Matar, C},
title = {Lentinula edodes Cultured Extract Intake at Puberty Mitigates Inflammatory Signals at the Mammary Glands by the Involvement of Epigenetic Mechanisms in BALB/c Mice.},
journal = {The breast journal},
volume = {2026},
number = {1},
pages = {e2122220},
doi = {10.1155/tbj/2122220},
pmid = {41915463},
issn = {1524-4741},
support = {532223-18//Natural Sciences and Engineering Research Council of Canada/ ; 2019-01497//AHCC Research Association, and New Frontiers in Research Fund-Exploration (NFRF/ ; //University of Ottawa/ ; },
mesh = {Animals ; Female ; Mice ; Mice, Inbred BALB C ; *Epigenesis, Genetic/drug effects ; DNA Methylation/drug effects ; *Mammary Glands, Animal/drug effects/metabolism ; Lipopolysaccharides ; *Shiitake Mushrooms/chemistry ; Sexual Maturation ; MicroRNAs/metabolism ; *Inflammation ; },
abstract = {Exposure to immune stress or lipopolysaccharide (LPS) during critical developmental stages like puberty may lead to gut microbiome dysbiosis and epigenetic dysregulation in mammary glands, affecting gene expression and potentially elevating breast cancer susceptibility in adulthood. Although LPS's adverse impacts on intestinal and brain functions are well-documented, its effects on mammary glands remain underexplored. Using an immunocompetent BALB/c mouse model, we administered an acute LPS dose (1.5 mg/kg body weight) during puberty. The study evaluated the long-term consequences of LPS exposure alone and combined with AHCC (Lentinula edodes cultured extract, 2 g/kg body weight/day) on DNA methylation patterns, cytokine profiles, and microRNA expression in mammary glands at 9 weeks of age. Analyses included DNA methylation sequencing, multiplex immunoassays, quantitative PCR, and image processing. Pubertal LPS exposure produced persistent molecular dysregulation in mammary glands, including differential DNA methylation (> 5% change vs. control; FDR-adjusted p < 0.05), elevated inflammatory mediators, and altered microRNA expression. Differentially methylated regions were enriched in regulatory features, with decreased methylation at transcription start sites, promoters, and 5' UTRs of genes implicated in mammary development and oncogenic signaling (including Vav3, Pdgfa, Pdgfc, Jag2, Hras, Ksr1, Il2rb, Il17b, and Il17rb) in the LPS group, whereas the AHCC + LPS group exhibited a shift toward hypermethylation at these loci (approximately 5%-10% decrease). Inflammatory profiling showed increased IL-17A/F (∼2-fold vs. control; p < 0.05), while microRNA analyses indicated reduced let-7a/c (∼30% vs. control; p < 0.05). Notably, miR-130a and miR-34a increased ∼1.5-fold across all treatment groups relative to control. Pubertal LPS exposure induces enduring epigenetic and inflammatory changes in mammary glands that may heighten breast cancer risk. AHCC's mitigating role indicates potential for dietary interventions to counteract these effects.},
}
MeSH Terms:
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Animals
Female
Mice
Mice, Inbred BALB C
*Epigenesis, Genetic/drug effects
DNA Methylation/drug effects
*Mammary Glands, Animal/drug effects/metabolism
Lipopolysaccharides
*Shiitake Mushrooms/chemistry
Sexual Maturation
MicroRNAs/metabolism
*Inflammation
RevDate: 2026-03-31
Phage-related symbiosis and antagonism shape gut ecosystem dynamics in Lachnospiraceae and Bacteroidaceae.
Cell reports, 45(4):117166 pii:S2211-1247(26)00244-5 [Epub ahead of print].
The human gut microbiota is shaped by intricate, yet poorly resolved interactions among bacteria, as well as their relationship to bacteriophages. However, resolving this complex interaction and dynamics has been limited by the challenges in genome recovery and functional characterization. We develop culture-enriched metagenomic co-barcoding sequencing (cMECOS), obtain 5,006 high- or medium-quality (HMQ) metagenome-assembled genomes (MAGs) and reconstruct bacteria-phage interaction networks via CRISPR spacer mapping. This framework uncovers two ecologically distinct, inter-specific bacterial networks: a Lachnospiraceae-dominated community associates with temperate phages and is characterized by metabolic cross-feeding and a Bacteroidaceae-dominated community linked to virulent phages and marked by resource competition. Both network architectures are disrupted in both inflammatory bowel disease (IBD) and obesity (OB), underscoring their role in ecosystem stability. Our work establishes cMECOS as a powerful platform for deciphering complex microbiome interactions and identifies phage-related bacterial networks as critical regulators of gut homeostasis, providing a foundation for phage-informed therapeutic development.
Additional Links: PMID-41915473
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@article {pmid41915473,
year = {2026},
author = {Zhao, Y and Li, J and Han, K and Chen, L and Zhuang, Q and Li, S and Hua, M and Li, N and Yue, J and Gu, C and Rong, C and Yang, D and Deng, Z and Huang, J and He, L and Zeng, H and Yu, Z and Chen, C},
title = {Phage-related symbiosis and antagonism shape gut ecosystem dynamics in Lachnospiraceae and Bacteroidaceae.},
journal = {Cell reports},
volume = {45},
number = {4},
pages = {117166},
doi = {10.1016/j.celrep.2026.117166},
pmid = {41915473},
issn = {2211-1247},
abstract = {The human gut microbiota is shaped by intricate, yet poorly resolved interactions among bacteria, as well as their relationship to bacteriophages. However, resolving this complex interaction and dynamics has been limited by the challenges in genome recovery and functional characterization. We develop culture-enriched metagenomic co-barcoding sequencing (cMECOS), obtain 5,006 high- or medium-quality (HMQ) metagenome-assembled genomes (MAGs) and reconstruct bacteria-phage interaction networks via CRISPR spacer mapping. This framework uncovers two ecologically distinct, inter-specific bacterial networks: a Lachnospiraceae-dominated community associates with temperate phages and is characterized by metabolic cross-feeding and a Bacteroidaceae-dominated community linked to virulent phages and marked by resource competition. Both network architectures are disrupted in both inflammatory bowel disease (IBD) and obesity (OB), underscoring their role in ecosystem stability. Our work establishes cMECOS as a powerful platform for deciphering complex microbiome interactions and identifies phage-related bacterial networks as critical regulators of gut homeostasis, providing a foundation for phage-informed therapeutic development.},
}
RevDate: 2026-03-31
Gut Microbiome, Immune Cells, and Heart Failure: A Multi-Omics Mendelian Randomization Study.
Cardiology pii:000550655 [Epub ahead of print].
INTRODUCTION: The global burden of heart failure is escalating, marked by persistently rising prevalence, incidence, and mortality. The emerging hypothesis that the gut microbiome, as a modifiable factor, influences HF pathogenesis through immune modulation.
METHODS: To examine the causal relationship, we conducted two-sample Mendelian randomization (MR) analyses using summary genetic data, which was obtained from genome-wide association studies (GWASs) of gut microbial taxa, immune cells, and HF. Single-cell RNA sequencing data and single-nucleus RNA sequencing from chronic heart failure and healthy samples were extracted for investigation. Expression quantitative trait loci (eQTL) MR analysis was used to integrate HF GWAS with eQTL from heart to confirm potential genes. We performed functional enrichment analysis to enrich their functions.
RESULTS: The analysis revealed that genus Blautia (p = 0.0287), genus Corynebactrium (p = 0.022), genus Demequina (p = 0.0064), genus Enterococcus (p = 0.0307), genus Eubacterium (p = 0.0234), genus F0482 (p = 0.0107), genus Leclercia (p = 0.0026), genus Prevotellamassilia (p = 0.0444), and genus Ruminococcus were causally linked to a higher risk of HF, while genus CAG-125 (p = 0.0443), genus CAG-245 (p = 0.0116), genus Fournierella (p = 0.0326), genus Roseibacillus (p = 0.028) protective factors for HF. Among differential microflora, genus Leclercia was significantly related to higher level of HVEM on terminally differentiated CD4+T-cell count (p = 0.0058). Moreover, HF patients underwent obviously increased NK/T cells. We identified positive association of EIF3A, RPL5, SLC25A51, HERC5, SUSD3, ZNF292, ZNF655, and DNAJC9 with increased risk of HF, whereas the expression of RMC1, CAMK2G, RPS26, ATP5PO displayed protective effect against HF by eQTL MR analysis; they were mainly enriched in myc-Targets-V1, IFN-γ-response, IFN-α-response, PI3K/AKT/mTOR signaling, TGF-beta signaling, allograft rejection, notch signaling pathways, angiogenesis, epithelial mesenchymal transition, UV-response-DN, hedgehog signaling, myogenesis.
CONCLUSION: Our multi-omics MR study uncovered the causality of gut microbiome on immune cells and HF. Genus Leclercia-related changes in T cells may present as a viable focus for HF. This offers new insights into mechanisms and therapy of gut microbiome-mediated HF.
Additional Links: PMID-41915616
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@article {pmid41915616,
year = {2026},
author = {Wei, Y and Ji, X and Mao, Y and Liu, Y and Li, Y},
title = {Gut Microbiome, Immune Cells, and Heart Failure: A Multi-Omics Mendelian Randomization Study.},
journal = {Cardiology},
volume = {},
number = {},
pages = {1-14},
doi = {10.1159/000550655},
pmid = {41915616},
issn = {1421-9751},
abstract = {INTRODUCTION: The global burden of heart failure is escalating, marked by persistently rising prevalence, incidence, and mortality. The emerging hypothesis that the gut microbiome, as a modifiable factor, influences HF pathogenesis through immune modulation.
METHODS: To examine the causal relationship, we conducted two-sample Mendelian randomization (MR) analyses using summary genetic data, which was obtained from genome-wide association studies (GWASs) of gut microbial taxa, immune cells, and HF. Single-cell RNA sequencing data and single-nucleus RNA sequencing from chronic heart failure and healthy samples were extracted for investigation. Expression quantitative trait loci (eQTL) MR analysis was used to integrate HF GWAS with eQTL from heart to confirm potential genes. We performed functional enrichment analysis to enrich their functions.
RESULTS: The analysis revealed that genus Blautia (p = 0.0287), genus Corynebactrium (p = 0.022), genus Demequina (p = 0.0064), genus Enterococcus (p = 0.0307), genus Eubacterium (p = 0.0234), genus F0482 (p = 0.0107), genus Leclercia (p = 0.0026), genus Prevotellamassilia (p = 0.0444), and genus Ruminococcus were causally linked to a higher risk of HF, while genus CAG-125 (p = 0.0443), genus CAG-245 (p = 0.0116), genus Fournierella (p = 0.0326), genus Roseibacillus (p = 0.028) protective factors for HF. Among differential microflora, genus Leclercia was significantly related to higher level of HVEM on terminally differentiated CD4+T-cell count (p = 0.0058). Moreover, HF patients underwent obviously increased NK/T cells. We identified positive association of EIF3A, RPL5, SLC25A51, HERC5, SUSD3, ZNF292, ZNF655, and DNAJC9 with increased risk of HF, whereas the expression of RMC1, CAMK2G, RPS26, ATP5PO displayed protective effect against HF by eQTL MR analysis; they were mainly enriched in myc-Targets-V1, IFN-γ-response, IFN-α-response, PI3K/AKT/mTOR signaling, TGF-beta signaling, allograft rejection, notch signaling pathways, angiogenesis, epithelial mesenchymal transition, UV-response-DN, hedgehog signaling, myogenesis.
CONCLUSION: Our multi-omics MR study uncovered the causality of gut microbiome on immune cells and HF. Genus Leclercia-related changes in T cells may present as a viable focus for HF. This offers new insights into mechanisms and therapy of gut microbiome-mediated HF.},
}
RevDate: 2026-03-31
Beyond the crop: the role of medicinal and aromatic plants in soil carbon sequestration and nitrogen cycling.
International journal of environmental health research [Epub ahead of print].
Medicinal and aromatic plants (MAPs) play a critical yet underexplored role in enhancing soil functionality through their unique phytochemical interactions and ecological adaptability. This review synthesizes current research on how MAPs influence soil carbon sequestration and nitrogen cycling, positioning them as multifunctional agents in sustainable agroecosystems. Unlike conventional crops, MAPs release complex secondary metabolites, such as flavonoids, alkaloids, terpenoids, and phenolics, which modulate microbial diversity, enzymatic activity, and nutrient transformation. These compounds shape the rhizosphere microbial communities, facilitate nitrogen fixation and mineralization, and contribute to soil organic matter (SOM) stabilization through rhizosphere priming and humus formation. Integrated approaches, such as intercropping, agroforestry, and organic amendments, enhance these benefits, while mitigating allelopathic effects and improving carbon and nitrogen fluxes. This review further explores technological innovations including remote sensing (RS), biochar applications, and nanotechnology, which support MAP-based climate-resilient agriculture. Case studies across diverse geographies demonstrate MAPs' potential to restore degraded soils, reduce greenhouse gas emissions, and improve phytochemical yields. Overall, MAPs offer a promising model for regenerative, low-input farming systems that align ecological integrity with economic viability. By actively engineering the soil environment, MAPs emerge not only as botanical resources but also as ecological catalysts in the transition to sustainable agriculture.
Additional Links: PMID-41915730
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@article {pmid41915730,
year = {2026},
author = {Negahban, M and Msaada, K},
title = {Beyond the crop: the role of medicinal and aromatic plants in soil carbon sequestration and nitrogen cycling.},
journal = {International journal of environmental health research},
volume = {},
number = {},
pages = {1-24},
doi = {10.1080/09603123.2026.2653197},
pmid = {41915730},
issn = {1369-1619},
abstract = {Medicinal and aromatic plants (MAPs) play a critical yet underexplored role in enhancing soil functionality through their unique phytochemical interactions and ecological adaptability. This review synthesizes current research on how MAPs influence soil carbon sequestration and nitrogen cycling, positioning them as multifunctional agents in sustainable agroecosystems. Unlike conventional crops, MAPs release complex secondary metabolites, such as flavonoids, alkaloids, terpenoids, and phenolics, which modulate microbial diversity, enzymatic activity, and nutrient transformation. These compounds shape the rhizosphere microbial communities, facilitate nitrogen fixation and mineralization, and contribute to soil organic matter (SOM) stabilization through rhizosphere priming and humus formation. Integrated approaches, such as intercropping, agroforestry, and organic amendments, enhance these benefits, while mitigating allelopathic effects and improving carbon and nitrogen fluxes. This review further explores technological innovations including remote sensing (RS), biochar applications, and nanotechnology, which support MAP-based climate-resilient agriculture. Case studies across diverse geographies demonstrate MAPs' potential to restore degraded soils, reduce greenhouse gas emissions, and improve phytochemical yields. Overall, MAPs offer a promising model for regenerative, low-input farming systems that align ecological integrity with economic viability. By actively engineering the soil environment, MAPs emerge not only as botanical resources but also as ecological catalysts in the transition to sustainable agriculture.},
}
RevDate: 2026-03-31
Influence of synbiotic supplementation on performance, fecal consistency, cecal microbiome, and egg quality of hens during late laying phase.
Poultry science, 105(6):106851 pii:S0032-5791(26)00480-3 [Epub ahead of print].
Hens in the late laying phase often experience age-related physiological constraints that may reduce production efficiency, eggshell quality, and welfare. This study evaluated the effects of dietary synbiotic supplementation on laying performance, egg quality, fecal characteristics, and the cecal microbiome of late-phase laying hens. A total of 240 Lohmann Brown hens (50 weeks old) were distributed into 20 replicates and randomly assigned to a corn-soybean control diet or the same diet supplemented with 100 mg/kg synbiotic (SYNLAC Prime®) for 22 weeks. Synbiotic supplementation did not affect egg production or egg mass but significantly reduced feed intake (P = 0.036). It also improved eggshell quality by decreasing the proportion of cracked eggs (P = 0.014) and increasing eggshell weight (P = 0.049) and shell thickness (P = 0.031). Fecal score and moisture content were not affected; however, synbiotic-fed hens showed lower fecal ammonia concentration (P = 0.033). Synbiotic supplementation increased both alpha and beta microbial diversity in the cecum. While microbial composition at higher taxonomic levels was largely unchanged, the relative abundances of Ruminococcaceae and Lachnospiraceae increased, whereas those of Bacteroidaceae and Clostridiaceae decreased. At the genus level, synbiotic supplementation increased Faecalibacterium, Ruminococcus, and Lactobacillus, while reducing Bacteroides and Alistipes. Functional prediction analysis indicated that synbiotic supplementation upregulated 12 cecal metabolic pathways and downregulated two pathways. Overall, synbiotic supplementation improved eggshell quality, promoted beneficial gut microbial populations, and reduced fecal ammonia emissions, suggesting its potential as a dietary strategy to support productivity and gut health in hens during the late laying phase.
