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ESP: PubMed Auto Bibliography 13 Nov 2025 at 01:54 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2025-11-12
Evaluating the Impact of Clear Dental Aligners on Dental and Periodontal Conditions, Oral Microbial Patterns, and the Immune System.
Advances in experimental medicine and biology, 1492:605-624.
Clear aligner therapy (CAT) has gained widespread adoption for managing malocclusions, primarily due to its aesthetic advantages, improved access for hygiene, and enhanced patient comfort relative to fixed appliances (FAs). However, CAT introduces a distinct intraoral environment that can influence microbial composition, biofilm development, and host immune responses. This chapter explores the effects of clear aligners on dental and periodontal health, oral microbial communities, and immunological parameters. Evidence indicates that CAT may facilitate plaque and biofilm accumulation, particularly on composite attachments, thereby increasing the risk of white spot lesions (WSLs), gingivitis, and dental caries. Despite these risks, aligners are generally associated with lower levels of pathogenic bacteria compared to FAs. Microbiome analyses of subgingival plaque and saliva reveal shifts in bacterial genera and phyla, although these changes are frequently non-pathogenic. CAT has demonstrated minimal negative effects on clinical periodontal indices, including the plaque index and gingival bleeding index, particularly when effective oral hygiene is maintained. Furthermore, aligners may reduce sustained immune activation by limiting plaque retention and aseptic inflammation, potentially decreasing the expression of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α. Although hypersensitivity reactions to aligner materials are infrequent, they warrant consideration. Overall, CAT appears to support periodontal health and promote a more stable oral microbial environment compared to FAs. Continued patient adherence to hygiene protocols and further long-term studies are necessary to fully evaluate systemic implications and optimize clinical outcomes.
Additional Links: PMID-41225118
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@article {pmid41225118,
year = {2026},
author = {Esmaeili, S and Shahbazi, S and Ziaei, H and Younessian, F},
title = {Evaluating the Impact of Clear Dental Aligners on Dental and Periodontal Conditions, Oral Microbial Patterns, and the Immune System.},
journal = {Advances in experimental medicine and biology},
volume = {1492},
number = {},
pages = {605-624},
pmid = {41225118},
issn = {0065-2598},
abstract = {Clear aligner therapy (CAT) has gained widespread adoption for managing malocclusions, primarily due to its aesthetic advantages, improved access for hygiene, and enhanced patient comfort relative to fixed appliances (FAs). However, CAT introduces a distinct intraoral environment that can influence microbial composition, biofilm development, and host immune responses. This chapter explores the effects of clear aligners on dental and periodontal health, oral microbial communities, and immunological parameters. Evidence indicates that CAT may facilitate plaque and biofilm accumulation, particularly on composite attachments, thereby increasing the risk of white spot lesions (WSLs), gingivitis, and dental caries. Despite these risks, aligners are generally associated with lower levels of pathogenic bacteria compared to FAs. Microbiome analyses of subgingival plaque and saliva reveal shifts in bacterial genera and phyla, although these changes are frequently non-pathogenic. CAT has demonstrated minimal negative effects on clinical periodontal indices, including the plaque index and gingival bleeding index, particularly when effective oral hygiene is maintained. Furthermore, aligners may reduce sustained immune activation by limiting plaque retention and aseptic inflammation, potentially decreasing the expression of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α. Although hypersensitivity reactions to aligner materials are infrequent, they warrant consideration. Overall, CAT appears to support periodontal health and promote a more stable oral microbial environment compared to FAs. Continued patient adherence to hygiene protocols and further long-term studies are necessary to fully evaluate systemic implications and optimize clinical outcomes.},
}
RevDate: 2025-11-12
Periodontal Disease and Osteoporosis: A Bidirectional Relationship.
Advances in experimental medicine and biology, 1492:163-178.
Osteoporosis (OP) and periodontitis (PD) are two prevalent diseases with significant public health implications, particularly among aging populations. Osteoporosis is a condition that can affect any bone, characterized by decreased bone mineral density (BMD) and deterioration of the bone architecture, resulting in weaker bones and a higher risk of fractures. Periodontitis is a chronic inflammatory condition affecting the supporting structures of the teeth, such as the gingiva, periodontal ligament, and alveolar bone, often leading to tooth loss if left untreated.Recent studies have suggested an interrelationship between these conditions, rooted in shared biological mechanisms. Both diseases involve an imbalance in bone remodeling processes, with excessive activity of osteoclasts over osteoblasts, leading to bone resorption. In osteoporosis, this imbalance is systemic, while in periodontitis, it is localized to the jawbone.Shared risk factors, such as aging, hormonal changes (e.g., postmenopausal estrogen deficiency), and lifestyle factors, like smoking and poor nutrition, further strengthen this association. Additionally, osteoporosis may exacerbate periodontitis by reducing alveolar bone density, while periodontal inflammation can elevate the expression of systemic biomarkers of bone resorption, influencing osteoporosis progression. Furthermore, dysbiosis of the gut and oral cavity microbial communities plays a critical role in both conditions. Gut dysbiosis can influence systemic inflammation and bone metabolism, exacerbating osteoporosis, while oral dysbiosis, marked by pathogenic shifts in the microbiota, triggers and perpetuates periodontal inflammation and alveolar bone loss. Understanding these interrelationships emphasizes the need for an integrated approach to preventing and managing these interconnected conditions.
Additional Links: PMID-41225098
PubMed:
Citation:
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@article {pmid41225098,
year = {2026},
author = {Contaldo, M},
title = {Periodontal Disease and Osteoporosis: A Bidirectional Relationship.},
journal = {Advances in experimental medicine and biology},
volume = {1492},
number = {},
pages = {163-178},
pmid = {41225098},
issn = {0065-2598},
abstract = {Osteoporosis (OP) and periodontitis (PD) are two prevalent diseases with significant public health implications, particularly among aging populations. Osteoporosis is a condition that can affect any bone, characterized by decreased bone mineral density (BMD) and deterioration of the bone architecture, resulting in weaker bones and a higher risk of fractures. Periodontitis is a chronic inflammatory condition affecting the supporting structures of the teeth, such as the gingiva, periodontal ligament, and alveolar bone, often leading to tooth loss if left untreated.Recent studies have suggested an interrelationship between these conditions, rooted in shared biological mechanisms. Both diseases involve an imbalance in bone remodeling processes, with excessive activity of osteoclasts over osteoblasts, leading to bone resorption. In osteoporosis, this imbalance is systemic, while in periodontitis, it is localized to the jawbone.Shared risk factors, such as aging, hormonal changes (e.g., postmenopausal estrogen deficiency), and lifestyle factors, like smoking and poor nutrition, further strengthen this association. Additionally, osteoporosis may exacerbate periodontitis by reducing alveolar bone density, while periodontal inflammation can elevate the expression of systemic biomarkers of bone resorption, influencing osteoporosis progression. Furthermore, dysbiosis of the gut and oral cavity microbial communities plays a critical role in both conditions. Gut dysbiosis can influence systemic inflammation and bone metabolism, exacerbating osteoporosis, while oral dysbiosis, marked by pathogenic shifts in the microbiota, triggers and perpetuates periodontal inflammation and alveolar bone loss. Understanding these interrelationships emphasizes the need for an integrated approach to preventing and managing these interconnected conditions.},
}
RevDate: 2025-11-12
Diabesity and Oral Immunity: Exploring the Interconnection.
Advances in experimental medicine and biology, 1492:121-139.
Diabesity-obesity and type 2 diabetes mellitus (T2DM)-has a profound effect on oral health, and modulation of the oral immune system may help in managing it. This review aims to elucidate the complex interconnection between diabesity, oral immunity, and oral health consequences. Diabesity affects metabolic homeostasis, leading to changes in the immune system within the oral cavity, and increases the incidence of chronic low-grade inflammation and oral diseases. Alterations in the oral microbiome and the breakdown of immune homeostasis further contribute to oral health problems. The reciprocal relationship between diabesity and oral diseases and how inflammation in the oral cavity can worsen systemic metabolic diseases are also described. Apart from periodontal diseases, diabesity increases susceptibility to dental caries, xerostomia, and oral mucosal lesions. Novel treatment strategies are presented with special emphasis on nutrition, lifestyle changes, new drugs, and immunomodulating therapies. The possibility of using a personalized medicine approach in the prevention and treatment of oral diseases in diabesity patients is discussed with regard to genetic and epigenetic factors, biomarkers, and genetic profiles. A combined strategy focusing on both systemic metabolic and oral immunomodulation is recommended to advance the knowledge of diabesity in oral health and thus improve the oral health and quality of life (QoL) of patients with diabesity.
Additional Links: PMID-41225096
PubMed:
Citation:
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@article {pmid41225096,
year = {2026},
author = {Nehaoua, A and Gasmi, A and Noor, S and Benahmed, AG},
title = {Diabesity and Oral Immunity: Exploring the Interconnection.},
journal = {Advances in experimental medicine and biology},
volume = {1492},
number = {},
pages = {121-139},
pmid = {41225096},
issn = {0065-2598},
abstract = {Diabesity-obesity and type 2 diabetes mellitus (T2DM)-has a profound effect on oral health, and modulation of the oral immune system may help in managing it. This review aims to elucidate the complex interconnection between diabesity, oral immunity, and oral health consequences. Diabesity affects metabolic homeostasis, leading to changes in the immune system within the oral cavity, and increases the incidence of chronic low-grade inflammation and oral diseases. Alterations in the oral microbiome and the breakdown of immune homeostasis further contribute to oral health problems. The reciprocal relationship between diabesity and oral diseases and how inflammation in the oral cavity can worsen systemic metabolic diseases are also described. Apart from periodontal diseases, diabesity increases susceptibility to dental caries, xerostomia, and oral mucosal lesions. Novel treatment strategies are presented with special emphasis on nutrition, lifestyle changes, new drugs, and immunomodulating therapies. The possibility of using a personalized medicine approach in the prevention and treatment of oral diseases in diabesity patients is discussed with regard to genetic and epigenetic factors, biomarkers, and genetic profiles. A combined strategy focusing on both systemic metabolic and oral immunomodulation is recommended to advance the knowledge of diabesity in oral health and thus improve the oral health and quality of life (QoL) of patients with diabesity.},
}
RevDate: 2025-11-12
The Oral Microbiome, Oral Hyperpermeability, and Periodontitis in Metabolic Syndrome.
Advances in experimental medicine and biology, 1492:101-120.
The links between the oral microbiome, oral hyperpermeability, periodontitis, and metabolic syndrome (MetS) are good examples of the oral-systemic health connection. The oral microbiota is involved in host defense and metabolism. Oral dysbiosis disrupts periodontal homeostasis, increases the permeability of the oral mucosa, and triggers systemic inflammation, thus leading to MetS. On the other hand, metabolic disorders can change the environmental conditions in the oral cavity and exacerbate dysbiosis and periodontitis. Oral hyperpermeability is evidently a key player in this oral-systemic connection, allowing passage of oral bacteria, their by-products, and inflammatory mediators into the systemic circulation. It triggers the low-grade, chronic inflammation commonly seen in MetS and may exacerbate insulin resistance and other metabolic changes. Thus, periodontitis-a chronic inflammatory disease-is both a result and a cause of MetS. The classification of periodontitis as both a diagnostic marker and a treatment target in metabolic risk enhances the opportunity for the assessment and control of MetS. New-generation therapies targeting oral permeability and dysbiosis, such as barrier-strengthening agents, precision probiotics, and advanced antimicrobial agents, are potential strategies to address the oral-systemic health link. The concept of oral-systemic healthcare, incorporating both dental and medical care, is an emerging model of care delivery systems. Such strategies, including salivary risk management (SRM), targeted interventions, and patient education, may contribute to the enhancement of general health, particularly among individuals with or at risk of MetS.
Additional Links: PMID-41225095
PubMed:
Citation:
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@article {pmid41225095,
year = {2026},
author = {Nehaoua, A and Gasmi, A and Noor, S and Benahmed, AG},
title = {The Oral Microbiome, Oral Hyperpermeability, and Periodontitis in Metabolic Syndrome.},
journal = {Advances in experimental medicine and biology},
volume = {1492},
number = {},
pages = {101-120},
pmid = {41225095},
issn = {0065-2598},
abstract = {The links between the oral microbiome, oral hyperpermeability, periodontitis, and metabolic syndrome (MetS) are good examples of the oral-systemic health connection. The oral microbiota is involved in host defense and metabolism. Oral dysbiosis disrupts periodontal homeostasis, increases the permeability of the oral mucosa, and triggers systemic inflammation, thus leading to MetS. On the other hand, metabolic disorders can change the environmental conditions in the oral cavity and exacerbate dysbiosis and periodontitis. Oral hyperpermeability is evidently a key player in this oral-systemic connection, allowing passage of oral bacteria, their by-products, and inflammatory mediators into the systemic circulation. It triggers the low-grade, chronic inflammation commonly seen in MetS and may exacerbate insulin resistance and other metabolic changes. Thus, periodontitis-a chronic inflammatory disease-is both a result and a cause of MetS. The classification of periodontitis as both a diagnostic marker and a treatment target in metabolic risk enhances the opportunity for the assessment and control of MetS. New-generation therapies targeting oral permeability and dysbiosis, such as barrier-strengthening agents, precision probiotics, and advanced antimicrobial agents, are potential strategies to address the oral-systemic health link. The concept of oral-systemic healthcare, incorporating both dental and medical care, is an emerging model of care delivery systems. Such strategies, including salivary risk management (SRM), targeted interventions, and patient education, may contribute to the enhancement of general health, particularly among individuals with or at risk of MetS.},
}
RevDate: 2025-11-12
Introduction to Oral Immunity.
Advances in experimental medicine and biology, 1492:3-21.
The oral immune system functions as a primary line of defense, composed of oral epithelial barriers, salivary antimicrobial factors, and various innate and adaptive immune components to prevent pathogen entry. Resident immune cells in oral tissues help maintain tolerance to commensal microorganisms while simultaneously responding to harmful external stimuli and contributing to systemic immune regulation. This chapter provides a comprehensive overview of the immunological components and their functions in the oral cavity, emphasizing the dual role of maintaining tolerance to commensal microbes and dietary antigens while initiating protective responses against pathogens. Any disruptions in this balance, such as oral dysbiosis or immune dysregulation, can lead to the development of local inflammatory conditions; it may also contribute to systemic immune disturbances and related pathologies. Immune mechanisms also regulate craniofacial development and postnatal bone remodeling and regeneration, mainly through cytokine-mediated signaling pathways and interactions between stem cells and immune cells. Several local and systemic immunological pathways are often dysregulated in oral inflammatory conditions, which makes them important therapeutic targets. Therapeutic strategies targeting these pathways include immune checkpoint inhibitors, microbiome-directed interventions, stem cell-based therapies, and salivary diagnostics for real-time and noninvasive immune profiling. These offer promising approaches for restoring oral and systemic immune balance. Finally, this chapter has reviewed recent technological advances, such as single-cell RNA sequencing (scRNA-seq), spatial transcriptomics, metagenomics, and multi-omics integration, in the context of oral immunity. These novel techniques are transforming oral immunology, since they enable high-resolution characterization of cellular, microbial, and molecular interactions, and support the transition toward establishing more precise diagnosis and treatment plans. These findings suggest that oral immunity plays a critical role in linking local mucosal defense and systemic immune responses. Therefore, understanding oral immune mechanisms in health and inflammatory conditions is important for revealing disease pathogenesis and guiding targeted interventions.
Additional Links: PMID-41225090
PubMed:
Citation:
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@article {pmid41225090,
year = {2026},
author = {Ziaei, H and Rezaei, N},
title = {Introduction to Oral Immunity.},
journal = {Advances in experimental medicine and biology},
volume = {1492},
number = {},
pages = {3-21},
pmid = {41225090},
issn = {0065-2598},
abstract = {The oral immune system functions as a primary line of defense, composed of oral epithelial barriers, salivary antimicrobial factors, and various innate and adaptive immune components to prevent pathogen entry. Resident immune cells in oral tissues help maintain tolerance to commensal microorganisms while simultaneously responding to harmful external stimuli and contributing to systemic immune regulation. This chapter provides a comprehensive overview of the immunological components and their functions in the oral cavity, emphasizing the dual role of maintaining tolerance to commensal microbes and dietary antigens while initiating protective responses against pathogens. Any disruptions in this balance, such as oral dysbiosis or immune dysregulation, can lead to the development of local inflammatory conditions; it may also contribute to systemic immune disturbances and related pathologies. Immune mechanisms also regulate craniofacial development and postnatal bone remodeling and regeneration, mainly through cytokine-mediated signaling pathways and interactions between stem cells and immune cells. Several local and systemic immunological pathways are often dysregulated in oral inflammatory conditions, which makes them important therapeutic targets. Therapeutic strategies targeting these pathways include immune checkpoint inhibitors, microbiome-directed interventions, stem cell-based therapies, and salivary diagnostics for real-time and noninvasive immune profiling. These offer promising approaches for restoring oral and systemic immune balance. Finally, this chapter has reviewed recent technological advances, such as single-cell RNA sequencing (scRNA-seq), spatial transcriptomics, metagenomics, and multi-omics integration, in the context of oral immunity. These novel techniques are transforming oral immunology, since they enable high-resolution characterization of cellular, microbial, and molecular interactions, and support the transition toward establishing more precise diagnosis and treatment plans. These findings suggest that oral immunity plays a critical role in linking local mucosal defense and systemic immune responses. Therefore, understanding oral immune mechanisms in health and inflammatory conditions is important for revealing disease pathogenesis and guiding targeted interventions.},
}
RevDate: 2025-11-12
Integrative multi-omics identifies coordinated alterations in the gut microbiome and in plasma and aqueous humor metabolomes in high myopic cataract.
Scientific reports, 15(1):39636.
Growing evidence suggests that chronic inflammation contributes to the development of myopia, but the biological link between systemic processes and ocular changes remains poorly understood. In this study, we explored the gut-retina axis using a multi-omics approach in patients with high myopic cataract (HMC) compared with age-related cataract (ARC) controls. Fecal 16S rDNA sequencing revealed distinct microbial signatures in HMC, notably the enrichment of Lactobacillales and depletion of Roseburia, taxa associated with systemic inflammatory status. Metabolomic profiling of plasma and aqueous humor (AH) identified widespread alterations, with enrichment analyses highlighting pathways related to steroid hormone biosynthesis, PPAR signaling, and amino acid metabolism. Several metabolites correlated with axial length, and 4-phenolsulfonic acid in plasma and 5'-N-ethylcarboxamidoadenosine in AH showed the strongest discriminatory potential between HMC and ARC groups. While these findings are associative and require validation in larger, longitudinal cohorts, they suggest that systemic and ocular metabolic disturbances are closely linked to established high myopia. This study provides novel insights into the potential role of the gut-retina axis in myopia pathogenesis.
Additional Links: PMID-41224847
PubMed:
Citation:
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@article {pmid41224847,
year = {2025},
author = {Gu, X and Ruan, X and Yang, W and He, J and Tang, L and Niu, D and Ma, B},
title = {Integrative multi-omics identifies coordinated alterations in the gut microbiome and in plasma and aqueous humor metabolomes in high myopic cataract.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {39636},
pmid = {41224847},
issn = {2045-2322},
support = {2025JC-YBQN-1258//Natural Science Foundation of Shaanxi Province/ ; 2023-JC-QN-0885//Natural Science Foundation of Shaanxi Province/ ; ZR2023QH479//Natural Science Foundation of Shandong Province/ ; },
abstract = {Growing evidence suggests that chronic inflammation contributes to the development of myopia, but the biological link between systemic processes and ocular changes remains poorly understood. In this study, we explored the gut-retina axis using a multi-omics approach in patients with high myopic cataract (HMC) compared with age-related cataract (ARC) controls. Fecal 16S rDNA sequencing revealed distinct microbial signatures in HMC, notably the enrichment of Lactobacillales and depletion of Roseburia, taxa associated with systemic inflammatory status. Metabolomic profiling of plasma and aqueous humor (AH) identified widespread alterations, with enrichment analyses highlighting pathways related to steroid hormone biosynthesis, PPAR signaling, and amino acid metabolism. Several metabolites correlated with axial length, and 4-phenolsulfonic acid in plasma and 5'-N-ethylcarboxamidoadenosine in AH showed the strongest discriminatory potential between HMC and ARC groups. While these findings are associative and require validation in larger, longitudinal cohorts, they suggest that systemic and ocular metabolic disturbances are closely linked to established high myopia. This study provides novel insights into the potential role of the gut-retina axis in myopia pathogenesis.},
}
RevDate: 2025-11-12
The Gut Microbiome as a Modulator of Traumatic Brain Injury Pathology and Symptoms.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 45(46): pii:45/46/e1337252025.
Traumatic brain injuries (TBIs) affect millions annually, leading to devastating neurobehavioral consequences and increasing risk for neurodegenerative and psychiatric diseases. However, therapies are lacking. Starting in 2018, dysbiosis of the gut microbiome was identified as an acute, and potentially chronic, pathology originating from TBI. Recent studies established that the microbiome contributes to the evolution of TBI pathology and functional impairments. The gut microbiome is the collection of microorganisms that inhabit the stomach through colon and is indicated as a contributor to myriad neurological and psychiatric conditions. This makes it an intriguing target to understand in the context of TBI. Thus, this review focuses on the evidence establishing the gut as a modulator of TBI and the major potential mechanisms by which this occurs. This includes regulation of food processing into host-usable nutrients, inflammatory signaling, and vagus nerve modulation. Each of these areas provides potential for future therapeutic development and intervention but there are also multiple areas where microbiome-TBI science could be improved.
Additional Links: PMID-41224658
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@article {pmid41224658,
year = {2025},
author = {Vonder Haar, C and Celorrio, M and Martens, KM and Friess, SH and Villapol, S and Urban, RJ and Pyles, R and Mychasiuk, R and Simon, D and Dave, A},
title = {The Gut Microbiome as a Modulator of Traumatic Brain Injury Pathology and Symptoms.},
journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
volume = {45},
number = {46},
pages = {},
doi = {10.1523/JNEUROSCI.1337-25.2025},
pmid = {41224658},
issn = {1529-2401},
abstract = {Traumatic brain injuries (TBIs) affect millions annually, leading to devastating neurobehavioral consequences and increasing risk for neurodegenerative and psychiatric diseases. However, therapies are lacking. Starting in 2018, dysbiosis of the gut microbiome was identified as an acute, and potentially chronic, pathology originating from TBI. Recent studies established that the microbiome contributes to the evolution of TBI pathology and functional impairments. The gut microbiome is the collection of microorganisms that inhabit the stomach through colon and is indicated as a contributor to myriad neurological and psychiatric conditions. This makes it an intriguing target to understand in the context of TBI. Thus, this review focuses on the evidence establishing the gut as a modulator of TBI and the major potential mechanisms by which this occurs. This includes regulation of food processing into host-usable nutrients, inflammatory signaling, and vagus nerve modulation. Each of these areas provides potential for future therapeutic development and intervention but there are also multiple areas where microbiome-TBI science could be improved.},
}
RevDate: 2025-11-12
Unraveling the Causal Relationship Between Gut Microbiota and Chronic Hepatitis B: A Large-scale Mediation Mendelian Randomization Analysis.
Microbial pathogenesis pii:S0882-4010(25)00904-0 [Epub ahead of print].
Observational evidence links gut microbiota dysbiosis to chronic hepatitis B (CHB) progression, but causal mechanisms remain unclear. Genome-wide association study (GWAS) data for gut microbiota were sourced from the MiBioGen Consortium and Dutch Microbiome Project, with CHB outcome data from the GWAS Catalog. Initial analyses used two-sample and reverse Mendelian randomization (MR) to explore causality between gut microbiota and CHB. Further two-step and multivariable MR analyses revealed mediation by cytokines, metabolites, and immune cells. The study identified 16 microbial taxa causally related to CHB. Bifidobacterium longum (β = -0.298, p = 0.037), Bacteroides coprocola (β = -0.256, p = 0.014), and Bacteroides salyersiae (β = -0.119, p = 0.022) were linked to reduced CHB risk. Ten taxa, including Butyrivibrio (β = 0.164, p = 0.009), Butyrivibrio crossotus (β = 0.227, p = 0.009), Eggerthella sp. id.819 (β = 0.251, p = 0.039), Bacteroides xylanisolvens (β = 0.282, p = 0.026), Dorea longicatena (β = 0.284, p = 0.035), and Prevotella copri (β = 0.349, p = 0.045), were associated with increased CHB risk. Multi-omics analyses identified 1 cytokine, 10 metabolites, and 24 immune cells as key mediators linking gut microbiota to CHB outcomes. These findings confirm a causal relationship, uncover underlying mechanisms, and enhance understanding of the gut-liver axis in CHB etiology and pathology.
Additional Links: PMID-41224159
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@article {pmid41224159,
year = {2025},
author = {Yuan, T and Chen, J and Yang, J and Pu, J and Lu, Y and Zheng, H and Xu, J},
title = {Unraveling the Causal Relationship Between Gut Microbiota and Chronic Hepatitis B: A Large-scale Mediation Mendelian Randomization Analysis.},
journal = {Microbial pathogenesis},
volume = {},
number = {},
pages = {108179},
doi = {10.1016/j.micpath.2025.108179},
pmid = {41224159},
issn = {1096-1208},
abstract = {Observational evidence links gut microbiota dysbiosis to chronic hepatitis B (CHB) progression, but causal mechanisms remain unclear. Genome-wide association study (GWAS) data for gut microbiota were sourced from the MiBioGen Consortium and Dutch Microbiome Project, with CHB outcome data from the GWAS Catalog. Initial analyses used two-sample and reverse Mendelian randomization (MR) to explore causality between gut microbiota and CHB. Further two-step and multivariable MR analyses revealed mediation by cytokines, metabolites, and immune cells. The study identified 16 microbial taxa causally related to CHB. Bifidobacterium longum (β = -0.298, p = 0.037), Bacteroides coprocola (β = -0.256, p = 0.014), and Bacteroides salyersiae (β = -0.119, p = 0.022) were linked to reduced CHB risk. Ten taxa, including Butyrivibrio (β = 0.164, p = 0.009), Butyrivibrio crossotus (β = 0.227, p = 0.009), Eggerthella sp. id.819 (β = 0.251, p = 0.039), Bacteroides xylanisolvens (β = 0.282, p = 0.026), Dorea longicatena (β = 0.284, p = 0.035), and Prevotella copri (β = 0.349, p = 0.045), were associated with increased CHB risk. Multi-omics analyses identified 1 cytokine, 10 metabolites, and 24 immune cells as key mediators linking gut microbiota to CHB outcomes. These findings confirm a causal relationship, uncover underlying mechanisms, and enhance understanding of the gut-liver axis in CHB etiology and pathology.},
}
RevDate: 2025-11-12
The Effects of Prenatal GenX (HFPO-DA) Exposure on Gut Microbiota and Metabolic Function in Pregnant Rats and Their Offspring.
Environmental pollution (Barking, Essex : 1987) pii:S0269-7491(25)01737-3 [Epub ahead of print].
Hexafluoropropylene oxide dimer acid [(HFPO-DA), GenX] is listed as Substances of Very High Concern (SVHC) by the Commission of Member States (MSC) in 2019. The threat of GenX to human health, especially to sensitive populations such as pregnant women, infants and children cannot be ignored. We aimed to investigate the effects of GenX on the intestinal barrier function and gut microbiota of both pregnant rats and their offspring. We subsequently performed a metabolomic analysis of the maternal gut to investigate the metabolic disruptions associated with GenX exposure. Pregnant Sprague-Dawley rats (n = 12/group) received GenX once daily by gavage at 0, 1, 10, or 100 mg/kg body weight from gestational day (GD) 0.5 through GD 19.5. We observed intestinal tissue damage and changes in the gut microbiota in both pregnant rats and their offspring. Additionally, we performed untargeted LC/MS metabolomic analysis on the intestinal tissues of the pregnant rats. The intestinal barrier function of the pregnant rats was impaired. The results of 16S rRNA gene sequencing indicate that GenX alters the gut microbiota diversity and composition in both pregnant rats and their offspring. The metabolites of pregnant rats were also found to be significantly altered, and these metabolites are mainly associated with amino acid metabolism, carbohydrate metabolism, and lipid metabolism. Collectively, Exposure to GenX disrupts the intestinal barrier function of pregnant rats, exacerbates microbiome toxicity, and disturbs the gut microbiome-metabolome homeostasis.
Additional Links: PMID-41224068
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PubMed:
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@article {pmid41224068,
year = {2025},
author = {Han, W and Zhang, X and Li, D and Liu, W and He, Y and Shang, H and Yang, Z and Liu, H and Zhu, W},
title = {The Effects of Prenatal GenX (HFPO-DA) Exposure on Gut Microbiota and Metabolic Function in Pregnant Rats and Their Offspring.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {127363},
doi = {10.1016/j.envpol.2025.127363},
pmid = {41224068},
issn = {1873-6424},
abstract = {Hexafluoropropylene oxide dimer acid [(HFPO-DA), GenX] is listed as Substances of Very High Concern (SVHC) by the Commission of Member States (MSC) in 2019. The threat of GenX to human health, especially to sensitive populations such as pregnant women, infants and children cannot be ignored. We aimed to investigate the effects of GenX on the intestinal barrier function and gut microbiota of both pregnant rats and their offspring. We subsequently performed a metabolomic analysis of the maternal gut to investigate the metabolic disruptions associated with GenX exposure. Pregnant Sprague-Dawley rats (n = 12/group) received GenX once daily by gavage at 0, 1, 10, or 100 mg/kg body weight from gestational day (GD) 0.5 through GD 19.5. We observed intestinal tissue damage and changes in the gut microbiota in both pregnant rats and their offspring. Additionally, we performed untargeted LC/MS metabolomic analysis on the intestinal tissues of the pregnant rats. The intestinal barrier function of the pregnant rats was impaired. The results of 16S rRNA gene sequencing indicate that GenX alters the gut microbiota diversity and composition in both pregnant rats and their offspring. The metabolites of pregnant rats were also found to be significantly altered, and these metabolites are mainly associated with amino acid metabolism, carbohydrate metabolism, and lipid metabolism. Collectively, Exposure to GenX disrupts the intestinal barrier function of pregnant rats, exacerbates microbiome toxicity, and disturbs the gut microbiome-metabolome homeostasis.},
}
RevDate: 2025-11-12
From molecules to models: A holistic review of autism spectrum disorder mechanisms and research tools.
Neurobiology of disease pii:S0969-9961(25)00404-8 [Epub ahead of print].
Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by persistent deficits in social communication and interaction, as well as restricted, repetitive patterns of behavior, interests, or activities. These features are associated with atypical early brain development and connectivity. While ASD has been traditionally associated with molecular genetic alterations, recent research highlights the significant contribution of various environmental factors to the pathophysiology of the disorder. Pathogenic genetic variations in key regulatory genes remain central to ASD risk; however, environmental influences such as advanced maternal or paternal age, poor maternal health during pregnancy, gestational diabetes mellitus, alterations in the early-life gut microbiome, and other perinatal or early childhood environmental exposures have all been associated with an increased likelihood of developing ASD. This review synthesizes recent advances in our understanding of ASD by providing a comprehensive analysis of the disorder's diverse pathophysiological mechanisms from multiple perspectives. Specifically, this paper discusses neurophysiological, behavioral, and post-mortem findings, and explores the utility of widely used animal models in ASD research. Particular attention is given to dysregulation of key metabolic pathways and the role of the gut-brain axis in ASD. The review also evaluates both established and emerging pharmacotherapeutic approaches, highlighting significant cellular, histological, and behavioral alterations associated with ASD. Collectively, these insights provide a foundation for developing novel tools to understand the molecular pathways of these genes and its implication of novel therapeutic opportunities for individuals with ASD.