Additional Links: PMID-41916054
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@article {pmid41916054,
year = {2026},
author = {Pongmanee, K and Rassmidatta, K and Lee, TY and Lin, JS and Chaosap, C and Adeyemi, KD and Ruangpanit, Y},
title = {Influence of synbiotic supplementation on performance, fecal consistency, cecal microbiome, and egg quality of hens during late laying phase.},
journal = {Poultry science},
volume = {105},
number = {6},
pages = {106851},
doi = {10.1016/j.psj.2026.106851},
pmid = {41916054},
issn = {1525-3171},
abstract = {Hens in the late laying phase often experience age-related physiological constraints that may reduce production efficiency, eggshell quality, and welfare. This study evaluated the effects of dietary synbiotic supplementation on laying performance, egg quality, fecal characteristics, and the cecal microbiome of late-phase laying hens. A total of 240 Lohmann Brown hens (50 weeks old) were distributed into 20 replicates and randomly assigned to a corn-soybean control diet or the same diet supplemented with 100 mg/kg synbiotic (SYNLAC Prime®) for 22 weeks. Synbiotic supplementation did not affect egg production or egg mass but significantly reduced feed intake (P = 0.036). It also improved eggshell quality by decreasing the proportion of cracked eggs (P = 0.014) and increasing eggshell weight (P = 0.049) and shell thickness (P = 0.031). Fecal score and moisture content were not affected; however, synbiotic-fed hens showed lower fecal ammonia concentration (P = 0.033). Synbiotic supplementation increased both alpha and beta microbial diversity in the cecum. While microbial composition at higher taxonomic levels was largely unchanged, the relative abundances of Ruminococcaceae and Lachnospiraceae increased, whereas those of Bacteroidaceae and Clostridiaceae decreased. At the genus level, synbiotic supplementation increased Faecalibacterium, Ruminococcus, and Lactobacillus, while reducing Bacteroides and Alistipes. Functional prediction analysis indicated that synbiotic supplementation upregulated 12 cecal metabolic pathways and downregulated two pathways. Overall, synbiotic supplementation improved eggshell quality, promoted beneficial gut microbial populations, and reduced fecal ammonia emissions, suggesting its potential as a dietary strategy to support productivity and gut health in hens during the late laying phase.},
}
RevDate: 2026-03-31
Higher ultra-processed food consumption is associated with higher likelihood of paediatric-onset multiple sclerosis.
Multiple sclerosis and related disorders, 109:107159 pii:S2211-0348(26)00195-1 [Epub ahead of print].
BACKGROUND: Diets are increasingly dominated by ultra-processed foods, which have been linked to several chronic diseases. Emerging evidence suggests an association between ultra-processed food consumption and inflammatory diseases, including multiple sclerosis (MS).
OBJECTIVE: To assess associations between consumption of ultra-processed foods and paediatric-onset MS (PoMS).
METHODS: We used data from the microbiome sub-study of the Canadian Pediatric Demyelinating Disease Network Study for PoMS cases (symptom onset aged <18 years) and unaffected controls. Data on consumption of ultra-processed foods (defined within the Nova system) were derived from dietary intake data collected using the Block Kids Food Screener. Dietary contribution of ultra-processed foods (% of total grams consumed per day) was estimated. Logistic regression models were used to examine associations between ultra-processed food consumption (continuous and tertiles) and likelihood of PoMS. Models were adjusted for age at dietary data collection, sex, race, region of residence, and total energy intake.
RESULTS: Dietary data were collected from PoMS participants (females=57, males=23) aged 5-28 years and controls (females=30, males=16) aged 8-26 years. Each additional 10% in ultra-processed food consumption was associated with a 35% higher odds of being a PoMS participant (adjusted odds ratio [aOR]=1.35, 95% CI 1.05, 1.73). Participants in the highest (versus lowest) tertile for ultra-processed food consumption had over five times higher odds of being a PoMS participant (aOR=5.30, 95% CI 1.36, 20.70).
CONCLUSION: Participants with PoMS reported greater consumption of ultra-processed foods compared to unaffected peers. More comprehensive longitudinal dietary histories are required to better understand this observation.
Additional Links: PMID-41916081
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@article {pmid41916081,
year = {2026},
author = {Machado, P and Mazahery, H and Black, LJ and Tremlett, H and Daly, A and Pham, NM and Tessema, GA and Zhu, F and Banwell, B and Bar-Or, A and Marrie, RA and Bernstein, CN and Mirza, AI and Yeh, EA and Waubant, E and O'Mahony, J and Dunlop, E and , },
title = {Higher ultra-processed food consumption is associated with higher likelihood of paediatric-onset multiple sclerosis.},
journal = {Multiple sclerosis and related disorders},
volume = {109},
number = {},
pages = {107159},
doi = {10.1016/j.msard.2026.107159},
pmid = {41916081},
issn = {2211-0356},
abstract = {BACKGROUND: Diets are increasingly dominated by ultra-processed foods, which have been linked to several chronic diseases. Emerging evidence suggests an association between ultra-processed food consumption and inflammatory diseases, including multiple sclerosis (MS).
OBJECTIVE: To assess associations between consumption of ultra-processed foods and paediatric-onset MS (PoMS).
METHODS: We used data from the microbiome sub-study of the Canadian Pediatric Demyelinating Disease Network Study for PoMS cases (symptom onset aged <18 years) and unaffected controls. Data on consumption of ultra-processed foods (defined within the Nova system) were derived from dietary intake data collected using the Block Kids Food Screener. Dietary contribution of ultra-processed foods (% of total grams consumed per day) was estimated. Logistic regression models were used to examine associations between ultra-processed food consumption (continuous and tertiles) and likelihood of PoMS. Models were adjusted for age at dietary data collection, sex, race, region of residence, and total energy intake.
RESULTS: Dietary data were collected from PoMS participants (females=57, males=23) aged 5-28 years and controls (females=30, males=16) aged 8-26 years. Each additional 10% in ultra-processed food consumption was associated with a 35% higher odds of being a PoMS participant (adjusted odds ratio [aOR]=1.35, 95% CI 1.05, 1.73). Participants in the highest (versus lowest) tertile for ultra-processed food consumption had over five times higher odds of being a PoMS participant (aOR=5.30, 95% CI 1.36, 20.70).
CONCLUSION: Participants with PoMS reported greater consumption of ultra-processed foods compared to unaffected peers. More comprehensive longitudinal dietary histories are required to better understand this observation.},
}
RevDate: 2026-03-31
Ageing of the Oral Mucosa: Mechanisms and Consequences.
International dental journal, 76(3):109482 pii:S0020-6539(26)00078-X [Epub ahead of print].
Oral mucosal ageing represents a fundamental reprogramming of the tissue microenvironment, a dynamic process that underlies the functional decline and heightened disease susceptibility observed in the elderly. This review synthesises current evidence to reconceptualise oral mucosal ageing as an active reprogramming of the tissue microenvironment, delineating the interplay between structural, molecular, and immunological changes, and exploring how these alterations drive functional decline and increase susceptibility to age-related oral diseases. Through a comprehensive analysis of experimental and clinical studies from human and animal models, we demonstrate that the ageing process fundamentally transforms the oral mucosa. Key findings include structural changes such as epithelial atrophy, extracellular matrix remodelling, and salivary gland degeneration, driven molecularly by genomic instability, accumulation of proinflammatory senescent cells, stem cell exhaustion, and dysregulated stress responses. These are compounded by an immunological state of 'inflammaging' and functional decline in innate and adaptive immunity, further exacerbated by shifts in the oral microbiome. Collectively, these deficits lead to impaired regeneration, diminished sensory function, and reduced salivary secretion, creating a permissive landscape for chronic oral diseases. In conclusion, oral mucosal ageing is a dynamic process of microenvironmental reprogramming driven by cellular senescence, immunosenescence, and structural decay. This actively underpins the heightened vulnerability to oral disease in the elderly, providing a mechanistic foundation for developing targeted interventions to preserve oral health in ageing populations.
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@article {pmid41916092,
year = {2026},
author = {Qiu, C and Jie, W and Qian, Y and Lu, X and Chen, Y and Si, M},
title = {Ageing of the Oral Mucosa: Mechanisms and Consequences.},
journal = {International dental journal},
volume = {76},
number = {3},
pages = {109482},
doi = {10.1016/j.identj.2026.109482},
pmid = {41916092},
issn = {1875-595X},
abstract = {Oral mucosal ageing represents a fundamental reprogramming of the tissue microenvironment, a dynamic process that underlies the functional decline and heightened disease susceptibility observed in the elderly. This review synthesises current evidence to reconceptualise oral mucosal ageing as an active reprogramming of the tissue microenvironment, delineating the interplay between structural, molecular, and immunological changes, and exploring how these alterations drive functional decline and increase susceptibility to age-related oral diseases. Through a comprehensive analysis of experimental and clinical studies from human and animal models, we demonstrate that the ageing process fundamentally transforms the oral mucosa. Key findings include structural changes such as epithelial atrophy, extracellular matrix remodelling, and salivary gland degeneration, driven molecularly by genomic instability, accumulation of proinflammatory senescent cells, stem cell exhaustion, and dysregulated stress responses. These are compounded by an immunological state of 'inflammaging' and functional decline in innate and adaptive immunity, further exacerbated by shifts in the oral microbiome. Collectively, these deficits lead to impaired regeneration, diminished sensory function, and reduced salivary secretion, creating a permissive landscape for chronic oral diseases. In conclusion, oral mucosal ageing is a dynamic process of microenvironmental reprogramming driven by cellular senescence, immunosenescence, and structural decay. This actively underpins the heightened vulnerability to oral disease in the elderly, providing a mechanistic foundation for developing targeted interventions to preserve oral health in ageing populations.},
}
RevDate: 2026-03-31
Aging enhances the ecological toxicity of polyethylene microplastics to marine medaka larvae (Oryzias melastigma).
Journal of environmental management, 404:129493 pii:S0301-4797(26)00953-9 [Epub ahead of print].
Microplastics (MPs), widely distributed in marine environments, pose urgent ecological risks as emerging contaminants. However, current ecological risk assessments are largely based on the commercially produced MPs, which poorly represent in natural settings. Here, we simulated the natural aging of polyethylene MPs (PE-MPs) using ultraviolet radiation (UV) and Fenton reactions, characterized the resultant physicochemical changes, and assessed their ecological toxicity in marine medaka larvae over a 30-day exposure experiment. Short-term aging via UV and Fenton reactions primarily altered the physical properties of PE, including surface morphology, hydrophobicity, and Zeta potential. Both original and aged PE induced intestinal damage and oxidative stress in the larvae, indicating that aged PE retains its toxicity. In contrast, aged PE significantly altered the microbial community structure in the fish intestines: Roseibacillus was significantly enriched in the UV-aged polyethylene (UVPE) exposure group, while Ruegeria and Pseudomonas were enriched in the Fenton-aged polyethylene (FPE) exposure group. Functional predictions of the intestinal microbial communities indicated that exposure to FPE resulted in the upregulation of metabolism-related functions, whereas exposure to UVPE significantly downregulated similar functions. Such upregulation likely reflects microbiome reprogramming under stress rather than improved health. Overall, our study demonstrated that aged PE exhibited pronounced toxicity to marine fish and their larvae by altering gut microbiota, and thus significantly impacting energy metabolism and nutrient absorption, leading to detrimental effects on their growth and development. These findings further underscore the enhanced ecological toxicity effects of aged MPs on marine organisms, highlighting the need for better assessments of the adverse impacts of MPs in marine environments.
Additional Links: PMID-41916240
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@article {pmid41916240,
year = {2026},
author = {Wen, S and Liu, J and Lin, B and Li, N and Diao, X},
title = {Aging enhances the ecological toxicity of polyethylene microplastics to marine medaka larvae (Oryzias melastigma).},
journal = {Journal of environmental management},
volume = {404},
number = {},
pages = {129493},
doi = {10.1016/j.jenvman.2026.129493},
pmid = {41916240},
issn = {1095-8630},
abstract = {Microplastics (MPs), widely distributed in marine environments, pose urgent ecological risks as emerging contaminants. However, current ecological risk assessments are largely based on the commercially produced MPs, which poorly represent in natural settings. Here, we simulated the natural aging of polyethylene MPs (PE-MPs) using ultraviolet radiation (UV) and Fenton reactions, characterized the resultant physicochemical changes, and assessed their ecological toxicity in marine medaka larvae over a 30-day exposure experiment. Short-term aging via UV and Fenton reactions primarily altered the physical properties of PE, including surface morphology, hydrophobicity, and Zeta potential. Both original and aged PE induced intestinal damage and oxidative stress in the larvae, indicating that aged PE retains its toxicity. In contrast, aged PE significantly altered the microbial community structure in the fish intestines: Roseibacillus was significantly enriched in the UV-aged polyethylene (UVPE) exposure group, while Ruegeria and Pseudomonas were enriched in the Fenton-aged polyethylene (FPE) exposure group. Functional predictions of the intestinal microbial communities indicated that exposure to FPE resulted in the upregulation of metabolism-related functions, whereas exposure to UVPE significantly downregulated similar functions. Such upregulation likely reflects microbiome reprogramming under stress rather than improved health. Overall, our study demonstrated that aged PE exhibited pronounced toxicity to marine fish and their larvae by altering gut microbiota, and thus significantly impacting energy metabolism and nutrient absorption, leading to detrimental effects on their growth and development. These findings further underscore the enhanced ecological toxicity effects of aged MPs on marine organisms, highlighting the need for better assessments of the adverse impacts of MPs in marine environments.},
}
RevDate: 2026-03-31
Diversity-triggered 2-naphthoic acid exudation recruits keystone microbial taxa to promote soybean drought tolerance.
Cell host & microbe pii:S1931-3128(26)00089-2 [Epub ahead of print].
Rhizosphere microbiomes are essential for plant growth and stress tolerance, yet how microbial diversity shapes drought resilience in soybean remains unclear. Here, we demonstrate that high rhizosphere microbial diversity, generated via dilution-to-extinction manipulation of soil microbiome diversity, improves soybean performance under drought. Integrated metabolomic and transcriptomic analyses identify 2-naphthoic acid as a diversity-induced root exudate that accumulates exclusively under drought. This metabolite selectively recruits Sinorhizobium CS204 via chemotaxis and ATP-binding cassette (ABC) transporter-mediated uptake, as confirmed by in vitro substrate utilization assays and targeted mutant construction. Molecular docking and microscale thermophoresis reveal direct interactions between this metabolite and nitrogen-cycling proteins, enhancing denitrification and nitrogen fixation of S.CS204. Co-application of 2-naphthoic acid and S.CS204 significantly improves plant nutrient acquisition and photosynthesis under drought. Collectively, our study underscores the pivotal role of rhizosphere microbial diversity in triggering the exudation of root metabolites to recruit keystone taxa, establishing microbe-plant synergies that bolster drought tolerance.
Additional Links: PMID-41916289
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@article {pmid41916289,
year = {2026},
author = {Chen, S and Wang, Y and Chen, B and Hou, X and Liu, S and He, S and Qi, J and Peng, Z and Pan, H and Liang, C and Wei, G and Jiao, S},
title = {Diversity-triggered 2-naphthoic acid exudation recruits keystone microbial taxa to promote soybean drought tolerance.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.03.002},
pmid = {41916289},
issn = {1934-6069},
abstract = {Rhizosphere microbiomes are essential for plant growth and stress tolerance, yet how microbial diversity shapes drought resilience in soybean remains unclear. Here, we demonstrate that high rhizosphere microbial diversity, generated via dilution-to-extinction manipulation of soil microbiome diversity, improves soybean performance under drought. Integrated metabolomic and transcriptomic analyses identify 2-naphthoic acid as a diversity-induced root exudate that accumulates exclusively under drought. This metabolite selectively recruits Sinorhizobium CS204 via chemotaxis and ATP-binding cassette (ABC) transporter-mediated uptake, as confirmed by in vitro substrate utilization assays and targeted mutant construction. Molecular docking and microscale thermophoresis reveal direct interactions between this metabolite and nitrogen-cycling proteins, enhancing denitrification and nitrogen fixation of S.CS204. Co-application of 2-naphthoic acid and S.CS204 significantly improves plant nutrient acquisition and photosynthesis under drought. Collectively, our study underscores the pivotal role of rhizosphere microbial diversity in triggering the exudation of root metabolites to recruit keystone taxa, establishing microbe-plant synergies that bolster drought tolerance.},
}
RevDate: 2026-03-31
A microbiome-derived olfactory signal regulates inter-male aggression and social dominance in mice.