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@article {pmid41223972,
year = {2025},
author = {Gullapalli, S and Baldado, L and Szobody, MW and Murambadoro, AK and Valdez, KG and Bellamkonda, A and Gonzalez, D and Ghumman, U and Anand, N and Potter-Baker, K and Gadad, BS},
title = {From molecules to models: A holistic review of autism spectrum disorder mechanisms and research tools.},
journal = {Neurobiology of disease},
volume = {},
number = {},
pages = {107187},
doi = {10.1016/j.nbd.2025.107187},
pmid = {41223972},
issn = {1095-953X},
abstract = {Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by persistent deficits in social communication and interaction, as well as restricted, repetitive patterns of behavior, interests, or activities. These features are associated with atypical early brain development and connectivity. While ASD has been traditionally associated with molecular genetic alterations, recent research highlights the significant contribution of various environmental factors to the pathophysiology of the disorder. Pathogenic genetic variations in key regulatory genes remain central to ASD risk; however, environmental influences such as advanced maternal or paternal age, poor maternal health during pregnancy, gestational diabetes mellitus, alterations in the early-life gut microbiome, and other perinatal or early childhood environmental exposures have all been associated with an increased likelihood of developing ASD. This review synthesizes recent advances in our understanding of ASD by providing a comprehensive analysis of the disorder's diverse pathophysiological mechanisms from multiple perspectives. Specifically, this paper discusses neurophysiological, behavioral, and post-mortem findings, and explores the utility of widely used animal models in ASD research. Particular attention is given to dysregulation of key metabolic pathways and the role of the gut-brain axis in ASD. The review also evaluates both established and emerging pharmacotherapeutic approaches, highlighting significant cellular, histological, and behavioral alterations associated with ASD. Collectively, these insights provide a foundation for developing novel tools to understand the molecular pathways of these genes and its implication of novel therapeutic opportunities for individuals with ASD.},
}
RevDate: 2025-11-12
Food grade titanium dioxide is related to gut dysbiosis, but not markers of intestinal inflammation nor permeability in healthy, young adults.
NanoImpact pii:S2452-0748(25)00054-0 [Epub ahead of print].
Titanium dioxide is a white pigment used in products such as foods and pharmaceuticals. Limitations exist in our understanding of titanium dioxide (TiO2) oral exposure by adults and whether chronic exposure impacts gut health. The aims of this study were to estimate oral exposure of TiO2 by quantifying stool content, and determine its association with the gut microbiome, intestinal permeability, and gut inflammation among healthy adults. This longitudinal analysis included stool collection at three time points from adults (18-30 y). TiO2 concentration in stool was measured using Inductively Coupled Plasma Mass Spectrometry. Gut microbiota were assessed using 16S rRNA sequencing. Microbiome Multivariate Association with Linear Models (MaAsLin2) identified gut microbiota associated with stool TiO2. Intestinal inflammation was assessed from stool concentrations of calprotectin, lactoferrin, and myeloperoxidase and gut permeability from alpha-1-antitrypsin using enzyme-linked immune-sorbent assays. Dietary intake was assessed from three 24-h dietary recalls. Differences in intestinal biomarkers between high and low TiO2 groups (stratified at median, 0.22 μg/mg stool) were tested by student's t-test, and across quartiles of TiO2 by ANCOVA. Beta diversity showed clustering between the lowest and highest quartiles of TiO2, P < 0.02. Thirteen microbial taxa were differentially abundant in any of the quartiles of TiO2 compared to the lowest. No differences in biomarkers of gut health were detected following adjustment. In healthy adults, higher stool TiO2 concentration is related to gut dysbiosis, but not to higher levels of gut inflammation nor permeability. Future studies should evaluate TiO2 in the stool of adults with impaired gut health.
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@article {pmid41223969,
year = {2025},
author = {Merrill, LC and Thomas, E and Wright, JR and Lamendella, R and Bhandari, S and Bello, D and Kelleher, SL and Tucker, KL and Mangano, KM},
title = {Food grade titanium dioxide is related to gut dysbiosis, but not markers of intestinal inflammation nor permeability in healthy, young adults.},
journal = {NanoImpact},
volume = {},
number = {},
pages = {100594},
doi = {10.1016/j.impact.2025.100594},
pmid = {41223969},
issn = {2452-0748},
abstract = {Titanium dioxide is a white pigment used in products such as foods and pharmaceuticals. Limitations exist in our understanding of titanium dioxide (TiO2) oral exposure by adults and whether chronic exposure impacts gut health. The aims of this study were to estimate oral exposure of TiO2 by quantifying stool content, and determine its association with the gut microbiome, intestinal permeability, and gut inflammation among healthy adults. This longitudinal analysis included stool collection at three time points from adults (18-30 y). TiO2 concentration in stool was measured using Inductively Coupled Plasma Mass Spectrometry. Gut microbiota were assessed using 16S rRNA sequencing. Microbiome Multivariate Association with Linear Models (MaAsLin2) identified gut microbiota associated with stool TiO2. Intestinal inflammation was assessed from stool concentrations of calprotectin, lactoferrin, and myeloperoxidase and gut permeability from alpha-1-antitrypsin using enzyme-linked immune-sorbent assays. Dietary intake was assessed from three 24-h dietary recalls. Differences in intestinal biomarkers between high and low TiO2 groups (stratified at median, 0.22 μg/mg stool) were tested by student's t-test, and across quartiles of TiO2 by ANCOVA. Beta diversity showed clustering between the lowest and highest quartiles of TiO2, P < 0.02. Thirteen microbial taxa were differentially abundant in any of the quartiles of TiO2 compared to the lowest. No differences in biomarkers of gut health were detected following adjustment. In healthy adults, higher stool TiO2 concentration is related to gut dysbiosis, but not to higher levels of gut inflammation nor permeability. Future studies should evaluate TiO2 in the stool of adults with impaired gut health.},
}
RevDate: 2025-11-12
Recent Insights on Dental Caries Microbiota in Pediatric Patients with Inborn Errors of Immunity.
Advances in experimental medicine and biology, 1492:291-313.
Inborn errors of immunity (IEIs) are genetic disorders that impair immune defense and regulation, increasing susceptibility to infections, including those in the oral cavity. The oral microbiota plays a vital role in maintaining oral health, and in pediatric patients with IEIs, disruptions in this balance can lead to dental caries and other oral diseases. This chapter provides a comprehensive analysis of the relationship between immune deficiencies and oral microbiota dysbiosis, focusing on dental caries in children with IEIs. Omics technologies, particularly metagenomics, have enhanced understanding of the microbial diversity and metabolic activities within the oral microbiota of the patients. Key findings reveal that compromised immune responses in children with IEIs disrupt the balance of oral bacteria, making them more prone to dental caries. The chapter highlights the importance of an interdisciplinary approach, integrating microbiology, immunology, dentistry, and bioinformatics, to uncover the complex interactions between the oral microbiome and the immune system. The insights gained from this research will contribute to the development of personalized therapeutic strategies, improving the dental and overall health of pediatric patients with IEIs.
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@article {pmid41225104,
year = {2026},
author = {Kars, G and Alkebsi, BLA and Keleş, S and Altan, H and Özer, H and Holyavkin, C and Karaselek, MA},
title = {Recent Insights on Dental Caries Microbiota in Pediatric Patients with Inborn Errors of Immunity.},
journal = {Advances in experimental medicine and biology},
volume = {1492},
number = {},
pages = {291-313},
pmid = {41225104},
issn = {0065-2598},
abstract = {Inborn errors of immunity (IEIs) are genetic disorders that impair immune defense and regulation, increasing susceptibility to infections, including those in the oral cavity. The oral microbiota plays a vital role in maintaining oral health, and in pediatric patients with IEIs, disruptions in this balance can lead to dental caries and other oral diseases. This chapter provides a comprehensive analysis of the relationship between immune deficiencies and oral microbiota dysbiosis, focusing on dental caries in children with IEIs. Omics technologies, particularly metagenomics, have enhanced understanding of the microbial diversity and metabolic activities within the oral microbiota of the patients. Key findings reveal that compromised immune responses in children with IEIs disrupt the balance of oral bacteria, making them more prone to dental caries. The chapter highlights the importance of an interdisciplinary approach, integrating microbiology, immunology, dentistry, and bioinformatics, to uncover the complex interactions between the oral microbiome and the immune system. The insights gained from this research will contribute to the development of personalized therapeutic strategies, improving the dental and overall health of pediatric patients with IEIs.},
}
RevDate: 2025-11-12
Examining Oral Microbial Communities at the Gingival Interface During Health and Inflammatory Diseases.
Advances in experimental medicine and biology, 1492:41-58.
The subgingival environment is a unique ecological niche where host-microbe interactions continuously occur, ultimately determining the balance that characterizes periodontal health or the disequilibrium featured in periodontal diseases. Importantly, knowledge of the subgingival microbiome has expanded dramatically due to the extensive use of next-generation sequencing techniques in both periodontal health and diseases, making it necessary to summarize and contextualize evidence from these types of studies. Consequently, this chapter first explores the anatomical and histological characteristics of the subgingival area and provides an overview of the microbial communities and immune surveillance mechanisms unraveling in this space and during periodontal health. Then, focus is placed on better defining periodontal inflammation as a main driver of microbial dysbiosis during disease. The subgingival microbiome in gingivitis and periodontitis is further analyzed, focusing on the environmental changes triggered by periodontal inflammation, as inflammation and tissue destruction lead to dramatic environmental changes that are associated with distinct microbial shifts. The microbial transition from health to gingivitis is explored in detail, discussing evidence stemming from studies dedicated to natural and experimental gingivitis. Finally, the dynamics of subgingival microbial communities in periodontitis and their connection with inflammation are explored, acknowledging the bidirectional nature of this relationship and highlighting its importance in determining health and disease in this setting.
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@article {pmid41225092,
year = {2026},
author = {Abusleme, L and Arce, M and Dutzan, N},
title = {Examining Oral Microbial Communities at the Gingival Interface During Health and Inflammatory Diseases.},
journal = {Advances in experimental medicine and biology},
volume = {1492},
number = {},
pages = {41-58},
pmid = {41225092},
issn = {0065-2598},
abstract = {The subgingival environment is a unique ecological niche where host-microbe interactions continuously occur, ultimately determining the balance that characterizes periodontal health or the disequilibrium featured in periodontal diseases. Importantly, knowledge of the subgingival microbiome has expanded dramatically due to the extensive use of next-generation sequencing techniques in both periodontal health and diseases, making it necessary to summarize and contextualize evidence from these types of studies. Consequently, this chapter first explores the anatomical and histological characteristics of the subgingival area and provides an overview of the microbial communities and immune surveillance mechanisms unraveling in this space and during periodontal health. Then, focus is placed on better defining periodontal inflammation as a main driver of microbial dysbiosis during disease. The subgingival microbiome in gingivitis and periodontitis is further analyzed, focusing on the environmental changes triggered by periodontal inflammation, as inflammation and tissue destruction lead to dramatic environmental changes that are associated with distinct microbial shifts. The microbial transition from health to gingivitis is explored in detail, discussing evidence stemming from studies dedicated to natural and experimental gingivitis. Finally, the dynamics of subgingival microbial communities in periodontitis and their connection with inflammation are explored, acknowledging the bidirectional nature of this relationship and highlighting its importance in determining health and disease in this setting.},
}
RevDate: 2025-11-12
A lysine-restricted diet ameliorates obesity via enrichment of Parabacteroides goldsteinii and 1,4-methylimidazoleacetic acid.
Nature communications, 16(1):9953.
The effects of dietary amino acid restriction on obesity may be related to the gut microbiome, but its role and mechanism in lysine-restricted diet (LRD) on childhood obesity is largely undefined. Herein, we show that blood lysine levels are elevated in children with obesity compared to healthy controls. Using young mice, we show that LRD ameliorates obesity via gut microbiota modulation. We further identify Parabacteroides goldsteinii (P. goldsteinii) as a candidate contributor and validate that its supplementation reduces obesity phenotype. Metabolomics reveals that P. goldsteinii increases 1,4-methylimidazoleacetic acid (MIAA), a metabolite linked to decreased body weight in animal models. Mechanistically, we show that MIAA inhibits the expression of the demethylase FTO, leading to increased m[6]A modifications on Slc2a4 mRNA via the reader protein YTHDC1. Collectively, these findings suggest a role for P. goldsteinii and its metabolite MIAA on LRD-mediated obesity reduction, potentially via the FTO-SLC2A4 axis to restrict adipose tissue expansion.
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@article {pmid41224764,
year = {2025},
author = {Zhao, F and Zou, Z and Liu, Z and Wang, J and Wu, Y and Zhang, J and Liu, Q and Liang, W and Yao, J and Jiang, X and Routledge, MN and Khan, A and Zhang, H and Qiu, J and Chen, C},
title = {A lysine-restricted diet ameliorates obesity via enrichment of Parabacteroides goldsteinii and 1,4-methylimidazoleacetic acid.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {9953},
pmid = {41224764},
issn = {2041-1723},
support = {82473594//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {The effects of dietary amino acid restriction on obesity may be related to the gut microbiome, but its role and mechanism in lysine-restricted diet (LRD) on childhood obesity is largely undefined. Herein, we show that blood lysine levels are elevated in children with obesity compared to healthy controls. Using young mice, we show that LRD ameliorates obesity via gut microbiota modulation. We further identify Parabacteroides goldsteinii (P. goldsteinii) as a candidate contributor and validate that its supplementation reduces obesity phenotype. Metabolomics reveals that P. goldsteinii increases 1,4-methylimidazoleacetic acid (MIAA), a metabolite linked to decreased body weight in animal models. Mechanistically, we show that MIAA inhibits the expression of the demethylase FTO, leading to increased m[6]A modifications on Slc2a4 mRNA via the reader protein YTHDC1. Collectively, these findings suggest a role for P. goldsteinii and its metabolite MIAA on LRD-mediated obesity reduction, potentially via the FTO-SLC2A4 axis to restrict adipose tissue expansion.},
}
RevDate: 2025-11-12
Integration of metagenome-assembled genomes with clinical isolates expands the genomic landscape of gut-associated Klebsiella pneumoniae.
Nature communications, 16(1):9959.
Klebsiella pneumoniae is an opportunistic pathogen causing diseases ranging from gastrointestinal disorders to severe liver abscesses. While clinical isolates of K. pneumoniae have been extensively studied, less is known about asymptomatic variants colonizing the human gut across diverse populations. Developments in genome-resolved metagenomics have offered unprecedented access to metagenome-assembled genomes (MAGs), expanding the known bacterial diversity within the gut microbiome. Here we analysed 656 human gut-derived K. pneumoniae genomes (317 MAGs, 339 isolates) from 29 countries to investigate the population structure and genomic landscape of gut-associated lineages. Over 60% of MAGs were found to belong to new sequence types, highlighting a large uncharacterized diversity of K. pneumoniae missing among sequenced clinical isolates. In particular, integrating MAGs nearly doubled gut-associated K. pneumoniae phylogenetic diversity, and uncovered 86 MAGs with >0.5% genomic distance compared to 20,792 Klebsiella isolate genomes from various sources. Pan-genome analyses identified 214 genes exclusively detected among MAGs, with 107 predicted to encode putative virulence factors. Notably, combining MAGs and isolates revealed genomic signatures linked to health and disease and more accurately classified disease and carriage states compared to isolates alone. These findings showcase the value of metagenomics to understand pathogen evolution and diversity with implications for public health surveillance strategies.
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@article {pmid41224755,
year = {2025},
author = {Gupta, S and Almeida, A},
title = {Integration of metagenome-assembled genomes with clinical isolates expands the genomic landscape of gut-associated Klebsiella pneumoniae.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {9959},
pmid = {41224755},
issn = {2041-1723},
support = {MR/W016184/1//RCUK | Medical Research Council (MRC)/ ; },
abstract = {Klebsiella pneumoniae is an opportunistic pathogen causing diseases ranging from gastrointestinal disorders to severe liver abscesses. While clinical isolates of K. pneumoniae have been extensively studied, less is known about asymptomatic variants colonizing the human gut across diverse populations. Developments in genome-resolved metagenomics have offered unprecedented access to metagenome-assembled genomes (MAGs), expanding the known bacterial diversity within the gut microbiome. Here we analysed 656 human gut-derived K. pneumoniae genomes (317 MAGs, 339 isolates) from 29 countries to investigate the population structure and genomic landscape of gut-associated lineages. Over 60% of MAGs were found to belong to new sequence types, highlighting a large uncharacterized diversity of K. pneumoniae missing among sequenced clinical isolates. In particular, integrating MAGs nearly doubled gut-associated K. pneumoniae phylogenetic diversity, and uncovered 86 MAGs with >0.5% genomic distance compared to 20,792 Klebsiella isolate genomes from various sources. Pan-genome analyses identified 214 genes exclusively detected among MAGs, with 107 predicted to encode putative virulence factors. Notably, combining MAGs and isolates revealed genomic signatures linked to health and disease and more accurately classified disease and carriage states compared to isolates alone. These findings showcase the value of metagenomics to understand pathogen evolution and diversity with implications for public health surveillance strategies.},
}
RevDate: 2025-11-12
Localized glutamine leakage shapes root microbiome.
Trends in microbiology pii:S0966-842X(25)00330-0 [Epub ahead of print].
Root exudates are vital for guiding microbial dynamics in the rhizosphere. Nevertheless, the key component in root exudates responsible for defining the root microbiome has remained obscure. Tsai et al. recently offered insights into how Casparian strips prevent glutamine leakage from the vasculature, thereby shaping the root microbiome.
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@article {pmid41224620,
year = {2025},
author = {Wu, Q and Wang, D and Fu, ZQ and Que, Y},
title = {Localized glutamine leakage shapes root microbiome.},
journal = {Trends in microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tim.2025.11.004},
pmid = {41224620},
issn = {1878-4380},
abstract = {Root exudates are vital for guiding microbial dynamics in the rhizosphere. Nevertheless, the key component in root exudates responsible for defining the root microbiome has remained obscure. Tsai et al. recently offered insights into how Casparian strips prevent glutamine leakage from the vasculature, thereby shaping the root microbiome.},
}
RevDate: 2025-11-12
Microbiome Studies in Chronic Pelvic Pain: Addressing Key Methodological Concerns (Letter-to-the-Editor).
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@article {pmid41223963,
year = {2025},
author = {Shafi Rahu, S and Kassem, A and Ullah, S and Parveen, S and Ramzan, H},
title = {Microbiome Studies in Chronic Pelvic Pain: Addressing Key Methodological Concerns (Letter-to-the-Editor).},
journal = {American journal of obstetrics and gynecology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ajog.2025.10.016},
pmid = {41223963},
issn = {1097-6868},
}
RevDate: 2025-11-12
Methodological Considerations in Microbiome Studies of Chronic Pelvic Pain (Reply to Letter-to-the-Editor).
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@article {pmid41223959,
year = {2025},
author = {Cardaillac, C and Trottier, C and Neunlist, M},
title = {Methodological Considerations in Microbiome Studies of Chronic Pelvic Pain (Reply to Letter-to-the-Editor).},
journal = {American journal of obstetrics and gynecology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ajog.2025.10.017},
pmid = {41223959},
issn = {1097-6868},
}
RevDate: 2025-11-12
A repository of the salivary metabolome and its key drivers in 1436 European children.
EBioMedicine, 122:106019 pii:S2352-3964(25)00463-3 [Epub ahead of print].
BACKGROUND: Saliva is an emerging but understudied biofluid in metabolomics, offering a similar window into biological information as blood, while enabling repetitive and non-invasive sampling.
METHODS: In this observational study, we comprehensively analysed the salivary metabolome of 965 children and adolescents (7-17y) from two exploratory cohorts in Europe, using ultra-high performance liquid chromatography coupled to high-resolution mass spectrometry. Preprocessed data were assessed via (partial) Spearman correlation, Mummichog-based pathway enrichment, and univariate (Welsh t-test, one-way ANOVA, Wilcoxon or Kruskal-Wallis rank-sum test) analyses. All p-values were corrected using the Benjamini-Hochberg procedure. Associations with age, anthropometrics, mental wellbeing, lifestyle, dietary intake and microbiome were explored. Key metabolite associations were validated in two independent cohorts (8-18y, n = 471), yielding a total study population of 1436 participants.
FINDINGS: Over 3500 untargeted features and 188 targeted metabolites were consistently detected in the pooled quality control saliva of the exploratory cohorts. Weight status (|ρ| < 0.255) and age (|ρ| < 0.341) reflected the salivary metabolome best, compared to mental wellbeing (|ρ| < 0.227) and lifestyle factors (|ρ| < 0.185). Multiple metabolites, especially (acetylated) amino acids and derivatives were elevated in participants with overweight or obesity and those experiencing high psychological stress, mirroring blood-based studies. In addition, these metabolites correlated with Bacteroidota, Pseudomonadota, Actinomycetota and Bacillota (|ρ| < 0.423) phyla, suggesting oral microbiome disturbances. Notably, the artificial sweetener acesulfame K, detected for the first time in children and adolescents' saliva, was associated with excess weight (|ρ| < 0.243), psychological stress (|ρ| < 0.148), specific food and/or beverage consumption (|ρ| < 0.348) and Bacillota spp. (|ρ| < 0.196).
INTERPRETATION: Our findings reinforce and expand upon previous blood-based studies, while revealing novel salivary biomarkers and, as such, provide a high-quality repository of the paediatric salivary metabolome for future studies exploring its association with children and adolescent's health.
FUNDING: FAME and OPERA were supported by the Research Foundation Flanders, Ghent University, and the European Research Council. PANIC was funded by Finnish national agencies and foundations. Fin-HIT was funded by the Folkhälsan Research Foundation and the Päivikki and Sakari Sohlberg Foundation.
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@article {pmid41223785,
year = {2025},
author = {De Paepe, E and Callemeyn, E and De Windt, K and Wijnant, K and Plekhova, V and Pomian, B and Vangeenderhuysen, P and De Henauw, S and Michels, N and Viljakainen, H and Leppänen, MH and Lakka, TA and Van De Maele, K and Baeck, N and De Bruyne, R and Lefere, S and Geerts, A and Vynck, M and Vanhaecke, L},
title = {A repository of the salivary metabolome and its key drivers in 1436 European children.},
journal = {EBioMedicine},
volume = {122},
number = {},
pages = {106019},
doi = {10.1016/j.ebiom.2025.106019},
pmid = {41223785},
issn = {2352-3964},
abstract = {BACKGROUND: Saliva is an emerging but understudied biofluid in metabolomics, offering a similar window into biological information as blood, while enabling repetitive and non-invasive sampling.
METHODS: In this observational study, we comprehensively analysed the salivary metabolome of 965 children and adolescents (7-17y) from two exploratory cohorts in Europe, using ultra-high performance liquid chromatography coupled to high-resolution mass spectrometry. Preprocessed data were assessed via (partial) Spearman correlation, Mummichog-based pathway enrichment, and univariate (Welsh t-test, one-way ANOVA, Wilcoxon or Kruskal-Wallis rank-sum test) analyses. All p-values were corrected using the Benjamini-Hochberg procedure. Associations with age, anthropometrics, mental wellbeing, lifestyle, dietary intake and microbiome were explored. Key metabolite associations were validated in two independent cohorts (8-18y, n = 471), yielding a total study population of 1436 participants.
FINDINGS: Over 3500 untargeted features and 188 targeted metabolites were consistently detected in the pooled quality control saliva of the exploratory cohorts. Weight status (|ρ| < 0.255) and age (|ρ| < 0.341) reflected the salivary metabolome best, compared to mental wellbeing (|ρ| < 0.227) and lifestyle factors (|ρ| < 0.185). Multiple metabolites, especially (acetylated) amino acids and derivatives were elevated in participants with overweight or obesity and those experiencing high psychological stress, mirroring blood-based studies. In addition, these metabolites correlated with Bacteroidota, Pseudomonadota, Actinomycetota and Bacillota (|ρ| < 0.423) phyla, suggesting oral microbiome disturbances. Notably, the artificial sweetener acesulfame K, detected for the first time in children and adolescents' saliva, was associated with excess weight (|ρ| < 0.243), psychological stress (|ρ| < 0.148), specific food and/or beverage consumption (|ρ| < 0.348) and Bacillota spp. (|ρ| < 0.196).
INTERPRETATION: Our findings reinforce and expand upon previous blood-based studies, while revealing novel salivary biomarkers and, as such, provide a high-quality repository of the paediatric salivary metabolome for future studies exploring its association with children and adolescent's health.
FUNDING: FAME and OPERA were supported by the Research Foundation Flanders, Ghent University, and the European Research Council. PANIC was funded by Finnish national agencies and foundations. Fin-HIT was funded by the Folkhälsan Research Foundation and the Päivikki and Sakari Sohlberg Foundation.},
}
RevDate: 2025-11-12
Use of selective decontamination of the digestive tract in burn patients: A European survey.
Burns : journal of the International Society for Burn Injuries, 52(1):107774 pii:S0305-4179(25)00403-6 [Epub ahead of print].
BACKGROUND: Infectious complications are a major cause of morbidity and mortality in burn patients. Selective decontamination of the digestive tract (SDD) is a prophylactic antimicrobial strategy aimed at suppressing potential pathogenic microorganisms in the gut microbiome. This study aimed to assess the values and preferences for the use of SDD in burn centres across Europe and to evaluate clinicians' interest in further research on its efficacy.
METHODS: We circulated a survey on the values and preferences for the use of SDD between March and October 2024, targeting surgeons, anaesthesiologists, and intensivists at European burn centres. The survey comprised 13 questions focusing on SDD usage criteria, regimens, and willingness to participate in a multicentre randomised clinical trial. Data were analysed and presented descriptively.
RESULTS: We invited 45 burn centres to participate; 22 responded (49 % response rate). Among these, 27 % (6/22) reported routine use of SDD, primarily for patients with extensive burns or those requiring intensive care. Most centres using SDD (5/6) administered a combination of enteral and intravenous antibiotics and/or antifungals, while one centre (1/6) relied on enteral antimicrobials alone. The most common regimen included intravenous cefotaxime combined with enteral polymyxin E, tobramycin, and amphotericin B or nystatin. Notably, 82 % (18/22) of respondents expressed interest in participating in a multicentre randomised clinical trial on SDD in burn patients.
CONCLUSION: A minority of European burn centres routinely used SDD, while the majority did not. Among those that used SDD, treatment regimens were largely aligned with practices commonly used in ICU patients. Notably, there was significant interest among European burn centres in participating in future clinical trials comparing SDD versus no SDD in burn patients.
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@article {pmid41223769,
year = {2025},
author = {Tsuchiya, EA and Krag, M and Møller, MH and Vestergaard, MR and Haase, N and Helleberg, M and Holmgaard, R and Heiberg, J},
title = {Use of selective decontamination of the digestive tract in burn patients: A European survey.},
journal = {Burns : journal of the International Society for Burn Injuries},
volume = {52},
number = {1},
pages = {107774},
doi = {10.1016/j.burns.2025.107774},
pmid = {41223769},
issn = {1879-1409},
abstract = {BACKGROUND: Infectious complications are a major cause of morbidity and mortality in burn patients. Selective decontamination of the digestive tract (SDD) is a prophylactic antimicrobial strategy aimed at suppressing potential pathogenic microorganisms in the gut microbiome. This study aimed to assess the values and preferences for the use of SDD in burn centres across Europe and to evaluate clinicians' interest in further research on its efficacy.
METHODS: We circulated a survey on the values and preferences for the use of SDD between March and October 2024, targeting surgeons, anaesthesiologists, and intensivists at European burn centres. The survey comprised 13 questions focusing on SDD usage criteria, regimens, and willingness to participate in a multicentre randomised clinical trial. Data were analysed and presented descriptively.
RESULTS: We invited 45 burn centres to participate; 22 responded (49 % response rate). Among these, 27 % (6/22) reported routine use of SDD, primarily for patients with extensive burns or those requiring intensive care. Most centres using SDD (5/6) administered a combination of enteral and intravenous antibiotics and/or antifungals, while one centre (1/6) relied on enteral antimicrobials alone. The most common regimen included intravenous cefotaxime combined with enteral polymyxin E, tobramycin, and amphotericin B or nystatin. Notably, 82 % (18/22) of respondents expressed interest in participating in a multicentre randomised clinical trial on SDD in burn patients.
CONCLUSION: A minority of European burn centres routinely used SDD, while the majority did not. Among those that used SDD, treatment regimens were largely aligned with practices commonly used in ICU patients. Notably, there was significant interest among European burn centres in participating in future clinical trials comparing SDD versus no SDD in burn patients.},
}
RevDate: 2025-11-12
Phenolic acids: An emerging player in Plant-Microbe interactions.
Journal of plant physiology, 315:154640 pii:S0176-1617(25)00222-6 [Epub ahead of print].
Phenolic acids (PAs) are important secondary metabolites that mediate plant-microbe communication and function as plant defenders, plant growth promoters, rhizosphere microbial recruiters, and interferers of microbial quorum sensing. Against the backdrop of cutting-edge biotechnologies in genomics and metabolomics, this review synthesizes frontier research on the functions and mechanisms of PAs in the aforementioned aspects, following a brief summary of their biosynthesis and chemical structures in plants. Finally, the review also suggests further research priorities, including manipulating PAs to reshape the rhizosphere microbiome, developing functional root exudate databases for precision breeding, and investigating the degradation of PAs by prebiotics to enhance agricultural sustainability. We advocate for multidisciplinary studies that integrate metabolomics, genomics, and ecology, as they offer diverse perspectives on plant-microbe interactions and provide valuable ecological insights and potential applications for sustainable agriculture.
Additional Links: PMID-41223720
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@article {pmid41223720,
year = {2025},
author = {Tingting, P and Qiqi, H and Caihong, B and Shijian, X and Xinfang, Z},
title = {Phenolic acids: An emerging player in Plant-Microbe interactions.},
journal = {Journal of plant physiology},
volume = {315},
number = {},
pages = {154640},
doi = {10.1016/j.jplph.2025.154640},
pmid = {41223720},
issn = {1618-1328},
abstract = {Phenolic acids (PAs) are important secondary metabolites that mediate plant-microbe communication and function as plant defenders, plant growth promoters, rhizosphere microbial recruiters, and interferers of microbial quorum sensing. Against the backdrop of cutting-edge biotechnologies in genomics and metabolomics, this review synthesizes frontier research on the functions and mechanisms of PAs in the aforementioned aspects, following a brief summary of their biosynthesis and chemical structures in plants. Finally, the review also suggests further research priorities, including manipulating PAs to reshape the rhizosphere microbiome, developing functional root exudate databases for precision breeding, and investigating the degradation of PAs by prebiotics to enhance agricultural sustainability. We advocate for multidisciplinary studies that integrate metabolomics, genomics, and ecology, as they offer diverse perspectives on plant-microbe interactions and provide valuable ecological insights and potential applications for sustainable agriculture.},
}
RevDate: 2025-11-12
Toward indole postbiotics precision therapy via AI-powered drug delivery technologies.
Current opinion in immunology, 98:102692 pii:S0952-7915(25)00168-2 [Epub ahead of print].
Recent advancements in microbiome research have revealed the restorative capacities of postbiotics, including indole and its derivatives generated via bacterial tryptophan metabolism. Widespread in prokaryotic and eukaryotic communities, indole and its derivatives are uniquely suited to promote host physiology and homeostasis at the host/microbe interface. In addition to suppressing the bacterial pathogenesis, the antioxidant, anti-inflammatory, antidiabetic, antihypertensive, immunomodulatory, and metabolic activities of indole and its derivatives make these postbiotics an attractive therapeutic option. However, their clinical translation is impeded by pharmacokinetic constraints, structural promiscuity, and formulation difficulties. This review examines the current status of indole bioactivities, identifies translational challenges, and suggests the use of artificial intelligence as a method for establishing a comprehensive framework for future translational development.
Additional Links: PMID-41223607
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@article {pmid41223607,
year = {2025},
author = {Matteo, P and Marilena, P and Anna, WP and Maurizio, R and Giovagnoli, S},
title = {Toward indole postbiotics precision therapy via AI-powered drug delivery technologies.},
journal = {Current opinion in immunology},
volume = {98},
number = {},
pages = {102692},
doi = {10.1016/j.coi.2025.102692},
pmid = {41223607},
issn = {1879-0372},
abstract = {Recent advancements in microbiome research have revealed the restorative capacities of postbiotics, including indole and its derivatives generated via bacterial tryptophan metabolism. Widespread in prokaryotic and eukaryotic communities, indole and its derivatives are uniquely suited to promote host physiology and homeostasis at the host/microbe interface. In addition to suppressing the bacterial pathogenesis, the antioxidant, anti-inflammatory, antidiabetic, antihypertensive, immunomodulatory, and metabolic activities of indole and its derivatives make these postbiotics an attractive therapeutic option. However, their clinical translation is impeded by pharmacokinetic constraints, structural promiscuity, and formulation difficulties. This review examines the current status of indole bioactivities, identifies translational challenges, and suggests the use of artificial intelligence as a method for establishing a comprehensive framework for future translational development.},
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
Dominance of Zygosaccharomyces and shifts in bacterial pathways: Effects of antimicrobials on composition and diversity of the Ceratitis capitata bacterial and fungal microbiome.
PloS one, 20(11):e0335811 pii:PONE-D-25-35691.
The Mediterranean fruit fly (Ceratitis capitata Wied.) is an agricultural pest of significant economic importance. This species has been globally managed using the Sterile Insect Technique (SIT). Insects, including tephritid flies, harbor a diverse gut microbiota that plays critical roles in their physiology, behavior, and overall fitness, suggesting that microbial communities may profoundly influence the biology of this pest. The aim of this study was to characterize the fungal and bacterial gut microbial communities of C. capitata from Tucumán, Argentina, and to assess their response to antimicrobial treatment using amplicon-based 16S rRNA gene and ITS region sequencing. Both control and treated flies were dominated by Proteobacteria (bacteria) and Zygosaccharomyces (fungi). Antimicrobial treatment induced significant shifts in bacterial and fungal composition, reducing diversity and altering gut community structure. Untreated flies exhibited a diverse and structured bacterial gut community dominated by the family Enterobacteriaceae, while antibiotic-treated communities were dominated by Rhizobiaceae. Despite these shifts, fungal communities in both treated and untreated groups were consistently dominated by the genus Zygosaccharomyces. Functional predictions revealed notable changes in metabolic pathways following antibiotic treatment, including increased gene abundance for ABC transporters and the phosphotransferase system, and decreased representation of genes involved in antibiotic biosynthesis and two-component systems. These results indicate significant alterations in bacterial metabolism and stress response mechanisms induced by the treatment. Such changes may help explain the underperformance of irradiated, mass-reared males within the context of SIT. This study provides new insights into the structural and functional dynamics of the C. capitata gut microbiome under disturbance. These findings have implications for understanding the ecological roles of microbial communities in this pest and their potential impact on fly health and fitness. Identification of dominant gut bacterial and fungal groups may support the development of probiotic diets, enhancing the efficiency of SIT application.
Additional Links: PMID-41223178
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@article {pmid41223178,
year = {2025},
author = {Rasuk, MC and Palladini, A and Moyano, A and Díaz, V and Giudice, A and Castillo, G and Abraham, S and Rull, J and Poehlein, A and Daniel, R and Dib, JR},
title = {Dominance of Zygosaccharomyces and shifts in bacterial pathways: Effects of antimicrobials on composition and diversity of the Ceratitis capitata bacterial and fungal microbiome.},
journal = {PloS one},
volume = {20},
number = {11},
pages = {e0335811},
doi = {10.1371/journal.pone.0335811},
pmid = {41223178},
issn = {1932-6203},
mesh = {Animals ; *Ceratitis capitata/microbiology/drug effects ; *Zygosaccharomyces/drug effects/genetics ; RNA, Ribosomal, 16S/genetics ; *Gastrointestinal Microbiome/drug effects ; *Microbiota/drug effects ; *Anti-Infective Agents/pharmacology ; *Bacteria/genetics/drug effects/classification ; Male ; },
abstract = {The Mediterranean fruit fly (Ceratitis capitata Wied.) is an agricultural pest of significant economic importance. This species has been globally managed using the Sterile Insect Technique (SIT). Insects, including tephritid flies, harbor a diverse gut microbiota that plays critical roles in their physiology, behavior, and overall fitness, suggesting that microbial communities may profoundly influence the biology of this pest. The aim of this study was to characterize the fungal and bacterial gut microbial communities of C. capitata from Tucumán, Argentina, and to assess their response to antimicrobial treatment using amplicon-based 16S rRNA gene and ITS region sequencing. Both control and treated flies were dominated by Proteobacteria (bacteria) and Zygosaccharomyces (fungi). Antimicrobial treatment induced significant shifts in bacterial and fungal composition, reducing diversity and altering gut community structure. Untreated flies exhibited a diverse and structured bacterial gut community dominated by the family Enterobacteriaceae, while antibiotic-treated communities were dominated by Rhizobiaceae. Despite these shifts, fungal communities in both treated and untreated groups were consistently dominated by the genus Zygosaccharomyces. Functional predictions revealed notable changes in metabolic pathways following antibiotic treatment, including increased gene abundance for ABC transporters and the phosphotransferase system, and decreased representation of genes involved in antibiotic biosynthesis and two-component systems. These results indicate significant alterations in bacterial metabolism and stress response mechanisms induced by the treatment. Such changes may help explain the underperformance of irradiated, mass-reared males within the context of SIT. This study provides new insights into the structural and functional dynamics of the C. capitata gut microbiome under disturbance. These findings have implications for understanding the ecological roles of microbial communities in this pest and their potential impact on fly health and fitness. Identification of dominant gut bacterial and fungal groups may support the development of probiotic diets, enhancing the efficiency of SIT application.},
}
MeSH Terms:
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Animals
*Ceratitis capitata/microbiology/drug effects
*Zygosaccharomyces/drug effects/genetics
RNA, Ribosomal, 16S/genetics
*Gastrointestinal Microbiome/drug effects
*Microbiota/drug effects
*Anti-Infective Agents/pharmacology
*Bacteria/genetics/drug effects/classification
Male
RevDate: 2025-11-12
CmpDate: 2025-11-12
Microbiota-Derived SCFAs in Multiple Sclerosis: From Immune Priming to Neurodegeneration.
Molecular neurobiology, 63(1):31.
Multiple sclerosis (MS) is a chronic, immune-mediated neuroinflammatory and neurodegenerative disorder characterized by demyelination, axonal injury, and widespread disruption of central nervous system (CNS) integrity. Clinically heterogeneous and often presenting in young adults-especially women-MS manifests with motor deficits, cognitive impairment, depression, fatigue, sexual and sensory dysfunctions, and autonomic disturbances. Despite advances in immunotherapies, including disease-modifying agents and monoclonal antibodies, current treatments inadequately address progressive neurodegeneration or restore neuronal integrity. Traditional risk factors such as Epstein-Barr virus infection, vitamin D deficiency, smoking, and childhood obesity only partially explain disease onset, reflecting the multifactorial and elusive nature of MS pathogenesis. Recent research has turned attention toward the gut-brain axis, particularly the role of intestinal dysbiosis and microbial metabolites in modulating systemic and CNS inflammation. Among these, short-chain fatty acids (SCFAs)-produced through microbial fermentation of dietary fibres-have emerged as pivotal regulators of immune homeostasis, neuroinflammation, and glial function. Furthermore, MS patients consistently exhibit a depletion of SCFA-producing bacteria, implicating these metabolites development and progression of MS. In the prodromal phase, SCFAs influence gut immune priming and tolerance; in relapsing-remitting MS, they modulate T cell differentiation, cytokine profiles, and remyelination processes; and in progressive MS, they support mitochondrial function, reduce oxidative stress, and influence neuroglial dynamics. While SCFAs show promise as diagnostic biomarkers and adjunctive therapeutic targets, their context-dependent, bidirectional effects necessitate a precision-medicine approach. This review synthesizes current insights into the stage-specific roles of SCFAs across the MS disease continuum. The present work not only elucidates the mechanistic underpinnings of SCFA action in MS but also outlines future directions for microbiota-centred interventions tailored to disease stage and individual microbiome profiles.
Additional Links: PMID-41222739
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@article {pmid41222739,
year = {2025},
author = {Sharma, VK},
title = {Microbiota-Derived SCFAs in Multiple Sclerosis: From Immune Priming to Neurodegeneration.},
journal = {Molecular neurobiology},
volume = {63},
number = {1},
pages = {31},
pmid = {41222739},
issn = {1559-1182},
mesh = {Humans ; *Multiple Sclerosis/immunology/microbiology/metabolism/pathology ; Animals ; *Gastrointestinal Microbiome ; *Fatty Acids, Volatile/metabolism ; *Nerve Degeneration/metabolism/immunology ; },
abstract = {Multiple sclerosis (MS) is a chronic, immune-mediated neuroinflammatory and neurodegenerative disorder characterized by demyelination, axonal injury, and widespread disruption of central nervous system (CNS) integrity. Clinically heterogeneous and often presenting in young adults-especially women-MS manifests with motor deficits, cognitive impairment, depression, fatigue, sexual and sensory dysfunctions, and autonomic disturbances. Despite advances in immunotherapies, including disease-modifying agents and monoclonal antibodies, current treatments inadequately address progressive neurodegeneration or restore neuronal integrity. Traditional risk factors such as Epstein-Barr virus infection, vitamin D deficiency, smoking, and childhood obesity only partially explain disease onset, reflecting the multifactorial and elusive nature of MS pathogenesis. Recent research has turned attention toward the gut-brain axis, particularly the role of intestinal dysbiosis and microbial metabolites in modulating systemic and CNS inflammation. Among these, short-chain fatty acids (SCFAs)-produced through microbial fermentation of dietary fibres-have emerged as pivotal regulators of immune homeostasis, neuroinflammation, and glial function. Furthermore, MS patients consistently exhibit a depletion of SCFA-producing bacteria, implicating these metabolites development and progression of MS. In the prodromal phase, SCFAs influence gut immune priming and tolerance; in relapsing-remitting MS, they modulate T cell differentiation, cytokine profiles, and remyelination processes; and in progressive MS, they support mitochondrial function, reduce oxidative stress, and influence neuroglial dynamics. While SCFAs show promise as diagnostic biomarkers and adjunctive therapeutic targets, their context-dependent, bidirectional effects necessitate a precision-medicine approach. This review synthesizes current insights into the stage-specific roles of SCFAs across the MS disease continuum. The present work not only elucidates the mechanistic underpinnings of SCFA action in MS but also outlines future directions for microbiota-centred interventions tailored to disease stage and individual microbiome profiles.},
}
MeSH Terms:
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Humans
*Multiple Sclerosis/immunology/microbiology/metabolism/pathology
Animals
*Gastrointestinal Microbiome
*Fatty Acids, Volatile/metabolism
*Nerve Degeneration/metabolism/immunology
RevDate: 2025-11-12
Gut microbiome dysbiosis and antimicrobial resistance in the Middle East: a converging public health crisis in conflict and fragile settings.
Archives of microbiology, 208(1):15.
Additional Links: PMID-41222715
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Citation:
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@article {pmid41222715,
year = {2025},
author = {Almutawif, YA and Khan, NU},
title = {Gut microbiome dysbiosis and antimicrobial resistance in the Middle East: a converging public health crisis in conflict and fragile settings.},
journal = {Archives of microbiology},
volume = {208},
number = {1},
pages = {15},
pmid = {41222715},
issn = {1432-072X},
}
RevDate: 2025-11-12
Ketone ester supplementation protects from experimental colitis via improved goblet cell differentiation and function.
European journal of nutrition, 64(8):316.
PURPOSE: A ketogenic diet (KD), high in fat and low in carbohydrates, induces ketosis characterized by elevated circulating ketone bodies. While both KD and ketone bodies have demonstrated therapeutic potential in various pathophysiological conditions, their effect on inflammatory bowel diseases remains controversial. This study aimed to investigate the impact of a KD and ketone ester (KE), an ingestible form of ketone bodies, on intestinal inflammation.
METHODS: Acute dextran sodium sulfate (DSS)- and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced murine colitis models were used to evaluate and compare the effects of KD feeding and KE supplementation on intestinal inflammation, the mucus barrier and gut microbiota composition.
RESULTS: KD feeding did not significantly affect colitis activity, whereas KE supplementation alleviated colitis in both models investigated. KE-induced mitigation of colitis was associated with increased mucin2 expression, indicating enhanced colonic mucus barrier integrity. KE supplementation also improved goblet cell function and differentiation, as evidenced by increased goblet cell numbers and the upregulation of goblet cell differentiation markers. Furthermore, 16S rRNA sequencing analysis revealed that KE supplementation resulted in higher abundances of mucus-degrading Akkermansia, a genus believed to play a key role in maintaining intestinal homeostasis.
CONCLUSION: The present study suggests that KE represent an effective anti-inflammatory dietary supplement in the context of acute colitis, potentially by modulating mucin2 expression, goblet cell differentiation, and the abundance of Akkermansia. Although promising, these findings remain preliminary, and further investigations are needed to explore the therapeutic potential of KE as a dietary supplement in patients with inflammatory bowel disease.
Additional Links: PMID-41222705
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Citation:
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@article {pmid41222705,
year = {2025},
author = {Rohwer, N and Sander, A and Ocvirk, S and Wiebel, M and Kühl, AA and Schebb, NH and Grune, T and Weylandt, KH},
title = {Ketone ester supplementation protects from experimental colitis via improved goblet cell differentiation and function.},
journal = {European journal of nutrition},
volume = {64},
number = {8},
pages = {316},
pmid = {41222705},
issn = {1436-6215},
abstract = {PURPOSE: A ketogenic diet (KD), high in fat and low in carbohydrates, induces ketosis characterized by elevated circulating ketone bodies. While both KD and ketone bodies have demonstrated therapeutic potential in various pathophysiological conditions, their effect on inflammatory bowel diseases remains controversial. This study aimed to investigate the impact of a KD and ketone ester (KE), an ingestible form of ketone bodies, on intestinal inflammation.
METHODS: Acute dextran sodium sulfate (DSS)- and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced murine colitis models were used to evaluate and compare the effects of KD feeding and KE supplementation on intestinal inflammation, the mucus barrier and gut microbiota composition.
RESULTS: KD feeding did not significantly affect colitis activity, whereas KE supplementation alleviated colitis in both models investigated. KE-induced mitigation of colitis was associated with increased mucin2 expression, indicating enhanced colonic mucus barrier integrity. KE supplementation also improved goblet cell function and differentiation, as evidenced by increased goblet cell numbers and the upregulation of goblet cell differentiation markers. Furthermore, 16S rRNA sequencing analysis revealed that KE supplementation resulted in higher abundances of mucus-degrading Akkermansia, a genus believed to play a key role in maintaining intestinal homeostasis.
CONCLUSION: The present study suggests that KE represent an effective anti-inflammatory dietary supplement in the context of acute colitis, potentially by modulating mucin2 expression, goblet cell differentiation, and the abundance of Akkermansia. Although promising, these findings remain preliminary, and further investigations are needed to explore the therapeutic potential of KE as a dietary supplement in patients with inflammatory bowel disease.},
}
RevDate: 2025-11-12
Sand fly gut microbiota in Leishmania transmission: roles, interactions, and paratransgenic prospects.
Archives of microbiology, 208(1):16.
Additional Links: PMID-41222703
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Citation:
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@article {pmid41222703,
year = {2025},
author = {Chowdhury, S and Mishra, N and Pawar, H},
title = {Sand fly gut microbiota in Leishmania transmission: roles, interactions, and paratransgenic prospects.},
journal = {Archives of microbiology},
volume = {208},
number = {1},
pages = {16},
pmid = {41222703},
issn = {1432-072X},
}
RevDate: 2025-11-12
Exploring the microbial basis of postbiotic and paraprobiotic therapy in ulcerative colitis.
Archives of microbiology, 208(1):13.
Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by disrupted mucosal integrity and immune dysregulation. Emerging evidence increasingly supports postbiotics and paraprobiotics as safer, mechanistically targeted alternatives to conventional therapies such as corticosteroids and biologics. Unlike live probiotics, these non-viable microbial derivatives act through defined immune-metabolic pathways that enhance epithelial barrier function, rebalance gut dysbiosis, and modulate oxidative and inflammatory signalling without infection risk or viability concerns. Preclinical studies demonstrate their capacity to inhibit NF-κB activation, promote regulatory T-cell responses, and restore tight-junction integrity, while early clinical investigations suggest symptom improvement and mucosal healing in subsets of UC patients. Despite these advances, translation remains constrained by limited human trials, lack of standardized formulations, dose-response variability, and regulatory ambiguity. This review critically examines mechanistic, preclinical, and clinical findings on postbiotic and para probiotic interventions in UC, highlighting both their therapeutic promise and the translational gaps that must be bridged for clinical implementation.
Additional Links: PMID-41222696
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@article {pmid41222696,
year = {2025},
author = {Pavithra, N and Devi, M and Nirenjen, S and Keerthana, B and Kumar, VKG and Yogalakshmi, R and Priyadharshni, MG and Harikrishnan, N},
title = {Exploring the microbial basis of postbiotic and paraprobiotic therapy in ulcerative colitis.},
journal = {Archives of microbiology},
volume = {208},
number = {1},
pages = {13},
pmid = {41222696},
issn = {1432-072X},
abstract = {Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by disrupted mucosal integrity and immune dysregulation. Emerging evidence increasingly supports postbiotics and paraprobiotics as safer, mechanistically targeted alternatives to conventional therapies such as corticosteroids and biologics. Unlike live probiotics, these non-viable microbial derivatives act through defined immune-metabolic pathways that enhance epithelial barrier function, rebalance gut dysbiosis, and modulate oxidative and inflammatory signalling without infection risk or viability concerns. Preclinical studies demonstrate their capacity to inhibit NF-κB activation, promote regulatory T-cell responses, and restore tight-junction integrity, while early clinical investigations suggest symptom improvement and mucosal healing in subsets of UC patients. Despite these advances, translation remains constrained by limited human trials, lack of standardized formulations, dose-response variability, and regulatory ambiguity. This review critically examines mechanistic, preclinical, and clinical findings on postbiotic and para probiotic interventions in UC, highlighting both their therapeutic promise and the translational gaps that must be bridged for clinical implementation.},
}
RevDate: 2025-11-12
Transcription regulator TrtA modulates oxygen stress response in Treponema denticola.
Applied and environmental microbiology [Epub ahead of print].
Periodontitis is caused by dysbiosis of the subgingival microbiome. Treponema denticola is an obligate anaerobe frequently detected in advanced periodontal lesions. However, the mechanism by which T. denticola evades oxygen stress remains unclear. TDE_0127 (trtA) encodes a potential transcriptional regulator in T. denticola and is upregulated in response to oxygen exposure. However, its exact function is unclear. This study aimed to investigate the involvement of TrtA in the oxygen stress response of T. denticola. trtA expression increased under oxygen exposure. RNA-seq analysis revealed that the expression levels of 38 genes, including that encoding internalin-related protein, were significantly upregulated under anaerobic conditions, and 153 genes, including those encoding peroxiredoxin and dentilisin, were significantly downregulated (|log2(mutant/wild type)| >1.5, false discovery rate <0.05) in the trtA-deletion mutant. Under aerobic conditions, peroxiredoxin expression was lower and the viable cell proportion was significantly lower in the trtA-deletion mutant than in the wild-type strain (P < 0.001), suggesting that TrtA is involved in oxygen resistance via peroxiredoxin regulation. In contrast, internalin-related protein expression in the trtA-deletion mutant increased. Inactivation of internalin-related protein reduced the intracellular invasion of gingival keratinocytes, and quantitative reverse transcription PCR analysis showed that internalin-related protein expression in the wild-type strain decreased under oxygen exposure, suggesting that it is under TrtA regulation. Although dentilisin expression was downregulated in the trtA-deletion mutant, direct interaction was not elucidated. These results suggest that TrtA is involved in oxygen stress resistance and intracellular invasion in T. denticola.IMPORTANCETreponema denticola is prevalent in advanced periodontal lesions and is involved in the pathogenesis and progression of periodontitis. During dysbiosis of the subgingival microbiome, T. denticola resists the effects of environmental oxygen and H2O2 released from commensal bacteria. In other periodontopathic bacteria, genes encoding master regulators of oxygen stress, such as OxyR, have been detected in the genome. However, an ortholog of such a regulator is yet to be detected in the genome of T. denticola. Herein, we show, for the first time, that TrtA is involved in the oxygen stress response of T. denticola. The expression of 153 genes was attenuated in the trtA-deletion mutant, indicating that TrtA influences a broad range of cellular processes. TrtA regulates the oxygen stress response in part through peroxiredoxin. In addition, internalin-related protein, which may participate in the host cell invasion by T. denticola, is under the control of TrtA.
Additional Links: PMID-41222288
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PubMed:
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@article {pmid41222288,
year = {2025},
author = {Kitamura, Y and Kikuchi, Y and Kokubu, E and Yamashita, K and Yonezawa, H and Saito, A and Ishihara, K},
title = {Transcription regulator TrtA modulates oxygen stress response in Treponema denticola.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0075025},
doi = {10.1128/aem.00750-25},
pmid = {41222288},
issn = {1098-5336},
abstract = {Periodontitis is caused by dysbiosis of the subgingival microbiome. Treponema denticola is an obligate anaerobe frequently detected in advanced periodontal lesions. However, the mechanism by which T. denticola evades oxygen stress remains unclear. TDE_0127 (trtA) encodes a potential transcriptional regulator in T. denticola and is upregulated in response to oxygen exposure. However, its exact function is unclear. This study aimed to investigate the involvement of TrtA in the oxygen stress response of T. denticola. trtA expression increased under oxygen exposure. RNA-seq analysis revealed that the expression levels of 38 genes, including that encoding internalin-related protein, were significantly upregulated under anaerobic conditions, and 153 genes, including those encoding peroxiredoxin and dentilisin, were significantly downregulated (|log2(mutant/wild type)| >1.5, false discovery rate <0.05) in the trtA-deletion mutant. Under aerobic conditions, peroxiredoxin expression was lower and the viable cell proportion was significantly lower in the trtA-deletion mutant than in the wild-type strain (P < 0.001), suggesting that TrtA is involved in oxygen resistance via peroxiredoxin regulation. In contrast, internalin-related protein expression in the trtA-deletion mutant increased. Inactivation of internalin-related protein reduced the intracellular invasion of gingival keratinocytes, and quantitative reverse transcription PCR analysis showed that internalin-related protein expression in the wild-type strain decreased under oxygen exposure, suggesting that it is under TrtA regulation. Although dentilisin expression was downregulated in the trtA-deletion mutant, direct interaction was not elucidated. These results suggest that TrtA is involved in oxygen stress resistance and intracellular invasion in T. denticola.IMPORTANCETreponema denticola is prevalent in advanced periodontal lesions and is involved in the pathogenesis and progression of periodontitis. During dysbiosis of the subgingival microbiome, T. denticola resists the effects of environmental oxygen and H2O2 released from commensal bacteria. In other periodontopathic bacteria, genes encoding master regulators of oxygen stress, such as OxyR, have been detected in the genome. However, an ortholog of such a regulator is yet to be detected in the genome of T. denticola. Herein, we show, for the first time, that TrtA is involved in the oxygen stress response of T. denticola. The expression of 153 genes was attenuated in the trtA-deletion mutant, indicating that TrtA influences a broad range of cellular processes. TrtA regulates the oxygen stress response in part through peroxiredoxin. In addition, internalin-related protein, which may participate in the host cell invasion by T. denticola, is under the control of TrtA.},
}
RevDate: 2025-11-12
Age and antibiotic use influence longitudinal dynamics of the upper respiratory microbiome in children with recurrent acute otitis media.
mSphere [Epub ahead of print].
UNLABELLED: The upper respiratory tract (URT) microbiome has emerged as a key component of acute otitis media (AOM) pathophysiology; however, few studies conducted to date have evaluated URT microbiome composition in children with recurrent AOM (rAOM). We collected serial nasopharyngeal samples from a cohort of 58 children, 6 to 35 months of age, over a one-year period. Samples were analyzed using 16S rRNA sequencing and PCR-based assays for common otopathogens and respiratory viruses. Age was strongly associated with differential abundance of specific genera, including increased abundance of genera associated with respiratory health (e.g., Dolosigranulum, Corynebacterium). In contrast, samples collected during AOM episodes or within 30 days of receipt of an antibiotic had a lower relative abundance of these genera. Further, the number of antibiotic-free days prior to sample collection was associated with global changes in microbiome composition. Unsupervised clustering identified three microbiome profiles that differed by incidence of AOM, bacterial otopathogen burden, symptom score, and number of antibiotic-free days prior to sample collection. Increasing age was associated with transition to profiles characterized by lower incidence of AOM and bacterial otopathogen burden, while antibiotic use was associated with transition to a profile associated with greater incidence of AOM. Our findings indicate that alterations of the microbiome associated with aging may contribute to decreased incidence of AOM as children age, while systemic antibiotic use may induce dysbiosis, thereby enhancing AOM susceptibility.
IMPORTANCE: Ear infections are the most common bacterial infection among young children and the leading cause of healthcare visits and antibiotic prescriptions. This study explores the connection between the microbiome of the nose-the community of microorganisms that live in different areas of the human body-and recurrent ear infections in young children. An analysis of nasal swabs collected from 58 children over a year showed that as children age, they tend to have fewer bacterial pathogens and more species that are associated with a healthy state in their microbiomes. These more mature microbiomes were associated with fewer ear infections. In contrast, recent use of antibiotics was associated with microbiomes that had more bacterial pathogens and that were associated with greater ear infection incidence. Overall, these findings indicate that the microbiome may be a key factor in reduced ear infections as children age.
Additional Links: PMID-41222257
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@article {pmid41222257,
year = {2025},
author = {Hurst, JH and Xing, Y and Dong, Q and Hoberman, A and Gao, X and Shaikh, N},
title = {Age and antibiotic use influence longitudinal dynamics of the upper respiratory microbiome in children with recurrent acute otitis media.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0046825},
doi = {10.1128/msphere.00468-25},
pmid = {41222257},
issn = {2379-5042},
abstract = {UNLABELLED: The upper respiratory tract (URT) microbiome has emerged as a key component of acute otitis media (AOM) pathophysiology; however, few studies conducted to date have evaluated URT microbiome composition in children with recurrent AOM (rAOM). We collected serial nasopharyngeal samples from a cohort of 58 children, 6 to 35 months of age, over a one-year period. Samples were analyzed using 16S rRNA sequencing and PCR-based assays for common otopathogens and respiratory viruses. Age was strongly associated with differential abundance of specific genera, including increased abundance of genera associated with respiratory health (e.g., Dolosigranulum, Corynebacterium). In contrast, samples collected during AOM episodes or within 30 days of receipt of an antibiotic had a lower relative abundance of these genera. Further, the number of antibiotic-free days prior to sample collection was associated with global changes in microbiome composition. Unsupervised clustering identified three microbiome profiles that differed by incidence of AOM, bacterial otopathogen burden, symptom score, and number of antibiotic-free days prior to sample collection. Increasing age was associated with transition to profiles characterized by lower incidence of AOM and bacterial otopathogen burden, while antibiotic use was associated with transition to a profile associated with greater incidence of AOM. Our findings indicate that alterations of the microbiome associated with aging may contribute to decreased incidence of AOM as children age, while systemic antibiotic use may induce dysbiosis, thereby enhancing AOM susceptibility.
IMPORTANCE: Ear infections are the most common bacterial infection among young children and the leading cause of healthcare visits and antibiotic prescriptions. This study explores the connection between the microbiome of the nose-the community of microorganisms that live in different areas of the human body-and recurrent ear infections in young children. An analysis of nasal swabs collected from 58 children over a year showed that as children age, they tend to have fewer bacterial pathogens and more species that are associated with a healthy state in their microbiomes. These more mature microbiomes were associated with fewer ear infections. In contrast, recent use of antibiotics was associated with microbiomes that had more bacterial pathogens and that were associated with greater ear infection incidence. Overall, these findings indicate that the microbiome may be a key factor in reduced ear infections as children age.},
}
RevDate: 2025-11-12
The Link between Modifiable Risk Factors and Myeloid Disorders-From Plate to Pathogenesis.
Blood cancer discovery pii:767197 [Epub ahead of print].
UNLABELLED: Clonal hematopoiesis of indeterminate potential, myelodysplastic syndromes, and acute myeloid leukemia are myeloid cell disorders that exist on a spectrum. Modifiable risk factors, including obesity, insulin resistance, physical activity, dietary patterns, smoking, and the microbiome, have been implicated in myeloid cell disorder pathogenesis. Although the connection between these modifiable risk factors and their association with myeloid disorders has been studied, as of September 2025, no clinical trials are ongoing that evaluate whether lifestyle interventions can alter myeloid disorder disease progression. This article reviews myeloid disorders and their association with inflammation and how lifestyle interventions may influence disease progression.
SIGNIFICANCE: Myeloid disorders are associated with inflammation and metabolic disorders such as obesity and diabetes mellitus. Dietary and lifestyle modifications may directly influence the pathogenesis, development, and survival by addressing inflammatory and metabolic pathways. However, additional preclinical research and large prospective clinical trials are needed to confirm these findings. This review provides an overview on myeloid disorder pathogenesis and modifiable factors that influence it, which may guide future research to reduce the myeloid disorder burden and improve outcomes for patients with clonal hematopoiesis of indeterminate potential, myelodysplastic syndromes, and acute myeloid leukemia.
Additional Links: PMID-41222150
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@article {pmid41222150,
year = {2025},
author = {Weinreb, JT and Abdel-Wahab, O and Shah, UA},
title = {The Link between Modifiable Risk Factors and Myeloid Disorders-From Plate to Pathogenesis.},
journal = {Blood cancer discovery},
volume = {},
number = {},
pages = {OF1-OF10},
doi = {10.1158/2643-3230.BCD-25-0056},
pmid = {41222150},
issn = {2643-3249},
abstract = {UNLABELLED: Clonal hematopoiesis of indeterminate potential, myelodysplastic syndromes, and acute myeloid leukemia are myeloid cell disorders that exist on a spectrum. Modifiable risk factors, including obesity, insulin resistance, physical activity, dietary patterns, smoking, and the microbiome, have been implicated in myeloid cell disorder pathogenesis. Although the connection between these modifiable risk factors and their association with myeloid disorders has been studied, as of September 2025, no clinical trials are ongoing that evaluate whether lifestyle interventions can alter myeloid disorder disease progression. This article reviews myeloid disorders and their association with inflammation and how lifestyle interventions may influence disease progression.
SIGNIFICANCE: Myeloid disorders are associated with inflammation and metabolic disorders such as obesity and diabetes mellitus. Dietary and lifestyle modifications may directly influence the pathogenesis, development, and survival by addressing inflammatory and metabolic pathways. However, additional preclinical research and large prospective clinical trials are needed to confirm these findings. This review provides an overview on myeloid disorder pathogenesis and modifiable factors that influence it, which may guide future research to reduce the myeloid disorder burden and improve outcomes for patients with clonal hematopoiesis of indeterminate potential, myelodysplastic syndromes, and acute myeloid leukemia.},
}
RevDate: 2025-11-12
A synthetic gut microbiota provides an understanding of the maintenance and functional impact of phage.
mBio [Epub ahead of print].
UNLABELLED: Phages are under intense study as therapeutics and mediators of microbial community behavior; however, tractable models are needed to study phages in the context of the mammalian gut. To address this gap, we isolated phages against members of a synthetic gut microbial community (sFMT), identifying the Bacteroides uniformis JEB00023 (DSM 6597) phage HKP09. While resistance to HKP09 was observable within hours of infection in monoculture, high titers of HKP09 were maintained in vitro and in gnotobiotic mouse models over extended periods. Sequencing of resistant B. uniformis lines revealed phase variation upstream of a capsular polysaccharide locus driving the generation of resistant and sensitive subpopulations, thus demonstrating a mechanism allowing stable coexistence of both virus and bacterial host. Communities infected in vitro and in vivo with HKP09 showed transiently reduced loads of B. uniformis DSM 6597. Its impact in the gut was distinct from communities constructed without its host B. uniformis strain (sFMT∆JEB00023). Rather than a compensatory increase in closely related Bacteroides strains, the most significant impacts were observed on distantly related strains, demonstrating that phage perturbations more broadly impact community structure in ways not easily predicted by phylogeny or simple strain exclusion. Metabolomic analyses of the feces of HKP09-infected sFMT-colonized gnotobiotic animals demonstrated altered abundances of amino acids and microbial fermentation products compared to uninfected mice and those colonized with sFMT∆JEB00023. Taken together, these data provide a controlled model for studying phages in the context of the mammalian gut, providing mechanistic insights into phage-host dynamics and their consequences on the function of microbial communities.
IMPORTANCE: Phages are key members of the gut microbiome, but the understanding of their biological significance for host health lags behind their bacterial hosts. In this study, we demonstrate the use of a phage-infection model using defined, synthetic microbial communities that colonize the intestinal tract of mice. We uncovered that spontaneous inversions in the genome of Bacteroides uniformis perpetually generate subpopulations, which are either sensitive or resistant to phage infection, allowing for the coexistence of predator and prey in this species. Phage infection demonstrated broad impacts on community structure and metabolism in animals, which are not easily predicted by the exclusion of the viral host. This research demonstrates a tractable approach through which the impacts of phage on both the microbiome and mammalian host can be deciphered.