Current biology : CB pii:S0960-9822(26)00298-8 [Epub ahead of print].
Many species use microbiome-derived metabolites as chemosensory cues, yet the chemicals involved and the sensory pathways that detect and process them remain poorly understood. Trimethylamine (TMA) is a volatile metabolite that is produced by the gut microbiome and selectively accumulated in the urine of sexually mature male mice. Here, we show that TMA regulates inter-male aggression and social dominance by activating trace amine-associated receptor 5 (TAAR5) in the main olfactory system. In wild-type mice, early aggressive behavior during male-male encounters strongly predicts eventual social status: dominant males initiate more attacks, whereas subordinate males display more defensive behaviors. Deletion of TAAR5 eliminated this asymmetry, with dominant and subordinate mice showing similar levels of aggressive and defensive behaviors. Strikingly, restoring TAAR5 expression in olfactory sensory neurons (OSNs) rescued the behavioral asymmetry, indicating that this effect is mediated by the main olfactory system and arguing against contributions from proposed TAAR5 expression in the brain. Finally, pharmacological suppression of microbial TMA production reduced inter-male aggression, and this effect was reversed by painting treated males with TMA, showing that microbiome-derived TMA is the key volatile ligand for TAAR5 in this context. Taken together, our findings identify TMA as a critical olfactory cue that signals the presence of sexually mature males and facilitates social hierarchy formation. More broadly, our results demonstrate that a microbiome-derived metabolite can shape mammalian social interactions through the main olfactory system and uncover a previously unrecognized role for the TAAR family in regulating social behavior.
Additional Links: PMID-41916309
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@article {pmid41916309,
year = {2026},
author = {Cichy, A and Dewan, A and He, Z and Fitzgerald, C and Ratkowski, M and Krasewicz, J and Ozarkar, V and Kaye, S and Teng, T and Zhang, J and Feinstein, P and Bozza, T},
title = {A microbiome-derived olfactory signal regulates inter-male aggression and social dominance in mice.},
journal = {Current biology : CB},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cub.2026.03.009},
pmid = {41916309},
issn = {1879-0445},
abstract = {Many species use microbiome-derived metabolites as chemosensory cues, yet the chemicals involved and the sensory pathways that detect and process them remain poorly understood. Trimethylamine (TMA) is a volatile metabolite that is produced by the gut microbiome and selectively accumulated in the urine of sexually mature male mice. Here, we show that TMA regulates inter-male aggression and social dominance by activating trace amine-associated receptor 5 (TAAR5) in the main olfactory system. In wild-type mice, early aggressive behavior during male-male encounters strongly predicts eventual social status: dominant males initiate more attacks, whereas subordinate males display more defensive behaviors. Deletion of TAAR5 eliminated this asymmetry, with dominant and subordinate mice showing similar levels of aggressive and defensive behaviors. Strikingly, restoring TAAR5 expression in olfactory sensory neurons (OSNs) rescued the behavioral asymmetry, indicating that this effect is mediated by the main olfactory system and arguing against contributions from proposed TAAR5 expression in the brain. Finally, pharmacological suppression of microbial TMA production reduced inter-male aggression, and this effect was reversed by painting treated males with TMA, showing that microbiome-derived TMA is the key volatile ligand for TAAR5 in this context. Taken together, our findings identify TMA as a critical olfactory cue that signals the presence of sexually mature males and facilitates social hierarchy formation. More broadly, our results demonstrate that a microbiome-derived metabolite can shape mammalian social interactions through the main olfactory system and uncover a previously unrecognized role for the TAAR family in regulating social behavior.},
}
RevDate: 2026-04-01
Probiotic treatment rescues behavioral deficits and gut microbial abnormalities induced by preconceptional stress in mothers and offspring.
Brain, behavior, and immunity, 136:106571 pii:S0889-1591(26)00319-3 [Epub ahead of print].
Depression and anxiety during pregnancy are major public health concerns with lasting consequences for mother and child. Although the gut microbiome contributes to stress and mood regulation, its role in preconceptional stress and transgenerational outcomes remains unclear. Here, we examined behavioral, microbial, and thalamic transcriptional effects of preconceptional social isolation rearing (SIR) in female mice and tested whether maternal probiotic supplementation mitigates these alterations. SIR females displayed increased anxiety-like and social-avoidant behavior, reduced gut microbial diversity, depletion of Odoribacter, Tuzzerella, and Alloprevotella, and enrichment of Bacteroides and Lachnospiraceae. A multispecies probiotic (Lactobacillus rhamnosus HN001, L. acidophilus La-14, Bifidobacterium lactis HN019) reversed these behavioral and microbial changes. Adult offspring of SIR dams showed sex-dependent behavioral deficits and microbial alterations partly reflecting maternal patterns. Prenatal SIR was associated with reduced thalamic Bdnf expression in offspring and altered Grin2a/2b selectively in males. In contrast, prenatal probiotic exposure exerted broader transcriptional effects and restored Bdnf levels in SIR offspring. SIR-induced increases in Lachnospiraceae were transmitted to offspring, whereas reductions in Ruminococcaceae were normalized by maternal probiotic treatment. Predicted functional profiling indicated sex-dependent modulation of microbial pathways related to tryptophan and central carbon metabolism. These findings demonstrate enduring transgenerational effects of preconceptional stress on the gut-brain axis and support maternal probiotic supplementation as a potential strategy to mitigate stress-induced dysregulation.
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@article {pmid41916434,
year = {2026},
author = {Iachizzi, M and Zajac, N and Ruiz, JL and Güller, T and Rabin, R and Schalbetter, S and de Cillis, F and Moccia, MD and Cattaneo, A and Cryan, JF and Richetto, J},
title = {Probiotic treatment rescues behavioral deficits and gut microbial abnormalities induced by preconceptional stress in mothers and offspring.},
journal = {Brain, behavior, and immunity},
volume = {136},
number = {},
pages = {106571},
doi = {10.1016/j.bbi.2026.106571},
pmid = {41916434},
issn = {1090-2139},
abstract = {Depression and anxiety during pregnancy are major public health concerns with lasting consequences for mother and child. Although the gut microbiome contributes to stress and mood regulation, its role in preconceptional stress and transgenerational outcomes remains unclear. Here, we examined behavioral, microbial, and thalamic transcriptional effects of preconceptional social isolation rearing (SIR) in female mice and tested whether maternal probiotic supplementation mitigates these alterations. SIR females displayed increased anxiety-like and social-avoidant behavior, reduced gut microbial diversity, depletion of Odoribacter, Tuzzerella, and Alloprevotella, and enrichment of Bacteroides and Lachnospiraceae. A multispecies probiotic (Lactobacillus rhamnosus HN001, L. acidophilus La-14, Bifidobacterium lactis HN019) reversed these behavioral and microbial changes. Adult offspring of SIR dams showed sex-dependent behavioral deficits and microbial alterations partly reflecting maternal patterns. Prenatal SIR was associated with reduced thalamic Bdnf expression in offspring and altered Grin2a/2b selectively in males. In contrast, prenatal probiotic exposure exerted broader transcriptional effects and restored Bdnf levels in SIR offspring. SIR-induced increases in Lachnospiraceae were transmitted to offspring, whereas reductions in Ruminococcaceae were normalized by maternal probiotic treatment. Predicted functional profiling indicated sex-dependent modulation of microbial pathways related to tryptophan and central carbon metabolism. These findings demonstrate enduring transgenerational effects of preconceptional stress on the gut-brain axis and support maternal probiotic supplementation as a potential strategy to mitigate stress-induced dysregulation.},
}
RevDate: 2026-03-31
Innovative soil seeding with waste-derived microbial inoculums: Enhancing plastic biodegradation and Revealing microbiome shifts.
Bioresource technology pii:S0960-8524(26)00604-8 [Epub ahead of print].
Plastic waste accumulation in terrestrial ecosystems poses a global environmental challenge, demanding sustainable alternatives to conventional disposal. Aerobic biodegradation is promising, yet most studies rely on composting systems, often overlooking different polymer types and how seeding soil with waste-derived inoculums affect polymer breakdown. This study developed an innovative soil-seeding approach using microbe-rich inoculums derived from real waste streams: compost (Comp.), activated sludge (AS), plastic-contaminated soil (PCS), and oil-contaminated soil (OCS) to enhance biodegradation of starch, compostable bioplastic (CBP), and the mineralization of linear low-density polyethylene (LLDPE). Biodegradation was evaluated under controlled soil conditions, and microbial community responses were characterized through metataxonomic profiling. Starch exhibited the highest biodegradation (71-100%), followed by CBP (31-56%) and LLDPE mineralization (12-22%). OCS and PCS significantly enhanced CBP and LLDPE degradation, respectively, corresponding to differences in organic content and carbon-to-nitrogen ratios. Shifts in microbial composition revealed polymer-specific microbial drivers, including Bacilli (Bacillaceae, Paenibacillus) and Chaetomium for starch, and Actinobacteriota, Acidimicrobiia, Mycobacterium, and Nocardioides for CBP, particularly in OCS. LLDPE degradation remained low but was modestly improved in Comp- and PCS-amended soils. Overall, this study demonstrates that targeted soil-seeding with waste-derived inoculums can substantially influence polymer degradation and microbial succession, providing a practical strategy to accelerate biodegradation in natural soils and informing future sustainable plastic-management approaches.
Additional Links: PMID-41916460
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@article {pmid41916460,
year = {2026},
author = {Asiri, F and Kishk, M and Karam, H and Al-Muhanna, K and Al-Najdi, F and Al-Enezi, A and Al-Khalifah, N and Hejji, AB and Al-Salameen, F and Al-Salem, SM},
title = {Innovative soil seeding with waste-derived microbial inoculums: Enhancing plastic biodegradation and Revealing microbiome shifts.},
journal = {Bioresource technology},
volume = {},
number = {},
pages = {134523},
doi = {10.1016/j.biortech.2026.134523},
pmid = {41916460},
issn = {1873-2976},
abstract = {Plastic waste accumulation in terrestrial ecosystems poses a global environmental challenge, demanding sustainable alternatives to conventional disposal. Aerobic biodegradation is promising, yet most studies rely on composting systems, often overlooking different polymer types and how seeding soil with waste-derived inoculums affect polymer breakdown. This study developed an innovative soil-seeding approach using microbe-rich inoculums derived from real waste streams: compost (Comp.), activated sludge (AS), plastic-contaminated soil (PCS), and oil-contaminated soil (OCS) to enhance biodegradation of starch, compostable bioplastic (CBP), and the mineralization of linear low-density polyethylene (LLDPE). Biodegradation was evaluated under controlled soil conditions, and microbial community responses were characterized through metataxonomic profiling. Starch exhibited the highest biodegradation (71-100%), followed by CBP (31-56%) and LLDPE mineralization (12-22%). OCS and PCS significantly enhanced CBP and LLDPE degradation, respectively, corresponding to differences in organic content and carbon-to-nitrogen ratios. Shifts in microbial composition revealed polymer-specific microbial drivers, including Bacilli (Bacillaceae, Paenibacillus) and Chaetomium for starch, and Actinobacteriota, Acidimicrobiia, Mycobacterium, and Nocardioides for CBP, particularly in OCS. LLDPE degradation remained low but was modestly improved in Comp- and PCS-amended soils. Overall, this study demonstrates that targeted soil-seeding with waste-derived inoculums can substantially influence polymer degradation and microbial succession, providing a practical strategy to accelerate biodegradation in natural soils and informing future sustainable plastic-management approaches.},
}
RevDate: 2026-03-31
Commonly prescribed drugs as risk factors for Clostridioides difficile infections: a Swedish population-based case-control study.
Gut pii:gutjnl-2025-337629 [Epub ahead of print].
BACKGROUND: Clostridioides difficile infections (CDIs) are associated with antibiotic use, although the link with other drugs remains underexplored.
OBJECTIVES: To investigate the association between antibiotic and non-antibiotic drugs with microbiome-modulating activity on new occurrences of CDI.
DESIGN: We conducted a Swedish population-based case-control study from 2006 to 2019 including 42 921 cases matched with 355 159 population controls on age and sex, obtained from multiple linked Swedish registries. The effect of antibiotic and non-antibiotic use within 30 days from the index date on CDI occurrence was estimated using multivariable conditional logistic regression additionally with a lasso penalty. Models were adjusted for age and sex by design and for Charlson Comorbidity Index and concomitant drug use, providing adjusted ORs (aORs) with 95% CIs.
RESULTS: Antibiotics with the greatest CDI risk were lincosamides (aOR=31.4, 95% CI 27.9 to 35.3), combinations of penicillins (aOR=19.8, 95% CI 15.9 to 24.5), sulfonamides and trimethoprim, and cephalosporins, though no association for tetracyclines. Among non-antibiotic drugs, we found decreased risks of CDI for lipid-modifiers (aOR=0.8, 95% CI 0.8 to 0.8) and aspirin (aOR=0.8, 95% CI 0.7 to 0.8) and increased risks for antidiarrhoeals (aOR=7.3, 95% CI 6.8 to 7.8), corticosteroids (aOR=2.4, 95% CI 2.3 to 2.5), proton-pump inhibitors (PPIs) (aOR=1.8, 95% CI 1.7 to 1.8), nervous system drugs, constipation drugs, histamine H2-receptor antagonists, antidepressants, and beta blockers, but no significant risk for non-steroidal anti-inflammatory drugs.
CONCLUSIONS: We found varying effects of antibiotics on CDI, providing evidence for ongoing efforts in prudent prescribing decisions and antimicrobial stewardship. We confirmed PPI as a main risk factor for CDI and provided new evidence for other non-antibiotic drugs as potentially important risk factors considering their high prescription prevalence.
Additional Links: PMID-41916675
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PubMed:
Citation:
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@article {pmid41916675,
year = {2026},
author = {Boven, A and Vranken, H and Vlieghe, E and Boleij, A and Fall, K and Engstrand, L and Brusselaers, N},
title = {Commonly prescribed drugs as risk factors for Clostridioides difficile infections: a Swedish population-based case-control study.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2025-337629},
pmid = {41916675},
issn = {1468-3288},
abstract = {BACKGROUND: Clostridioides difficile infections (CDIs) are associated with antibiotic use, although the link with other drugs remains underexplored.
OBJECTIVES: To investigate the association between antibiotic and non-antibiotic drugs with microbiome-modulating activity on new occurrences of CDI.
DESIGN: We conducted a Swedish population-based case-control study from 2006 to 2019 including 42 921 cases matched with 355 159 population controls on age and sex, obtained from multiple linked Swedish registries. The effect of antibiotic and non-antibiotic use within 30 days from the index date on CDI occurrence was estimated using multivariable conditional logistic regression additionally with a lasso penalty. Models were adjusted for age and sex by design and for Charlson Comorbidity Index and concomitant drug use, providing adjusted ORs (aORs) with 95% CIs.
RESULTS: Antibiotics with the greatest CDI risk were lincosamides (aOR=31.4, 95% CI 27.9 to 35.3), combinations of penicillins (aOR=19.8, 95% CI 15.9 to 24.5), sulfonamides and trimethoprim, and cephalosporins, though no association for tetracyclines. Among non-antibiotic drugs, we found decreased risks of CDI for lipid-modifiers (aOR=0.8, 95% CI 0.8 to 0.8) and aspirin (aOR=0.8, 95% CI 0.7 to 0.8) and increased risks for antidiarrhoeals (aOR=7.3, 95% CI 6.8 to 7.8), corticosteroids (aOR=2.4, 95% CI 2.3 to 2.5), proton-pump inhibitors (PPIs) (aOR=1.8, 95% CI 1.7 to 1.8), nervous system drugs, constipation drugs, histamine H2-receptor antagonists, antidepressants, and beta blockers, but no significant risk for non-steroidal anti-inflammatory drugs.
CONCLUSIONS: We found varying effects of antibiotics on CDI, providing evidence for ongoing efforts in prudent prescribing decisions and antimicrobial stewardship. We confirmed PPI as a main risk factor for CDI and provided new evidence for other non-antibiotic drugs as potentially important risk factors considering their high prescription prevalence.},
}
RevDate: 2026-03-31
CmpDate: 2026-03-31
Association between soft drink consumption and depression mediated by gut microbiome: a perspective.
East Asian archives of psychiatry : official journal of the Hong Kong College of Psychiatrists = Dong Ya jing shen ke xue zhi : Xianggang jing shen ke yi xue yuan qi kan, 36(1):56-59.