Additional Links: PMID-41222145
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PubMed:
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@article {pmid41222145,
year = {2025},
author = {Koo, H and Heber, K and Tian, S and Connolly, ST and Hao, F and Zhao, J and Swencki-Underwood, B and Patterson, AD and Townsend, GE and Bisanz, JE},
title = {A synthetic gut microbiota provides an understanding of the maintenance and functional impact of phage.},
journal = {mBio},
volume = {},
number = {},
pages = {e0234125},
doi = {10.1128/mbio.02341-25},
pmid = {41222145},
issn = {2150-7511},
abstract = {UNLABELLED: Phages are under intense study as therapeutics and mediators of microbial community behavior; however, tractable models are needed to study phages in the context of the mammalian gut. To address this gap, we isolated phages against members of a synthetic gut microbial community (sFMT), identifying the Bacteroides uniformis JEB00023 (DSM 6597) phage HKP09. While resistance to HKP09 was observable within hours of infection in monoculture, high titers of HKP09 were maintained in vitro and in gnotobiotic mouse models over extended periods. Sequencing of resistant B. uniformis lines revealed phase variation upstream of a capsular polysaccharide locus driving the generation of resistant and sensitive subpopulations, thus demonstrating a mechanism allowing stable coexistence of both virus and bacterial host. Communities infected in vitro and in vivo with HKP09 showed transiently reduced loads of B. uniformis DSM 6597. Its impact in the gut was distinct from communities constructed without its host B. uniformis strain (sFMT∆JEB00023). Rather than a compensatory increase in closely related Bacteroides strains, the most significant impacts were observed on distantly related strains, demonstrating that phage perturbations more broadly impact community structure in ways not easily predicted by phylogeny or simple strain exclusion. Metabolomic analyses of the feces of HKP09-infected sFMT-colonized gnotobiotic animals demonstrated altered abundances of amino acids and microbial fermentation products compared to uninfected mice and those colonized with sFMT∆JEB00023. Taken together, these data provide a controlled model for studying phages in the context of the mammalian gut, providing mechanistic insights into phage-host dynamics and their consequences on the function of microbial communities.
IMPORTANCE: Phages are key members of the gut microbiome, but the understanding of their biological significance for host health lags behind their bacterial hosts. In this study, we demonstrate the use of a phage-infection model using defined, synthetic microbial communities that colonize the intestinal tract of mice. We uncovered that spontaneous inversions in the genome of Bacteroides uniformis perpetually generate subpopulations, which are either sensitive or resistant to phage infection, allowing for the coexistence of predator and prey in this species. Phage infection demonstrated broad impacts on community structure and metabolism in animals, which are not easily predicted by the exclusion of the viral host. This research demonstrates a tractable approach through which the impacts of phage on both the microbiome and mammalian host can be deciphered.},
}
RevDate: 2025-11-12
Dominant effects of the immediate environment on the gut microbiome of mice used in biomedical research.
mSystems [Epub ahead of print].
Studies using genetically engineered mouse (GEM) models are often performed over extended periods. The microbiomes of GEM colonies are expected to retain some of the microbial features present in the founder mice used to generate each GEM model and to acquire new features through dietary and environmental sources. The rate at which these processes occur over time likely varies between institutions. To assess the relative effect size of environment on the microbiome of GEMs used in biomedical research, we performed 16S rRNA metabarcoding of fecal samples from 275 distinct GEM lines (n = 351) maintained by 139 different laboratories at 84 different research institutions in 34 U.S. states or districts and seven other countries, and compared intra-strain, inter-strain, inter-lab, and inter-institution similarities. Reference data from mice harboring supplier-origin (SO) microbiomes (n = 1,171) were used to determine the relative contribution and nature of microbes from known and unknown sources. Paradoxically, the data indicate that the immediate laboratory-level environment is the dominant factor shaping the microbiome of GEM models, but that the microbiome of GEMs develops similarities in beta-diversity, regardless of other factors. Related to this, we detected an unexpectedly high prevalence and abundance of Helicobacter spp. in GEM microbiomes, the abundance of which correlated significantly with the abundance of multiple resident taxa colonizing the mucosa. These findings suggest a higher prevalence of Helicobacter spp. in laboratory mice than previously appreciated, and the possibility of positive and negative interactions with other taxa is found to affect GEM model phenotypes.IMPORTANCEThere are concerns regarding the reproducibility and predictive value of mouse models of human disease. Notwithstanding those legitimate concerns, genetically engineered mouse (GEM) models provide an invaluable platform to investigate gene function or effects of environmental factors in a biological system. The microbiome of GEM models significantly influences model phenotypes and thus represents a possible source of poor reproducibility. While the microbiome is often incorporated in research investigating disease mechanisms using GEMs, limited information is available regarding the similarity of the microbiome of GEM models within and between research labs at the same institution, or across institutions. Moreover, while the microbiome of founder mice from different suppliers is known to differ, the degree to which features present in supplier-origin microbiomes are retained in GEM colonies throughout experimentation is unclear. These data demonstrate the robust effect of lab-level environment and the need for sample collection concurrent with phenotyping.
Additional Links: PMID-41222144
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@article {pmid41222144,
year = {2025},
author = {Ericsson, AC and McAdams, ZL and Dorfmeyer, RA and Hart, ML and O'Neill-Blair, A and Amos-Landgraf, J and Franklin, CL},
title = {Dominant effects of the immediate environment on the gut microbiome of mice used in biomedical research.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0111225},
doi = {10.1128/msystems.01112-25},
pmid = {41222144},
issn = {2379-5077},
abstract = {Studies using genetically engineered mouse (GEM) models are often performed over extended periods. The microbiomes of GEM colonies are expected to retain some of the microbial features present in the founder mice used to generate each GEM model and to acquire new features through dietary and environmental sources. The rate at which these processes occur over time likely varies between institutions. To assess the relative effect size of environment on the microbiome of GEMs used in biomedical research, we performed 16S rRNA metabarcoding of fecal samples from 275 distinct GEM lines (n = 351) maintained by 139 different laboratories at 84 different research institutions in 34 U.S. states or districts and seven other countries, and compared intra-strain, inter-strain, inter-lab, and inter-institution similarities. Reference data from mice harboring supplier-origin (SO) microbiomes (n = 1,171) were used to determine the relative contribution and nature of microbes from known and unknown sources. Paradoxically, the data indicate that the immediate laboratory-level environment is the dominant factor shaping the microbiome of GEM models, but that the microbiome of GEMs develops similarities in beta-diversity, regardless of other factors. Related to this, we detected an unexpectedly high prevalence and abundance of Helicobacter spp. in GEM microbiomes, the abundance of which correlated significantly with the abundance of multiple resident taxa colonizing the mucosa. These findings suggest a higher prevalence of Helicobacter spp. in laboratory mice than previously appreciated, and the possibility of positive and negative interactions with other taxa is found to affect GEM model phenotypes.IMPORTANCEThere are concerns regarding the reproducibility and predictive value of mouse models of human disease. Notwithstanding those legitimate concerns, genetically engineered mouse (GEM) models provide an invaluable platform to investigate gene function or effects of environmental factors in a biological system. The microbiome of GEM models significantly influences model phenotypes and thus represents a possible source of poor reproducibility. While the microbiome is often incorporated in research investigating disease mechanisms using GEMs, limited information is available regarding the similarity of the microbiome of GEM models within and between research labs at the same institution, or across institutions. Moreover, while the microbiome of founder mice from different suppliers is known to differ, the degree to which features present in supplier-origin microbiomes are retained in GEM colonies throughout experimentation is unclear. These data demonstrate the robust effect of lab-level environment and the need for sample collection concurrent with phenotyping.},
}
RevDate: 2025-11-12
Distinct gut microbiome shifts in the NICU influence later atopic dermatitis development.
Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology, 36(11):e70239.
Additional Links: PMID-41221992
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PubMed:
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@article {pmid41221992,
year = {2025},
author = {Robbins, ES and McCauley, KE and Strength, R and Namasivayam, S and Angelova, AG and Prasad, R and Patel, A and Deopujari, V and Burns, AS and Mistry, S and Baveja, R and Baker, RL and Frischmeyer-Guerrerio, PA and Levy, S and Hourigan, SK},
title = {Distinct gut microbiome shifts in the NICU influence later atopic dermatitis development.},
journal = {Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology},
volume = {36},
number = {11},
pages = {e70239},
doi = {10.1111/pai.70239},
pmid = {41221992},
issn = {1399-3038},
support = {//National Eczema Association/ ; //Division of Intramural Research, National Institute of Allergy and Infectious Diseases/ ; },
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
Persistent human-associated microbial signatures in burial soils from the 17th and 18th century New York African burial ground.
ISME communications, 5(1):ycaf181.
Understanding the long-term persistence of human-associated microbial signatures in burial soils offers a untapped insights into historical human health, decomposition, and ecological transformation. This study investigates whether centuries-old burial soils retain distinguishable microbial evidence of human decomposition using 16S rRNA gene sequencing on 81 samples from the New York African Burial Ground (NYABG), a 17th and 18th century cemetery for free and enslaved Africans. Comparative analyses against six control soils from nearby urban parks were conducted using QIIME2, ALDEx2, and ANCOM. Burial soils exhibited significantly greater alpha diversity (Faith's PD, Shannon, observed ASVs; P < .01) and distinct beta diversity patterns (Bray-Curtis, UniFrac; PERMANOVA P = .001). Enrichment of Firmicutes, Actinobacteriota, and gut-associated genera such as Bacillus and Ruminococcus characterized burial soils, whereas oligotrophic taxa dominated controls. Tentative identifications of human-associated pathogenic genera (e.g. Fusobacterium periodonticum, Prevotella pleuritidis) were observed exclusively in burial soils, suggesting their origin from the interred individuals but requiring further validation. These findings demonstrate that soil microbiomes reflect host-associated microbial communities long after decomposition, providing a scalable, nondestructive approach for reconstructing ancient microbial communities and host-associated health signatures. This work establishes the NYABG burial soil microbiome as a valuable model for microbial archaeology and introduces a replicable framework for integrating environmental microbiology, bioarchaeology, and historical epidemiology through the lens of postmortem microbial ecology.
Additional Links: PMID-41221507
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Citation:
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@article {pmid41221507,
year = {2025},
author = {Clinton, CK and Jackson, FLC},
title = {Persistent human-associated microbial signatures in burial soils from the 17th and 18th century New York African burial ground.},
journal = {ISME communications},
volume = {5},
number = {1},
pages = {ycaf181},
pmid = {41221507},
issn = {2730-6151},
abstract = {Understanding the long-term persistence of human-associated microbial signatures in burial soils offers a untapped insights into historical human health, decomposition, and ecological transformation. This study investigates whether centuries-old burial soils retain distinguishable microbial evidence of human decomposition using 16S rRNA gene sequencing on 81 samples from the New York African Burial Ground (NYABG), a 17th and 18th century cemetery for free and enslaved Africans. Comparative analyses against six control soils from nearby urban parks were conducted using QIIME2, ALDEx2, and ANCOM. Burial soils exhibited significantly greater alpha diversity (Faith's PD, Shannon, observed ASVs; P < .01) and distinct beta diversity patterns (Bray-Curtis, UniFrac; PERMANOVA P = .001). Enrichment of Firmicutes, Actinobacteriota, and gut-associated genera such as Bacillus and Ruminococcus characterized burial soils, whereas oligotrophic taxa dominated controls. Tentative identifications of human-associated pathogenic genera (e.g. Fusobacterium periodonticum, Prevotella pleuritidis) were observed exclusively in burial soils, suggesting their origin from the interred individuals but requiring further validation. These findings demonstrate that soil microbiomes reflect host-associated microbial communities long after decomposition, providing a scalable, nondestructive approach for reconstructing ancient microbial communities and host-associated health signatures. This work establishes the NYABG burial soil microbiome as a valuable model for microbial archaeology and introduces a replicable framework for integrating environmental microbiology, bioarchaeology, and historical epidemiology through the lens of postmortem microbial ecology.},
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
Double-edged effects of aquatic environmental biofilms on Batrachochytrium dendrobatidis growth and inhibition.
ISME communications, 5(1):ycaf185.
Batrachochytrium dendrobatidis (Bd) is an aquatic chytrid fungus that infects amphibians and has the potential to remain viable outside of hosts. However, the role of aquatic microbiota in influencing Bd growth and survival remains insufficiently understood. In this study, we demonstrated that in the absence of amphibian hosts, aquatic environmental (AE) biofilms supported the development of Bd, allowing it to complete its life cycle for a short period; whereas aquatic planktonic microorganisms did not. However, exposure of Bd zoospores to AE biofilms or planktonic microorganisms resulted in a significant reduction in Bd DNA within a week. These results suggest a dual role of aquatic biofilms in both supporting Bd growth and inhibiting it simultaneously. Moreover, Bd monolayers, composed mainly of zoosporangia, rapidly declined when exposed to AE planktonic microorganisms. Laboratory-formulated nutrients further enhanced the Bd-inhibitory effect of AE microbiota, suggesting that competition for shared nutrients plays a role in this interaction. This study advances our understanding of the complex interactions between Bd and aquatic microbial communities, underscores the ecological significance of biofilm-associated environments, and supports the potential of microbiota-informed interventions for controlling chytridiomycosis in amphibians.
Additional Links: PMID-41221506
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@article {pmid41221506,
year = {2025},
author = {Chen, R and Nordheim-Maestas, CL and Briggs, CJ},
title = {Double-edged effects of aquatic environmental biofilms on Batrachochytrium dendrobatidis growth and inhibition.},
journal = {ISME communications},
volume = {5},
number = {1},
pages = {ycaf185},
pmid = {41221506},
issn = {2730-6151},
abstract = {Batrachochytrium dendrobatidis (Bd) is an aquatic chytrid fungus that infects amphibians and has the potential to remain viable outside of hosts. However, the role of aquatic microbiota in influencing Bd growth and survival remains insufficiently understood. In this study, we demonstrated that in the absence of amphibian hosts, aquatic environmental (AE) biofilms supported the development of Bd, allowing it to complete its life cycle for a short period; whereas aquatic planktonic microorganisms did not. However, exposure of Bd zoospores to AE biofilms or planktonic microorganisms resulted in a significant reduction in Bd DNA within a week. These results suggest a dual role of aquatic biofilms in both supporting Bd growth and inhibiting it simultaneously. Moreover, Bd monolayers, composed mainly of zoosporangia, rapidly declined when exposed to AE planktonic microorganisms. Laboratory-formulated nutrients further enhanced the Bd-inhibitory effect of AE microbiota, suggesting that competition for shared nutrients plays a role in this interaction. This study advances our understanding of the complex interactions between Bd and aquatic microbial communities, underscores the ecological significance of biofilm-associated environments, and supports the potential of microbiota-informed interventions for controlling chytridiomycosis in amphibians.},
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
Dynamic multi-omics mechanisms underpinning retinol tolerance: stage-specific reconstruction of skin barrier function and host-microbiome metabolic interactions.
Frontiers in microbiology, 16:1668712.
BACKGROUND: Retinol remains an essential component in anti-aging skincare; however, a subset of users develop intolerance, characterized by compromised barrier integrity and inflammation. The temporal dynamics of how skin microbiota and host metabolism co-evolve during retinol tolerance establishment remain poorly understood.
METHODS: We conducted a prospective 28-day longitudinal study with 18 Chinese women (aged 25-40): 9 retinol-intolerant subjects monitored at baseline, adverse reaction phase, and tolerance establishment, while baseline data from 9 retinol-tolerant individuals served as controls. We integrated cutaneous phenotypic measurements, metagenomic sequencing, and untargeted metabolomics.
RESULTS: In the intolerant group, skin phenotype assessment revealed a distinct biphasic response-an acute phase marked by increased stratum corneum hydration, reduced sebum secretion, lower skin pH, and improved wrinkle metrics, followed by a re-equilibration phase characterized by sustained barrier restoration. Metagenomic profiling of 969 microbial species demonstrated that, although overall microbial α-diversity remained stable across time points in both groups, key taxa in the intolerant group exhibited transient "rise-and-fall" dynamics. At baseline, the intolerant group exhibited overrepresentation of Cutibacterium acnes, whereas the tolerant group was enriched in potentially protective species, including Sphingomonas hankookensis and Acinetobacter johnsonii. Untargeted metabolomics showed marked temporal fluctuations with an initial phase of metabolic turbulence, followed by partial recovery. During the early adverse reaction phase in intolerant subjects, lipid and fatty acid metabolic pathways-specifically, glycerophospholipid, linoleic acid, α-linolenic acid, and ether lipid metabolism-were significantly upregulated, concomitant with the suppression of TCA cycle and sphingolipid activity. Conversely, as tolerance was established, enhanced activity in the TCA cycle, sphingolipid, ascorbate, and pentose metabolism pathways-coupled with a reduction in pro-inflammatory arachidonic acid derivatives-indicated metabolic reconstitution and restoration of barrier integrity.
DISCUSSION: Integrated multi-omics correlation analyses further underscored the tightly interconnected regulation of host-microbe energy metabolism, antioxidant defenses, and membrane repair in response to retinol-induced stress. These findings elucidate the temporal interplay between host and microbial processes underpinning retinol tolerance and highlight baseline biomarkers that may facilitate personalized skincare interventions.
Additional Links: PMID-41221399
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@article {pmid41221399,
year = {2025},
author = {Huang, Y and Zhou, Q and Gui, M and Guo, D and Cheng, J and Ma, W and Shu, P and Liu, X},
title = {Dynamic multi-omics mechanisms underpinning retinol tolerance: stage-specific reconstruction of skin barrier function and host-microbiome metabolic interactions.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1668712},
pmid = {41221399},
issn = {1664-302X},
abstract = {BACKGROUND: Retinol remains an essential component in anti-aging skincare; however, a subset of users develop intolerance, characterized by compromised barrier integrity and inflammation. The temporal dynamics of how skin microbiota and host metabolism co-evolve during retinol tolerance establishment remain poorly understood.
METHODS: We conducted a prospective 28-day longitudinal study with 18 Chinese women (aged 25-40): 9 retinol-intolerant subjects monitored at baseline, adverse reaction phase, and tolerance establishment, while baseline data from 9 retinol-tolerant individuals served as controls. We integrated cutaneous phenotypic measurements, metagenomic sequencing, and untargeted metabolomics.
RESULTS: In the intolerant group, skin phenotype assessment revealed a distinct biphasic response-an acute phase marked by increased stratum corneum hydration, reduced sebum secretion, lower skin pH, and improved wrinkle metrics, followed by a re-equilibration phase characterized by sustained barrier restoration. Metagenomic profiling of 969 microbial species demonstrated that, although overall microbial α-diversity remained stable across time points in both groups, key taxa in the intolerant group exhibited transient "rise-and-fall" dynamics. At baseline, the intolerant group exhibited overrepresentation of Cutibacterium acnes, whereas the tolerant group was enriched in potentially protective species, including Sphingomonas hankookensis and Acinetobacter johnsonii. Untargeted metabolomics showed marked temporal fluctuations with an initial phase of metabolic turbulence, followed by partial recovery. During the early adverse reaction phase in intolerant subjects, lipid and fatty acid metabolic pathways-specifically, glycerophospholipid, linoleic acid, α-linolenic acid, and ether lipid metabolism-were significantly upregulated, concomitant with the suppression of TCA cycle and sphingolipid activity. Conversely, as tolerance was established, enhanced activity in the TCA cycle, sphingolipid, ascorbate, and pentose metabolism pathways-coupled with a reduction in pro-inflammatory arachidonic acid derivatives-indicated metabolic reconstitution and restoration of barrier integrity.
DISCUSSION: Integrated multi-omics correlation analyses further underscored the tightly interconnected regulation of host-microbe energy metabolism, antioxidant defenses, and membrane repair in response to retinol-induced stress. These findings elucidate the temporal interplay between host and microbial processes underpinning retinol tolerance and highlight baseline biomarkers that may facilitate personalized skincare interventions.},
}
RevDate: 2025-11-12
Lactobacillus casei's Antitumor Potential in Colorectal Cancer: Exploring Mechanisms-A Systematic Review.
BioMed research international, 2025:4216722.
Colorectal cancer (CRC) is the third most common cancer worldwide. Around 1.8 million people were diagnosed with CRC in 2018, and 881,000 died. The limitations of chemotherapy and radiotherapy, as well as the uncertainty of CRC-specific therapies, encourage the development of alternative CRC prevention, treatment, and control measures. Probiotics are being studied as a strategy for preventing and treating CRC due to their potential health benefits. Lactobacillus casei (L. casei) shows promise in reducing tumor growth and cancer cell survival in CRC, according to recent studies. Due to the varying efficiency of probiotics depending on the specific strain, substantial research has been conducted on the L. casei strains to explore their potential anticancer effects in CRC. In this study, we aimed to conduct a systematic review of exploring the various mechanisms of L. casei strains to facilitate the development of effective probiotic supplements to complement standard CRC therapy. We conducted a meticulous search on Scopus, PubMed, Embase, and Web of Science. Initial research resulted in 433 records, from which 412 papers were excluded by reason. The remaining 21 papers were categorized into four topics. These papers discuss several mechanisms involved in anticancer properties against CRC, including apoptosis induction and antiproliferation activity, immunomodulation, gut microbiome, intestinal barrier function modulation, and detoxifying carcinogens. Our findings suggest that using the potential strains of L. casei in combination therapy and targeted therapy, along with conventional drugs, could be a promising approach against CRC.
Additional Links: PMID-41221154
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@article {pmid41221154,
year = {2025},
author = {Abdorrashidi, M and Heiat, M and Yeganeh, AV and Tohidinia, A and Alizadeh, A and Ramazani, A and Gholizadeh, H and Pouraskar, T and Peypar, MH},
title = {Lactobacillus casei's Antitumor Potential in Colorectal Cancer: Exploring Mechanisms-A Systematic Review.},
journal = {BioMed research international},
volume = {2025},
number = {},
pages = {4216722},
pmid = {41221154},
issn = {2314-6141},
abstract = {Colorectal cancer (CRC) is the third most common cancer worldwide. Around 1.8 million people were diagnosed with CRC in 2018, and 881,000 died. The limitations of chemotherapy and radiotherapy, as well as the uncertainty of CRC-specific therapies, encourage the development of alternative CRC prevention, treatment, and control measures. Probiotics are being studied as a strategy for preventing and treating CRC due to their potential health benefits. Lactobacillus casei (L. casei) shows promise in reducing tumor growth and cancer cell survival in CRC, according to recent studies. Due to the varying efficiency of probiotics depending on the specific strain, substantial research has been conducted on the L. casei strains to explore their potential anticancer effects in CRC. In this study, we aimed to conduct a systematic review of exploring the various mechanisms of L. casei strains to facilitate the development of effective probiotic supplements to complement standard CRC therapy. We conducted a meticulous search on Scopus, PubMed, Embase, and Web of Science. Initial research resulted in 433 records, from which 412 papers were excluded by reason. The remaining 21 papers were categorized into four topics. These papers discuss several mechanisms involved in anticancer properties against CRC, including apoptosis induction and antiproliferation activity, immunomodulation, gut microbiome, intestinal barrier function modulation, and detoxifying carcinogens. Our findings suggest that using the potential strains of L. casei in combination therapy and targeted therapy, along with conventional drugs, could be a promising approach against CRC.},
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
Primary sclerosing cholangitis: a narrative review of diagnostic and prognostic biomarkers.
Translational gastroenterology and hepatology, 10:72.
BACKGROUND AND OBJECTIVE: Primary sclerosing cholangitis (PSC) is an autoimmune biliary fibrosing disease characterized by inflammation and injury of the intra- and/or extrahepatic bile ducts. The pathogenesis of PSC is poorly understood but is believed to be multifactorial, involving genetic predisposition, immunological dysregulation, and environmental influences. These may include disturbances in the gut-liver axis such as immune dysfunction in the colon and liver, alterations in the fecal and biliary microbiome, conjugation of bile acids into toxic species, and compromised intestinal epithelial integrity due to colitis, resulting in translocation of bacterial byproducts to the liver. There is a critical need for diagnostic and prognostic biomarkers that would enhance management and outcomes for patients with PSC. Additionally, validation of such biomarkers could serve as measurable endpoints when conducting future clinical trials. This aim of this paper is to review the available literature on candidate diagnostic and prognostic biomarkers in the adult and pediatric PSC populations.
METHODS: Original studies investigating biomarkers in serum, bile, and tissue published until November 2024 were systematically searched on PubMed, with a specific focus on newer studies published in the past 10 years and pediatric studies. Small studies with fewer than 10 patients in each study group, animal model studies, and studies with a focus on biomarkers for cholangiocarcinoma were excluded.
KEY CONTENT AND FINDINGS: Diagnostic and prognostic biomarkers summarized in this review include autoantibodies, markers of innate and adaptive immune responses, extracellular vesicles, epigenetic modifications, microbiome, proteins involved in lipid metabolism and bile acid homeostasis, and markers of fibrogenesis. Novel concepts for future biomarker discovery and implementation, including the potential for insights to be gained from the pediatric PSC population, are explored.
CONCLUSIONS: There is a critical need for further biomarker discovery for PSC as it will provide clues to disease pathogenesis and uncover candidate targets for therapeutic intervention.
Additional Links: PMID-41221136
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@article {pmid41221136,
year = {2025},
author = {Rolfes, PS and de Zoeten, EF and Forman, L and Mack, CL},
title = {Primary sclerosing cholangitis: a narrative review of diagnostic and prognostic biomarkers.},
journal = {Translational gastroenterology and hepatology},
volume = {10},
number = {},
pages = {72},
pmid = {41221136},
issn = {2415-1289},
abstract = {BACKGROUND AND OBJECTIVE: Primary sclerosing cholangitis (PSC) is an autoimmune biliary fibrosing disease characterized by inflammation and injury of the intra- and/or extrahepatic bile ducts. The pathogenesis of PSC is poorly understood but is believed to be multifactorial, involving genetic predisposition, immunological dysregulation, and environmental influences. These may include disturbances in the gut-liver axis such as immune dysfunction in the colon and liver, alterations in the fecal and biliary microbiome, conjugation of bile acids into toxic species, and compromised intestinal epithelial integrity due to colitis, resulting in translocation of bacterial byproducts to the liver. There is a critical need for diagnostic and prognostic biomarkers that would enhance management and outcomes for patients with PSC. Additionally, validation of such biomarkers could serve as measurable endpoints when conducting future clinical trials. This aim of this paper is to review the available literature on candidate diagnostic and prognostic biomarkers in the adult and pediatric PSC populations.
METHODS: Original studies investigating biomarkers in serum, bile, and tissue published until November 2024 were systematically searched on PubMed, with a specific focus on newer studies published in the past 10 years and pediatric studies. Small studies with fewer than 10 patients in each study group, animal model studies, and studies with a focus on biomarkers for cholangiocarcinoma were excluded.
KEY CONTENT AND FINDINGS: Diagnostic and prognostic biomarkers summarized in this review include autoantibodies, markers of innate and adaptive immune responses, extracellular vesicles, epigenetic modifications, microbiome, proteins involved in lipid metabolism and bile acid homeostasis, and markers of fibrogenesis. Novel concepts for future biomarker discovery and implementation, including the potential for insights to be gained from the pediatric PSC population, are explored.
CONCLUSIONS: There is a critical need for further biomarker discovery for PSC as it will provide clues to disease pathogenesis and uncover candidate targets for therapeutic intervention.},
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
Intestinal Dysbiosis Caused by Epithelial Fabp6 Gene Disruption Exacerbates Gut Inflammatory Disease.
Immune network, 25(5):e35.
Ileal lipid binding protein (Ilbp), encoded by Fabp6 gene, plays a critical role in intracellular transport of bile acids (BAs) from apical to basolateral side of ileal enterocytes, maintaining BA homeostasis within enterohepatic circulation. However, pathophysiological consequences of Ilbp deficiency remain largely unexplored. Here, we demonstrate that disruption of BA balance, caused by intestinal epithelial cell (IEC)-specific Fabp6 gene knockout (Fabp6 [ΔIEC]), exacerbates dextran sulfate sodium (DSS)-induced gut inflammation. Fecal microbiota transplantation from Fabp6 [ΔIEC] mice to germ free recipient mice replicated the adverse effects observed in Fabp6 [ΔIEC] mice, which were mitigated when these mice were co-housed with control (Fabp6 [f/f]) mice. Metagenomic analysis identified Ligilactobacillus murinus as a primarily diminished strain in Fabp6 [ΔIEC] mice. Oral administration of L. murinus isolated from feces of Fabp6 [f/f] mice ameliorated DSS-induced colitis in Fabp6 [ΔIEC] mice by restoring epithelial barrier integrity and lowering pro-inflammatory cytokines IL-1β, IL-6 and TNF-α. Furthermore, daily administration of taurodeoxycholic acid-one of the BAs reduced in Fabp6 [ΔIEC] mice and that promotes the growth of L. murinus in an in vitro growth assay-also exhibited a protective effect against DSS-induced colitis through a similar mechanism. These findings suggest that deficiency of specific BAs due to epithelial Fabp6 deletion leads to gut dysbiosis, predisposing the host to inflammatory disease.
Additional Links: PMID-41220843
PubMed:
Citation:
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@article {pmid41220843,
year = {2025},
author = {Kwon, K and Kim, M and Jung, Y and Yoon, MY and Lee, JY and Yoon, SS and Rho, M and Chung, YW and Ryu, JH},
title = {Intestinal Dysbiosis Caused by Epithelial Fabp6 Gene Disruption Exacerbates Gut Inflammatory Disease.},
journal = {Immune network},
volume = {25},
number = {5},
pages = {e35},
pmid = {41220843},
issn = {1598-2629},
abstract = {Ileal lipid binding protein (Ilbp), encoded by Fabp6 gene, plays a critical role in intracellular transport of bile acids (BAs) from apical to basolateral side of ileal enterocytes, maintaining BA homeostasis within enterohepatic circulation. However, pathophysiological consequences of Ilbp deficiency remain largely unexplored. Here, we demonstrate that disruption of BA balance, caused by intestinal epithelial cell (IEC)-specific Fabp6 gene knockout (Fabp6 [ΔIEC]), exacerbates dextran sulfate sodium (DSS)-induced gut inflammation. Fecal microbiota transplantation from Fabp6 [ΔIEC] mice to germ free recipient mice replicated the adverse effects observed in Fabp6 [ΔIEC] mice, which were mitigated when these mice were co-housed with control (Fabp6 [f/f]) mice. Metagenomic analysis identified Ligilactobacillus murinus as a primarily diminished strain in Fabp6 [ΔIEC] mice. Oral administration of L. murinus isolated from feces of Fabp6 [f/f] mice ameliorated DSS-induced colitis in Fabp6 [ΔIEC] mice by restoring epithelial barrier integrity and lowering pro-inflammatory cytokines IL-1β, IL-6 and TNF-α. Furthermore, daily administration of taurodeoxycholic acid-one of the BAs reduced in Fabp6 [ΔIEC] mice and that promotes the growth of L. murinus in an in vitro growth assay-also exhibited a protective effect against DSS-induced colitis through a similar mechanism. These findings suggest that deficiency of specific BAs due to epithelial Fabp6 deletion leads to gut dysbiosis, predisposing the host to inflammatory disease.},
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
Oral microbial alterations by smoking and metabolic factors in esophageal squamous cell carcinoma.
Journal of gastrointestinal oncology, 16(5):1796-1811.
BACKGROUND: It is important to understand how clinical factors affect microbial profiles, but few studies have evaluated these associations in patients with esophageal squamous cell carcinoma (ESCC). This study aimed to analyze differences in the oral microbiome between patients with ESCC and healthy controls, with subgroup analyses stratified by clinical and metabolic factors.
METHODS: From December 2021 to May 2023, oral swab samples and clinical data were collected from participants at five tertiary medical centers. Clinical data included age, sex, body mass index (BMI), smoking history, metabolic profiles such as cholesterol, triglycerides (TG), low-density lipoprotein (LDL), and high-density lipoprotein, and endoscopic findings. Sequencing and taxa abundance analyses were performed to compare oral microbiota between patients with ESCC and controls. Subgroup analyses were conducted to explore the impact of clinical factors on microbial community composition and diversity.
RESULTS: No significant differences in α- or β-diversity were observed between ESCC patients (n=21) and controls (n=20). However, subgroup analyses revealed distinct microbial patterns. Haemophilus parainfluenzae was less abundant in younger and low-LDL ESCC patients compared to controls, while Veillonella dispar was more abundant in older and high-LDL ESCC patients. Streptococcus infantis was less abundant in ESCC patients under 65 years compared to controls, and in smoking patients compared to non-smoking patients.
CONCLUSIONS: The oral microorganisms H. parainfluenzae, V. dispar, and S. infantis may serve as potential biomarkers influenced by metabolic factors in ESCC.
Additional Links: PMID-41220770
PubMed:
Citation:
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@article {pmid41220770,
year = {2025},
author = {Jung, K and Joo, M and Nam, K and Cho, JH and Cho, YS and Nam, S and Nam, SY},
title = {Oral microbial alterations by smoking and metabolic factors in esophageal squamous cell carcinoma.},
journal = {Journal of gastrointestinal oncology},
volume = {16},
number = {5},
pages = {1796-1811},
pmid = {41220770},
issn = {2078-6891},
abstract = {BACKGROUND: It is important to understand how clinical factors affect microbial profiles, but few studies have evaluated these associations in patients with esophageal squamous cell carcinoma (ESCC). This study aimed to analyze differences in the oral microbiome between patients with ESCC and healthy controls, with subgroup analyses stratified by clinical and metabolic factors.
METHODS: From December 2021 to May 2023, oral swab samples and clinical data were collected from participants at five tertiary medical centers. Clinical data included age, sex, body mass index (BMI), smoking history, metabolic profiles such as cholesterol, triglycerides (TG), low-density lipoprotein (LDL), and high-density lipoprotein, and endoscopic findings. Sequencing and taxa abundance analyses were performed to compare oral microbiota between patients with ESCC and controls. Subgroup analyses were conducted to explore the impact of clinical factors on microbial community composition and diversity.
RESULTS: No significant differences in α- or β-diversity were observed between ESCC patients (n=21) and controls (n=20). However, subgroup analyses revealed distinct microbial patterns. Haemophilus parainfluenzae was less abundant in younger and low-LDL ESCC patients compared to controls, while Veillonella dispar was more abundant in older and high-LDL ESCC patients. Streptococcus infantis was less abundant in ESCC patients under 65 years compared to controls, and in smoking patients compared to non-smoking patients.
CONCLUSIONS: The oral microorganisms H. parainfluenzae, V. dispar, and S. infantis may serve as potential biomarkers influenced by metabolic factors in ESCC.},
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
Exploring mucosal cytopathology through the lens of the microbiome in Sjögren's syndrome.
CytoJournal, 22:76.
Additional Links: PMID-41220569
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Citation:
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@article {pmid41220569,
year = {2025},
author = {Zeppieri, M and Foti, R and Gagliano, C},
title = {Exploring mucosal cytopathology through the lens of the microbiome in Sjögren's syndrome.},
journal = {CytoJournal},
volume = {22},
number = {},
pages = {76},
pmid = {41220569},
issn = {0974-5963},
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
The Role Played by Imidazole Propionic Acid in Modulating Gut-Heart Axis and the Development of Atherosclerosis: An Explorative Review.
Cureus, 17(10):e94362.
Recent studies have demonstrated the significant role of the normal human microbial component, also known as gut microbiome/gut microbiota (GM). Dysbiosis, or imbalance of GM, can predispose to systemic diseases, including cardiovascular disease (CVD). The GMs' influence extends further to cardiometabolic health, with microbial metabolites playing a pivotal role in these interactions. Traditional risk factors like hyperlipidemia and hypertension are now complemented by emerging evidence implicating GM-derived metabolites in the pathogenesis of atherosclerosis (ATS). Imidazole propionic acid (ImP), a metabolite of histidine derived from GM, has emerged as a significant mediator linking GM dysbiosis to ATS and CVD, or coronary artery disease (CAD). This comprehensive review synthesizes current knowledge on ImP's biosynthesis, molecular mechanisms, clinical relevance, and therapeutic potential, emphasizing its role in the gut-heart axis and cardiovascular pathology. Appropriate keywords, including "microbes", "dysbiosis", "gut microbiota/gut microbiome and cardiovascular disorders", "atherosclerosis and microbes", and "microbial metabolites", among others, were used to extract relevant studies in PubMed and Google Scholar from inception to date. ImP bridges microbial dysbiosis and CVD through endothelial dysfunction, inflammation, and metabolic disturbances. Its production is modifiable by diet and GM composition, positioning ImP as both a biomarker and therapeutic target in ATS and heart failure. Advancing understanding of ImP's biology and clinical impact will enable novel interventions to reduce the global burden of atherosclerotic cardiovascular disease (ASCVD), marking a change in basic assumptions in cardiovascular medicine centered on the gut-heart axis.
Additional Links: PMID-41220438
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Citation:
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@article {pmid41220438,
year = {2025},
author = {Pinnelli, VB and Ca, J and Kandi, V and P, S and Gr, M and Hussain, MH and As, A and R, K and Jp, R and T, SB and Vadakedath, S},
title = {The Role Played by Imidazole Propionic Acid in Modulating Gut-Heart Axis and the Development of Atherosclerosis: An Explorative Review.},
journal = {Cureus},
volume = {17},
number = {10},
pages = {e94362},
pmid = {41220438},
issn = {2168-8184},
abstract = {Recent studies have demonstrated the significant role of the normal human microbial component, also known as gut microbiome/gut microbiota (GM). Dysbiosis, or imbalance of GM, can predispose to systemic diseases, including cardiovascular disease (CVD). The GMs' influence extends further to cardiometabolic health, with microbial metabolites playing a pivotal role in these interactions. Traditional risk factors like hyperlipidemia and hypertension are now complemented by emerging evidence implicating GM-derived metabolites in the pathogenesis of atherosclerosis (ATS). Imidazole propionic acid (ImP), a metabolite of histidine derived from GM, has emerged as a significant mediator linking GM dysbiosis to ATS and CVD, or coronary artery disease (CAD). This comprehensive review synthesizes current knowledge on ImP's biosynthesis, molecular mechanisms, clinical relevance, and therapeutic potential, emphasizing its role in the gut-heart axis and cardiovascular pathology. Appropriate keywords, including "microbes", "dysbiosis", "gut microbiota/gut microbiome and cardiovascular disorders", "atherosclerosis and microbes", and "microbial metabolites", among others, were used to extract relevant studies in PubMed and Google Scholar from inception to date. ImP bridges microbial dysbiosis and CVD through endothelial dysfunction, inflammation, and metabolic disturbances. Its production is modifiable by diet and GM composition, positioning ImP as both a biomarker and therapeutic target in ATS and heart failure. Advancing understanding of ImP's biology and clinical impact will enable novel interventions to reduce the global burden of atherosclerotic cardiovascular disease (ASCVD), marking a change in basic assumptions in cardiovascular medicine centered on the gut-heart axis.},
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
Correction: MicrobiomeKG: bridging microbiome research and host health through knowledge graphs.
Frontiers in systems biology, 5:1710604 pii:1710604.
[This corrects the article DOI: 10.3389/fsysb.2025.1544432.].
Additional Links: PMID-41220422
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@article {pmid41220422,
year = {2025},
author = {, },
title = {Correction: MicrobiomeKG: bridging microbiome research and host health through knowledge graphs.},
journal = {Frontiers in systems biology},
volume = {5},
number = {},
pages = {1710604},
doi = {10.3389/fsysb.2025.1710604},
pmid = {41220422},
issn = {2674-0702},
abstract = {[This corrects the article DOI: 10.3389/fsysb.2025.1544432.].},
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
Therapeutic Potential Targeting Gut Microbiota Modulation With Emphasis on Lactobacillus spp. in Common Metabolic Disorders: A Systematic Review.
Scientifica, 2025:3367875.
Metabolic disorders are complex conditions that arise from abnormal biochemical reactions, disrupting normal metabolic processes. The most prevalent metabolic disorders include obesity, Type 2 diabetes mellitus (T2DM), cardiovascular disease (CVD), nonalcoholic fatty liver disease (NAFLD), and inflammatory bowel disease (IBD). Despite extensive research, no definitive therapeutic strategy has been established for a complete cure. Emerging evidence suggests that gut microbiome dysbiosis plays a critical role in the pathogenesis of these disorders, as maintaining microbial homeostasis is essential for metabolic health. Short-chain fatty acids (SCFAs) are a key metabolite produced by gut microbiota and exhibit significant therapeutic potential by serving as an energy source for colonocytes, enhancing gut barrier integrity, and modulating inflammation. Our analysis reveals that targeted microbial modulation, particularly through SCFA-producing probiotics and prebiotics, consistently benefits host metabolism and reduces systemic inflammation across multiple conditions. This review highlights the importance of gut microbiota as a viable therapeutic target and underscore the need for further clinical trials to validate microbiome-based interventions in metabolic disease management.
Additional Links: PMID-41220421
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Citation:
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@article {pmid41220421,
year = {2025},
author = {Rahaman, MM and Wangchuk, P and Sarker, S},
title = {Therapeutic Potential Targeting Gut Microbiota Modulation With Emphasis on Lactobacillus spp. in Common Metabolic Disorders: A Systematic Review.},
journal = {Scientifica},
volume = {2025},
number = {},
pages = {3367875},
pmid = {41220421},
issn = {2090-908X},
abstract = {Metabolic disorders are complex conditions that arise from abnormal biochemical reactions, disrupting normal metabolic processes. The most prevalent metabolic disorders include obesity, Type 2 diabetes mellitus (T2DM), cardiovascular disease (CVD), nonalcoholic fatty liver disease (NAFLD), and inflammatory bowel disease (IBD). Despite extensive research, no definitive therapeutic strategy has been established for a complete cure. Emerging evidence suggests that gut microbiome dysbiosis plays a critical role in the pathogenesis of these disorders, as maintaining microbial homeostasis is essential for metabolic health. Short-chain fatty acids (SCFAs) are a key metabolite produced by gut microbiota and exhibit significant therapeutic potential by serving as an energy source for colonocytes, enhancing gut barrier integrity, and modulating inflammation. Our analysis reveals that targeted microbial modulation, particularly through SCFA-producing probiotics and prebiotics, consistently benefits host metabolism and reduces systemic inflammation across multiple conditions. This review highlights the importance of gut microbiota as a viable therapeutic target and underscore the need for further clinical trials to validate microbiome-based interventions in metabolic disease management.},
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
From obesity to cancer: Gut microbiome mechanisms, biomarkers, and U.S. public health strategies.
Oncoscience, 12:175-188.
BACKGROUND: Obesity, metabolic syndrome, and colorectal cancer (CRC) remain major public health challenges in the United States, collectively driving substantial morbidity, mortality, and economic burden. Beyond diet and genetics, the gut microbiome has emerged as a pivotal determinant of host metabolism, immunity, and carcinogenesis, influenced by both environmental and behavioral factors.
OBJECTIVE: This review synthesizes current evidence linking gut microbial dysbiosis to obesity, metabolic syndrome, and CRC, emphasizing mechanistic pathways, environmental modifiers, and translational opportunities relevant to U.S. public health and precision medicine.
METHODS: Comprehensive searches of PubMed and Scopus (2000-2025) identified large epidemiologic studies, mechanistic experiments, and clinical trials, prioritizing research from U.S. populations and nationally representative databases including NHANES, SEER, and the Nurses' Health Study.
RESULTS: Microbial alterations such as enrichment of Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis, and colibactin-producing Escherichia coli contribute to CRC initiation and progression. In obesity and metabolic syndrome, shifts in Firmicutes-to-Bacteroidetes ratios, altered short-chain fatty acid metabolism, and endotoxin-mediated inflammation disrupt metabolic homeostasis. Environmental and lifestyle exposures, including air pollutants, smoking, and Westernized diets, modulate microbial ecology across the aerodigestive tract, affecting disease susceptibility. The emerging discipline of Molecular Pathological Epidemiology (MPE) integrates lifestyle, microbiome, and biomarker data to elucidate exposure-outcome relationships, enabling personalized prevention and therapeutic strategies.
CONCLUSIONS: The gut microbiome functions as both a biomarker and therapeutic target across metabolic and neoplastic diseases. Integrating microbiome science with environmental epidemiology and MPE frameworks offers transformative potential for precision prevention and equitable public health strategies in the U.S.
Additional Links: PMID-41220415
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Citation:
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@article {pmid41220415,
year = {2025},
author = {Moseeb, HM and Aizaz, MM and Aiza, K and Hafsa, TH and Sania, M and Kamran, Z and Shamama, ZT and Usama, AM and Maroof, QP and Feroze, F and Ahmed, R and Ammara, N and Mahima, G},
title = {From obesity to cancer: Gut microbiome mechanisms, biomarkers, and U.S. public health strategies.},
journal = {Oncoscience},
volume = {12},
number = {},
pages = {175-188},
pmid = {41220415},
issn = {2331-4737},
abstract = {BACKGROUND: Obesity, metabolic syndrome, and colorectal cancer (CRC) remain major public health challenges in the United States, collectively driving substantial morbidity, mortality, and economic burden. Beyond diet and genetics, the gut microbiome has emerged as a pivotal determinant of host metabolism, immunity, and carcinogenesis, influenced by both environmental and behavioral factors.
OBJECTIVE: This review synthesizes current evidence linking gut microbial dysbiosis to obesity, metabolic syndrome, and CRC, emphasizing mechanistic pathways, environmental modifiers, and translational opportunities relevant to U.S. public health and precision medicine.
METHODS: Comprehensive searches of PubMed and Scopus (2000-2025) identified large epidemiologic studies, mechanistic experiments, and clinical trials, prioritizing research from U.S. populations and nationally representative databases including NHANES, SEER, and the Nurses' Health Study.
RESULTS: Microbial alterations such as enrichment of Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis, and colibactin-producing Escherichia coli contribute to CRC initiation and progression. In obesity and metabolic syndrome, shifts in Firmicutes-to-Bacteroidetes ratios, altered short-chain fatty acid metabolism, and endotoxin-mediated inflammation disrupt metabolic homeostasis. Environmental and lifestyle exposures, including air pollutants, smoking, and Westernized diets, modulate microbial ecology across the aerodigestive tract, affecting disease susceptibility. The emerging discipline of Molecular Pathological Epidemiology (MPE) integrates lifestyle, microbiome, and biomarker data to elucidate exposure-outcome relationships, enabling personalized prevention and therapeutic strategies.
CONCLUSIONS: The gut microbiome functions as both a biomarker and therapeutic target across metabolic and neoplastic diseases. Integrating microbiome science with environmental epidemiology and MPE frameworks offers transformative potential for precision prevention and equitable public health strategies in the U.S.},
}
RevDate: 2025-11-12
Modelling Metabolic Disorders with Stem Cell-Derived Gut and Liver Organoids: Insights into Probiotic Therapies.
Recent advances in food, nutrition & agriculture pii:RAFNA-EPUB-151684 [Epub ahead of print].
Metabolic disorders, such as non-alcoholic fatty liver disease (NAFLD), type 2 diabetes, and obesity, are increasingly linked to disruptions in the gut-liver axis and microbiome. Probiotics have gained attention for modulating metabolic health, but their translation from preclinical to clinical use remains limited. Stem cell-derived liver and gut organoids provide advanced in vitro platforms for studying host-microbe interactions and evaluating probiotic therapies in a physiologically relevant context. This review systematically synthesized studies published between 2014 and 2025, obtained from PubMed, Scopus, and Web of Science, focusing on the generation, biological relevance, and translational applications of liver and gut organoids in probiotic therapy research. Key inclusion criteria were studies demonstrating organoid-based modelling of metabolic diseases, microbiome interactions, and high-throughput screening approaches. Gut and liver organoids successfully replicated key tissue functions and host-microbiota dynamics. Probiotics, such as Lactobacillus rhamnosus and Bifidobacterium breve, have been shown to improve gut barrier function, reduce hepatic lipid accumulation, and modulate inflammatory signalling. Integration with high-throughput screening and microbiome co-culture platforms will enhance their predictive value. Organoid-based models bridge the gap between traditional in vitro systems and human clinical relevance, providing detailed insights into the action of probiotics on metabolic pathways. However, challenges remain in terms of reproducibility, vascular and immune integration, and clinical translatability. Stem cell-derived gut and liver organoids represent promising tools for advancing probioticbased therapies in metabolic diseases. Their continued refinement could have a significant impact on personalized medicine and accelerate therapeutic development.
Additional Links: PMID-41220390
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@article {pmid41220390,
year = {2025},
author = {Chauhan, SB and Garg, T and Jain, C and Singh, I},
title = {Modelling Metabolic Disorders with Stem Cell-Derived Gut and Liver Organoids: Insights into Probiotic Therapies.},
journal = {Recent advances in food, nutrition & agriculture},
volume = {},
number = {},
pages = {},
doi = {10.2174/012772574X399047251006043349},
pmid = {41220390},
issn = {2772-5758},
abstract = {Metabolic disorders, such as non-alcoholic fatty liver disease (NAFLD), type 2 diabetes, and obesity, are increasingly linked to disruptions in the gut-liver axis and microbiome. Probiotics have gained attention for modulating metabolic health, but their translation from preclinical to clinical use remains limited. Stem cell-derived liver and gut organoids provide advanced in vitro platforms for studying host-microbe interactions and evaluating probiotic therapies in a physiologically relevant context. This review systematically synthesized studies published between 2014 and 2025, obtained from PubMed, Scopus, and Web of Science, focusing on the generation, biological relevance, and translational applications of liver and gut organoids in probiotic therapy research. Key inclusion criteria were studies demonstrating organoid-based modelling of metabolic diseases, microbiome interactions, and high-throughput screening approaches. Gut and liver organoids successfully replicated key tissue functions and host-microbiota dynamics. Probiotics, such as Lactobacillus rhamnosus and Bifidobacterium breve, have been shown to improve gut barrier function, reduce hepatic lipid accumulation, and modulate inflammatory signalling. Integration with high-throughput screening and microbiome co-culture platforms will enhance their predictive value. Organoid-based models bridge the gap between traditional in vitro systems and human clinical relevance, providing detailed insights into the action of probiotics on metabolic pathways. However, challenges remain in terms of reproducibility, vascular and immune integration, and clinical translatability. Stem cell-derived gut and liver organoids represent promising tools for advancing probioticbased therapies in metabolic diseases. Their continued refinement could have a significant impact on personalized medicine and accelerate therapeutic development.},
}
RevDate: 2025-11-12
Translating Gut Microbiota into Diagnostics: A Multidimensional Approach for the Diagnosis of Inflammatory Bowel Disease.
Gut and liver pii:gnl250360 [Epub ahead of print].
The gut microbiota has emerged as a key factor in the pathophysiology of inflammatory bowel disease (IBD), providing novel opportunities for diagnostic innovation. Traditional biomarkers, such as C-reactive protein and fecal calprotectin, are widely used in clinical practice; however, their ability to reflect disease complexity and microbial dysregulation remains limited. Recent advances in metagenomics and multi-omics integration have enabled high-resolution profiling of microbial communities and their functional capacities and associated metabolites. Differential abundance analysis and machine learning models have been used to identify microbial biomarkers that can distinguish patients with IBD from healthy individuals. Multicohort studies integrating microbiome and metabolomic data have further improved diagnostic accuracy and generalizability. Transcriptomic and proteomic analyses provide complementary insights into host-microbe interactions and disease mechanisms. In this review, we explored the potential of metagenomic biodata as diagnostic markers for IBD, with an emphasis on a multidimensional analytical approach. We highlight the recent developments in sequencing technologies, computational pipelines for microbial feature selection, and machine learning strategies applied to biomarker discovery. The integration of multi-omics data deepens our understanding of host-microbe interactions and facilitates the development of microbiota-informed diagnostic tools. As multidimensional microbial profiling evolves, its clinical utility for the diagnosis and stratification of IBD requires further investigation.
Additional Links: PMID-41220286
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@article {pmid41220286,
year = {2025},
author = {Lee, JY and Yoo, JH and Kim, JE and Bae, JW and Lee, CK},
title = {Translating Gut Microbiota into Diagnostics: A Multidimensional Approach for the Diagnosis of Inflammatory Bowel Disease.},
journal = {Gut and liver},
volume = {},
number = {},
pages = {},
doi = {10.5009/gnl250360},
pmid = {41220286},
issn = {2005-1212},
abstract = {The gut microbiota has emerged as a key factor in the pathophysiology of inflammatory bowel disease (IBD), providing novel opportunities for diagnostic innovation. Traditional biomarkers, such as C-reactive protein and fecal calprotectin, are widely used in clinical practice; however, their ability to reflect disease complexity and microbial dysregulation remains limited. Recent advances in metagenomics and multi-omics integration have enabled high-resolution profiling of microbial communities and their functional capacities and associated metabolites. Differential abundance analysis and machine learning models have been used to identify microbial biomarkers that can distinguish patients with IBD from healthy individuals. Multicohort studies integrating microbiome and metabolomic data have further improved diagnostic accuracy and generalizability. Transcriptomic and proteomic analyses provide complementary insights into host-microbe interactions and disease mechanisms. In this review, we explored the potential of metagenomic biodata as diagnostic markers for IBD, with an emphasis on a multidimensional analytical approach. We highlight the recent developments in sequencing technologies, computational pipelines for microbial feature selection, and machine learning strategies applied to biomarker discovery. The integration of multi-omics data deepens our understanding of host-microbe interactions and facilitates the development of microbiota-informed diagnostic tools. As multidimensional microbial profiling evolves, its clinical utility for the diagnosis and stratification of IBD requires further investigation.},
}
RevDate: 2025-11-12
Fecal calprotectin and other biomarkers are not prospectively associated with food protein-induced allergic proctocolitis.
Journal of pediatric gastroenterology and nutrition [Epub ahead of print].
OBJECTIVES: Diagnosis of food protein-induced allergic proctocolitis (FPIAP) is challenging due to the lack of noninvasive biomarkers. We evaluated fecal calprotectin, eosinophil-derived neurotoxin (EDN), and zonulin as potential biomarkers for diagnosing FPIAP, while also examining normal ranges in healthy infants under 12 months.
METHODS: We analyzed 214 stool samples from 115 infants (63 with clinically diagnosed FPIAP) over the first year of life from a large prospective observational cohort. We examined the range for each biomarker in infants over time and compared biomarker concentrations in infants with and without FPIAP using linear mixed-effects modeling. We also compared biomarker concentrations to existing 16S rRNA microbiome profiles using MaAsLin2.
RESULTS: Concentrations of calprotectin, EDN, and zonulin were not associated with FPIAP at the time of diagnosis (p = 0.81, p = 0.74, p = 0.24, nor longitudinally (p = 0.356, p = 0.0791, p = 0.333). Calprotectin was found to decrease significantly over the first 12 months of life for both groups (p < 0.001), while EDN and zonulin did not significantly change (p = 0.903, p = 0.043). There was no associated dysbiosis or microbial signature with any of the three biomarkers.
CONCLUSION: Concentrations of calprotectin, EDN, and zonulin were not associated with clinically diagnosed FPIAP in our cohort. Very high levels of calprotectin are noted in early infancy in asymptomatic healthy infants, and we provide normal ranges across the first year of life for all three biomarkers. This study does not support the use of fecal calprotectin, EDN, or zonulin for diagnosis of FPIAP.
Additional Links: PMID-41220250
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@article {pmid41220250,
year = {2025},
author = {Sun, T and Virkud, YV and Kirpas, M and Gregory, K and De Paz, J and O'Connell, I and Yassour, M and Shreffler, W and Yuan, Q and Martin, V},
title = {Fecal calprotectin and other biomarkers are not prospectively associated with food protein-induced allergic proctocolitis.},
journal = {Journal of pediatric gastroenterology and nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1002/jpn3.70257},
pmid = {41220250},
issn = {1536-4801},
support = {//None/ ; },
abstract = {OBJECTIVES: Diagnosis of food protein-induced allergic proctocolitis (FPIAP) is challenging due to the lack of noninvasive biomarkers. We evaluated fecal calprotectin, eosinophil-derived neurotoxin (EDN), and zonulin as potential biomarkers for diagnosing FPIAP, while also examining normal ranges in healthy infants under 12 months.
METHODS: We analyzed 214 stool samples from 115 infants (63 with clinically diagnosed FPIAP) over the first year of life from a large prospective observational cohort. We examined the range for each biomarker in infants over time and compared biomarker concentrations in infants with and without FPIAP using linear mixed-effects modeling. We also compared biomarker concentrations to existing 16S rRNA microbiome profiles using MaAsLin2.
RESULTS: Concentrations of calprotectin, EDN, and zonulin were not associated with FPIAP at the time of diagnosis (p = 0.81, p = 0.74, p = 0.24, nor longitudinally (p = 0.356, p = 0.0791, p = 0.333). Calprotectin was found to decrease significantly over the first 12 months of life for both groups (p < 0.001), while EDN and zonulin did not significantly change (p = 0.903, p = 0.043). There was no associated dysbiosis or microbial signature with any of the three biomarkers.
CONCLUSION: Concentrations of calprotectin, EDN, and zonulin were not associated with clinically diagnosed FPIAP in our cohort. Very high levels of calprotectin are noted in early infancy in asymptomatic healthy infants, and we provide normal ranges across the first year of life for all three biomarkers. This study does not support the use of fecal calprotectin, EDN, or zonulin for diagnosis of FPIAP.},
}
RevDate: 2025-11-11
A comprehensive narrative review on precision medicine approach to hypertension: exploring the role of genetics, epigenetics, microbiome, and artificial intelligence.
Journal of health, population, and nutrition, 44(1):394.
Hypertension (HTN) impacts approximately 1.28 billion individuals globally and poses a great burden of disease. The objectives of this study are to explore the role of genetics, epigenetics, microbiome, and artificial intelligence (AI) in the management of HTN. A thorough literature search was conducted across various databases including PubMed, Google Scholar, Web of Science (WoS), and Medline to retrieve articles related to the role of genetics, epigenetics, microbiome, and AI in the precision medicine of HTN. Genes-including ACE, NOS3, ADD1, CYP11B2, NPPA, and NPPB-have a profound impact on blood pressure (BP) regulation in our body and polymorphism in these key genes can lead to HTN. Up or down-regulation of genes by epigenetic factors such as miRNA-155, miRNA-210, and miRNA-122 can significantly contribute to the development of HTN. These genetic and epigenetic factors can also be used as specific targets for gene editing and gene therapy for long-term management of HTN. However, the implementation of these techniques has not been possible in clinical settings due to lack of human studies and safety concerns related to unpredictable DNA alterations, nucleotide deletions, and loss of allele-specific chromosomes. Modulation of gut microbiome through oral supplements, fecal microbiota transplant (FMT), and dietary interventions has emerged as one the most effective and safe techniques for managing HTN in human models. AI-based cutting-edge models have helped curate personalized diet plans based on an individual's unique microbiome, genomic information, and physiological conditions leading to a reduction in BMI, fat, BP, and heart rate while improving overall cardiac health and gut microbial diversity. Despite the significant advantages offered by AI-based medicine, ethical concerns-related to data privacy, bias, and discrimination-and ineffective models have led to limited integration of AI in precision medicine of HTN. The integration of genetics, epigenetics, microbiome, and AI-based models can play a key role in improving the current landscape of precision medicine of HTN. These cutting-edge techniques can lead to a shift from the current one-size-fits all approach to more personalized treatment plan however further research in human models is needed to determine the safety and true efficacy of these techniques. Additionally, new AI-models need to be developed that address ethical concerns and are effective in real-world clinical settings.
Additional Links: PMID-41219783
PubMed:
Citation:
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@article {pmid41219783,
year = {2025},
author = {Sami, A and Ashraf, R and Nisar, S and Mustehsan, ZH and Javed, MA and Ozsahin, DU and Waheed, Y},
title = {A comprehensive narrative review on precision medicine approach to hypertension: exploring the role of genetics, epigenetics, microbiome, and artificial intelligence.},
journal = {Journal of health, population, and nutrition},
volume = {44},
number = {1},
pages = {394},
pmid = {41219783},
issn = {2072-1315},
abstract = {Hypertension (HTN) impacts approximately 1.28 billion individuals globally and poses a great burden of disease. The objectives of this study are to explore the role of genetics, epigenetics, microbiome, and artificial intelligence (AI) in the management of HTN. A thorough literature search was conducted across various databases including PubMed, Google Scholar, Web of Science (WoS), and Medline to retrieve articles related to the role of genetics, epigenetics, microbiome, and AI in the precision medicine of HTN. Genes-including ACE, NOS3, ADD1, CYP11B2, NPPA, and NPPB-have a profound impact on blood pressure (BP) regulation in our body and polymorphism in these key genes can lead to HTN. Up or down-regulation of genes by epigenetic factors such as miRNA-155, miRNA-210, and miRNA-122 can significantly contribute to the development of HTN. These genetic and epigenetic factors can also be used as specific targets for gene editing and gene therapy for long-term management of HTN. However, the implementation of these techniques has not been possible in clinical settings due to lack of human studies and safety concerns related to unpredictable DNA alterations, nucleotide deletions, and loss of allele-specific chromosomes. Modulation of gut microbiome through oral supplements, fecal microbiota transplant (FMT), and dietary interventions has emerged as one the most effective and safe techniques for managing HTN in human models. AI-based cutting-edge models have helped curate personalized diet plans based on an individual's unique microbiome, genomic information, and physiological conditions leading to a reduction in BMI, fat, BP, and heart rate while improving overall cardiac health and gut microbial diversity. Despite the significant advantages offered by AI-based medicine, ethical concerns-related to data privacy, bias, and discrimination-and ineffective models have led to limited integration of AI in precision medicine of HTN. The integration of genetics, epigenetics, microbiome, and AI-based models can play a key role in improving the current landscape of precision medicine of HTN. These cutting-edge techniques can lead to a shift from the current one-size-fits all approach to more personalized treatment plan however further research in human models is needed to determine the safety and true efficacy of these techniques. Additionally, new AI-models need to be developed that address ethical concerns and are effective in real-world clinical settings.},
}
RevDate: 2025-11-11
Gut Microbiota and Chronic Kidney Disease: A Complex Interplay with Implications for Diagnosis and Treatment.
Probiotics and antimicrobial proteins [Epub ahead of print].
Chronic kidney disease (CKD) progresses over the years with a steady loss of renal function, often culminating in renal failure. While diabetes and hypertension are the major drivers, the exact underlying molecular mechanism for CKD remains only partially understood. Emerging research has revealed a new paradigm, linking microbiota imbalance or dysbiosis with CKD. Dysbiosis leads to the development of uremic toxins, which aggravate kidney damage, inflammation, and metabolic disruptions that accelerate disease progression. This review explores the complex interactions between dysbiosis, uremic toxins, and the major risk factors, namely, diabetes and hypertension. Microbiome-targeted interventions, such as dietary interventions, probiotics, prebiotics, synbiotics, and fecal microbiota transplantation (FMT), are discussed with an emphasis on their therapeutic relevance in influencing renal health. Additionally, the potential of genetic engineering, particularly CRISPR-based systems, to develop 'smart bacteria' designed to restore gut health is also examined. Future perspectives highlight the need for personalized therapies targeting the gut-kidney axis. Incorporating microbiome modulation into standard CKD treatments holds the potential to slow disease progression, enhance recovery, and improve the quality of life for patients.
Additional Links: PMID-41219653
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Citation:
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@article {pmid41219653,
year = {2025},
author = {Lamba, JK and Tandon, C and Tandon, S},
title = {Gut Microbiota and Chronic Kidney Disease: A Complex Interplay with Implications for Diagnosis and Treatment.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {41219653},
issn = {1867-1314},
abstract = {Chronic kidney disease (CKD) progresses over the years with a steady loss of renal function, often culminating in renal failure. While diabetes and hypertension are the major drivers, the exact underlying molecular mechanism for CKD remains only partially understood. Emerging research has revealed a new paradigm, linking microbiota imbalance or dysbiosis with CKD. Dysbiosis leads to the development of uremic toxins, which aggravate kidney damage, inflammation, and metabolic disruptions that accelerate disease progression. This review explores the complex interactions between dysbiosis, uremic toxins, and the major risk factors, namely, diabetes and hypertension. Microbiome-targeted interventions, such as dietary interventions, probiotics, prebiotics, synbiotics, and fecal microbiota transplantation (FMT), are discussed with an emphasis on their therapeutic relevance in influencing renal health. Additionally, the potential of genetic engineering, particularly CRISPR-based systems, to develop 'smart bacteria' designed to restore gut health is also examined. Future perspectives highlight the need for personalized therapies targeting the gut-kidney axis. Incorporating microbiome modulation into standard CKD treatments holds the potential to slow disease progression, enhance recovery, and improve the quality of life for patients.},
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
Gut microbiome variation in juvenile blue tits in a European urban mosaic.