This perspective synthesises current evidence on the association between soft drink consumption and depression, with emphasis on the gut microbiome as a potential mediating mechanism. PubMed, Scopus, and Google Scholar were searched using the following terms: 'soft drinks', 'sugar-sweetened beverages', 'carbonated beverages', 'soda', 'depression', 'depressive symptoms', 'mental health', 'gut microbiome', 'microbiota', and 'gut-brain axis'. Peer-reviewed original articles published in English between January 2000 and October 2025 were included if they involved human participants of any age (sample size ≥50 for observational studies), assessed soft drink or sugar-sweetened beverage consumption, and measured depression diagnosis, depressive symptoms, or depression severity. Associations between soft drink consumption and increased depression risk were consistently shown across multiple study designs and populations. Evidence for artificially sweetened beverages was less consistent and suggested potentially distinct, non-sugar-related pathways. A multicentre cohort study of 932 participants revealed that soft drink consumption predicted the major depressive disorder diagnosis (odds ratio = 1.081), with stronger effects in women (odds ratio = 1.167). Eggerthella partially mediated the soft drink-depression association, explaining approximately 4% of the association. Soft drink consumption is associated with increased depression risk through multiple biological pathways involving inflammation, metabolic dysregulation, and gut microbiome alterations. Modest effect sizes suggest the involvement of multiple interconnected mechanisms. Public health interventions to limit sugar-sweetened beverage consumption are recommended to improve physical and mental health. Healthcare providers should consider dietary assessment and counselling as part of depression prevention and treatment strategies.
Additional Links: PMID-41916943
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PubMed:
Citation:
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@article {pmid41916943,
year = {2026},
author = {Sailesh, SS},
title = {Association between soft drink consumption and depression mediated by gut microbiome: a perspective.},
journal = {East Asian archives of psychiatry : official journal of the Hong Kong College of Psychiatrists = Dong Ya jing shen ke xue zhi : Xianggang jing shen ke yi xue yuan qi kan},
volume = {36},
number = {1},
pages = {56-59},
doi = {10.12809/eaap25136},
pmid = {41916943},
issn = {2224-7041},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Carbonated Beverages/adverse effects ; *Depression/etiology/epidemiology/microbiology ; *Sugar-Sweetened Beverages/adverse effects ; Female ; },
abstract = {This perspective synthesises current evidence on the association between soft drink consumption and depression, with emphasis on the gut microbiome as a potential mediating mechanism. PubMed, Scopus, and Google Scholar were searched using the following terms: 'soft drinks', 'sugar-sweetened beverages', 'carbonated beverages', 'soda', 'depression', 'depressive symptoms', 'mental health', 'gut microbiome', 'microbiota', and 'gut-brain axis'. Peer-reviewed original articles published in English between January 2000 and October 2025 were included if they involved human participants of any age (sample size ≥50 for observational studies), assessed soft drink or sugar-sweetened beverage consumption, and measured depression diagnosis, depressive symptoms, or depression severity. Associations between soft drink consumption and increased depression risk were consistently shown across multiple study designs and populations. Evidence for artificially sweetened beverages was less consistent and suggested potentially distinct, non-sugar-related pathways. A multicentre cohort study of 932 participants revealed that soft drink consumption predicted the major depressive disorder diagnosis (odds ratio = 1.081), with stronger effects in women (odds ratio = 1.167). Eggerthella partially mediated the soft drink-depression association, explaining approximately 4% of the association. Soft drink consumption is associated with increased depression risk through multiple biological pathways involving inflammation, metabolic dysregulation, and gut microbiome alterations. Modest effect sizes suggest the involvement of multiple interconnected mechanisms. Public health interventions to limit sugar-sweetened beverage consumption are recommended to improve physical and mental health. Healthcare providers should consider dietary assessment and counselling as part of depression prevention and treatment strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology
*Carbonated Beverages/adverse effects
*Depression/etiology/epidemiology/microbiology
*Sugar-Sweetened Beverages/adverse effects
Female
RevDate: 2026-03-31
Cultivation system and plant health influence root-associated bacterial community structure and interaction networks in strawberry.
Scientific reports pii:10.1038/s41598-026-45642-7 [Epub ahead of print].
Strawberry is cultivated in both soil-based field and substrate-based soilless hydroponic systems, yet how cultivation context shapes root-associated bacterial communities and their interaction architecture remains unclear. We compared root-associated bacterial communities from field root-associated soil and hydroponic root-adhering substrate under asymptomatic and symptomatic conditions using 16S rRNA gene amplicon sequencing. Cultivation system was the primary driver of community structure, clearly separating field and hydroponic samples. Field communities were enriched in Firmicutes and Actinobacteria, such as Bacillaceae and Nocardioidaceae, whereas hydroponic communities showed higher relative abundances of Proteobacteria, Bacteroidetes, Planctomycetes, and Verrucomicrobia, including Chitinophagaceae and Sphingomonadaceae. Differential abundance and Random Forest analyses revealed consistent enrichment of Bacillus-associated ASVs in field samples, whereas asymptomatic and symptomatic communities showed greater compositional differentiation in hydroponic than in field samples.. Co-occurrence network analysis further demonstrated that hydroponic communities contained more taxa and interactions but exhibited lower density and clustering compared to field communities, indicating reduced structural cohesion. These findings demonstrate that cultivation system strongly influences both the composition and structural organization of strawberry root-associated bacterial communities, with implications for microbiome-informed disease management in intensive production systems.
Additional Links: PMID-41917102
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PubMed:
Citation:
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@article {pmid41917102,
year = {2026},
author = {Roy, M and Han, D and Lee, D and Kang, B and Choi, K},
title = {Cultivation system and plant health influence root-associated bacterial community structure and interaction networks in strawberry.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-45642-7},
pmid = {41917102},
issn = {2045-2322},
support = {(RS-2023-00251252 and 2020R1A6A1A03047729)//National Research Foundation of Korea/ ; (RS-2025-02613089)//Rural Development Administration/ ; },
abstract = {Strawberry is cultivated in both soil-based field and substrate-based soilless hydroponic systems, yet how cultivation context shapes root-associated bacterial communities and their interaction architecture remains unclear. We compared root-associated bacterial communities from field root-associated soil and hydroponic root-adhering substrate under asymptomatic and symptomatic conditions using 16S rRNA gene amplicon sequencing. Cultivation system was the primary driver of community structure, clearly separating field and hydroponic samples. Field communities were enriched in Firmicutes and Actinobacteria, such as Bacillaceae and Nocardioidaceae, whereas hydroponic communities showed higher relative abundances of Proteobacteria, Bacteroidetes, Planctomycetes, and Verrucomicrobia, including Chitinophagaceae and Sphingomonadaceae. Differential abundance and Random Forest analyses revealed consistent enrichment of Bacillus-associated ASVs in field samples, whereas asymptomatic and symptomatic communities showed greater compositional differentiation in hydroponic than in field samples.. Co-occurrence network analysis further demonstrated that hydroponic communities contained more taxa and interactions but exhibited lower density and clustering compared to field communities, indicating reduced structural cohesion. These findings demonstrate that cultivation system strongly influences both the composition and structural organization of strawberry root-associated bacterial communities, with implications for microbiome-informed disease management in intensive production systems.},
}
RevDate: 2026-03-31
Context-dependent indirect effects mediate ecological transitions between parasitism and mutualism.
Communications biology pii:10.1038/s42003-026-09945-9 [Epub ahead of print].
Symbiotic interactions frequently shift along a mutualism-parasitism continuum, altering host fitness, population dynamics, and microbial community structure with ecological context. Here, we integrate field surveys, reciprocal breeding experiments, feeding assays, and microbiome profiling to dissect interactions between phoretic mite (Poecilochirus carabi), nematode (Rhomborhabditis regina), and their burying beetle host (Nicrophorus nepalensis) during reproduction. We show that high nematode densities reduce beetle offspring survival during metamorphosis, but co-occurring mites mitigate these costs by preying on nematodes and suppressing vertical transmission, thereby enhancing beetle fitness. Both mites and nematodes are equally effective at suppressing bacterial loads on carrion, but mites drive greater shifts in carcass microbiome composition. Carcasses exposed to both symbionts display the most pronounced shifts in bacterial communities, suggesting that inter-symbiont interactions have cascading effects on host-associated microbiota. Intriguingly, in the absence of nematodes, mites impose fitness costs on their beetle hosts. These results demonstrate that the net effects of mites on beetle fitness emerge largely through indirect, density-dependent interactions with nematodes and microbial competitors. By integrating macro-symbiont and microbiome perspectives, our study highlights how phoresy extends beyond passive dispersal to actively restructure host-symbiont networks, highlighting the overlooked potential of indirect effects in driving context-dependent mutualism within multisymbiotic systems.
Additional Links: PMID-41917200
Publisher:
PubMed:
Citation:
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@article {pmid41917200,
year = {2026},
author = {Lee, YH and Lin, WJ and Tsai, MT and Lan, B and Chu, YL and Yang, JI and Sun, SJ},
title = {Context-dependent indirect effects mediate ecological transitions between parasitism and mutualism.},
journal = {Communications biology},
volume = {},
number = {},
pages = {},
doi = {10.1038/s42003-026-09945-9},
pmid = {41917200},
issn = {2399-3642},
support = {Academic Research-Career Development Project (Sprout Research Projects; 114L7869)//National Taiwan University (NTU)/ ; },
abstract = {Symbiotic interactions frequently shift along a mutualism-parasitism continuum, altering host fitness, population dynamics, and microbial community structure with ecological context. Here, we integrate field surveys, reciprocal breeding experiments, feeding assays, and microbiome profiling to dissect interactions between phoretic mite (Poecilochirus carabi), nematode (Rhomborhabditis regina), and their burying beetle host (Nicrophorus nepalensis) during reproduction. We show that high nematode densities reduce beetle offspring survival during metamorphosis, but co-occurring mites mitigate these costs by preying on nematodes and suppressing vertical transmission, thereby enhancing beetle fitness. Both mites and nematodes are equally effective at suppressing bacterial loads on carrion, but mites drive greater shifts in carcass microbiome composition. Carcasses exposed to both symbionts display the most pronounced shifts in bacterial communities, suggesting that inter-symbiont interactions have cascading effects on host-associated microbiota. Intriguingly, in the absence of nematodes, mites impose fitness costs on their beetle hosts. These results demonstrate that the net effects of mites on beetle fitness emerge largely through indirect, density-dependent interactions with nematodes and microbial competitors. By integrating macro-symbiont and microbiome perspectives, our study highlights how phoresy extends beyond passive dispersal to actively restructure host-symbiont networks, highlighting the overlooked potential of indirect effects in driving context-dependent mutualism within multisymbiotic systems.},
}
RevDate: 2026-04-01
CmpDate: 2026-04-01
New Trends and Challenges in Academic Research on Adolescent Growth and Development.
Advances in experimental medicine and biology, 1505:411-420.
Adolescence is a critical period for physical and psychological growth and development when individuals undergo a burst growth in physical size, hormonal re-adjustment, and brain development. In recent years, research studies have changed from descriptive growth charts toward focusing on the roles of multiple factors that affect adolescent health, including epigenetic regulators, genetic traits, social stressors, and gut microbiota. Compared to traditional factors like nutrition and hormones, environmental factors, personalized genomics, social media exposure, and gut-microbiome, etc. are increasing recognized as novel critical regulators of adolescent health. Currently, the goal of academic research in adolescence is to understand the interactions and underlying mechanisms of these factors and to develop targeted interventions for addressing adolescent health issues. Therefore, this chapter mainly discusses the new trends, key challenges, and translational research potential in these rapidly advancing field of adolescent growth and development.
Additional Links: PMID-41917642
PubMed:
Citation:
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@article {pmid41917642,
year = {2026},
author = {Gao, J and Ren, X and Hu, Y and Li, G and Yang, T and Xiao, J},
title = {New Trends and Challenges in Academic Research on Adolescent Growth and Development.},
journal = {Advances in experimental medicine and biology},
volume = {1505},
number = {},
pages = {411-420},
pmid = {41917642},
issn = {0065-2598},
mesh = {Humans ; Adolescent ; *Adolescent Development/physiology ; *Adolescent Health/trends ; Gastrointestinal Microbiome/physiology ; Epigenesis, Genetic ; *Biomedical Research/trends ; },
abstract = {Adolescence is a critical period for physical and psychological growth and development when individuals undergo a burst growth in physical size, hormonal re-adjustment, and brain development. In recent years, research studies have changed from descriptive growth charts toward focusing on the roles of multiple factors that affect adolescent health, including epigenetic regulators, genetic traits, social stressors, and gut microbiota. Compared to traditional factors like nutrition and hormones, environmental factors, personalized genomics, social media exposure, and gut-microbiome, etc. are increasing recognized as novel critical regulators of adolescent health. Currently, the goal of academic research in adolescence is to understand the interactions and underlying mechanisms of these factors and to develop targeted interventions for addressing adolescent health issues. Therefore, this chapter mainly discusses the new trends, key challenges, and translational research potential in these rapidly advancing field of adolescent growth and development.},
}
MeSH Terms:
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Humans
Adolescent
*Adolescent Development/physiology
*Adolescent Health/trends
Gastrointestinal Microbiome/physiology
Epigenesis, Genetic
*Biomedical Research/trends
RevDate: 2026-04-01
Inside the Gut-Mind Connection: Mind-Body Medicine Meets the Microbiome Revolution.
Journal of integrative and complementary medicine [Epub ahead of print].
Additional Links: PMID-41917750
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PubMed:
Citation:
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@article {pmid41917750,
year = {2026},
author = {Yeh, GY and Wayne, PM and Mehta, D},
title = {Inside the Gut-Mind Connection: Mind-Body Medicine Meets the Microbiome Revolution.},
journal = {Journal of integrative and complementary medicine},
volume = {},
number = {},
pages = {27683605261438880},
doi = {10.1177/27683605261438880},
pmid = {41917750},
issn = {2768-3613},
}
RevDate: 2026-04-01
Tryptophan metabolism mediated by the gut microbiota inhibits pyroptosis via the AhR signaling pathway to maintain intestinal epithelial homeostasis.
Microbiome pii:10.1186/s40168-026-02408-7 [Epub ahead of print].
BACKGROUND: The intestinal epithelial barrier protects the gut from pathogen invasion as well as exposure to food antigens and toxins. Increasing evidence has linked the gut microbiota to the function of the intestinal epithelial barrier. Fecal microbiota transplantation (FMT) can treat various intestinal diseases by reshaping the gut microbiota. However, the mechanisms by which FMT exerts its effects across different gastrointestinal conditions remain unclear. Moreover, its limitations are significant, including issues related to donor selection, the complexity of the microbiome, potential infection risks, inconsistent clinical responses, and ethical and legal considerations. Therefore, exploring the microbes and metabolites that mediate the effects of FMT as a replacement for traditional FMT is of great importance. In this study, we aim to investigate the gut microbiota and its metabolites to support the therapeutic role of FMT in intestinal barrier damage and elucidate its potential molecular mechanisms.
RESULTS: Our findings indicate that FMT prevents Lipopolysaccharide (LPS)-induced pyroptosis and damage to the colonic epithelial barrier. Mechanistically, FMT treatment reprograms the composition of gut microbiota, increasing the relative abundance of Lactobacillus reuteri and the levels of tryptophan metabolites (ILA, IAld, and IAA) in the colon, thereby inhibiting pyroptosis and protecting the intestinal epithelial barrier. Importantly, the AhR/NLRP3 axis is essential for the pyroptosis-inhibitory effects of Lactobacillus reuteri and its tryptophan metabolites.
CONCLUSIONS: Our results provide the first evidence that targeting the regulation of Lactobacillus reuteri and tryptophan metabolism is a promising strategy for inhibiting pyroptosis and improving intestinal epithelial homeostasis.