Scientific reports, 15(1):39474.
Urbanisation transforms natural environments, impacting not only wild animals living in cities but also the microorganisms they are hosting. To better understand urban-driven variation in microbiological composition and diversity in the gut of birds developing in urban areas, we collected faecal samples from blue tit Cyanistes caeruleus nestlings using nestboxes distributed across the capital city of Warsaw, Poland. Sampling included a variety of urban habitats, a suburban village and a natural forest area. Microbiome analysis revealed a pattern of reduced alpha diversity and significant shifts in beta diversity in urbanised settings, driven by impervious surface coverage. Additionally, we observed that this effect was year-dependent, therefore highlighting the importance of temporal replication in ecological research. Furthermore, comparing two cavity types (natural and human-made), we demonstrated that artificial nestboxes, a tool widely used in field ecology, can impact the microbiome assembly in nestlings.
Additional Links: PMID-41219297
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Citation:
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@article {pmid41219297,
year = {2025},
author = {Fus, L and Jünemann, S and Di Lecce, I and Sudyka, J and Szulkin, M and Maraci, Ö},
title = {Gut microbiome variation in juvenile blue tits in a European urban mosaic.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {39474},
pmid = {41219297},
issn = {2045-2322},
mesh = {Animals ; *Gastrointestinal Microbiome ; *Passeriformes/microbiology ; Feces/microbiology ; Poland ; Ecosystem ; Biodiversity ; Urbanization ; Cities ; },
abstract = {Urbanisation transforms natural environments, impacting not only wild animals living in cities but also the microorganisms they are hosting. To better understand urban-driven variation in microbiological composition and diversity in the gut of birds developing in urban areas, we collected faecal samples from blue tit Cyanistes caeruleus nestlings using nestboxes distributed across the capital city of Warsaw, Poland. Sampling included a variety of urban habitats, a suburban village and a natural forest area. Microbiome analysis revealed a pattern of reduced alpha diversity and significant shifts in beta diversity in urbanised settings, driven by impervious surface coverage. Additionally, we observed that this effect was year-dependent, therefore highlighting the importance of temporal replication in ecological research. Furthermore, comparing two cavity types (natural and human-made), we demonstrated that artificial nestboxes, a tool widely used in field ecology, can impact the microbiome assembly in nestlings.},
}
MeSH Terms:
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Animals
*Gastrointestinal Microbiome
*Passeriformes/microbiology
Feces/microbiology
Poland
Ecosystem
Biodiversity
Urbanization
Cities
RevDate: 2025-11-11
Interaction between serum levels of Porphyromonas gingivalis immunoglobulin G and lutein/zeaxanthin is associated with risk for age-related macular degeneration.
Scientific reports, 15(1):39400.
Porphyromonas gingivalis (P. gingivalis) functions as a catalyst bacterium in the development of periodontitis, and the serum antibody level against P. gingivalis is considered a surrogate marker for the activity level of periodontopathic microbiota. The chronic systemic inflammation induced by P. gingivalis elevates the risk of various systemic and neurodegenerative disorders, including atherosclerosis, diabetes, and Alzheimer's disease. Although the connection between human microbiota and age-related macular degeneration (AMD) remains relatively unexplored, it is noteworthy that AMD shares risk factors and etiological mechanisms with diseases related to P. gingivalis. To investigate the potential association between periodontopathic microbiota and AMD occurrence, we conducted a candidate microbe approach case-control study in the Third National Health and Nutrition Examination Survey (NHANES-III). Our hypothesis was tested by examining the correlation between serum P. gingivalis immunoglobulin G (IgG) levels and AMD. Comparing the lowest IgG category (≤ 57 enzyme-linked immunosorbent assay units (EU)) with higher categories revealed escalating risks: the second higher category (58-65 EU) conferred almost a 30% increased risk (odds ratio (OR) = 1.28, 95% confidence interval (CI): 1.17 to 1.4), the third higher category (66-119 EU) conferred nearly a 60% increase (OR = 1.58, 95% CI: 1.46 to 1.72), and the highest category (> 119 EU) conveyed over a two-fold risk (OR = 2.04, 95% CI: 1.62 to 2.58) of early AMD. Consistent with current evidence that host nutritional status critically modulates immune responses to the microbiota and influences human health, our analysis indicates that sustaining elevated serum levels of lutein/zeaxanthin (≥ 0.35 µmol/L or ≥ 20 µg/dL) might potentially mitigate the P. gingivalis-related AMD risk by as much as 35% (P for interaction < 0.0001). Although the precise mechanism requires additional exploration, these findings suggest a connection between nutrients related to eye health and humoral response to P. gingivalis.Significance statement: While humoral response to P. gingivalis indicates an impact on age-related macular degeneration, nutritional factors may modulate the associated risk.
Additional Links: PMID-41219247
PubMed:
Citation:
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@article {pmid41219247,
year = {2025},
author = {Chiu, CJ and Chiu, ES and Chang, ML},
title = {Interaction between serum levels of Porphyromonas gingivalis immunoglobulin G and lutein/zeaxanthin is associated with risk for age-related macular degeneration.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {39400},
pmid = {41219247},
issn = {2045-2322},
support = {RO1EY021826 and R21EY028209/GF/NIH HHS/United States ; },
abstract = {Porphyromonas gingivalis (P. gingivalis) functions as a catalyst bacterium in the development of periodontitis, and the serum antibody level against P. gingivalis is considered a surrogate marker for the activity level of periodontopathic microbiota. The chronic systemic inflammation induced by P. gingivalis elevates the risk of various systemic and neurodegenerative disorders, including atherosclerosis, diabetes, and Alzheimer's disease. Although the connection between human microbiota and age-related macular degeneration (AMD) remains relatively unexplored, it is noteworthy that AMD shares risk factors and etiological mechanisms with diseases related to P. gingivalis. To investigate the potential association between periodontopathic microbiota and AMD occurrence, we conducted a candidate microbe approach case-control study in the Third National Health and Nutrition Examination Survey (NHANES-III). Our hypothesis was tested by examining the correlation between serum P. gingivalis immunoglobulin G (IgG) levels and AMD. Comparing the lowest IgG category (≤ 57 enzyme-linked immunosorbent assay units (EU)) with higher categories revealed escalating risks: the second higher category (58-65 EU) conferred almost a 30% increased risk (odds ratio (OR) = 1.28, 95% confidence interval (CI): 1.17 to 1.4), the third higher category (66-119 EU) conferred nearly a 60% increase (OR = 1.58, 95% CI: 1.46 to 1.72), and the highest category (> 119 EU) conveyed over a two-fold risk (OR = 2.04, 95% CI: 1.62 to 2.58) of early AMD. Consistent with current evidence that host nutritional status critically modulates immune responses to the microbiota and influences human health, our analysis indicates that sustaining elevated serum levels of lutein/zeaxanthin (≥ 0.35 µmol/L or ≥ 20 µg/dL) might potentially mitigate the P. gingivalis-related AMD risk by as much as 35% (P for interaction < 0.0001). Although the precise mechanism requires additional exploration, these findings suggest a connection between nutrients related to eye health and humoral response to P. gingivalis.Significance statement: While humoral response to P. gingivalis indicates an impact on age-related macular degeneration, nutritional factors may modulate the associated risk.},
}
RevDate: 2025-11-11
Gut microbiome in IBD: past, present and the future.
Gut pii:gutjnl-2025-335626 [Epub ahead of print].
IBD has become a global disease in the 21st century that shifts through four epidemiological stages. Alterations in the gut microbiome consisting of a complex multikingdom community of bacteria, fungi and viruses are strongly linked to disease pathogenesis. Advances in sequencing technologies, multiomics integration and experimental approaches have shed new insights into host-microbiota interactions in IBD and characterised mechanisms through which the microbiota and its metabolites contribute to disease. We review the evolution of microbiome-based research, with a focus on genetic and environmental factors affecting the gut microbiota, the role of cross-kingdom microbiome and their bioproducts in disease development and new strategies by which microbiome-based approaches can be used to diagnose, monitor, prevent and treat IBD.
Additional Links: PMID-41219057
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PubMed:
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@article {pmid41219057,
year = {2025},
author = {Zhang, J and Mak, JWY and Ng, SC},
title = {Gut microbiome in IBD: past, present and the future.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2025-335626},
pmid = {41219057},
issn = {1468-3288},
abstract = {IBD has become a global disease in the 21st century that shifts through four epidemiological stages. Alterations in the gut microbiome consisting of a complex multikingdom community of bacteria, fungi and viruses are strongly linked to disease pathogenesis. Advances in sequencing technologies, multiomics integration and experimental approaches have shed new insights into host-microbiota interactions in IBD and characterised mechanisms through which the microbiota and its metabolites contribute to disease. We review the evolution of microbiome-based research, with a focus on genetic and environmental factors affecting the gut microbiota, the role of cross-kingdom microbiome and their bioproducts in disease development and new strategies by which microbiome-based approaches can be used to diagnose, monitor, prevent and treat IBD.},
}
RevDate: 2025-11-11
Your FLORA Matters: Microbiome Modulation in Psoriatic Arthritis.
Additional Links: PMID-41218800
Publisher:
PubMed:
Citation:
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@article {pmid41218800,
year = {2025},
author = {Dumas, E and Elewaut, D},
title = {Your FLORA Matters: Microbiome Modulation in Psoriatic Arthritis.},
journal = {Arthritis & rheumatology (Hoboken, N.J.)},
volume = {},
number = {},
pages = {},
doi = {10.1002/art.43450},
pmid = {41218800},
issn = {2326-5205},
}
RevDate: 2025-11-11
Assessing the impact of broiler genotype on cecal and tracheal microbiome composition using full-length 16S rRNA sequencing.
Poultry science, 104(12):106072 pii:S0032-5791(25)01312-4 [Epub ahead of print].
This study examined the tracheal and cecal microbiome composition across three broiler chicken genotypes including a heritage New Hampshire × Columbian cross (NHC) and modern Ross × Ross 308 (R308) and Ross YP × Ross 708 (R708) broilers, using full-length 16S rRNA sequencing. Birds were reared in floor pens, and at 56 d of age, cecal and tracheal samples were collected from 8 birds per genotype and subjected to DNA extraction followed by PCR amplification of full-length 16S rRNA. Obtained amplified PCR product was sequenced using MinION. A total of 1.8 million reads for tracheal samples and 1.2 million reads for ceca samples were obtained from 24 birds. Despite similar alpha diversity matrixes (Shannon, Simpson, Pielou's evenness, and Chao1) across genotypes in both tracheal and cecal samples, beta diversity analysis revealed significant differences in community composition. Tracheal and cecal microbiota varied significantly among genotypes, particularly NHC with the R308 and R708 groups. At the phylum level, Bacillota (Firmicutes) dominated both tracheal and cecal samples across genotypes. In the trachea, NHC and R708 birds exhibited high relative abundance of Enterococcus cecorum, while Jeotgalicoccus meleagridis dominated R308. Differential abundance analysis showed higher abundance of potentially beneficial bacteria such as Limosilactobacillus pontis and Aerococcus viridans in R308 and R708, while NHC birds had higher levels of species like Merdibacter massiliensis and Agathobaculum butyriciproducens. Cecal microbiome analysis revealed genotype-specific enrichment of species, with NHC birds showing higher abundance of potential pathogens like Shigella boydii and Escherichia fergusonii compared to R708. In contrast, R308 birds harboured more potentially beneficial taxa, including Lactobacillus acidophilus and Limosilactobacillus vaginalis, compared to R708. Pairwise comparisons further highlighted Intestinibacter bartlettii and other potentially beneficial microbes being significantly enriched in R308 over R708. Overall, while microbial richness remained consistent, significant genotype-associated differences in bacterial community structure and genotype-specific microbial abundance were observed, emphasizing the influence of host genetics on microbiota composition and potential implications for poultry health and performance.
Additional Links: PMID-41218558
Publisher:
PubMed:
Citation:
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@article {pmid41218558,
year = {2025},
author = {Poudel, S and Rahman, FA and Granados, EAF and Adhikari, Y and Naeem, M and Rochell, SJ and Bourassa, D},
title = {Assessing the impact of broiler genotype on cecal and tracheal microbiome composition using full-length 16S rRNA sequencing.},
journal = {Poultry science},
volume = {104},
number = {12},
pages = {106072},
doi = {10.1016/j.psj.2025.106072},
pmid = {41218558},
issn = {1525-3171},
abstract = {This study examined the tracheal and cecal microbiome composition across three broiler chicken genotypes including a heritage New Hampshire × Columbian cross (NHC) and modern Ross × Ross 308 (R308) and Ross YP × Ross 708 (R708) broilers, using full-length 16S rRNA sequencing. Birds were reared in floor pens, and at 56 d of age, cecal and tracheal samples were collected from 8 birds per genotype and subjected to DNA extraction followed by PCR amplification of full-length 16S rRNA. Obtained amplified PCR product was sequenced using MinION. A total of 1.8 million reads for tracheal samples and 1.2 million reads for ceca samples were obtained from 24 birds. Despite similar alpha diversity matrixes (Shannon, Simpson, Pielou's evenness, and Chao1) across genotypes in both tracheal and cecal samples, beta diversity analysis revealed significant differences in community composition. Tracheal and cecal microbiota varied significantly among genotypes, particularly NHC with the R308 and R708 groups. At the phylum level, Bacillota (Firmicutes) dominated both tracheal and cecal samples across genotypes. In the trachea, NHC and R708 birds exhibited high relative abundance of Enterococcus cecorum, while Jeotgalicoccus meleagridis dominated R308. Differential abundance analysis showed higher abundance of potentially beneficial bacteria such as Limosilactobacillus pontis and Aerococcus viridans in R308 and R708, while NHC birds had higher levels of species like Merdibacter massiliensis and Agathobaculum butyriciproducens. Cecal microbiome analysis revealed genotype-specific enrichment of species, with NHC birds showing higher abundance of potential pathogens like Shigella boydii and Escherichia fergusonii compared to R708. In contrast, R308 birds harboured more potentially beneficial taxa, including Lactobacillus acidophilus and Limosilactobacillus vaginalis, compared to R708. Pairwise comparisons further highlighted Intestinibacter bartlettii and other potentially beneficial microbes being significantly enriched in R308 over R708. Overall, while microbial richness remained consistent, significant genotype-associated differences in bacterial community structure and genotype-specific microbial abundance were observed, emphasizing the influence of host genetics on microbiota composition and potential implications for poultry health and performance.},
}
RevDate: 2025-11-11
Bioengineered polymeric mesh with imaging contrast for enhanced urogynaecological applications.
Biomaterials advances, 180:214478 pii:S2772-9508(25)00305-X [Epub ahead of print].
Pelvic floor disorders affect up to 50 % of women, with prevalence increasing significantly in those over 65. While transvaginal mesh (TVM) implantation remains a common treatment, its use has been associated with complications, including inflammation, infection, and poor integration, prompting the need for safer alternatives. This study introduces a novel composite mesh designed to enhance clinical outcomes by significantly improving the mechanical properties of the TVM, its biocompatibility, and enabling its visibility. The mesh consists of polymethylmethacrylate and thermoplastic polyurethane, with embedded iodine-doped carbon nanoparticles for contrast-enhanced computed tomography (CT) imaging and coated with a phosphorylcholine-based polymer to reduce protein adsorption and hence support tissue regeneration. The composite mesh showed a tensile modulus of approximately 2.7 MPa, closely matching vaginal tissue, and reduced non-specific protein adsorption by ~78 %. In vitro analysis confirmed high biocompatibility and minimal protein adsorption. Conducted in vivo mouse studies showed no adverse overall health effects or systemic inflammation based on spleen weight; however, elevations in some cytokine levels in the iodinated mesh group indicate a potential area for optimisation of mesh properties. Fecal microbiome diversity was stable in both sham and iodinated groups. Further, the mesh mimics native tissue mechanics and enables clear CT visibility for at least 14 days post-implantation, allowing non-invasive monitoring. This novel TVM presents a multifunctional platform able to address key limitations of conventional TVMs by improving CT imaging, minimising inflammation, and supporting integration, offering a promising solution for safer and more effective pelvic floor repair.
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@article {pmid41218467,
year = {2025},
author = {Houshyar, S and Quigley, A and Cole, I and Yin, H and Zizhou, R and Saha, T and Pirogova, E and Yeung, JM and Mohsenipour, M and Mirabedini, A and Subejano, E and Shindler, AE and Wood, JL and Franks, AE and Hill-Yardin, EL},
title = {Bioengineered polymeric mesh with imaging contrast for enhanced urogynaecological applications.},
journal = {Biomaterials advances},
volume = {180},
number = {},
pages = {214478},
doi = {10.1016/j.bioadv.2025.214478},
pmid = {41218467},
issn = {2772-9508},
abstract = {Pelvic floor disorders affect up to 50 % of women, with prevalence increasing significantly in those over 65. While transvaginal mesh (TVM) implantation remains a common treatment, its use has been associated with complications, including inflammation, infection, and poor integration, prompting the need for safer alternatives. This study introduces a novel composite mesh designed to enhance clinical outcomes by significantly improving the mechanical properties of the TVM, its biocompatibility, and enabling its visibility. The mesh consists of polymethylmethacrylate and thermoplastic polyurethane, with embedded iodine-doped carbon nanoparticles for contrast-enhanced computed tomography (CT) imaging and coated with a phosphorylcholine-based polymer to reduce protein adsorption and hence support tissue regeneration. The composite mesh showed a tensile modulus of approximately 2.7 MPa, closely matching vaginal tissue, and reduced non-specific protein adsorption by ~78 %. In vitro analysis confirmed high biocompatibility and minimal protein adsorption. Conducted in vivo mouse studies showed no adverse overall health effects or systemic inflammation based on spleen weight; however, elevations in some cytokine levels in the iodinated mesh group indicate a potential area for optimisation of mesh properties. Fecal microbiome diversity was stable in both sham and iodinated groups. Further, the mesh mimics native tissue mechanics and enables clear CT visibility for at least 14 days post-implantation, allowing non-invasive monitoring. This novel TVM presents a multifunctional platform able to address key limitations of conventional TVMs by improving CT imaging, minimising inflammation, and supporting integration, offering a promising solution for safer and more effective pelvic floor repair.},
}
RevDate: 2025-11-11
Plasma metabolic profiling identifies elevated hippurate as a potential biomarker of methotrexate non-response in juvenile idiopathic arthritis.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 193:118755 pii:S0753-3322(25)00949-7 [Epub ahead of print].
BACKGROUND / PURPOSE: Methotrexate (MTX) continues to be the first-line disease-modifying antirheumatic drug (DMARD) in the treatment of juvenile idiopathic arthritis (JIA). However, response to MTX is often delayed and variable, requiring the initiation of second-line therapies, most notably biologic DMARDs. Recognizing the goal of early initiation of effective therapy in the treatment of JIA, there remains a need to identify predictive biomarkers to guide drug selection in the treatment of JIA. This study uses a plasma metabolomic profiling approach to identify metabolic biomarkers associated with MTX non-response in JIA.
METHODS: A multi-platform ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) approach was used to obtain a 902 plasma metabolite profile in pretreatment samples from patients with JIA initiating MTX therapy (n = 60) in a single-center, prospective observational study. The cohort consisted of 67 % female patients, with a median age of 10.75 years. Patients were classified as responders (n = 45) or non-responders (n = 15), with non-response defined as the need to add or switch to a biologic DMARD within the first six months of therapy. Unpaired univariate analysis was performed using MetaboAnalyst 5.0 to identify significant metabolites (p < 0.05). Enrichment analysis was conducted using Chemical Similarity Enrichment Analysis (ChemRich) and identified chemical clusters that differed between the groups using an FDR-adjusted p-value (q-value) threshold of 0.05. A metabolic network map was generated using MetaMapp and visualized using Cytoscape 3.9.1. Receiver operator characteristic (ROC) curve analyses were conducted to identify metabolites that effectively discriminate MTX responders and non-responders. Biomarker performance was assessed based on the ROC Area Under the Curve (AUC). Regression modeling was used to investigate the independent association between the identified metabolites, while controlling for clinical covariates, including baseline 71-joint count, Juvenile Arthritis Disease Activity Score (JADAS-71), and Active Joint Count (AJC).
RESULTS: Out of 902 pretreatment plasma metabolites measured, 63 were found to significantly differ based on MTX response. Chemical cluster analysis identified six metabolite clusters as significant, including indoles, sugar alcohols, xanthines, trimethylammonium compounds, glycodeoxycholic acid, and dipeptides. Metabolic pathway analysis reveals that tryptophan, lipids, amino acids, and nucleic acids are key pathways that differ between MTX responders and non-responders. ROC analysis identified eight metabolites with an AUC > 0.75, which included multiple metabolites related to gut microbial metabolism, such as hippurate, indole-2-one, indolepropionate, anthranilate, phenylacetylglutamine, p-cresol sulfate, and several unidentified metabolites. Increased plasma hippurate levels were found to be the most discriminating metabolite (AUC=0.781). Multivariate models that included baseline JADAS-71, AJC, and hippurate levels demonstrated that increased plasma hippurate levels were independently associated with MTX non-response at 6 months.
CONCLUSION: These findings support plasma metabolomic differences associated with the response to MTX in JIA. The identification of hippurate, indoles, and other gut microbial-derived metabolites continues to draw attention to the potential relationship between the gut microbiome and MTX treatment response in JIA.
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@article {pmid41218338,
year = {2025},
author = {Kumar, A and Becker, ML and Funk, RS},
title = {Plasma metabolic profiling identifies elevated hippurate as a potential biomarker of methotrexate non-response in juvenile idiopathic arthritis.},
journal = {Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie},
volume = {193},
number = {},
pages = {118755},
doi = {10.1016/j.biopha.2025.118755},
pmid = {41218338},
issn = {1950-6007},
abstract = {BACKGROUND / PURPOSE: Methotrexate (MTX) continues to be the first-line disease-modifying antirheumatic drug (DMARD) in the treatment of juvenile idiopathic arthritis (JIA). However, response to MTX is often delayed and variable, requiring the initiation of second-line therapies, most notably biologic DMARDs. Recognizing the goal of early initiation of effective therapy in the treatment of JIA, there remains a need to identify predictive biomarkers to guide drug selection in the treatment of JIA. This study uses a plasma metabolomic profiling approach to identify metabolic biomarkers associated with MTX non-response in JIA.
METHODS: A multi-platform ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) approach was used to obtain a 902 plasma metabolite profile in pretreatment samples from patients with JIA initiating MTX therapy (n = 60) in a single-center, prospective observational study. The cohort consisted of 67 % female patients, with a median age of 10.75 years. Patients were classified as responders (n = 45) or non-responders (n = 15), with non-response defined as the need to add or switch to a biologic DMARD within the first six months of therapy. Unpaired univariate analysis was performed using MetaboAnalyst 5.0 to identify significant metabolites (p < 0.05). Enrichment analysis was conducted using Chemical Similarity Enrichment Analysis (ChemRich) and identified chemical clusters that differed between the groups using an FDR-adjusted p-value (q-value) threshold of 0.05. A metabolic network map was generated using MetaMapp and visualized using Cytoscape 3.9.1. Receiver operator characteristic (ROC) curve analyses were conducted to identify metabolites that effectively discriminate MTX responders and non-responders. Biomarker performance was assessed based on the ROC Area Under the Curve (AUC). Regression modeling was used to investigate the independent association between the identified metabolites, while controlling for clinical covariates, including baseline 71-joint count, Juvenile Arthritis Disease Activity Score (JADAS-71), and Active Joint Count (AJC).
RESULTS: Out of 902 pretreatment plasma metabolites measured, 63 were found to significantly differ based on MTX response. Chemical cluster analysis identified six metabolite clusters as significant, including indoles, sugar alcohols, xanthines, trimethylammonium compounds, glycodeoxycholic acid, and dipeptides. Metabolic pathway analysis reveals that tryptophan, lipids, amino acids, and nucleic acids are key pathways that differ between MTX responders and non-responders. ROC analysis identified eight metabolites with an AUC > 0.75, which included multiple metabolites related to gut microbial metabolism, such as hippurate, indole-2-one, indolepropionate, anthranilate, phenylacetylglutamine, p-cresol sulfate, and several unidentified metabolites. Increased plasma hippurate levels were found to be the most discriminating metabolite (AUC=0.781). Multivariate models that included baseline JADAS-71, AJC, and hippurate levels demonstrated that increased plasma hippurate levels were independently associated with MTX non-response at 6 months.
CONCLUSION: These findings support plasma metabolomic differences associated with the response to MTX in JIA. The identification of hippurate, indoles, and other gut microbial-derived metabolites continues to draw attention to the potential relationship between the gut microbiome and MTX treatment response in JIA.},
}
RevDate: 2025-11-11
The cervicovaginal microbiome associates with spatially restricted host transcriptional signatures throughout the human ectocervical epithelium and submucosa.
PLoS pathogens, 21(11):e1013677 pii:PPATHOGENS-D-25-01489 [Epub ahead of print].
The cervicovaginal microbiome is a key biological determinant of human immunodeficiency virus (HIV) susceptibility, but its underlying impact on the ectocervical transcriptional landscape is unclear. Ectocervical tissue samples from Kenyan female sex workers were categorized into pre-defined cervicovaginal microbiome groups based on dominant compositions: Lactobacillus crispatus/acidophilus, Lactobacillus iners, Gardnerella, and 'highly diverse'. The tissue samples (n = 21) were assessed using spatial transcriptomics, revealing three epithelial, one mixed border, and nine submucosal gene clusters. Differential gene expression analysis across the microbiome groups and gene clusters identified 3,771 unique genes. The highly diverse microbiome group associated with the largest differences, mostly located near the epithelial basal membrane, encompassing genes involved in epithelial maintenance, submucosal extracellular matrix structures, and immune function. The L. crispatus/acidophilus-dominated group was identified by genes involved in active immune engagement, supporting mucosal barrier integrity. Weighted gene co-expression analysis confirmed tissue-wide altered gene expression associated with all microbiome groups and with individual bacterial taxa. Despite the assumption that microbiome colonization is restricted to the luminal surface, the transcriptional landscape was affected throughout the mucosa, with the most pronounced effect near both sides of the basal membrane. This broad association with the mucosal barrier integrity could affect susceptibility to HIV acquisition.
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@article {pmid41218071,
year = {2025},
author = {Kaldhusdal, V and Franzén Boger, M and Burgener, AD and Lajoie, J and Omollo, K and Kimani, J and Tjernlund, A and Fowke, KR and Kwon, DS and Edfeldt, G and Broliden, K},
title = {The cervicovaginal microbiome associates with spatially restricted host transcriptional signatures throughout the human ectocervical epithelium and submucosa.},
journal = {PLoS pathogens},
volume = {21},
number = {11},
pages = {e1013677},
doi = {10.1371/journal.ppat.1013677},
pmid = {41218071},
issn = {1553-7374},
abstract = {The cervicovaginal microbiome is a key biological determinant of human immunodeficiency virus (HIV) susceptibility, but its underlying impact on the ectocervical transcriptional landscape is unclear. Ectocervical tissue samples from Kenyan female sex workers were categorized into pre-defined cervicovaginal microbiome groups based on dominant compositions: Lactobacillus crispatus/acidophilus, Lactobacillus iners, Gardnerella, and 'highly diverse'. The tissue samples (n = 21) were assessed using spatial transcriptomics, revealing three epithelial, one mixed border, and nine submucosal gene clusters. Differential gene expression analysis across the microbiome groups and gene clusters identified 3,771 unique genes. The highly diverse microbiome group associated with the largest differences, mostly located near the epithelial basal membrane, encompassing genes involved in epithelial maintenance, submucosal extracellular matrix structures, and immune function. The L. crispatus/acidophilus-dominated group was identified by genes involved in active immune engagement, supporting mucosal barrier integrity. Weighted gene co-expression analysis confirmed tissue-wide altered gene expression associated with all microbiome groups and with individual bacterial taxa. Despite the assumption that microbiome colonization is restricted to the luminal surface, the transcriptional landscape was affected throughout the mucosa, with the most pronounced effect near both sides of the basal membrane. This broad association with the mucosal barrier integrity could affect susceptibility to HIV acquisition.},
}
RevDate: 2025-11-11
Exploring the gut microbiota of Pacific white shrimp (Litopenaeus vannamei) suffering pale shrimp disease.
PloS one, 20(11):e0336700 pii:PONE-D-25-37306.
Pale shrimp disease is an emerging threat in Thailand, characterized by pale body coloration in Pacific white shrimp (Litopenaeus vannamei). Although the etiology had been identified as Photobacterium damselae subsp. damselae, the disease effects on gut microbiome remain poorly understood. This study investigated changes in the gut microbiota of Pacific white shrimp suffering from pale shrimp disease (diseased group) compared to disease-free shrimp (healthy group) collected from Surat Thani Province, Thailand. DNA extracted from the intestinal samples was subjected to 16S rRNA metagenomic sequencing, followed by taxonomic identification, diversity analyses, and functional prediction of the metabolic pathways. Despite a limited number of biological replicates, the occurrence of pale shrimp disease was able to reveal alterations in intestinal microbial composition, diversities, and functional features compared to the healthy shrimp. In most cases, the intestinal microbiota of the diseased shrimp were dominated by only 2 genera of bacteria, i.e., Photobacterium (54.63-70.53%) and Vibrio (24.94-26.12%), which together accounted for 79.58-95.47% of the total bacterial community. α-diversity, as indicated by the observed features, Shannon, and Simpson indices, was significantly decreased, and dominance was significantly increased in the diseased shrimp compared to healthy shrimp. Likewise, β-diversity was significantly different between groups; PCoA of un-weighted and weighted UniFrac clearly distinguished intestinal microbiota of the shrimp into 2 clusters, and ANOSIM of these data revealed statistical differences between groups, suggesting different microbiota communities between healthy and diseased shrimp. Moreover, diseased shrimp had significantly higher predicted functional features associated with bacterial virulence factors and antibacterial resistance. These exploratory findings suggest an association among pale shrimp disease, gut microbiota dysbiosis, and the proliferation of opportunistic taxa, particularly Photobacterium.
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@article {pmid41218045,
year = {2025},
author = {Kitsanayanyong, L and Chongprachavat, N and Rairat, T and Keetanon, A and Wimanhaemin, P and Chuchird, N},
title = {Exploring the gut microbiota of Pacific white shrimp (Litopenaeus vannamei) suffering pale shrimp disease.},
journal = {PloS one},
volume = {20},
number = {11},
pages = {e0336700},
doi = {10.1371/journal.pone.0336700},
pmid = {41218045},
issn = {1932-6203},
abstract = {Pale shrimp disease is an emerging threat in Thailand, characterized by pale body coloration in Pacific white shrimp (Litopenaeus vannamei). Although the etiology had been identified as Photobacterium damselae subsp. damselae, the disease effects on gut microbiome remain poorly understood. This study investigated changes in the gut microbiota of Pacific white shrimp suffering from pale shrimp disease (diseased group) compared to disease-free shrimp (healthy group) collected from Surat Thani Province, Thailand. DNA extracted from the intestinal samples was subjected to 16S rRNA metagenomic sequencing, followed by taxonomic identification, diversity analyses, and functional prediction of the metabolic pathways. Despite a limited number of biological replicates, the occurrence of pale shrimp disease was able to reveal alterations in intestinal microbial composition, diversities, and functional features compared to the healthy shrimp. In most cases, the intestinal microbiota of the diseased shrimp were dominated by only 2 genera of bacteria, i.e., Photobacterium (54.63-70.53%) and Vibrio (24.94-26.12%), which together accounted for 79.58-95.47% of the total bacterial community. α-diversity, as indicated by the observed features, Shannon, and Simpson indices, was significantly decreased, and dominance was significantly increased in the diseased shrimp compared to healthy shrimp. Likewise, β-diversity was significantly different between groups; PCoA of un-weighted and weighted UniFrac clearly distinguished intestinal microbiota of the shrimp into 2 clusters, and ANOSIM of these data revealed statistical differences between groups, suggesting different microbiota communities between healthy and diseased shrimp. Moreover, diseased shrimp had significantly higher predicted functional features associated with bacterial virulence factors and antibacterial resistance. These exploratory findings suggest an association among pale shrimp disease, gut microbiota dysbiosis, and the proliferation of opportunistic taxa, particularly Photobacterium.},
}
RevDate: 2025-11-11
[Connective tissue diseases: development predictors, multimorbidity variants, physical treatment methods. (Literature review)].
Voprosy kurortologii, fizioterapii, i lechebnoi fizicheskoi kultury, 102(5):56-62.
UNLABELLED: Connective tissue diseases, such as systemic lupus erythematosus, systemic scleroderma and dermatomyositis are heterogeneous autoimmune diseases with damage to the skin, vessels and internal organs, immune dysregulation, fibrosis. The relevance of their study is due to high multimorbidity, including cardiovascular, oncological and neuropsychiatric complications (pulmonary hypertension develops in 30-40% of patients with scleroderma, paraneoplastic syndromes are recorded in 40% of patients with dermatomyositis). Increase in knowledge of genetic and epigenetic factors triggering debut of connective tissue diseases emphasizes the need for an interdisciplinary approach and personalization of therapy.
OBJECTIVE: To analyze the modern data on pathogenesis, genetic predictors, clinical complications and comorbid conditions, methods of treatment of the connective tissue diseases, as well as to evaluate the promising research directions for improving diagnosis and therapy.
MATERIAL AND METHODS: A review of scientific publications and clinical studies presented in international abstract databases for the period from 2013 to 2025 involving more than 700 thousand patients was carried out. Data on genetic biomarkers, epidemiological factors, effectiveness of physical methods of treatment of the connective tissue diseases and innovative approaches were systematized.
RESULTS: Key genetic (polymorphisms of HLA class II, TRAF1-C5, TNFSF4, antibodies to MDA5) and epigenetic risk factors (insolation, smoking, vitamin D deficiency) of the connective tissue diseases have been identified. Effectiveness of physical therapy for improvement of the function of joints and lungs, phototherapy for correction of skin manifestations has been proven. Autologous stem cell transplantation has shown effectiveness in refractory forms. Personalization of biomarker-based therapy improves patients' quality of life. The main challenges have been established: resistance to therapy, risk of infections during immunosuppression. The investigation of gut microbiome and development of targeted drugs inhibiting TGF-β and interleukin-6 have been recognized as promising directions.
CONCLUSION: Connective tissue diseases require early diagnosis, interdisciplinary strategy and integration of pharmacological and non-drug methods. Physical treatment methods demonstrate proven effectiveness in the context of a comprehensive approach to therapy. Physical therapy with a high level of evidence (I, A) improves the function of joints and lungs, as well as contributes to the reduction of fibrosis severity. UVA-1 phototherapy is a method of choice for improving the skin elasticity in scleroderma and skin forms of the connective tissue diseases by inhibiting TGF-β and collagen synthesis. Ultrasound therapy in combination with hyaluronidase, high-intensity dye laser therapy are indicated for reduction of the vascular disorders in tissues. Cryotherapy (whole-body and local), electrophoresis with corticosteroids have a local anti-inflammatory effect, complement the range of non-drug interventions, improving the quality of life of patients, but require individualization of parameters. Personalization of treatment based on genetic markers, as well as the introduction of innovative methods (targeted therapy) can reduce the risk of complications, but problems of resistance and iatrogenic effects remain. Further research should be aimed at the study of the role of microbiome and development of pathogenetically substantiated drugs.
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@article {pmid41217799,
year = {2025},
author = {Ponomarenko, IG and Ponomarenko, GN},
title = {[Connective tissue diseases: development predictors, multimorbidity variants, physical treatment methods. (Literature review)].},
journal = {Voprosy kurortologii, fizioterapii, i lechebnoi fizicheskoi kultury},
volume = {102},
number = {5},
pages = {56-62},
doi = {10.17116/kurort202510205156},
pmid = {41217799},
issn = {0042-8787},
abstract = {UNLABELLED: Connective tissue diseases, such as systemic lupus erythematosus, systemic scleroderma and dermatomyositis are heterogeneous autoimmune diseases with damage to the skin, vessels and internal organs, immune dysregulation, fibrosis. The relevance of their study is due to high multimorbidity, including cardiovascular, oncological and neuropsychiatric complications (pulmonary hypertension develops in 30-40% of patients with scleroderma, paraneoplastic syndromes are recorded in 40% of patients with dermatomyositis). Increase in knowledge of genetic and epigenetic factors triggering debut of connective tissue diseases emphasizes the need for an interdisciplinary approach and personalization of therapy.
OBJECTIVE: To analyze the modern data on pathogenesis, genetic predictors, clinical complications and comorbid conditions, methods of treatment of the connective tissue diseases, as well as to evaluate the promising research directions for improving diagnosis and therapy.
MATERIAL AND METHODS: A review of scientific publications and clinical studies presented in international abstract databases for the period from 2013 to 2025 involving more than 700 thousand patients was carried out. Data on genetic biomarkers, epidemiological factors, effectiveness of physical methods of treatment of the connective tissue diseases and innovative approaches were systematized.
RESULTS: Key genetic (polymorphisms of HLA class II, TRAF1-C5, TNFSF4, antibodies to MDA5) and epigenetic risk factors (insolation, smoking, vitamin D deficiency) of the connective tissue diseases have been identified. Effectiveness of physical therapy for improvement of the function of joints and lungs, phototherapy for correction of skin manifestations has been proven. Autologous stem cell transplantation has shown effectiveness in refractory forms. Personalization of biomarker-based therapy improves patients' quality of life. The main challenges have been established: resistance to therapy, risk of infections during immunosuppression. The investigation of gut microbiome and development of targeted drugs inhibiting TGF-β and interleukin-6 have been recognized as promising directions.
CONCLUSION: Connective tissue diseases require early diagnosis, interdisciplinary strategy and integration of pharmacological and non-drug methods. Physical treatment methods demonstrate proven effectiveness in the context of a comprehensive approach to therapy. Physical therapy with a high level of evidence (I, A) improves the function of joints and lungs, as well as contributes to the reduction of fibrosis severity. UVA-1 phototherapy is a method of choice for improving the skin elasticity in scleroderma and skin forms of the connective tissue diseases by inhibiting TGF-β and collagen synthesis. Ultrasound therapy in combination with hyaluronidase, high-intensity dye laser therapy are indicated for reduction of the vascular disorders in tissues. Cryotherapy (whole-body and local), electrophoresis with corticosteroids have a local anti-inflammatory effect, complement the range of non-drug interventions, improving the quality of life of patients, but require individualization of parameters. Personalization of treatment based on genetic markers, as well as the introduction of innovative methods (targeted therapy) can reduce the risk of complications, but problems of resistance and iatrogenic effects remain. Further research should be aimed at the study of the role of microbiome and development of pathogenetically substantiated drugs.},
}
RevDate: 2025-11-11
Oral probiotic and postbiotic supplementation enhances the abundance of Lactobacillus acidophilus, Lactobacillus johnsonii, and Limosilactobacillus reuteri in both canine skin and gastrointestinal microbiota: insights from long-read 16S rRNA gene sequencing.
Veterinary research communications, 50(1):29.
Oral daily probiotic and postbiotic supplementation (ODPPS) is a promising strategy for canine skin and gut health. Despite growing interest, the effects of ODPPS on the composition of the canine gut and skin microbiota remain largely unexplored. The advent of full-length 16S rRNA gene sequencing has opened new avenues in microbiome research, significantly enhancing the accuracy and completeness of microbial community profiling. This study employed PacBio long-read sequencing to profile longitudinal changes in canine fecal microbiota composition during ODPPS. Then, we evaluated the parallel dynamics between fecal and skin microbiota responses to ODPPS, addressing a critical gap in understanding systemic microbiome interactions in dogs. By Day 90, fecal microbiota composition shifted significantly (PERMANOVA p = 0.05), with increased beneficial bacteria by Day 30 and further by Day 90. In both axillae and fecal microbiota, ODPPS supplementation increased the relative abundance of beneficial species including Lactobacillus acidophilus, Lactobacillus johnsonii, and Limosilactobacillus reuteri. A significant positive Pearson correlation was found between the relative abundances of these bacteria in the skin and fecal microbiota (p = 0.05), suggesting a coordinated microbial response across body sites. The results highlight the significance of Lactobacillus acidophilus as a core probiotic strain, demonstrating exceptional capacity for colonisation and establishment in both the gastrointestinal and skin niches of dogs. These findings show the systemic influence of ODPPS in shaping microbial communities across both sites and support its use to promote overall canine health. Collectively, our results offer robust evidence for the dual benefits of daily oral ODPPS on both skin and gut microbiota.
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@article {pmid41217655,
year = {2025},
author = {Mohammadi Dehcheshmeh, M and Grant, L and Ebrahimie, E and Khabiri, A and Hemmatzadeh, F and Shipstone, M and Trott, DJ},
title = {Oral probiotic and postbiotic supplementation enhances the abundance of Lactobacillus acidophilus, Lactobacillus johnsonii, and Limosilactobacillus reuteri in both canine skin and gastrointestinal microbiota: insights from long-read 16S rRNA gene sequencing.},
journal = {Veterinary research communications},
volume = {50},
number = {1},
pages = {29},
pmid = {41217655},
issn = {1573-7446},
abstract = {Oral daily probiotic and postbiotic supplementation (ODPPS) is a promising strategy for canine skin and gut health. Despite growing interest, the effects of ODPPS on the composition of the canine gut and skin microbiota remain largely unexplored. The advent of full-length 16S rRNA gene sequencing has opened new avenues in microbiome research, significantly enhancing the accuracy and completeness of microbial community profiling. This study employed PacBio long-read sequencing to profile longitudinal changes in canine fecal microbiota composition during ODPPS. Then, we evaluated the parallel dynamics between fecal and skin microbiota responses to ODPPS, addressing a critical gap in understanding systemic microbiome interactions in dogs. By Day 90, fecal microbiota composition shifted significantly (PERMANOVA p = 0.05), with increased beneficial bacteria by Day 30 and further by Day 90. In both axillae and fecal microbiota, ODPPS supplementation increased the relative abundance of beneficial species including Lactobacillus acidophilus, Lactobacillus johnsonii, and Limosilactobacillus reuteri. A significant positive Pearson correlation was found between the relative abundances of these bacteria in the skin and fecal microbiota (p = 0.05), suggesting a coordinated microbial response across body sites. The results highlight the significance of Lactobacillus acidophilus as a core probiotic strain, demonstrating exceptional capacity for colonisation and establishment in both the gastrointestinal and skin niches of dogs. These findings show the systemic influence of ODPPS in shaping microbial communities across both sites and support its use to promote overall canine health. Collectively, our results offer robust evidence for the dual benefits of daily oral ODPPS on both skin and gut microbiota.},
}
RevDate: 2025-11-11
Lower Respiratory Tract Bacterial Profiles Are Associated With Respiratory Severity and Bronchopulmonary Dysplasia in Neonates.
Pediatric pulmonology, 60(11):e71364.
INTRODUCTION: Bronchopulmonary dysplasia (BPD) is a major complication of prematurity, marked by heterogeneous pulmonary phenotypes and variable clinical outcomes. The airway microbiome may influence disease severity and progression, yet quantitative associations between airway pathogens and clinically relevant outcomes remain poorly understood.
METHODS: We conducted a retrospective analysis of 204 neonates who underwent flexible bronchoscopy with quantitative bronchoalveolar lavage (BAL) cultures in the NICU at the Children's Hospital of Philadelphia. Cultures yielding ≥ 10,000 colony-forming units per milliliter for a single bacterial species were classified as positive. Respiratory severity score (RSS), calculated as the product of mean airway pressure and fraction of inspired oxygen, served as the primary indicator of respiratory status. Linear, logistic, and negative binomial regression models were used to assess associations between bacterial species and clinical outcomes, adjusted for sex and race, with standard errors clustered at the patient level.
RESULTS: No bacterial species were significantly associated with RSS after correction for multiple testing. Klebsiella pneumoniae was associated with a diagnosis of BPD (adjusted p = 0.026), but no organisms were significantly associated with prolonged time to extubation. In secondary analyses, the presence of several organisms was significantly associated with higher MAP, including K. pneumoniae (β = 2.66, FDR-adjusted p = 0.014).
CONCLUSIONS: Multiple bacterial species identified on quantitative BAL culture were associated with higher mean airway pressure, and K. pneumoniae was additionally associated with BPD diagnosis. These findings support the potential utility of quantitative microbiologic data in risk stratification and management of neonatal respiratory disease.
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@article {pmid41217383,
year = {2025},
author = {Kelchtermans, J and Phinizy, P and Piccione, J and McGrath-Morrow, SA},
title = {Lower Respiratory Tract Bacterial Profiles Are Associated With Respiratory Severity and Bronchopulmonary Dysplasia in Neonates.},
journal = {Pediatric pulmonology},
volume = {60},
number = {11},
pages = {e71364},
doi = {10.1002/ppul.71364},
pmid = {41217383},
issn = {1099-0496},
support = {//This study was supported by the Parker B. Francis Fellowship Program. The study was funded by an Institute Development Fund and a K-readiness pilot grant from The Children's Hospital of Philadelphia. Research reported in this publication was supported by the National Institute of Environmental Health Sciences of the National Institutes of Health under grant number P30ES013508 and by the National Heart, Lung, and Blood Institute under grant number R01HL169859 and K08HL173625. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health./ ; },
abstract = {INTRODUCTION: Bronchopulmonary dysplasia (BPD) is a major complication of prematurity, marked by heterogeneous pulmonary phenotypes and variable clinical outcomes. The airway microbiome may influence disease severity and progression, yet quantitative associations between airway pathogens and clinically relevant outcomes remain poorly understood.
METHODS: We conducted a retrospective analysis of 204 neonates who underwent flexible bronchoscopy with quantitative bronchoalveolar lavage (BAL) cultures in the NICU at the Children's Hospital of Philadelphia. Cultures yielding ≥ 10,000 colony-forming units per milliliter for a single bacterial species were classified as positive. Respiratory severity score (RSS), calculated as the product of mean airway pressure and fraction of inspired oxygen, served as the primary indicator of respiratory status. Linear, logistic, and negative binomial regression models were used to assess associations between bacterial species and clinical outcomes, adjusted for sex and race, with standard errors clustered at the patient level.
RESULTS: No bacterial species were significantly associated with RSS after correction for multiple testing. Klebsiella pneumoniae was associated with a diagnosis of BPD (adjusted p = 0.026), but no organisms were significantly associated with prolonged time to extubation. In secondary analyses, the presence of several organisms was significantly associated with higher MAP, including K. pneumoniae (β = 2.66, FDR-adjusted p = 0.014).
CONCLUSIONS: Multiple bacterial species identified on quantitative BAL culture were associated with higher mean airway pressure, and K. pneumoniae was additionally associated with BPD diagnosis. These findings support the potential utility of quantitative microbiologic data in risk stratification and management of neonatal respiratory disease.},
}
RevDate: 2025-11-11
Sargassum fusiforme polysaccharides modulate gut microbiota and metabolites to regulate hyperlipidemia in mice fed a high-fat diet.
Applied and environmental microbiology [Epub ahead of print].
UNLABELLED: Hyperlipidemia complications caused by obesity are a hot issue threatening human health worldwide, and there is an urgent need to explore low-toxicity health foods for intervention. Sargassum fusiforme polysaccharides (SFPS) display cholesterol-lowering properties, but the underlying mechanism has not been elucidated. This study investigates the mechanisms by exploring changes in gut microbiota composition, gene expression, and metabolites in mice fed a high-fat diet after intervention with S. fusiforme fucoidan (SFF) and SFPS through 16S rRNA sequencing, transcriptomics, and non-targeted metabolomics. The experimental findings indicated that SFPS markedly enhanced the abundance of Akkermansia while concurrently reducing the levels of Actinobacteria, Erysipelotrichaceae, Bifidobacteriaceae, and Peptostreptococcaceae. This was achieved by upregulating the expression of Mt1, Prlr, and slc25a21 and downregulating SREBP-1, thereby inhibiting the cholesterol metabolism pathway. These changes resulted in increased hepatic production and fecal excretion of bile acids and reduced hepatic cholesterol. Our results shed light on the mechanisms behind the cholesterol- and lipid-lowering effects of SFPS, suggesting its potential as a therapeutic agent for hypercholesterolemia.
IMPORTANCE: Obesity and its associated metabolic disorders pose a global health challenge, necessitating safe and scalable interventions. This study demonstrated that polysaccharides from Sargassum fusiforme (SFPS), extracted via a novel non-alcoholic precipitation method, effectively ameliorate high-fat diet (HFD)-induced obesity by remodeling gut microbiota and restoring metabolic homeostasis. Integrating multi-omics approaches, we reveal that SFPS enriches beneficial taxa like Akkermansia while suppressing obesity-linked bacteria like Actinobacteria, Erysipelotrichaceae, and Bifidobacteriaceae; modulates cholesterol metabolism through gene regulation (e.g., downregulating Srebf1 and upregulating Mt1); and enhances bile acid excretion. Notably, SFPS exhibits efficacy comparable with the well-studied fucoidan (SFF); however, its cost-effective extraction method offers superior scalability for functional food development. These findings underscore the potential of SFPS as a prebiotic agent targeting the gut-liver axis, providing mechanistic insights into natural product-based strategies for metabolic disease management. This work advances our understanding of how polysaccharides interact with the host microbiome and metabolism, advancing dietary interventions for obesity management one step further.
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@article {pmid41217190,
year = {2025},
author = {Su, N and Han, S and Li, Z and Ling, X and Kong, L and Song, D},
title = {Sargassum fusiforme polysaccharides modulate gut microbiota and metabolites to regulate hyperlipidemia in mice fed a high-fat diet.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0144525},
doi = {10.1128/aem.01445-25},
pmid = {41217190},
issn = {1098-5336},
abstract = {UNLABELLED: Hyperlipidemia complications caused by obesity are a hot issue threatening human health worldwide, and there is an urgent need to explore low-toxicity health foods for intervention. Sargassum fusiforme polysaccharides (SFPS) display cholesterol-lowering properties, but the underlying mechanism has not been elucidated. This study investigates the mechanisms by exploring changes in gut microbiota composition, gene expression, and metabolites in mice fed a high-fat diet after intervention with S. fusiforme fucoidan (SFF) and SFPS through 16S rRNA sequencing, transcriptomics, and non-targeted metabolomics. The experimental findings indicated that SFPS markedly enhanced the abundance of Akkermansia while concurrently reducing the levels of Actinobacteria, Erysipelotrichaceae, Bifidobacteriaceae, and Peptostreptococcaceae. This was achieved by upregulating the expression of Mt1, Prlr, and slc25a21 and downregulating SREBP-1, thereby inhibiting the cholesterol metabolism pathway. These changes resulted in increased hepatic production and fecal excretion of bile acids and reduced hepatic cholesterol. Our results shed light on the mechanisms behind the cholesterol- and lipid-lowering effects of SFPS, suggesting its potential as a therapeutic agent for hypercholesterolemia.
IMPORTANCE: Obesity and its associated metabolic disorders pose a global health challenge, necessitating safe and scalable interventions. This study demonstrated that polysaccharides from Sargassum fusiforme (SFPS), extracted via a novel non-alcoholic precipitation method, effectively ameliorate high-fat diet (HFD)-induced obesity by remodeling gut microbiota and restoring metabolic homeostasis. Integrating multi-omics approaches, we reveal that SFPS enriches beneficial taxa like Akkermansia while suppressing obesity-linked bacteria like Actinobacteria, Erysipelotrichaceae, and Bifidobacteriaceae; modulates cholesterol metabolism through gene regulation (e.g., downregulating Srebf1 and upregulating Mt1); and enhances bile acid excretion. Notably, SFPS exhibits efficacy comparable with the well-studied fucoidan (SFF); however, its cost-effective extraction method offers superior scalability for functional food development. These findings underscore the potential of SFPS as a prebiotic agent targeting the gut-liver axis, providing mechanistic insights into natural product-based strategies for metabolic disease management. This work advances our understanding of how polysaccharides interact with the host microbiome and metabolism, advancing dietary interventions for obesity management one step further.},
}
RevDate: 2025-11-11
Colonizing the clinic: tracking bacterial succession and longitudinal dynamics in five new hospital departments over an entire year.
Microbiology spectrum [Epub ahead of print].
The development of hospital-associated microbial communities over time remains poorly characterized, particularly in terms of how microbial populations dynamically respond to changes in building function, the integration of molecular and cultivation-based data, and the early identification of intervention points for flexible, adaptive microbial control strategies. In this longitudinal study, we investigated microbiome dynamics across five newly built departments at the University Hospital of Graz, Austria, over one year. Surface samples were collected at seven time points: before and after hospital operation started. Alpha and beta diversity analyses revealed a distinct two-phase microbial transition, marked by an initial disruption followed by a gradual homogenization of microbial communities. The strongest driver of community change was the arrival of patients, which led to a significant shift in both diversity and taxonomic composition. While early time points were dominated by environmental taxa such as Acinetobacter and Pseudomonas, human-associated genera like Staphylococcus and Corynebacterium became more prevalent over time, particularly on frequently touched surfaces. Department-specific and surface-specific microbial signatures were observed, with outpatient and transplant departments showing more variability than surgical and intensive care units (ICUs). Propidium monoazide treatment indicated that Pseudomonas and Acinetobacter may persist as viable community members, whereas Staphylococcus and Corynebacterium likely reflect frequent human deposition. Cultivation data supported these findings, showing episodic contamination primarily linked to human contact. Phenotypic predictions revealed a decline in aerobic, Gram-negative, and potentially pathogenic bacteria over time, although these trends were less pronounced in the ICU. Together, our findings reveal a longitudinal homogenization of hospital microbiomes driven by human activity and highlight key taxa and surfaces that warrant targeted monitoring to improve hygiene protocols and infection control strategies.IMPORTANCEThis study provides crucial insights into how hospital environments transform microbially after new departments open, a process poorly understood until now. We reveal a two-phase microbial shift, starting with environmental bacteria like Acinetobacter and Pseudomonas before the hospital opens, then rapidly transitioning to human-associated microbes such as Staphylococcus and Corynebacterium once patients and staff arrive. Our findings highlight that human activity is the strongest driver of these changes, especially on frequently touched surfaces. This work is vital for developing targeted and adaptive hygiene concepts, improving infection control, and ultimately making hospital environments safer for patients and staff by focusing on specific surfaces and microbial groups that warrant continuous monitoring.
Additional Links: PMID-41217181
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PubMed:
Citation:
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@article {pmid41217181,
year = {2025},
author = {Weinberger, V and Neumann, C and Kumpitsch, C and Duller, S and Shinde, T and Mantaj, P and Schmidberger, L and Zurabishvili, T and Halmer, I and Cecovini, M and Vrbancic, S and Pepper, K and Schmon, E and Wenninger, J and Kamolz, L-P and Sendlhofer, G and Koskinen, K and Moissl-Eichinger, C and Mahnert, A},
title = {Colonizing the clinic: tracking bacterial succession and longitudinal dynamics in five new hospital departments over an entire year.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0217825},
doi = {10.1128/spectrum.02178-25},
pmid = {41217181},
issn = {2165-0497},
abstract = {The development of hospital-associated microbial communities over time remains poorly characterized, particularly in terms of how microbial populations dynamically respond to changes in building function, the integration of molecular and cultivation-based data, and the early identification of intervention points for flexible, adaptive microbial control strategies. In this longitudinal study, we investigated microbiome dynamics across five newly built departments at the University Hospital of Graz, Austria, over one year. Surface samples were collected at seven time points: before and after hospital operation started. Alpha and beta diversity analyses revealed a distinct two-phase microbial transition, marked by an initial disruption followed by a gradual homogenization of microbial communities. The strongest driver of community change was the arrival of patients, which led to a significant shift in both diversity and taxonomic composition. While early time points were dominated by environmental taxa such as Acinetobacter and Pseudomonas, human-associated genera like Staphylococcus and Corynebacterium became more prevalent over time, particularly on frequently touched surfaces. Department-specific and surface-specific microbial signatures were observed, with outpatient and transplant departments showing more variability than surgical and intensive care units (ICUs). Propidium monoazide treatment indicated that Pseudomonas and Acinetobacter may persist as viable community members, whereas Staphylococcus and Corynebacterium likely reflect frequent human deposition. Cultivation data supported these findings, showing episodic contamination primarily linked to human contact. Phenotypic predictions revealed a decline in aerobic, Gram-negative, and potentially pathogenic bacteria over time, although these trends were less pronounced in the ICU. Together, our findings reveal a longitudinal homogenization of hospital microbiomes driven by human activity and highlight key taxa and surfaces that warrant targeted monitoring to improve hygiene protocols and infection control strategies.IMPORTANCEThis study provides crucial insights into how hospital environments transform microbially after new departments open, a process poorly understood until now. We reveal a two-phase microbial shift, starting with environmental bacteria like Acinetobacter and Pseudomonas before the hospital opens, then rapidly transitioning to human-associated microbes such as Staphylococcus and Corynebacterium once patients and staff arrive. Our findings highlight that human activity is the strongest driver of these changes, especially on frequently touched surfaces. This work is vital for developing targeted and adaptive hygiene concepts, improving infection control, and ultimately making hospital environments safer for patients and staff by focusing on specific surfaces and microbial groups that warrant continuous monitoring.},
}
RevDate: 2025-11-11
Polyphenols of Ferula lehmanni Boiss. attenuate high-fat diet-induced liver injury by regulating lipid synthesis and remodeling the gut microbiota.
Food & function [Epub ahead of print].
High-fat diet (HFD)-induced liver injury, characterized by hepatic steatosis, inflammation, and oxidative stress, represents a significant global health challenge. Ferula lehmannii Boiss. (FLB), an edible and medicinal plant, is rich in polyphenols and has hepatoprotective effects, but the gut microbiota-mediated mechanism remains unclear. This study elucidates the protective effects of FLB polyphenols (FLBP) against HFD-induced liver injury via the gut microbiota. Chemical profiling and network pharmacology predicted FLBP's multitarget effects on lipid metabolism and inflammation. In vivo, FLBP attenuated hepatic steatosis by regulating lipogenic factors and energy metabolism, reducing oxidative stress and enhancing antioxidants. Gut microbiota analysis showed that FLBP restored gut microbial diversity, enriched beneficial bacteria abundance and promoted short-chain fatty acid (SCFA) production. Antibiotic-induced microbiota ablation abolished the hepatoprotective effects of FLBP, confirming the essential role of the gut microbiota. Collectively, our findings demonstrate that FLBP alleviates HFD-induced liver injury by regulating hepatic lipid synthesis and remodeling the gut microbiome, highlighting its potential as a dietary intervention for managing diet-related liver diseases.
Additional Links: PMID-41217033
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PubMed:
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@article {pmid41217033,
year = {2025},
author = {Ye, Y and Ge, J and He, W and Zhan, P and Wang, D and Wang, P and Tian, H and Liu, J},
title = {Polyphenols of Ferula lehmanni Boiss. attenuate high-fat diet-induced liver injury by regulating lipid synthesis and remodeling the gut microbiota.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d5fo03998c},
pmid = {41217033},
issn = {2042-650X},
abstract = {High-fat diet (HFD)-induced liver injury, characterized by hepatic steatosis, inflammation, and oxidative stress, represents a significant global health challenge. Ferula lehmannii Boiss. (FLB), an edible and medicinal plant, is rich in polyphenols and has hepatoprotective effects, but the gut microbiota-mediated mechanism remains unclear. This study elucidates the protective effects of FLB polyphenols (FLBP) against HFD-induced liver injury via the gut microbiota. Chemical profiling and network pharmacology predicted FLBP's multitarget effects on lipid metabolism and inflammation. In vivo, FLBP attenuated hepatic steatosis by regulating lipogenic factors and energy metabolism, reducing oxidative stress and enhancing antioxidants. Gut microbiota analysis showed that FLBP restored gut microbial diversity, enriched beneficial bacteria abundance and promoted short-chain fatty acid (SCFA) production. Antibiotic-induced microbiota ablation abolished the hepatoprotective effects of FLBP, confirming the essential role of the gut microbiota. Collectively, our findings demonstrate that FLBP alleviates HFD-induced liver injury by regulating hepatic lipid synthesis and remodeling the gut microbiome, highlighting its potential as a dietary intervention for managing diet-related liver diseases.},
}
RevDate: 2025-11-11
Establishment of a coculture system for Porphyromonas gingivalis and head and neck squamous cell carcinoma using spheroid culture and LATS inhibition.
FEBS open bio [Epub ahead of print].
Porphyromonas gingivalis (Pg) is a periodontal pathogen that has been implicated in the development and progression of head and neck squamous cell carcinoma (HNSCC). However, studying its interaction with HNSCC in vitro is challenging because of the obligatory anaerobic nature of Pg. To overcome this limitation, we developed a coculture system that enables the viability of both HNSCC cells and Pg using spheroid culture combined with Hippo pathway inhibition via treatment with a LATS1/2 inhibitor. In spheroid cultures, many HNSCC cell lines failed to grow in a normal medium. However, stable growth of these cells was achieved through Hippo pathway inhibition, which maintained the cells in an undifferentiated state. Furthermore, the addition of Pg to HNSCC spheroids maintained Pg viability in three out of four HNSCC cell lines, even after 3 days. Hippo pathway inhibition further enhanced Pg survival within the spheroids, likely by suppressing the differentiation-induced expression of antimicrobial genes S100A8 and S100A9. Coculturing HNSCC cells with Pg did not promote spheroid growth but induced p38 activation, leading to increased expression of the proinflammatory cytokines IL-1α and IL-8. Database analysis using The Cancer Microbiome Atlas corroborated these findings, showing upregulation of p38 phosphorylation, IL-1α, and IL-8 in Porphyromonas-positive HNSCC samples. These findings suggest that the established coculture system is a representative model of the clinical properties of Pg-positive HNSCC and can serve as a valuable tool for investigating the long-term interactions between HNSCC and viable Pg.
Additional Links: PMID-41216638
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PubMed:
Citation:
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@article {pmid41216638,
year = {2025},
author = {Nakajima, Y and Okazaki, S and Tamura, M and Sato, S and Imai, K},
title = {Establishment of a coculture system for Porphyromonas gingivalis and head and neck squamous cell carcinoma using spheroid culture and LATS inhibition.},
journal = {FEBS open bio},
volume = {},
number = {},
pages = {},
doi = {10.1002/2211-5463.70154},
pmid = {41216638},
issn = {2211-5463},
support = {SATO-2023-6//Sato Fund/ ; a Nihon University Research Grant-in-Aid for Early//Nihon University/ ; //the research grant of Nihon University/ ; //Mishima Kaiun Memorial Foundation/ ; //NSK Nakanishi Foundation/ ; DRC(B)-2023-6//Dental Research Center, Nihon University School of Dentistry/ ; DRC(B)-2024-6//Dental Research Center, Nihon University School of Dentistry/ ; DRC(B)-2025-6//Dental Research Center, Nihon University School of Dentistry/ ; JP22K07157//Japan Science and Technology Agency/ ; JP23K27810//Japan Science and Technology Agency/ ; JP24K22196//Japan Science and Technology Agency/ ; },
abstract = {Porphyromonas gingivalis (Pg) is a periodontal pathogen that has been implicated in the development and progression of head and neck squamous cell carcinoma (HNSCC). However, studying its interaction with HNSCC in vitro is challenging because of the obligatory anaerobic nature of Pg. To overcome this limitation, we developed a coculture system that enables the viability of both HNSCC cells and Pg using spheroid culture combined with Hippo pathway inhibition via treatment with a LATS1/2 inhibitor. In spheroid cultures, many HNSCC cell lines failed to grow in a normal medium. However, stable growth of these cells was achieved through Hippo pathway inhibition, which maintained the cells in an undifferentiated state. Furthermore, the addition of Pg to HNSCC spheroids maintained Pg viability in three out of four HNSCC cell lines, even after 3 days. Hippo pathway inhibition further enhanced Pg survival within the spheroids, likely by suppressing the differentiation-induced expression of antimicrobial genes S100A8 and S100A9. Coculturing HNSCC cells with Pg did not promote spheroid growth but induced p38 activation, leading to increased expression of the proinflammatory cytokines IL-1α and IL-8. Database analysis using The Cancer Microbiome Atlas corroborated these findings, showing upregulation of p38 phosphorylation, IL-1α, and IL-8 in Porphyromonas-positive HNSCC samples. These findings suggest that the established coculture system is a representative model of the clinical properties of Pg-positive HNSCC and can serve as a valuable tool for investigating the long-term interactions between HNSCC and viable Pg.},
}
RevDate: 2025-11-11
Microbiome dysbiosis and endometriosis: a systematic scoping review of current literature and knowledge gaps.