Additional Links: PMID-41917988
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PubMed:
Citation:
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@article {pmid41917988,
year = {2026},
author = {Liu, M and Li, S and Cui, Y and Zhu, X and Wang, Z and Sun, H and Li, D and Liu, B and Shi, Y},
title = {Tryptophan metabolism mediated by the gut microbiota inhibits pyroptosis via the AhR signaling pathway to maintain intestinal epithelial homeostasis.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02408-7},
pmid = {41917988},
issn = {2049-2618},
support = {CARS-34//Modern Agro-industry Technology Research System of China/ ; No. 244200510010//Science and Technology Innovation Leading Talent in Central Plains/ ; },
abstract = {BACKGROUND: The intestinal epithelial barrier protects the gut from pathogen invasion as well as exposure to food antigens and toxins. Increasing evidence has linked the gut microbiota to the function of the intestinal epithelial barrier. Fecal microbiota transplantation (FMT) can treat various intestinal diseases by reshaping the gut microbiota. However, the mechanisms by which FMT exerts its effects across different gastrointestinal conditions remain unclear. Moreover, its limitations are significant, including issues related to donor selection, the complexity of the microbiome, potential infection risks, inconsistent clinical responses, and ethical and legal considerations. Therefore, exploring the microbes and metabolites that mediate the effects of FMT as a replacement for traditional FMT is of great importance. In this study, we aim to investigate the gut microbiota and its metabolites to support the therapeutic role of FMT in intestinal barrier damage and elucidate its potential molecular mechanisms.
RESULTS: Our findings indicate that FMT prevents Lipopolysaccharide (LPS)-induced pyroptosis and damage to the colonic epithelial barrier. Mechanistically, FMT treatment reprograms the composition of gut microbiota, increasing the relative abundance of Lactobacillus reuteri and the levels of tryptophan metabolites (ILA, IAld, and IAA) in the colon, thereby inhibiting pyroptosis and protecting the intestinal epithelial barrier. Importantly, the AhR/NLRP3 axis is essential for the pyroptosis-inhibitory effects of Lactobacillus reuteri and its tryptophan metabolites.
CONCLUSIONS: Our results provide the first evidence that targeting the regulation of Lactobacillus reuteri and tryptophan metabolism is a promising strategy for inhibiting pyroptosis and improving intestinal epithelial homeostasis.},
}
RevDate: 2026-04-01
CmpDate: 2026-04-01
The Importance of Liver-Lung Communication in Pulmonary Vascular Diseases.
Comprehensive Physiology, 16(2):e70140.
In normal health, the liver and lungs enjoy a close anatomic, physiologic, and functional relationship. In the context of pulmonary vascular disease, however, there is accumulating evidence that the interplay between the gut microbiome, hepatic system, and pulmonary vasculature (so-called "gut-liver-lung" axis) plays an important role in driving disease pathogenesis and determining clinical outcomes. Despite recognizing the importance of the gut-liver-lung axis in pulmonary vascular disease however, little is known about the clinical characteristics, circulating factors, and physiologic pathways that mediate this important axis of communication. In this clinical and translationally focused review, we provide an overview of liver-lung communication in normal physiology, and contrast this with gut-liver-lung derangements in pulmonary arterial hypertension, portopulmonary hypertension, and hepatopulmonary syndrome. We conclude with identifying key gaps in knowledge that will need to be addressed in order to manipulate the gut-liver-lung axis to prevent worsening pulmonary vascular disease, develop novel therapeutics, and improve patient outcomes.
Additional Links: PMID-41918066
PubMed:
Citation:
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@article {pmid41918066,
year = {2026},
author = {Singh, N and DuBrock, HM and Prisco, SZ and Dai, Z and Zheng, Q and Fallon, MB and Thenappan, T and Ventetuolo, CE and Jose, A},
title = {The Importance of Liver-Lung Communication in Pulmonary Vascular Diseases.},
journal = {Comprehensive Physiology},
volume = {16},
number = {2},
pages = {e70140},
pmid = {41918066},
issn = {2040-4603},
support = {HL134625/HL/NHLBI NIH HHS/United States ; HL141268/HL/NHLBI NIH HHS/United States ; HL174007/HL/NHLBI NIH HHS/United States ; HL168166/HL/NHLBI NIH HHS/United States ; HL158596/HL/NHLBI NIH HHS/United States ; HL162794/HL/NHLBI NIH HHS/United States ; HL170096/HL/NHLBI NIH HHS/United States ; HL169509/HL/NHLBI NIH HHS/United States ; HL16497/HL/NHLBI NIH HHS/United States ; 23CDA1049093//American Heart Association/ ; },
mesh = {Humans ; *Lung/physiology/physiopathology ; *Liver/physiology/physiopathology ; Animals ; Hepatopulmonary Syndrome/physiopathology ; *Lung Diseases/physiopathology ; Gastrointestinal Microbiome/physiology ; Hypertension, Pulmonary/physiopathology ; },
abstract = {In normal health, the liver and lungs enjoy a close anatomic, physiologic, and functional relationship. In the context of pulmonary vascular disease, however, there is accumulating evidence that the interplay between the gut microbiome, hepatic system, and pulmonary vasculature (so-called "gut-liver-lung" axis) plays an important role in driving disease pathogenesis and determining clinical outcomes. Despite recognizing the importance of the gut-liver-lung axis in pulmonary vascular disease however, little is known about the clinical characteristics, circulating factors, and physiologic pathways that mediate this important axis of communication. In this clinical and translationally focused review, we provide an overview of liver-lung communication in normal physiology, and contrast this with gut-liver-lung derangements in pulmonary arterial hypertension, portopulmonary hypertension, and hepatopulmonary syndrome. We conclude with identifying key gaps in knowledge that will need to be addressed in order to manipulate the gut-liver-lung axis to prevent worsening pulmonary vascular disease, develop novel therapeutics, and improve patient outcomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Lung/physiology/physiopathology
*Liver/physiology/physiopathology
Animals
Hepatopulmonary Syndrome/physiopathology
*Lung Diseases/physiopathology
Gastrointestinal Microbiome/physiology
Hypertension, Pulmonary/physiopathology
RevDate: 2026-04-01
Compositional disparities and potential pathogenic mechanisms of the ocular microbiome in cataract patients: insights from high-throughput sequencing.
BMC microbiology pii:10.1186/s12866-026-05009-4 [Epub ahead of print].
Additional Links: PMID-41918094
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PubMed:
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@article {pmid41918094,
year = {2026},
author = {Liu, Y and Liu, W and Pu, J and Wang, Y and Kang, Z and Zheng, H and Chang, W and Zheng, X and Yang, Q and Xu, H and Feng, Z and Dong, K and Li, J},
title = {Compositional disparities and potential pathogenic mechanisms of the ocular microbiome in cataract patients: insights from high-throughput sequencing.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05009-4},
pmid = {41918094},
issn = {1471-2180},
support = {2023L118//Science and Technology Innovation Program for Higher Education Institutions of Shanxi Province/ ; 2024149//Laboratory Special Project of the Health Commission of Shanxi Province/ ; B202201//Doctoral Fund Project of Shanxi Eye Hospital/ ; 2024NITFID303//Independent Research Program of the National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases/ ; },
}
RevDate: 2026-04-01
CmpDate: 2026-04-01
Fiber: A New Myeloma Prevention Approach with Abundant Positive Effects.
Cancer discovery, 16(4):623-625.
In a recent study by Shah, Cogrossi, and colleagues, patients with overweight/obesity and pre-myeloma diseases (monoclonal gammopathy of undetermined significance or smoldering myeloma) were mailed 12 weeks of high-fiber meals, provided with nutritional counseling, and required to track their food intake and weight. The intervention was well tolerated and improved quality of life, metabolic health, gut microbiome composition, and immune system function while supporting stable or improved multiple myeloma disease trajectories. See related article by Shah et al., p. 697.
Additional Links: PMID-41918359
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PubMed:
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@article {pmid41918359,
year = {2026},
author = {Fairfield, H and Reagan, MR},
title = {Fiber: A New Myeloma Prevention Approach with Abundant Positive Effects.},
journal = {Cancer discovery},
volume = {16},
number = {4},
pages = {623-625},
doi = {10.1158/2159-8290.CD-26-0152},
pmid = {41918359},
issn = {2159-8290},
mesh = {Humans ; *Multiple Myeloma/prevention & control/diet therapy ; *Dietary Fiber/administration & dosage/therapeutic use ; Quality of Life ; Obesity/diet therapy/complications ; },
abstract = {In a recent study by Shah, Cogrossi, and colleagues, patients with overweight/obesity and pre-myeloma diseases (monoclonal gammopathy of undetermined significance or smoldering myeloma) were mailed 12 weeks of high-fiber meals, provided with nutritional counseling, and required to track their food intake and weight. The intervention was well tolerated and improved quality of life, metabolic health, gut microbiome composition, and immune system function while supporting stable or improved multiple myeloma disease trajectories. See related article by Shah et al., p. 697.},
}
MeSH Terms:
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Humans
*Multiple Myeloma/prevention & control/diet therapy
*Dietary Fiber/administration & dosage/therapeutic use
Quality of Life
Obesity/diet therapy/complications
RevDate: 2026-04-01
CmpDate: 2026-04-01
Microbial biodiversity in Tunisian olive grove soils: a reservoir of phytopathogenic fungi and potential beneficial microorganisms.
Frontiers in fungal biology, 7:1770745.
INTRODUCTION: Intercropping in olive orchards increases the risk of soil-borne fungal infections, particularly when associated crops are susceptible to the same pathogens. This study aimed to identify soil-borne microorganisms colonizing the roots and rhizosphere of olive trees in Tunisia intercropped with Solanaceae plants and to evaluate co-occurring bacterial communities for their potential to mitigate wilt disease and promote plant health.
MATERIAL AND METHODS: Endophytic fungi and bacteria were isolated from olive soils and roots collected from three olive orchards subjected to different intercropping systems. Fungal strains were molecularly identified at the species level using Internal Transcribed Spacer (ITS) and translation elongation factor 1-α (TEF1) gene sequencing, while bacterial strains were characterized by rep-PCR profiling and 16S rDNA sequencing. The pathogenicity of selected Fusarium strains was assessed by in vitro inoculation of detached olive leaves, olive twigs, and tomato seedlings. Antagonistic activity of bacterial strains against selected Fusarium species was evaluated using dual-culture assays, and bacteria-fungi interactions were further investigated by scanning electron microscopy (SEM).
RESULTS AND DISCUSSION: A total of 83 fungal and 40 bacterial strains were isolated. The fungal community was dominated by Fusarium species (62%), followed by Phoma (13%) and Alternaria (10%) species, while Verticillium dahliae was not detected at any site. The prevalence and virulence of Fusarium varied among olive groves, with the highest incidence observed at Sidi Bou Ali, where olive trees were intercropped with tomato, and the lowest at Kairouan, where potato intercropping was less frequent. Pathogenicity assays showed that 12 out of 15 of the tested Fusarium strains caused symptoms on both olive tissues and tomato seedlings. Bacterial communities were dominated by Bacillus species and Priestia megaterium. Bacillus species were particularly abundant at the site with the highest Fusarium pressure. The in vitro assay showed that several bacteria exhibited antagonistic activity against pathogenic fungi, with growth inhibition ranging from 8% to 68%, including volatile organic compound-mediated effects. SEM analyses revealed that Bacillus amyloliquefaciens inhibited fungal growth through biofilm formation and hyphal alteration.
Additional Links: PMID-41918498
PubMed:
Citation:
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@article {pmid41918498,
year = {2026},
author = {Belhedi, M and Sghaier-Hammami, B and Hammami, SBM and Ben Slema, S and De Bellis, P and Somma, S and Nafati, H and Hibar, K and Abi Saad, C and Moretti, A and Masiello, M},
title = {Microbial biodiversity in Tunisian olive grove soils: a reservoir of phytopathogenic fungi and potential beneficial microorganisms.},
journal = {Frontiers in fungal biology},
volume = {7},
number = {},
pages = {1770745},
pmid = {41918498},
issn = {2673-6128},
abstract = {INTRODUCTION: Intercropping in olive orchards increases the risk of soil-borne fungal infections, particularly when associated crops are susceptible to the same pathogens. This study aimed to identify soil-borne microorganisms colonizing the roots and rhizosphere of olive trees in Tunisia intercropped with Solanaceae plants and to evaluate co-occurring bacterial communities for their potential to mitigate wilt disease and promote plant health.
MATERIAL AND METHODS: Endophytic fungi and bacteria were isolated from olive soils and roots collected from three olive orchards subjected to different intercropping systems. Fungal strains were molecularly identified at the species level using Internal Transcribed Spacer (ITS) and translation elongation factor 1-α (TEF1) gene sequencing, while bacterial strains were characterized by rep-PCR profiling and 16S rDNA sequencing. The pathogenicity of selected Fusarium strains was assessed by in vitro inoculation of detached olive leaves, olive twigs, and tomato seedlings. Antagonistic activity of bacterial strains against selected Fusarium species was evaluated using dual-culture assays, and bacteria-fungi interactions were further investigated by scanning electron microscopy (SEM).
RESULTS AND DISCUSSION: A total of 83 fungal and 40 bacterial strains were isolated. The fungal community was dominated by Fusarium species (62%), followed by Phoma (13%) and Alternaria (10%) species, while Verticillium dahliae was not detected at any site. The prevalence and virulence of Fusarium varied among olive groves, with the highest incidence observed at Sidi Bou Ali, where olive trees were intercropped with tomato, and the lowest at Kairouan, where potato intercropping was less frequent. Pathogenicity assays showed that 12 out of 15 of the tested Fusarium strains caused symptoms on both olive tissues and tomato seedlings. Bacterial communities were dominated by Bacillus species and Priestia megaterium. Bacillus species were particularly abundant at the site with the highest Fusarium pressure. The in vitro assay showed that several bacteria exhibited antagonistic activity against pathogenic fungi, with growth inhibition ranging from 8% to 68%, including volatile organic compound-mediated effects. SEM analyses revealed that Bacillus amyloliquefaciens inhibited fungal growth through biofilm formation and hyphal alteration.},
}
RevDate: 2026-04-02
Multiparity as a Key Variable in Metabolism and Pregnancy Research.
Current opinion in physiology, 47:.
Parity is defined as the total number of pregnancies reaching ≥20 weeks of gestation. It is an important variable to consider in any metabolic studies involving maternal or offspring health, as multiparity has been identified as a potential driver of numerous aspects of reproduction, maternal-fetal programming, and the health of both maternal and offspring. Currently, it is understood that multiparity may increase the risk of maternal pregnancy complications, such as preeclampsia and gestational diabetes mellitus (GDM), which can have subsequent long-term effects on both the maternal and offspring. Although there are some differences in data between rodents and humans, multiparity has been shown to disrupt glucose homeostasis, decrease pancreatic beta-cell proliferation, alter cardiac hemodynamics, and change the composition of the gut microbiome. In this review, we discuss what is known in the current literature about the impact of multiparity on pregnancy outcomes, maternal health, and offspring health.
Additional Links: PMID-41918618
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Citation:
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@article {pmid41918618,
year = {2026},
author = {Her, TK and Pszczolkowski, VL and Chung, G and Woollett, LA and Alejandro, EU},
title = {Multiparity as a Key Variable in Metabolism and Pregnancy Research.},
journal = {Current opinion in physiology},
volume = {47},
number = {},
pages = {},
pmid = {41918618},
issn = {2468-8673},
support = {R01 DK136237/DK/NIDDK NIH HHS/United States ; },
abstract = {Parity is defined as the total number of pregnancies reaching ≥20 weeks of gestation. It is an important variable to consider in any metabolic studies involving maternal or offspring health, as multiparity has been identified as a potential driver of numerous aspects of reproduction, maternal-fetal programming, and the health of both maternal and offspring. Currently, it is understood that multiparity may increase the risk of maternal pregnancy complications, such as preeclampsia and gestational diabetes mellitus (GDM), which can have subsequent long-term effects on both the maternal and offspring. Although there are some differences in data between rodents and humans, multiparity has been shown to disrupt glucose homeostasis, decrease pancreatic beta-cell proliferation, alter cardiac hemodynamics, and change the composition of the gut microbiome. In this review, we discuss what is known in the current literature about the impact of multiparity on pregnancy outcomes, maternal health, and offspring health.},
}
RevDate: 2026-04-01
CmpDate: 2026-04-01
The neonatal lung microbiome: a dynamic determinant of respiratory health, disease, and novel therapeutics.
Frontiers in pediatrics, 14:1770578.
The neonatal lung, once considered sterile, is now recognized to harbor a dynamic and complex microbiome that plays a critical role in respiratory health and disease. This review synthesizes current evidence on the composition, development, and functional impact of the lung microbiome in neonates, with a focus on its involvement in key respiratory disorders such as bronchopulmonary dysplasia, respiratory syncytial virus infection, neonatal acute respiratory distress syndrome, cystic fibrosis, and asthma predisposition. We place particular emphasis on the bidirectional communication along the gut-lung axis as a central mechanism, wherein intestinal microbiota and their metabolites modulate pulmonary immunity and inflammation. Emerging multi-omics studies that integrate microbial data with host metabolomic and immune profiles are highlighted for their role in deciphering disease-specific dysbiotic signatures and mechanistic pathways. Critically, this review advances the discussion beyond association by evaluating the translational potential of the microbiome as both a diagnostic biomarker and a therapeutic target. We provide a critical appraisal of innovative microbiome-targeted strategies-including probiotics, postbiotics, phage therapy, and bacterial lysates-and discuss the unique challenges and future directions for translating these approaches into safe, effective clinical interventions for vulnerable neonates. By bridging foundational science with clinical implications, this work aims to inform the development of novel, ecology-informed therapeutics to prevent and mitigate neonatal respiratory diseases.
Additional Links: PMID-41918694
PubMed:
Citation:
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@article {pmid41918694,
year = {2026},
author = {Zheng, W and Liang, Y and Li, J},
title = {The neonatal lung microbiome: a dynamic determinant of respiratory health, disease, and novel therapeutics.},
journal = {Frontiers in pediatrics},
volume = {14},
number = {},
pages = {1770578},
pmid = {41918694},
issn = {2296-2360},
abstract = {The neonatal lung, once considered sterile, is now recognized to harbor a dynamic and complex microbiome that plays a critical role in respiratory health and disease. This review synthesizes current evidence on the composition, development, and functional impact of the lung microbiome in neonates, with a focus on its involvement in key respiratory disorders such as bronchopulmonary dysplasia, respiratory syncytial virus infection, neonatal acute respiratory distress syndrome, cystic fibrosis, and asthma predisposition. We place particular emphasis on the bidirectional communication along the gut-lung axis as a central mechanism, wherein intestinal microbiota and their metabolites modulate pulmonary immunity and inflammation. Emerging multi-omics studies that integrate microbial data with host metabolomic and immune profiles are highlighted for their role in deciphering disease-specific dysbiotic signatures and mechanistic pathways. Critically, this review advances the discussion beyond association by evaluating the translational potential of the microbiome as both a diagnostic biomarker and a therapeutic target. We provide a critical appraisal of innovative microbiome-targeted strategies-including probiotics, postbiotics, phage therapy, and bacterial lysates-and discuss the unique challenges and future directions for translating these approaches into safe, effective clinical interventions for vulnerable neonates. By bridging foundational science with clinical implications, this work aims to inform the development of novel, ecology-informed therapeutics to prevent and mitigate neonatal respiratory diseases.},
}
RevDate: 2026-04-01
CmpDate: 2026-04-01
Inflammation at the maternal-fetal interface: a perspective on interacting risk factors for preterm birth in sub-Saharan African women living with HIV.
Frontiers in immunology, 17:1741921.
Globally, approximately 10% of all babies are born prematurely. The vast majority of preterm births, defined as birth <37 weeks of gestation, occur in low- and middle-income countries (LMICs) in Asia and Africa. Furthermore, premature birth has become the leading cause of death in infants under the age of 5 years. Thus, to improve maternal and infant health outcomes, better diagnostics and intervention strategies are urgently needed. However, the multifactorial etiology of preterm birth provides a major obstacle in achieving this goal. A common factor to many adverse birth outcomes, including preterm birth, is aberrant immune activation at the maternal-fetal interface. The specific cause of immune activation, however, remains unknown. Both HIV and an anaerobe-rich vaginal microbiota have been independently identified as risk factors for preterm birth, and both factors also promote inflammation and immune activation at mucosal sites. The interplay of HIV and microbiota is widely acknowledged, although mostly in the context of the intestinal microbiome. This review will highlight how the regulatory function of macrophages at the maternal-fetal interface can be altered in response to HIV and antiretroviral therapy and to changes in vaginal microbiota. We proceed to discuss interactions between the various factors and propose a dual-hit model in which macrophages act as mediators of inflammation at the maternal-fetal interface in response to specific vaginal commensals and HIV infection in sub-Saharan African women with preterm birth outcomes.
Additional Links: PMID-41918737
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Citation:
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@article {pmid41918737,
year = {2026},
author = {Edwards, JS and De Paris, K},
title = {Inflammation at the maternal-fetal interface: a perspective on interacting risk factors for preterm birth in sub-Saharan African women living with HIV.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1741921},
pmid = {41918737},
issn = {1664-3224},
mesh = {Humans ; Female ; Pregnancy ; *HIV Infections/immunology/drug therapy/complications/epidemiology/virology ; *Premature Birth/immunology/epidemiology/etiology ; Risk Factors ; Africa South of the Sahara/epidemiology ; *Inflammation/immunology ; Vagina/microbiology/immunology ; *Pregnancy Complications, Infectious/immunology/virology ; Microbiota/immunology ; Macrophages/immunology ; Infant, Newborn ; *Maternal-Fetal Exchange/immunology ; },
abstract = {Globally, approximately 10% of all babies are born prematurely. The vast majority of preterm births, defined as birth <37 weeks of gestation, occur in low- and middle-income countries (LMICs) in Asia and Africa. Furthermore, premature birth has become the leading cause of death in infants under the age of 5 years. Thus, to improve maternal and infant health outcomes, better diagnostics and intervention strategies are urgently needed. However, the multifactorial etiology of preterm birth provides a major obstacle in achieving this goal. A common factor to many adverse birth outcomes, including preterm birth, is aberrant immune activation at the maternal-fetal interface. The specific cause of immune activation, however, remains unknown. Both HIV and an anaerobe-rich vaginal microbiota have been independently identified as risk factors for preterm birth, and both factors also promote inflammation and immune activation at mucosal sites. The interplay of HIV and microbiota is widely acknowledged, although mostly in the context of the intestinal microbiome. This review will highlight how the regulatory function of macrophages at the maternal-fetal interface can be altered in response to HIV and antiretroviral therapy and to changes in vaginal microbiota. We proceed to discuss interactions between the various factors and propose a dual-hit model in which macrophages act as mediators of inflammation at the maternal-fetal interface in response to specific vaginal commensals and HIV infection in sub-Saharan African women with preterm birth outcomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
Pregnancy
*HIV Infections/immunology/drug therapy/complications/epidemiology/virology
*Premature Birth/immunology/epidemiology/etiology
Risk Factors
Africa South of the Sahara/epidemiology
*Inflammation/immunology
Vagina/microbiology/immunology
*Pregnancy Complications, Infectious/immunology/virology
Microbiota/immunology
Macrophages/immunology
Infant, Newborn
*Maternal-Fetal Exchange/immunology
RevDate: 2026-04-01
CmpDate: 2026-04-01
Mitochondrial transplantation ameliorates experimental autoimmune encephalomyelitis by modulating the Th17/Treg balance and restoring metabolic homeostasis.
Frontiers in immunology, 17:1698136.
INTRODUCTION: Mitochondrial dysfunction has been increasingly implicated in the pathogenesis of multiple sclerosis (MS), contributing to oxidative stress, immune dysregulation, and neurodegeneration. Current therapies primarily target inflammation but do not adequately address mitochondrial impairment or progressive tissue damage. This study aimed to evaluate the therapeutic potential of mitochondrial transplantation in experimental autoimmune encephalomyelitis (EAE), a murine model of MS, by investigating its effects on immune modulation, mitochondrial function, and tissue integrity.
METHODS: EAE was induced in mice using myelin oligodendrocyte glycoprotein. Isolated mitochondria were administered intravenously, and clinical progression, spinal cord histology, immune cell populations, mitochondrial activity, fibrosis, and gut microbiota composition were assessed. Additionally, human peripheral blood mononuclear cells (PBMCs) from MS patients were co-cultured with mitochondria to examine ATP production, reactive oxygen species levels, and T cell differentiation.
RESULTS: Mitochondrial transplantation significantly reduced EAE severity, spinal cord inflammation, demyelination, and fibrosis. Treated mice showed increased regulatory T (Treg) cells, reduced T helper 17 (Th17) cells, improved mitochondrial biogenesis, and decreased oxidative stress. Gut microbiome analysis revealed beneficial compositional changes. In human PBMCs, mitochondrial transfer enhanced ATP synthesis, suppressed mitochondrial ROS, and promoted Treg differentiation while inhibiting pro-inflammatory cytokines.
DISCUSSION: Our findings suggest that mitochondrial transplantation restores mitochondrial function, rebalances immune responses, and mitigates neuroinflammation and fibrosis in EAE. This approach offers a novel therapeutic strategy for MS by addressing both metabolic and immunological drivers of disease progression.
Additional Links: PMID-41918738
PubMed:
Citation:
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@article {pmid41918738,
year = {2026},
author = {Lee, AR and Yang, SW and Lee, SY and Jeon, SB and Kang, HY and Choi, JW and Park, JH and Park, JH and Son, SB and Jeong, Y and Lee, JH and Kim, W and Cho, ML},
title = {Mitochondrial transplantation ameliorates experimental autoimmune encephalomyelitis by modulating the Th17/Treg balance and restoring metabolic homeostasis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1698136},
pmid = {41918738},
issn = {1664-3224},
mesh = {*Encephalomyelitis, Autoimmune, Experimental/therapy/immunology/metabolism/pathology ; Animals ; *Th17 Cells/immunology/metabolism ; *Mitochondria/transplantation/metabolism ; *T-Lymphocytes, Regulatory/immunology/metabolism ; Mice ; Humans ; Female ; Homeostasis ; Multiple Sclerosis/immunology/therapy/metabolism ; Oxidative Stress ; Mice, Inbred C57BL ; Gastrointestinal Microbiome ; Spinal Cord/pathology/immunology/metabolism ; Disease Models, Animal ; Reactive Oxygen Species/metabolism ; },
abstract = {INTRODUCTION: Mitochondrial dysfunction has been increasingly implicated in the pathogenesis of multiple sclerosis (MS), contributing to oxidative stress, immune dysregulation, and neurodegeneration. Current therapies primarily target inflammation but do not adequately address mitochondrial impairment or progressive tissue damage. This study aimed to evaluate the therapeutic potential of mitochondrial transplantation in experimental autoimmune encephalomyelitis (EAE), a murine model of MS, by investigating its effects on immune modulation, mitochondrial function, and tissue integrity.
METHODS: EAE was induced in mice using myelin oligodendrocyte glycoprotein. Isolated mitochondria were administered intravenously, and clinical progression, spinal cord histology, immune cell populations, mitochondrial activity, fibrosis, and gut microbiota composition were assessed. Additionally, human peripheral blood mononuclear cells (PBMCs) from MS patients were co-cultured with mitochondria to examine ATP production, reactive oxygen species levels, and T cell differentiation.
RESULTS: Mitochondrial transplantation significantly reduced EAE severity, spinal cord inflammation, demyelination, and fibrosis. Treated mice showed increased regulatory T (Treg) cells, reduced T helper 17 (Th17) cells, improved mitochondrial biogenesis, and decreased oxidative stress. Gut microbiome analysis revealed beneficial compositional changes. In human PBMCs, mitochondrial transfer enhanced ATP synthesis, suppressed mitochondrial ROS, and promoted Treg differentiation while inhibiting pro-inflammatory cytokines.
DISCUSSION: Our findings suggest that mitochondrial transplantation restores mitochondrial function, rebalances immune responses, and mitigates neuroinflammation and fibrosis in EAE. This approach offers a novel therapeutic strategy for MS by addressing both metabolic and immunological drivers of disease progression.},
}
MeSH Terms:
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hide MeSH Terms
*Encephalomyelitis, Autoimmune, Experimental/therapy/immunology/metabolism/pathology
Animals
*Th17 Cells/immunology/metabolism
*Mitochondria/transplantation/metabolism
*T-Lymphocytes, Regulatory/immunology/metabolism
Mice
Humans
Female
Homeostasis
Multiple Sclerosis/immunology/therapy/metabolism
Oxidative Stress
Mice, Inbred C57BL
Gastrointestinal Microbiome
Spinal Cord/pathology/immunology/metabolism
Disease Models, Animal
Reactive Oxygen Species/metabolism
RevDate: 2026-04-01
CmpDate: 2026-04-01
Presence of neutrophil extracellular traps (NETs) in different types of human urinary tract infections (UTI). A pilot study.
Frontiers in immunology, 17:1745166.
INTRODUCTION: Activated polymorphonuclear neutrophils (PMN) release neutrophil extracellular traps (NETs) composed of a web-like DNA core, concomitant with nuclear histones, granular peptides and enzymes. NETs in human urine and their potential role in human urinary tract infections (UTI) pathogenesis is still understudied. This pilot study aimed to analyze presence of NETs in urine samples of patients with different types of UTI.
METHODS: Urine and blood samples were collected from three cohorts: group (A) included females (n = 24) with cystitis (n = 10), pyelonephritis (n = 6), and asymptomatic bacteriuria (n = 8); group (B) composed of males with catheter-associated UTI (n = 20) and a control group (C) consisting of healthy patients of mixed gender (n = 20). NETs in urine samples were confirmed by immunofluorescence-based detection of neutrophil elastase and citrullinated histone. The presence of granular enzymes (myeloperoxidase, cathelicidin), calprotectin (subunits S100A8, S100A9) and CD15[+] PMN were detected by ELISA, western blot and flow cytometry, respectively. To study potential associations of NETs with the respective UTI microbiome, bacterial spectrum of each urine sample was estimated by 16S rRNA gene analysis.
RESULTS AND DISCUSSION: On average, 23.29% ± 16.89% of PMN forming NETs were detected in group A [subgroups cystitis (27.72% ± 17.88%), pyelonephritis (22.75% ± 12.91%), asymptomatic bacteriuria (18.17% ± 17.14%)] and 30.63% ± 17.88% in group B, with no differences observed between UTI groups, including patients with asymptomatic bacteriuria. For the control group (group C), a low incidence of NET-releasing cells was observed (0.32% ± 1.42%), resulting in a significant difference (p < 0.05) when compared to all UTI groups studied. Furthermore, different NET-phenotypes [i. e. spread NETs (sprNETs), diffuse NETs (diffNETs) and aggregated NETs (aggNETs)] were detected in both UTI groups. The presence of NET-associated proteins was confirmed in all UTI groups, but absent in the control samples. Microbiome analyses revealed a reduced microbial variability within UTI samples with the predominance of the bacterial family Enterobacteriaceae. Overall, PMN-derived NETs were consistently found in all UTI samples, suggesting a role of NETs in diverse UTI pathologies. Future studies should investigate its utility as an inflammatory biomarker in clinical human UTI.
Additional Links: PMID-41918743
PubMed:
Citation:
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@article {pmid41918743,
year = {2026},
author = {Schröder Alvarez, L and Conejeros, I and Espinosa, G and Salinas-Varas, C and Ott, B and Weigel, M and Imirzalioglu, C and Fritzenwanker, M and Windhorst, AC and Hain, T and Taubert, A and Hermosilla, C and Wagenlehner, F},
title = {Presence of neutrophil extracellular traps (NETs) in different types of human urinary tract infections (UTI). A pilot study.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1745166},
pmid = {41918743},
issn = {1664-3224},
mesh = {Humans ; *Extracellular Traps/immunology/metabolism ; Female ; Pilot Projects ; Male ; *Urinary Tract Infections/immunology/microbiology/urine ; Middle Aged ; Adult ; *Neutrophils/immunology/metabolism ; Aged ; Biomarkers ; Pyelonephritis/immunology/urine ; Bacteriuria/immunology ; },
abstract = {INTRODUCTION: Activated polymorphonuclear neutrophils (PMN) release neutrophil extracellular traps (NETs) composed of a web-like DNA core, concomitant with nuclear histones, granular peptides and enzymes. NETs in human urine and their potential role in human urinary tract infections (UTI) pathogenesis is still understudied. This pilot study aimed to analyze presence of NETs in urine samples of patients with different types of UTI.
METHODS: Urine and blood samples were collected from three cohorts: group (A) included females (n = 24) with cystitis (n = 10), pyelonephritis (n = 6), and asymptomatic bacteriuria (n = 8); group (B) composed of males with catheter-associated UTI (n = 20) and a control group (C) consisting of healthy patients of mixed gender (n = 20). NETs in urine samples were confirmed by immunofluorescence-based detection of neutrophil elastase and citrullinated histone. The presence of granular enzymes (myeloperoxidase, cathelicidin), calprotectin (subunits S100A8, S100A9) and CD15[+] PMN were detected by ELISA, western blot and flow cytometry, respectively. To study potential associations of NETs with the respective UTI microbiome, bacterial spectrum of each urine sample was estimated by 16S rRNA gene analysis.
RESULTS AND DISCUSSION: On average, 23.29% ± 16.89% of PMN forming NETs were detected in group A [subgroups cystitis (27.72% ± 17.88%), pyelonephritis (22.75% ± 12.91%), asymptomatic bacteriuria (18.17% ± 17.14%)] and 30.63% ± 17.88% in group B, with no differences observed between UTI groups, including patients with asymptomatic bacteriuria. For the control group (group C), a low incidence of NET-releasing cells was observed (0.32% ± 1.42%), resulting in a significant difference (p < 0.05) when compared to all UTI groups studied. Furthermore, different NET-phenotypes [i. e. spread NETs (sprNETs), diffuse NETs (diffNETs) and aggregated NETs (aggNETs)] were detected in both UTI groups. The presence of NET-associated proteins was confirmed in all UTI groups, but absent in the control samples. Microbiome analyses revealed a reduced microbial variability within UTI samples with the predominance of the bacterial family Enterobacteriaceae. Overall, PMN-derived NETs were consistently found in all UTI samples, suggesting a role of NETs in diverse UTI pathologies. Future studies should investigate its utility as an inflammatory biomarker in clinical human UTI.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Extracellular Traps/immunology/metabolism
Female
Pilot Projects
Male
*Urinary Tract Infections/immunology/microbiology/urine
Middle Aged
Adult
*Neutrophils/immunology/metabolism
Aged
Biomarkers
Pyelonephritis/immunology/urine
Bacteriuria/immunology
RevDate: 2026-04-01
CmpDate: 2026-04-01
Uremic Clearance Granules Regulate Immune Equilibrium via Gut Microbiome to Alleviate Chronic Renal Failure.
Biomaterials research, 30:0342.
Chronic renal failure (CRF) is the common end point of various chronic kidney diseases, and there is currently no specific drug for CRF. Effectively halting its progression remains a clinical challenge. Gut microbiota disorders are a key factor influencing immune dysfunction in chronic kidney disease patients. Intervening in gut microbiota to improve immune regulatory function in patients could serve as a new strategy for treating CRF with Traditional Chinese Medicine. Uremic Clearance Granules (UCG), a Traditional Chinese Medicine formulation, effectively attenuate CRF progression, but their active components and mechanisms remain undefined. This study investigates how UCG mitigate CRF via coordinated regulation of gut microbiota, metabolites, and the T helper 17 cells / regulatory T cell axis. Using an adenine-induced CRF mouse model, we combined gut microbiota depletion, fecal microbiota transplantation, 16S rRNA sequencing, and metabolomics to delineate the gut-kidney interactions underlying UCG efficacy. Flow cytometry quantified immune cell profiles in blood, and microbial intervention experiments verified the therapeutic role of Bifidobacterium animalis (B. animalis). In this study, we found that UCG treatment alleviated renal injury, reduced intestinal permeability, and up-regulated intestinal barrier markers. Microbiota depletion and fecal microbiota transplantation demonstrated that UCG's renoprotective effects depend on gut microbial modulation. Specifically, UCG ameliorates CRF through gut-kidney axis remodeling by enhancing B. animalis abundance and sophocarpine, thereby rebalancing T helper 17/regulatory T immunity and preserving renal function. These findings identify a microbiota-dependent immunometabolic mechanism for UCG and highlight a potential therapeutic strategy for CRF via the drug-microbiota axis.
Additional Links: PMID-41918843
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@article {pmid41918843,
year = {2026},
author = {Huang, Q and Liang, Z and Cui, Y and Diao, J and Zhou, T and Shi, L and Deng, Z and Wang, R and Yuan, H and Chen, K and Du, Y and Chen, A and Chen, J and Xiao, W},
title = {Uremic Clearance Granules Regulate Immune Equilibrium via Gut Microbiome to Alleviate Chronic Renal Failure.},
journal = {Biomaterials research},
volume = {30},
number = {},
pages = {0342},
pmid = {41918843},
issn = {1226-4601},
abstract = {Chronic renal failure (CRF) is the common end point of various chronic kidney diseases, and there is currently no specific drug for CRF. Effectively halting its progression remains a clinical challenge. Gut microbiota disorders are a key factor influencing immune dysfunction in chronic kidney disease patients. Intervening in gut microbiota to improve immune regulatory function in patients could serve as a new strategy for treating CRF with Traditional Chinese Medicine. Uremic Clearance Granules (UCG), a Traditional Chinese Medicine formulation, effectively attenuate CRF progression, but their active components and mechanisms remain undefined. This study investigates how UCG mitigate CRF via coordinated regulation of gut microbiota, metabolites, and the T helper 17 cells / regulatory T cell axis. Using an adenine-induced CRF mouse model, we combined gut microbiota depletion, fecal microbiota transplantation, 16S rRNA sequencing, and metabolomics to delineate the gut-kidney interactions underlying UCG efficacy. Flow cytometry quantified immune cell profiles in blood, and microbial intervention experiments verified the therapeutic role of Bifidobacterium animalis (B. animalis). In this study, we found that UCG treatment alleviated renal injury, reduced intestinal permeability, and up-regulated intestinal barrier markers. Microbiota depletion and fecal microbiota transplantation demonstrated that UCG's renoprotective effects depend on gut microbial modulation. Specifically, UCG ameliorates CRF through gut-kidney axis remodeling by enhancing B. animalis abundance and sophocarpine, thereby rebalancing T helper 17/regulatory T immunity and preserving renal function. These findings identify a microbiota-dependent immunometabolic mechanism for UCG and highlight a potential therapeutic strategy for CRF via the drug-microbiota axis.},
}
RevDate: 2026-04-01
CmpDate: 2026-04-01
MetaPepticon: automated prediction of anticancer peptides from microbial genomes and metagenomes.
PeerJ, 14:e20990.
BACKGROUND: Anticancer peptides (ACPs) are increasingly recognized as promising therapeutic candidates due to their ability to selectively target cancer cells. However, the systematic discovery of novel ACPs, particularly from high-throughput sequencing datasets, remains hindered by technical and methodological limitations. Current prediction frameworks require pre-extracted peptide sequences, involve manual preprocessing, and yield variable results, which restricts their applicability for large-scale, data-driven discovery.
METHODS: To address these limitations, we developed MetaPepticon, a modular, end-to-end pipeline for the discovery of ACP candidates from diverse sequencing inputs, including raw genomic, metagenomic, transcriptomic, and metatranscriptomic reads, as well as assembled contigs and peptide sequences. MetaPepticon automates quality control, filtering, assembly, small open reading frame prediction, ACP classification using multiple predictive algorithms, and in silico toxicity filtering.
RESULTS: MetaPepticon enables scalable and reproducible ACP prediction from raw sequences through integration of multiple predictors within a configurable agreement framework. Applied to 41,171 microbial genomes and 4,072,884 peptides, MetaPepticon identified 10,725 moderate-agreement ACP candidates, including 4,590 novel, non-toxic peptides. MetaPepticon expands the practical applicability of existing ACP prediction methods to high-throughput sequencing data and is freely available at: https://github.com/arikanlab/MetaPepticon.
Additional Links: PMID-41918857
PubMed:
Citation:
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@article {pmid41918857,
year = {2026},
author = {Erözden, AA and Tavşanlı, N and Demirel, G and Sanli, NO and Çalışkan, M and Arıkan, M},
title = {MetaPepticon: automated prediction of anticancer peptides from microbial genomes and metagenomes.},
journal = {PeerJ},
volume = {14},
number = {},
pages = {e20990},
pmid = {41918857},
issn = {2167-8359},
mesh = {*Peptides/genetics/pharmacology ; *Antineoplastic Agents/pharmacology ; *Metagenome ; Humans ; *Genome, Microbial ; *Software ; High-Throughput Nucleotide Sequencing ; Algorithms ; Computational Biology/methods ; },
abstract = {BACKGROUND: Anticancer peptides (ACPs) are increasingly recognized as promising therapeutic candidates due to their ability to selectively target cancer cells. However, the systematic discovery of novel ACPs, particularly from high-throughput sequencing datasets, remains hindered by technical and methodological limitations. Current prediction frameworks require pre-extracted peptide sequences, involve manual preprocessing, and yield variable results, which restricts their applicability for large-scale, data-driven discovery.
METHODS: To address these limitations, we developed MetaPepticon, a modular, end-to-end pipeline for the discovery of ACP candidates from diverse sequencing inputs, including raw genomic, metagenomic, transcriptomic, and metatranscriptomic reads, as well as assembled contigs and peptide sequences. MetaPepticon automates quality control, filtering, assembly, small open reading frame prediction, ACP classification using multiple predictive algorithms, and in silico toxicity filtering.
RESULTS: MetaPepticon enables scalable and reproducible ACP prediction from raw sequences through integration of multiple predictors within a configurable agreement framework. Applied to 41,171 microbial genomes and 4,072,884 peptides, MetaPepticon identified 10,725 moderate-agreement ACP candidates, including 4,590 novel, non-toxic peptides. MetaPepticon expands the practical applicability of existing ACP prediction methods to high-throughput sequencing data and is freely available at: https://github.com/arikanlab/MetaPepticon.},
}
MeSH Terms:
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*Peptides/genetics/pharmacology
*Antineoplastic Agents/pharmacology
*Metagenome
Humans
*Genome, Microbial
*Software
High-Throughput Nucleotide Sequencing
Algorithms
Computational Biology/methods
RevDate: 2026-04-01
CmpDate: 2026-04-01
Microbiome and metabolite signatures for cirrhosis to HCC risk stratification: progress, controversies, and gaps.
Frontiers in cellular and infection microbiology, 16:1793213.
The progression from cirrhosis to hepatocellular carcinoma (HCC) is a key outcome in the management of chronic liver disease. This process has a long incubation period and significant individual differences, making early warning still difficult. Clinical follow-up mainly relies on imaging examinations and alpha fetoprotein, but the ability to identify high risk precancerous states is limited. The imbalance of gut microbiota and its metabolites may occur earlier than the visible stage of tumors. They can affect barrier integrity, chronic inflammation, immune surveillance, and metabolic homeostasis through the gut liver axis, and participate in the formation of a pro tumor microenvironment. Therefore, such changes may provide more upstream risk stratification clues for the population with cirrhosis. This article summarizes previous research evidence and summarizes the common microbiome and metabolite characteristics of cirrhosis and high-risk populations, including a decrease in short chain fatty acid (SCFA) related symbiotic bacteria, an increase in inflammation related bacteria, bile acid spectrum shift, and other intestinal derived metabolite abnormalities. This article also outlines the key mechanisms that these features may correspond to, such as barrier damage and microbial translocation, immune suppression, etc. There are still significant uncertainties at present. The effect of SCFA is context dependent. Different etiologies, diets, medications, and complications can lead to significant confounding and affect cross cohort consistency. Subsequent research requires longitudinal cohort validation and the promotion of multi omics integration and the construction of interpretable predictive models to support clinical translation.
Additional Links: PMID-41918873
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@article {pmid41918873,
year = {2026},
author = {Duan, Y and Yang, M and Li, M and Sun, Y and Liu, S},
title = {Microbiome and metabolite signatures for cirrhosis to HCC risk stratification: progress, controversies, and gaps.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1793213},
pmid = {41918873},
issn = {2235-2988},
mesh = {Humans ; *Carcinoma, Hepatocellular/microbiology/metabolism/pathology/etiology ; *Liver Cirrhosis/microbiology/metabolism/complications/pathology ; *Gastrointestinal Microbiome ; *Liver Neoplasms/microbiology/metabolism/pathology/etiology ; Fatty Acids, Volatile/metabolism ; Risk Assessment ; Disease Progression ; Dysbiosis ; Bile Acids and Salts/metabolism ; },
abstract = {The progression from cirrhosis to hepatocellular carcinoma (HCC) is a key outcome in the management of chronic liver disease. This process has a long incubation period and significant individual differences, making early warning still difficult. Clinical follow-up mainly relies on imaging examinations and alpha fetoprotein, but the ability to identify high risk precancerous states is limited. The imbalance of gut microbiota and its metabolites may occur earlier than the visible stage of tumors. They can affect barrier integrity, chronic inflammation, immune surveillance, and metabolic homeostasis through the gut liver axis, and participate in the formation of a pro tumor microenvironment. Therefore, such changes may provide more upstream risk stratification clues for the population with cirrhosis. This article summarizes previous research evidence and summarizes the common microbiome and metabolite characteristics of cirrhosis and high-risk populations, including a decrease in short chain fatty acid (SCFA) related symbiotic bacteria, an increase in inflammation related bacteria, bile acid spectrum shift, and other intestinal derived metabolite abnormalities. This article also outlines the key mechanisms that these features may correspond to, such as barrier damage and microbial translocation, immune suppression, etc. There are still significant uncertainties at present. The effect of SCFA is context dependent. Different etiologies, diets, medications, and complications can lead to significant confounding and affect cross cohort consistency. Subsequent research requires longitudinal cohort validation and the promotion of multi omics integration and the construction of interpretable predictive models to support clinical translation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Carcinoma, Hepatocellular/microbiology/metabolism/pathology/etiology
*Liver Cirrhosis/microbiology/metabolism/complications/pathology
*Gastrointestinal Microbiome
*Liver Neoplasms/microbiology/metabolism/pathology/etiology
Fatty Acids, Volatile/metabolism
Risk Assessment
Disease Progression
Dysbiosis
Bile Acids and Salts/metabolism
RevDate: 2026-04-01
CmpDate: 2026-04-01
Integrative multi-omics analysis reveals probiotic-induced microbiota shifts in women with gestational diabetes.
Frontiers in cellular and infection microbiology, 16:1782744.
INTRODUCTION: Gestational diabetes mellitus (GDM) is a common pregnancy disorder. It is associated with impaired glucose tolerance and insulin resistance, increasing the potential risks for both maternal and fetal complications. GDM is associated with an increased risk of type 2 diabetes later in life. Management is a big issue in maternal health. New work has underscored the role of the gut microbiota in metabolism and immune function. This indicates that probiotics might exert their mode of action through modulating the microbiota and controlling metabolism.
METHODS: This study employs a multi-omics strategy to assess the impact of probiotic administration on gut microbiota composition, metabolomic profiles, and host gene expression in GDM women. Women with GDM received probiotics for 8 weeks. Metagenomic sequencing quantified alterations of gut microbiota composition and LC-MS provided untargeted metabolomics in serum and urine. Gene expression was analyzed by qRT-PCR in reference to other physiological factors such as insulin signaling, inflammation, oxidative stress, and gut barrier. Data integration was performed using Principal Component Analysis (PCA), Partial Least Squares Discriminant Analysis (PLS-DA), and network analysis, then pathway enrichment analysis was conducted with KEGG and MetaboAnalyst.
RESULTS: The supplementation of probiotics resulted in a significant change of gut microbiota (Lactobacillus 7.6-fold; Bifidobacterium 6.4-fold). Escherichia/Shigella was reduced. The amounts of short-chain fatty acids (SCFAs), especially butyrate and acetate, were increased 3.1 fold and 2.5 fold, respectively. In a gene expression assessment, the insulin receptor and AKT increased 2.5- and 1.9-fold higher, respectively, indicating greater insulin sensitivity. Levels of TNF-α and IL-6 decreased; however, genes related to gut barrier function (ZO-1, CLDN1) increased.
DISCUSSION: The administration of probiotic has a great impact on gut microbiome, metabolic activity, and host gene expression in women with GDM. Our data indicate that probiotics may represent a non-invasive and safe treatment for gestational diabetes through enhancing insulin sensitivity, anti-inflammatory environment, and gut health status. Larger confirmatory studies are needed to corroborate these findings and augment future clinical application of probiotics in GDM patients.
Additional Links: PMID-41918874
PubMed:
Citation:
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@article {pmid41918874,
year = {2026},
author = {Su, X and Yang, J and Le, Z and Xiao, J and Zhao, D},
title = {Integrative multi-omics analysis reveals probiotic-induced microbiota shifts in women with gestational diabetes.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1782744},
pmid = {41918874},
issn = {2235-2988},
mesh = {Humans ; Female ; *Probiotics/administration & dosage ; *Diabetes, Gestational/microbiology ; Pregnancy ; *Gastrointestinal Microbiome/drug effects ; Adult ; Metabolomics/methods ; Metagenomics ; Multiomics ; },
abstract = {INTRODUCTION: Gestational diabetes mellitus (GDM) is a common pregnancy disorder. It is associated with impaired glucose tolerance and insulin resistance, increasing the potential risks for both maternal and fetal complications. GDM is associated with an increased risk of type 2 diabetes later in life. Management is a big issue in maternal health. New work has underscored the role of the gut microbiota in metabolism and immune function. This indicates that probiotics might exert their mode of action through modulating the microbiota and controlling metabolism.
METHODS: This study employs a multi-omics strategy to assess the impact of probiotic administration on gut microbiota composition, metabolomic profiles, and host gene expression in GDM women. Women with GDM received probiotics for 8 weeks. Metagenomic sequencing quantified alterations of gut microbiota composition and LC-MS provided untargeted metabolomics in serum and urine. Gene expression was analyzed by qRT-PCR in reference to other physiological factors such as insulin signaling, inflammation, oxidative stress, and gut barrier. Data integration was performed using Principal Component Analysis (PCA), Partial Least Squares Discriminant Analysis (PLS-DA), and network analysis, then pathway enrichment analysis was conducted with KEGG and MetaboAnalyst.
RESULTS: The supplementation of probiotics resulted in a significant change of gut microbiota (Lactobacillus 7.6-fold; Bifidobacterium 6.4-fold). Escherichia/Shigella was reduced. The amounts of short-chain fatty acids (SCFAs), especially butyrate and acetate, were increased 3.1 fold and 2.5 fold, respectively. In a gene expression assessment, the insulin receptor and AKT increased 2.5- and 1.9-fold higher, respectively, indicating greater insulin sensitivity. Levels of TNF-α and IL-6 decreased; however, genes related to gut barrier function (ZO-1, CLDN1) increased.
DISCUSSION: The administration of probiotic has a great impact on gut microbiome, metabolic activity, and host gene expression in women with GDM. Our data indicate that probiotics may represent a non-invasive and safe treatment for gestational diabetes through enhancing insulin sensitivity, anti-inflammatory environment, and gut health status. Larger confirmatory studies are needed to corroborate these findings and augment future clinical application of probiotics in GDM patients.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
*Probiotics/administration & dosage
*Diabetes, Gestational/microbiology
Pregnancy
*Gastrointestinal Microbiome/drug effects
Adult
Metabolomics/methods
Metagenomics
Multiomics
RevDate: 2026-04-01
CmpDate: 2026-04-01
Airway microbial dysbiosis and oxidative mitochondrial DNA damage in the development of bronchopulmonary dysplasia.
ERJ open research, 12(2):.
BACKGROUND: This study investigated the association between airway microbiome composition, oxidative mitochondrial DNA (mtDNA) damage and the development of bronchopulmonary dysplasia (BPD) in preterm infants.
METHODS: A prospective cohort study enrolled 82 very low birth weight preterm infants (<32 weeks' gestation). Tracheal aspirates (TA) were collected at birth and on postnatal day 28. Airway microbial diversity and composition were assessed using 16S rRNA sequencing. Oxidative mtDNA damage was measured using 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in TA samples. We used PICRUSt2-based metagenome predictions from 16S rRNA gene sequencing of TA samples, with functional pathway annotations based on the Kyoto Encyclopedia of Genes and Genomes (KEGG) database.
RESULTS: Infants who developed BPD (n=25) had lower gestational age, birth weight and prolonged ventilatory support (p<0.05). Oxidative mtDNA damage was significantly higher in infants with BPD, particularly in moderate-to-severe cases (p<0.05). BPD was associated with reduced microbial alpha diversity and distinct beta diversity clustering. Infants with BPD exhibited higher relative abundance of Proteobacteria and lower relative abundance of Firmicutes, with enrichment of Stenotrophomonas, Acinetobacter and Serratia (p<0.05). By day 28, KEGG-based functional predictions revealed enrichment in microbial pathways related to bacterial motility proteins, circadian rhythm signalling pathway, MAPK signalling pathway and α-linolenic acid metabolism. Proteobacteria abundance correlated positively with oxidative mtDNA damage (r=0.49, p<0.01).
CONCLUSIONS: Airway microbial dysbiosis and oxidative mtDNA damage are strongly associated with BPD severity. Targeting oxidative stress and microbiome modulation may offer potential strategies for BPD prevention and management.
Additional Links: PMID-41918946
PubMed:
Citation:
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@article {pmid41918946,
year = {2026},
author = {Hsiao, CC and Chen, CH and Liu, CS and Wang, JY and Lin, CY and Yang, KD and Lee, CH and Lin, TT and Lin, CJ and Tsai, YG},
title = {Airway microbial dysbiosis and oxidative mitochondrial DNA damage in the development of bronchopulmonary dysplasia.},
journal = {ERJ open research},
volume = {12},
number = {2},
pages = {},
pmid = {41918946},
issn = {2312-0541},
abstract = {BACKGROUND: This study investigated the association between airway microbiome composition, oxidative mitochondrial DNA (mtDNA) damage and the development of bronchopulmonary dysplasia (BPD) in preterm infants.
METHODS: A prospective cohort study enrolled 82 very low birth weight preterm infants (<32 weeks' gestation). Tracheal aspirates (TA) were collected at birth and on postnatal day 28. Airway microbial diversity and composition were assessed using 16S rRNA sequencing. Oxidative mtDNA damage was measured using 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in TA samples. We used PICRUSt2-based metagenome predictions from 16S rRNA gene sequencing of TA samples, with functional pathway annotations based on the Kyoto Encyclopedia of Genes and Genomes (KEGG) database.
RESULTS: Infants who developed BPD (n=25) had lower gestational age, birth weight and prolonged ventilatory support (p<0.05). Oxidative mtDNA damage was significantly higher in infants with BPD, particularly in moderate-to-severe cases (p<0.05). BPD was associated with reduced microbial alpha diversity and distinct beta diversity clustering. Infants with BPD exhibited higher relative abundance of Proteobacteria and lower relative abundance of Firmicutes, with enrichment of Stenotrophomonas, Acinetobacter and Serratia (p<0.05). By day 28, KEGG-based functional predictions revealed enrichment in microbial pathways related to bacterial motility proteins, circadian rhythm signalling pathway, MAPK signalling pathway and α-linolenic acid metabolism. Proteobacteria abundance correlated positively with oxidative mtDNA damage (r=0.49, p<0.01).
CONCLUSIONS: Airway microbial dysbiosis and oxidative mtDNA damage are strongly associated with BPD severity. Targeting oxidative stress and microbiome modulation may offer potential strategies for BPD prevention and management.},
}
RevDate: 2026-04-02
Microbes first into the life rafts: preserving microbiomes to secure health in degrading ecosystems.
Sustainable microbiology [Epub ahead of print].
All organisms on the planet intrinsically rely on microbial ecosystems, and there are increasing calls from research communities to consider microbiota when administering personal or public health, ecosystem health, and the use of microbiota in personal or environmental health remediation, such as reducing the impacts of climate change, or protecting at-risk habitats which host rare microbiota. Through our collective work on the integral nature of microbiomes to host and environmental health, on health policy, and on the development of research and policy agendas, we have previously developed the concept of 'microbiome stewardship' and guidelines to promote consideration of microbial communities broadly or in specific scenarios. The practicality of stewarding one versus many microbiota is highly contextual, and will require different strategies for different scales of conservation. Here, we provide scientific arguments for the need for microbial stewardship, examples of possible solutions scaled to different ecological challenges or conservation goals, discourse on the logistical challenges which have been cited by research communities, and opportunities to use cutting-edge microbiome concepts and technology to implement large-scale interventions.
Additional Links: PMID-41918963
PubMed:
Citation:
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@article {pmid41918963,
year = {2026},
author = {Athithan, P and Ishaq, SL and Allen-Vercoe, E and O'Doherty, KC},
title = {Microbes first into the life rafts: preserving microbiomes to secure health in degrading ecosystems.},
journal = {Sustainable microbiology},
volume = {},
number = {},
pages = {},
pmid = {41918963},
issn = {2755-1970},
support = {R15 DK133826/DK/NIDDK NIH HHS/United States ; },
abstract = {All organisms on the planet intrinsically rely on microbial ecosystems, and there are increasing calls from research communities to consider microbiota when administering personal or public health, ecosystem health, and the use of microbiota in personal or environmental health remediation, such as reducing the impacts of climate change, or protecting at-risk habitats which host rare microbiota. Through our collective work on the integral nature of microbiomes to host and environmental health, on health policy, and on the development of research and policy agendas, we have previously developed the concept of 'microbiome stewardship' and guidelines to promote consideration of microbial communities broadly or in specific scenarios. The practicality of stewarding one versus many microbiota is highly contextual, and will require different strategies for different scales of conservation. Here, we provide scientific arguments for the need for microbial stewardship, examples of possible solutions scaled to different ecological challenges or conservation goals, discourse on the logistical challenges which have been cited by research communities, and opportunities to use cutting-edge microbiome concepts and technology to implement large-scale interventions.},
}
RevDate: 2026-04-01
CmpDate: 2026-04-01
Antimicrobial Peptides as Novel Ecological Approaches to Caries Prevention.
Drug design, development and therapy, 20:592732.
Antimicrobial strategies have consistently been a central theme in caries prevention research. Due to their potent antibacterial properties and the potential for multifunctionality through sequence modification, antimicrobial peptides (AMPs) are emerging as promising candidates for anticaries therapeutics. Traditional investigations primarily focused on the broad-spectrum bactericidal efficacy of AMPs to eradicate cariogenic bacteria; however, this approach may inadvertently harm the beneficial oral microbiome. With advancing knowledge of oral microecology, the focus has progressively shifted towards ecological approaches. These strategies aim to selectively modulate cariogenic populations or the disease-associated microbiota while preserving microbial diversity and maintaining ecological balance, as demonstrated in multispecies biofilm models and sequencing-based microbiome analyses. Current innovations include targeting specific pathogens, regulating virulence factors, utilizing bio-responsive mechanisms within the cariogenic microenvironment, and disrupting dental plaque biofilms. This article reviews the current progress and limitations of antimicrobial peptide-based ecological approaches to caries control and offers valuable insights for the future design and optimization of antimicrobial peptides with microecology regulating effects or other promising functions aiding caries prevention.
Additional Links: PMID-41918966
PubMed:
Citation:
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@article {pmid41918966,
year = {2026},
author = {Jiang, W and Liu, J and Chen, A and Zhao, T and Xu, Z and Xu, L and Du, Y and Guan, X and Ding, J and Liu, Y and Sun, D},
title = {Antimicrobial Peptides as Novel Ecological Approaches to Caries Prevention.},
journal = {Drug design, development and therapy},
volume = {20},
number = {},
pages = {592732},
pmid = {41918966},
issn = {1177-8881},
mesh = {*Dental Caries/prevention & control/microbiology ; Humans ; *Antimicrobial Peptides/pharmacology/chemistry ; Biofilms/drug effects ; Microbiota/drug effects ; *Anti-Bacterial Agents/pharmacology/chemistry ; },
abstract = {Antimicrobial strategies have consistently been a central theme in caries prevention research. Due to their potent antibacterial properties and the potential for multifunctionality through sequence modification, antimicrobial peptides (AMPs) are emerging as promising candidates for anticaries therapeutics. Traditional investigations primarily focused on the broad-spectrum bactericidal efficacy of AMPs to eradicate cariogenic bacteria; however, this approach may inadvertently harm the beneficial oral microbiome. With advancing knowledge of oral microecology, the focus has progressively shifted towards ecological approaches. These strategies aim to selectively modulate cariogenic populations or the disease-associated microbiota while preserving microbial diversity and maintaining ecological balance, as demonstrated in multispecies biofilm models and sequencing-based microbiome analyses. Current innovations include targeting specific pathogens, regulating virulence factors, utilizing bio-responsive mechanisms within the cariogenic microenvironment, and disrupting dental plaque biofilms. This article reviews the current progress and limitations of antimicrobial peptide-based ecological approaches to caries control and offers valuable insights for the future design and optimization of antimicrobial peptides with microecology regulating effects or other promising functions aiding caries prevention.},
}
MeSH Terms:
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hide MeSH Terms
*Dental Caries/prevention & control/microbiology
Humans
*Antimicrobial Peptides/pharmacology/chemistry
Biofilms/drug effects
Microbiota/drug effects
*Anti-Bacterial Agents/pharmacology/chemistry
RevDate: 2026-04-01
CmpDate: 2026-04-01
Strengths and limitations of in vitro and animal models to advance understanding of human diet‒microbiome interactions.
Gut microbes reports, 3(1):2636336.
The gut microbiome is a critical mediator of human health. As the intestinal microbiota is far more metabolically diverse than humans, it plays a significant role in the digestion of food, particularly food components that are nutritionally inaccessible to the human host. While no system can fully recapitulate the in vivo interactions of food, the host, and the gut microbiome in the human body, in vitro and animal model tools are critical for studying these complex relationships. Here, we review many of the common in vitro and animal models used to manipulate and study how the gut microbiome affects and is affected by diet. We focus on colonic fermentation systems, with or without small intestinal contribution, bioreactors with both microbial and host epithelial cell components, and animal models that have been developed to study these relationships. We will review the limitations of these systems while also discussing new innovations that seek to address these limitations.
Additional Links: PMID-41918983
PubMed:
Citation:
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@article {pmid41918983,
year = {2026},
author = {Weingarden, AR},
title = {Strengths and limitations of in vitro and animal models to advance understanding of human diet‒microbiome interactions.},
journal = {Gut microbes reports},
volume = {3},
number = {1},
pages = {2636336},
pmid = {41918983},
issn = {2993-3935},
abstract = {The gut microbiome is a critical mediator of human health. As the intestinal microbiota is far more metabolically diverse than humans, it plays a significant role in the digestion of food, particularly food components that are nutritionally inaccessible to the human host. While no system can fully recapitulate the in vivo interactions of food, the host, and the gut microbiome in the human body, in vitro and animal model tools are critical for studying these complex relationships. Here, we review many of the common in vitro and animal models used to manipulate and study how the gut microbiome affects and is affected by diet. We focus on colonic fermentation systems, with or without small intestinal contribution, bioreactors with both microbial and host epithelial cell components, and animal models that have been developed to study these relationships. We will review the limitations of these systems while also discussing new innovations that seek to address these limitations.},
}
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RJR Experience and Expertise
Researcher
Robbins holds BS, MS, and PhD degrees in the life sciences. He served as a tenured faculty member in the Zoology and Biological Science departments at Michigan State University. He is currently exploring the intersection between genomics, microbial ecology, and biodiversity — an area that promises to transform our understanding of the biosphere.
Educator
Robbins has extensive experience in college-level education: At MSU he taught introductory biology, genetics, and population genetics. At JHU, he was an instructor for a special course on biological database design. At FHCRC, he team-taught a graduate-level course on the history of genetics. At Bellevue College he taught medical informatics.
Administrator
Robbins has been involved in science administration at both the federal and the institutional levels. At NSF he was a program officer for database activities in the life sciences, at DOE he was a program officer for information infrastructure in the human genome project. At the Fred Hutchinson Cancer Research Center, he served as a vice president for fifteen years.
Technologist
Robbins has been involved with information technology since writing his first Fortran program as a college student. At NSF he was the first program officer for database activities in the life sciences. At JHU he held an appointment in the CS department and served as director of the informatics core for the Genome Data Base. At the FHCRC he was VP for Information Technology.
Publisher
While still at Michigan State, Robbins started his first publishing venture, founding a small company that addressed the short-run publishing needs of instructors in very large undergraduate classes. For more than 20 years, Robbins has been operating The Electronic Scholarly Publishing Project, a web site dedicated to the digital publishing of critical works in science, especially classical genetics.
Speaker
Robbins is well-known for his speaking abilities and is often called upon to provide keynote or plenary addresses at international meetings. For example, in July, 2012, he gave a well-received keynote address at the Global Biodiversity Informatics Congress, sponsored by GBIF and held in Copenhagen. The slides from that talk can be seen HERE.
Facilitator
Robbins is a skilled meeting facilitator. He prefers a participatory approach, with part of the meeting involving dynamic breakout groups, created by the participants in real time: (1) individuals propose breakout groups; (2) everyone signs up for one (or more) groups; (3) the groups with the most interested parties then meet, with reports from each group presented and discussed in a subsequent plenary session.
Designer
Robbins has been engaged with photography and design since the 1960s, when he worked for a professional photography laboratory. He now prefers digital photography and tools for their precision and reproducibility. He designed his first web site more than 20 years ago and he personally designed and implemented this web site. He engages in graphic design as a hobby.
RJR Picks from Around the Web (updated 11 MAY 2018 )
Old Science
Weird Science
Treating Disease with Fecal Transplantation
Fossils of miniature humans (hobbits) discovered in Indonesia
Paleontology
Dinosaur tail, complete with feathers, found preserved in amber.
Astronomy
Mysterious fast radio burst (FRB) detected in the distant universe.
Big Data & Informatics
Big Data: Buzzword or Big Deal?
Hacking the genome: Identifying anonymized human subjects using publicly available data.