Human reproduction open, 2025(4):hoaf061.
STUDY QUESTION: What is the evidence available concerning gut and reproductive tract microbiomes in patients with endometriosis and what are the methodological approaches employed in microbiome studies on endometriosis?
SUMMARY ANSWER: The taxonomic profiles exhibited pronounced heterogeneity within women with and also within women without endometriosis across reviewed studies for all the anatomical districts evaluated.
WHAT IS KNOWN ALREADY: Both human and animal studies support differences in the microbiome composition of individuals with and without endometriosis. Endometriosis onset occurs with variable symptoms and manifestations. The microbiome composition at different sites may contribute to this variability.
STUDY DESIGN SIZE DURATION: We used the scoping review methodology. Systematic searches of studies from the PubMed, EMBASE, and Web of Science databases published between 1 January 2016 and 1 November 2024 addressing endometriosis microbiome characterization in: (i) gut, (ii) vaginal fluid, (iii) cervical fluid, (iv) peritoneal fluid, (v) uterine fluid, (vi) ovarian cyst fluid, (vii) oropharyngeal fluid, and (viii) eutopic and (ix) ectopic tissues were performed using a combination of MeSH terms. References from relevant publications were systematically screened.
Results were reported in accordance with the PRISMA-ScR guidelines. Studies that did not report original data, not written in English or providing a review of the field were excluded. From the 2182 publications retrieved, 36 papers were selected and analyzed, focusing on sample characterization (patients, controls, tissues, and fluids) and methodologies used.
Sound evidence is lacking to support a specific gut dysbiosis profile in women with endometriosis. The largest metagenome study performed using shotgun sequencing and controlling for multiple hypotheses testing did not detect significant differences between women with and without the disease. For eutopic and ectopic tissue microbiomes, the literature is too scant to draw any conclusion. Some data suggest a possible enrichment of Streptococcus sp. in cervical fluid and of Pseudomonas sp. in peritoneal fluid and a depletion of Lachnospira sp. in stool/anal fluid of endometriosis patients. However, these findings may be explained by confounders or by intrinsic patient or population characteristics. We appraised the limitations of the studies and proposed suggestions for optimizing sequencing techniques and experimental designs.
The number of participants per study greatly varied and, with few exceptions, was typically low. Incomplete information on methodological approaches was broadly observed. The impact of participants' menstrual cycle phase, diet, and drug assumption was frequently not considered.
Standardization of research protocols to allow reproducibility is required, as well as collaborations to harmonize data analysis, interpretation, and, more importantly, health outcome prediction or improvement.
The review was funded by the Italian Ministry of Health: RF-2019-12369460, and Current Research IRCCS. P.Vi. serves as co-editor in Chief of Journal of Endometriosis and Uterine Disorders. E.S. serves as Editor in Chief of Human Reproduction Open and discloses research grants from Ferring, Ibsa, Gedeon Richter, and Theramex, and honoraria from Ibsa and Gedeon Richter. P.Ve. serves as Associate Editor for Human Reproduction Open; is a member of the Editorial Board of the Journal of Obstetrics and Gynaecology Canada, of the Italian Journal of Obstetrics and Gynaecology, and of the International Editorial Board of Acta Obstetricia et Gynecologica Scandinavica; has received royalties from Wolters Kluwer for chapters on endometriosis management in the clinical decision support resource UpToDate; and maintains both a public and private gynecological practice. All other authors declare they have no conflict of interest.
REGISTRATION NUMBER: 10.17605/OSF.IO/X6HBT at https://osf.io/registries.
Additional Links: PMID-41216332
PubMed:
Citation:
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@article {pmid41216332,
year = {2025},
author = {Facciotti, F and Di Stefano, G and Maragno, P and Ferraro, C and Dridi, D and Somigliana, E and Viganò, P and Vercellini, P and Casalechi, M},
title = {Microbiome dysbiosis and endometriosis: a systematic scoping review of current literature and knowledge gaps.},
journal = {Human reproduction open},
volume = {2025},
number = {4},
pages = {hoaf061},
pmid = {41216332},
issn = {2399-3529},
abstract = {STUDY QUESTION: What is the evidence available concerning gut and reproductive tract microbiomes in patients with endometriosis and what are the methodological approaches employed in microbiome studies on endometriosis?
SUMMARY ANSWER: The taxonomic profiles exhibited pronounced heterogeneity within women with and also within women without endometriosis across reviewed studies for all the anatomical districts evaluated.
WHAT IS KNOWN ALREADY: Both human and animal studies support differences in the microbiome composition of individuals with and without endometriosis. Endometriosis onset occurs with variable symptoms and manifestations. The microbiome composition at different sites may contribute to this variability.
STUDY DESIGN SIZE DURATION: We used the scoping review methodology. Systematic searches of studies from the PubMed, EMBASE, and Web of Science databases published between 1 January 2016 and 1 November 2024 addressing endometriosis microbiome characterization in: (i) gut, (ii) vaginal fluid, (iii) cervical fluid, (iv) peritoneal fluid, (v) uterine fluid, (vi) ovarian cyst fluid, (vii) oropharyngeal fluid, and (viii) eutopic and (ix) ectopic tissues were performed using a combination of MeSH terms. References from relevant publications were systematically screened.
Results were reported in accordance with the PRISMA-ScR guidelines. Studies that did not report original data, not written in English or providing a review of the field were excluded. From the 2182 publications retrieved, 36 papers were selected and analyzed, focusing on sample characterization (patients, controls, tissues, and fluids) and methodologies used.
Sound evidence is lacking to support a specific gut dysbiosis profile in women with endometriosis. The largest metagenome study performed using shotgun sequencing and controlling for multiple hypotheses testing did not detect significant differences between women with and without the disease. For eutopic and ectopic tissue microbiomes, the literature is too scant to draw any conclusion. Some data suggest a possible enrichment of Streptococcus sp. in cervical fluid and of Pseudomonas sp. in peritoneal fluid and a depletion of Lachnospira sp. in stool/anal fluid of endometriosis patients. However, these findings may be explained by confounders or by intrinsic patient or population characteristics. We appraised the limitations of the studies and proposed suggestions for optimizing sequencing techniques and experimental designs.
The number of participants per study greatly varied and, with few exceptions, was typically low. Incomplete information on methodological approaches was broadly observed. The impact of participants' menstrual cycle phase, diet, and drug assumption was frequently not considered.
Standardization of research protocols to allow reproducibility is required, as well as collaborations to harmonize data analysis, interpretation, and, more importantly, health outcome prediction or improvement.
The review was funded by the Italian Ministry of Health: RF-2019-12369460, and Current Research IRCCS. P.Vi. serves as co-editor in Chief of Journal of Endometriosis and Uterine Disorders. E.S. serves as Editor in Chief of Human Reproduction Open and discloses research grants from Ferring, Ibsa, Gedeon Richter, and Theramex, and honoraria from Ibsa and Gedeon Richter. P.Ve. serves as Associate Editor for Human Reproduction Open; is a member of the Editorial Board of the Journal of Obstetrics and Gynaecology Canada, of the Italian Journal of Obstetrics and Gynaecology, and of the International Editorial Board of Acta Obstetricia et Gynecologica Scandinavica; has received royalties from Wolters Kluwer for chapters on endometriosis management in the clinical decision support resource UpToDate; and maintains both a public and private gynecological practice. All other authors declare they have no conflict of interest.
REGISTRATION NUMBER: 10.17605/OSF.IO/X6HBT at https://osf.io/registries.},
}
RevDate: 2025-11-11
Gut microbial community plasticity as a climate shield mediating sea cucumber resilience to ocean acidification and warming.
ISME communications, 5(1):ycaf188.
Ocean acidification (OA) and ocean warming (OW) pose escalating threats to marine ecosystems, particularly to benthic organisms, such as sea cucumbers, that play pivotal roles in nutrient cycling and sediment health. Existing research mainly addresses sea cucumbers' physiological responses, overlooking gut microbial communities and metabolites in their stress adaptation. Herein, a mesocosm was constructed and analyzed by using integrated gut microbiome and metabolomics approaches to investigate the responses of sea cucumbers Apostichopus japonicus to OA and OW. Results revealed that microbial community plasticity underpins holobiont adaptation, with warming restructuring gut microbiota toward thermotolerant taxa, whereas acidification enriches alkalinity-modulating Rhodobacteraceae and Halioglobus sp. Metabolomic profiling identified 43 amino acid derivatives with significantly increased concentrations in OA and OW groups, including upregulated N-methyl-aspartic acid and γ-glutamyl peptides that stabilize macromolecules and enhance redox homeostasis. Conversely, antioxidative metabolites (e.g., ergothioneine, L-homocystine) are suppressed, reflecting trade-offs between energy allocation and stress protection. In OW group, the antioxidant synthesis pathway is shifted to energy metabolism related to heat tolerance, whereas in OA group, energy is preferentially used for alkalinity regulation pathways rather than oxidative stress defense. Changes in microbial community structure mechanistically explain the trends in metabolite concentrations, as the proliferation of Vibrio spp. in the OW group drives lysine catabolism, leading to a significant increase in L-saccharopine levels. Bacteroidetes reduction in the OA group correlates with L-homocystine downregulation, suggesting that pH-driven microbial interactions are disrupted. These findings demonstrate gut microbiota reshape community structure and metabolism to mitigate synergistic climate stress, emphasizing microbiome-mediated resilience in marine ecosystems amid global climate change.
Additional Links: PMID-41216323
PubMed:
Citation:
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@article {pmid41216323,
year = {2025},
author = {Shan, E and Yu, Z and Cong, X and Hou, C and Guo, X and Pang, L and Zhao, J and Wang, Q and Yuan, X},
title = {Gut microbial community plasticity as a climate shield mediating sea cucumber resilience to ocean acidification and warming.},
journal = {ISME communications},
volume = {5},
number = {1},
pages = {ycaf188},
pmid = {41216323},
issn = {2730-6151},
abstract = {Ocean acidification (OA) and ocean warming (OW) pose escalating threats to marine ecosystems, particularly to benthic organisms, such as sea cucumbers, that play pivotal roles in nutrient cycling and sediment health. Existing research mainly addresses sea cucumbers' physiological responses, overlooking gut microbial communities and metabolites in their stress adaptation. Herein, a mesocosm was constructed and analyzed by using integrated gut microbiome and metabolomics approaches to investigate the responses of sea cucumbers Apostichopus japonicus to OA and OW. Results revealed that microbial community plasticity underpins holobiont adaptation, with warming restructuring gut microbiota toward thermotolerant taxa, whereas acidification enriches alkalinity-modulating Rhodobacteraceae and Halioglobus sp. Metabolomic profiling identified 43 amino acid derivatives with significantly increased concentrations in OA and OW groups, including upregulated N-methyl-aspartic acid and γ-glutamyl peptides that stabilize macromolecules and enhance redox homeostasis. Conversely, antioxidative metabolites (e.g., ergothioneine, L-homocystine) are suppressed, reflecting trade-offs between energy allocation and stress protection. In OW group, the antioxidant synthesis pathway is shifted to energy metabolism related to heat tolerance, whereas in OA group, energy is preferentially used for alkalinity regulation pathways rather than oxidative stress defense. Changes in microbial community structure mechanistically explain the trends in metabolite concentrations, as the proliferation of Vibrio spp. in the OW group drives lysine catabolism, leading to a significant increase in L-saccharopine levels. Bacteroidetes reduction in the OA group correlates with L-homocystine downregulation, suggesting that pH-driven microbial interactions are disrupted. These findings demonstrate gut microbiota reshape community structure and metabolism to mitigate synergistic climate stress, emphasizing microbiome-mediated resilience in marine ecosystems amid global climate change.},
}
RevDate: 2025-11-11
A global deep terrestrial biosphere core microbiome.
ISME communications, 5(1):ycaf176.
The deep biosphere encompasses life beneath the Earth's surface and constitutes a substantial portion of the planet's microbial biomass. This study analyzed nucleic acid datasets from low-carbon and low-energy deep terrestrial subsurface groundwaters across four continents and revealed four core global populations. These populations exhibited metabolic strategies and adaptations reflecting depth and environmental constraints. Erythrobacter featured heterotrophic metabolism; Thiobacillus demonstrated sulfur oxidation coupled to denitrification along with carbon and nitrogen fixation; Methanobacteriaceae were methanogenic autotrophs using the Wood-Ljungdahl pathway (WL); and Candidatus Desulforudis audaxviator functioned as a sulfate-reducer also encoding the WL pathway. Depth-related adaptations suggested heterotrophic dominance at shallower depths with increasing contributions from autotrophy with depth. Finally, comparative genomics revealed minimal evolutionary changes among these populations, suggesting functional conservation since diverging from their ancestral lineages. These findings underscore a global deep biosphere core community.
Additional Links: PMID-41216320
PubMed:
Citation:
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@article {pmid41216320,
year = {2025},
author = {González-Rosales, C and Rezaei Somee, M and Buck, M and Bertilsson, S and Mehrshad, M and Dopson, M},
title = {A global deep terrestrial biosphere core microbiome.},
journal = {ISME communications},
volume = {5},
number = {1},
pages = {ycaf176},
pmid = {41216320},
issn = {2730-6151},
abstract = {The deep biosphere encompasses life beneath the Earth's surface and constitutes a substantial portion of the planet's microbial biomass. This study analyzed nucleic acid datasets from low-carbon and low-energy deep terrestrial subsurface groundwaters across four continents and revealed four core global populations. These populations exhibited metabolic strategies and adaptations reflecting depth and environmental constraints. Erythrobacter featured heterotrophic metabolism; Thiobacillus demonstrated sulfur oxidation coupled to denitrification along with carbon and nitrogen fixation; Methanobacteriaceae were methanogenic autotrophs using the Wood-Ljungdahl pathway (WL); and Candidatus Desulforudis audaxviator functioned as a sulfate-reducer also encoding the WL pathway. Depth-related adaptations suggested heterotrophic dominance at shallower depths with increasing contributions from autotrophy with depth. Finally, comparative genomics revealed minimal evolutionary changes among these populations, suggesting functional conservation since diverging from their ancestral lineages. These findings underscore a global deep biosphere core community.},
}
RevDate: 2025-11-11
Autecology of an oscillating population of a novel host-associated Phaeobacter species proliferating in marine bryozoans.
ISME communications, 5(1):ycaf178.
Phaeobacter are marine alphaprotebacteria capable of producing a potent antibacterial compound, tropodithietic acid. Here we demonstrate that they are part of the microbiome of marine bryozoans where they during warmer months reach 10[5] CFU/g. The levels exhibited a bimodal fluctuation, in both bryozoans and seawater across seasons. However, the population of Phaeobacter sp. was already established in the bryozoans prior to the peak in seawater and did not accumulate as a function of filter feeding on phytoplankton biomass, suggesting that the seawater population is likely seeded from the bryozoan-associated Phaeobacter sp. population rather than the opposite. By comparing whole-genome sequences of more than 100 bryozoan-associated Phaeobacter isolates sampled over a 12-year period, we found that all belonged to the same novel species and no systematic genetic changes occurred within it over the 12 year sampling period despite the fact that the population oscillated from below the limit of detection and across five orders of magnitude to 5.2 Log10 CFU g[-1] bryozoan within individual years and hence were subject to drift. All isolates had the genetic capacity to produce tropodithietic acid (TDA) and the algicidal compounds, roseobacticides. The genes encoding the enzymes for TDA biosynthesis remained stable over time, indicating a conserved phenotype important in the ecophysiology of the bacteria. TDA biosynthetic genes were actively transcribed within the bryozoan host further corroborating the notion that the secondary metabolites of this novel host-associated Phaeobacter sp. may be central to its role within the bryozoan microbiome.
Additional Links: PMID-41216319
PubMed:
Citation:
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@article {pmid41216319,
year = {2025},
author = {Bentzon-Tilia, M and Henriksen, NNSE and Schostag, MD and Andersen, AJC and Melchiorsen, J and Strube, ML and Gram, L},
title = {Autecology of an oscillating population of a novel host-associated Phaeobacter species proliferating in marine bryozoans.},
journal = {ISME communications},
volume = {5},
number = {1},
pages = {ycaf178},
pmid = {41216319},
issn = {2730-6151},
abstract = {Phaeobacter are marine alphaprotebacteria capable of producing a potent antibacterial compound, tropodithietic acid. Here we demonstrate that they are part of the microbiome of marine bryozoans where they during warmer months reach 10[5] CFU/g. The levels exhibited a bimodal fluctuation, in both bryozoans and seawater across seasons. However, the population of Phaeobacter sp. was already established in the bryozoans prior to the peak in seawater and did not accumulate as a function of filter feeding on phytoplankton biomass, suggesting that the seawater population is likely seeded from the bryozoan-associated Phaeobacter sp. population rather than the opposite. By comparing whole-genome sequences of more than 100 bryozoan-associated Phaeobacter isolates sampled over a 12-year period, we found that all belonged to the same novel species and no systematic genetic changes occurred within it over the 12 year sampling period despite the fact that the population oscillated from below the limit of detection and across five orders of magnitude to 5.2 Log10 CFU g[-1] bryozoan within individual years and hence were subject to drift. All isolates had the genetic capacity to produce tropodithietic acid (TDA) and the algicidal compounds, roseobacticides. The genes encoding the enzymes for TDA biosynthesis remained stable over time, indicating a conserved phenotype important in the ecophysiology of the bacteria. TDA biosynthetic genes were actively transcribed within the bryozoan host further corroborating the notion that the secondary metabolites of this novel host-associated Phaeobacter sp. may be central to its role within the bryozoan microbiome.},
}
RevDate: 2025-11-11
Dataset of rolling circle amplification (RCA) enriched metagenome of Cassava obtained through nanopore sequencing.
Data in brief, 63:112204.
The dataset presented here was obtained by sequencing selected historic herbarium cassava samples collected across Nigeria. Total DNA was extracted from the samples using the CTAB method, after which the samples were enriched by Rolling Circle Amplification (RCA) and then sequenced on the MinION. The dataset consists of raw sequencing data in FASTQ format reflecting microbial diversity in cassava leaf samples. Taxonomic classification of the samples using the Kraken2 PlusPFP-16 database revealed 12 kingdoms, 36 phyla, 67 classes, 154 orders, 273 families, 524 genera, and 895 species across the dataset, with a substantial proportion (77.9%) of reads remaining unclassified following host removal. The data is beneficial for exploring the microbiome diversity of cassava leaves across Nigeria, as well as serving as a reference for future microbial discovery, given the large number of unidentified reads in the dataset.
Additional Links: PMID-41215794
PubMed:
Citation:
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@article {pmid41215794,
year = {2025},
author = {Onile-Ere, O and Name, PE and Tibiri, EB and Tiendrébéogo, F and Pita, J and Mohammed, IU and Nkere, CK and Oranusi, S and Eni, A},
title = {Dataset of rolling circle amplification (RCA) enriched metagenome of Cassava obtained through nanopore sequencing.},
journal = {Data in brief},
volume = {63},
number = {},
pages = {112204},
pmid = {41215794},
issn = {2352-3409},
abstract = {The dataset presented here was obtained by sequencing selected historic herbarium cassava samples collected across Nigeria. Total DNA was extracted from the samples using the CTAB method, after which the samples were enriched by Rolling Circle Amplification (RCA) and then sequenced on the MinION. The dataset consists of raw sequencing data in FASTQ format reflecting microbial diversity in cassava leaf samples. Taxonomic classification of the samples using the Kraken2 PlusPFP-16 database revealed 12 kingdoms, 36 phyla, 67 classes, 154 orders, 273 families, 524 genera, and 895 species across the dataset, with a substantial proportion (77.9%) of reads remaining unclassified following host removal. The data is beneficial for exploring the microbiome diversity of cassava leaves across Nigeria, as well as serving as a reference for future microbial discovery, given the large number of unidentified reads in the dataset.},
}
RevDate: 2025-11-11
EUK nanozyme-loaded PL&GA coacervate droplets attenuate ulcerative colitis through restoring gut homeostasis and restricting intestinal cell ferroptosis.
Materials today. Bio, 35:102466.
Ulcerative colitis (UC), a prevalent form of inflammatory bowel disease (IBD), manifests as chronic diarrhea, abdominal pain, and bloody mucoid stools. Current treatment approaches for UC are typically limited by inadequate targeted delivery, premature gastrointestinal degradation, and systemic off-target effects. To address these challenges, we engineered PL&GA@EUK, EUK-134 nanozymes encapsulated in polylysine (PL) and glycyrrhizic acid (GA) coacervate droplets. PL&GA@EUK exhibited potent superoxide dismutase- and catalase-mimetic activities, scavenging hydroxyl radicals and demonstrating anti-inflammatory efficacy in both in vivo and in vitro models. In mice with dextran sulfate sodium-induced colitis, oral administration of PL&GA@EUK for 14 days significantly ameliorated the disease activity index and colonic damage. By maintaining the integrity of the intestinal mucosal barrier and modulating redox homeostasis, it protects the intestinal epithelial cells against ferroptosis, ultimately attenuating colitis progression. 16S rDNA sequencing revealed that PL&GA@EUK significantly enriched beneficial commensals, while suppressing opportunistic pathogens. Metabolomic analysis further indicated that it modulates lipid peroxidation-associated metabolites by regulating the biosynthesis of polyunsaturated fatty acids. Crucially, PL&GA@EUK achieved enhanced colon-targeted delivery with minimal systemic toxicity, thereby overcoming the key limitations of conventional treatments. The multifaceted mechanism of PL&GA@EUK, involving reactive oxygen species scavenging, gut microbiome remodeling, and ferroptosis suppression, underscores its immense promise for the clinical management of IBD.
Additional Links: PMID-41215769
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Citation:
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@article {pmid41215769,
year = {2025},
author = {Zhou, M and Lu, L and Xu, X and Zhou, Y and Fang, H and Wang, X and Li, D and Li, X and Hua, J and Liu, J and Li, Y and Jiang, L and Miao, Q and Wen, H and He, J and Yang, S},
title = {EUK nanozyme-loaded PL&GA coacervate droplets attenuate ulcerative colitis through restoring gut homeostasis and restricting intestinal cell ferroptosis.},
journal = {Materials today. Bio},
volume = {35},
number = {},
pages = {102466},
pmid = {41215769},
issn = {2590-0064},
abstract = {Ulcerative colitis (UC), a prevalent form of inflammatory bowel disease (IBD), manifests as chronic diarrhea, abdominal pain, and bloody mucoid stools. Current treatment approaches for UC are typically limited by inadequate targeted delivery, premature gastrointestinal degradation, and systemic off-target effects. To address these challenges, we engineered PL&GA@EUK, EUK-134 nanozymes encapsulated in polylysine (PL) and glycyrrhizic acid (GA) coacervate droplets. PL&GA@EUK exhibited potent superoxide dismutase- and catalase-mimetic activities, scavenging hydroxyl radicals and demonstrating anti-inflammatory efficacy in both in vivo and in vitro models. In mice with dextran sulfate sodium-induced colitis, oral administration of PL&GA@EUK for 14 days significantly ameliorated the disease activity index and colonic damage. By maintaining the integrity of the intestinal mucosal barrier and modulating redox homeostasis, it protects the intestinal epithelial cells against ferroptosis, ultimately attenuating colitis progression. 16S rDNA sequencing revealed that PL&GA@EUK significantly enriched beneficial commensals, while suppressing opportunistic pathogens. Metabolomic analysis further indicated that it modulates lipid peroxidation-associated metabolites by regulating the biosynthesis of polyunsaturated fatty acids. Crucially, PL&GA@EUK achieved enhanced colon-targeted delivery with minimal systemic toxicity, thereby overcoming the key limitations of conventional treatments. The multifaceted mechanism of PL&GA@EUK, involving reactive oxygen species scavenging, gut microbiome remodeling, and ferroptosis suppression, underscores its immense promise for the clinical management of IBD.},
}
RevDate: 2025-11-11
Gut microbiome, stress and interventional strategies using hardy animals.
Future science OA, 11(1):2583020.
The composition of the gut microbiota has been linked to acute stressors, suggesting that modulation of the gut microbiome is a potential avenue for enhancing human health and performance. The gut microbiome exerts its effects through several metabolites, which induce epigenetic and metabolic changes. Stress is a common occurrence in humans facing challenging environments such as military personnel and astronauts, but is not limited to humans. Among various species, crocodiles are well known for their "hardiness" and ability to achieve longevity, while surviving under stressful conditions. We speculated that their microbial gut flora produces substances contributing to their ability to resist stress, "wellbeing" and "longevity". Herein, we deliberate upon the stressors faced by individuals in testing conditions, and discuss potential avenues that can mitigate the gut microbiome compositional changes in order to augment human performance and overall health.
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@article {pmid41215695,
year = {2025},
author = {Siddiqui, R and Qaisar, R and Maciver, S and Khan, NA},
title = {Gut microbiome, stress and interventional strategies using hardy animals.},
journal = {Future science OA},
volume = {11},
number = {1},
pages = {2583020},
doi = {10.1080/20565623.2025.2583020},
pmid = {41215695},
issn = {2056-5623},
abstract = {The composition of the gut microbiota has been linked to acute stressors, suggesting that modulation of the gut microbiome is a potential avenue for enhancing human health and performance. The gut microbiome exerts its effects through several metabolites, which induce epigenetic and metabolic changes. Stress is a common occurrence in humans facing challenging environments such as military personnel and astronauts, but is not limited to humans. Among various species, crocodiles are well known for their "hardiness" and ability to achieve longevity, while surviving under stressful conditions. We speculated that their microbial gut flora produces substances contributing to their ability to resist stress, "wellbeing" and "longevity". Herein, we deliberate upon the stressors faced by individuals in testing conditions, and discuss potential avenues that can mitigate the gut microbiome compositional changes in order to augment human performance and overall health.},
}
RevDate: 2025-11-11
The Microbiome of the Seaweed Cultivar Ulva compressa (Chlorophyta) and Its Persistence Under Micropollutant Exposure.
Environmental microbiology reports, 17(6):e70230.
The green macroalga Ulva demonstrates exceptional growth rates, robustness, adaptability and potential for nitrogen and phosphorus removal; thus, it is a promising candidate for wastewater treatment and bioremediation. However, micropollutants in wastewater pose a potential threat to the holobiont. We explored the effects of emerging contaminants found in groundwater and wastewater on the microbiome of the cultivar Ulva compressa (conspecific with Ulva mutabilis). We identified the core microbiome by comparing the microbiome of the long-term cultivar (cultivated under laboratory conditions for over 70 years) with the native microbiome of U. compressa. Long-term cultivation was found to homogenise and reduce microbiome diversity; however, key functional taxa, including algal growth and morphogenesis-promoting bacteria, persisted. We subsequently challenged the core microbiome of the U. compressa cultivar with four antibiotics (chloramphenicol, erythromycin, oxytetracycline and sulfamethoxazole), two herbicides (atrazine, glyphosate) and three endocrine disruptors (bisphenol A, estradiol and ethinylestradiol). The micropollutants exerted distinct impacts, with antibiotics showing stronger effects than hormonal disruptors, which Ulva rapidly removes from the culture medium. In contrast, the microbiome did not contribute to the removal of these substances. These results indicate that although Ulva's microbiome is sensitive to environmental change, key functions with positive implications for aquaculture and ecosystem management are retained.
Additional Links: PMID-41215576
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PubMed:
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@article {pmid41215576,
year = {2025},
author = {Hardegen, J and Amend, G and Wichard, T},
title = {The Microbiome of the Seaweed Cultivar Ulva compressa (Chlorophyta) and Its Persistence Under Micropollutant Exposure.},
journal = {Environmental microbiology reports},
volume = {17},
number = {6},
pages = {e70230},
doi = {10.1111/1758-2229.70230},
pmid = {41215576},
issn = {1758-2229},
support = {//Graduietenakademie des Freistaats Thüringen/ ; 239748522//Deutsche Forschungsgemeinschaft/ ; 03ZU1214BB//Bundesministerium für Bildung und Forschung/ ; //European Cooperation in Science and Technology/ ; },
abstract = {The green macroalga Ulva demonstrates exceptional growth rates, robustness, adaptability and potential for nitrogen and phosphorus removal; thus, it is a promising candidate for wastewater treatment and bioremediation. However, micropollutants in wastewater pose a potential threat to the holobiont. We explored the effects of emerging contaminants found in groundwater and wastewater on the microbiome of the cultivar Ulva compressa (conspecific with Ulva mutabilis). We identified the core microbiome by comparing the microbiome of the long-term cultivar (cultivated under laboratory conditions for over 70 years) with the native microbiome of U. compressa. Long-term cultivation was found to homogenise and reduce microbiome diversity; however, key functional taxa, including algal growth and morphogenesis-promoting bacteria, persisted. We subsequently challenged the core microbiome of the U. compressa cultivar with four antibiotics (chloramphenicol, erythromycin, oxytetracycline and sulfamethoxazole), two herbicides (atrazine, glyphosate) and three endocrine disruptors (bisphenol A, estradiol and ethinylestradiol). The micropollutants exerted distinct impacts, with antibiotics showing stronger effects than hormonal disruptors, which Ulva rapidly removes from the culture medium. In contrast, the microbiome did not contribute to the removal of these substances. These results indicate that although Ulva's microbiome is sensitive to environmental change, key functions with positive implications for aquaculture and ecosystem management are retained.},
}
RevDate: 2025-11-11
Oral Bacterial Predator with "Catch-and-Kill" Functionality for Bacterial Enteritis via Selective Pathogen Capture and Sonodynamic Elimination.
ACS nano [Epub ahead of print].
Bacterial enteritis necessitates innovative therapeutic strategies to overcome the significant limitations posed by conventional antibiotics. Here, we introduce a pioneering antibacterial approach, employing a multifaceted "catch-and-kill" mechanism that synergistically integrates targeted pathogen capture, sonodynamic eradication, and toxin neutralization. We present SonoMMT, a microfluidically engineered sonosensitizer-montmorillonite complex. SonoMMT selectively adsorbs pathogenic bacteria and bacterial toxins, shields encapsulated sonosensitizers from gastric degradation, and enables sonodynamic therapy. Upon ultrasound activation, SonoMMT generates localized reactive oxygen species (ROS), efficiently eliminating captured pathogens and neutralizing residual toxins while preserving host cell integrity. In vitro assessments demonstrate robust antibacterial efficacy against bacteria. In vivo studies using a Salmonella typhimurium (S. typhimurium)-induced enteritis mouse model confirm that orally delivered SonoMMT significantly reduces bacterial loads, toxin levels, intestinal inflammation, and tissue damage. Moreover, gut microbiome analysis reveals beneficial shifts in microbial composition post-treatment, underscoring SonoMMT's dual action in pathogen clearance and microbiome restoration. Thus, SonoMMT represents a transformative advancement in bacterial enteritis management.
Additional Links: PMID-41215556
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PubMed:
Citation:
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@article {pmid41215556,
year = {2025},
author = {Chen, W and Zhu, J and Chen, K and Zhou, A and Li, J and Ning, X and Kong, D},
title = {Oral Bacterial Predator with "Catch-and-Kill" Functionality for Bacterial Enteritis via Selective Pathogen Capture and Sonodynamic Elimination.},
journal = {ACS nano},
volume = {},
number = {},
pages = {},
doi = {10.1021/acsnano.5c15064},
pmid = {41215556},
issn = {1936-086X},
abstract = {Bacterial enteritis necessitates innovative therapeutic strategies to overcome the significant limitations posed by conventional antibiotics. Here, we introduce a pioneering antibacterial approach, employing a multifaceted "catch-and-kill" mechanism that synergistically integrates targeted pathogen capture, sonodynamic eradication, and toxin neutralization. We present SonoMMT, a microfluidically engineered sonosensitizer-montmorillonite complex. SonoMMT selectively adsorbs pathogenic bacteria and bacterial toxins, shields encapsulated sonosensitizers from gastric degradation, and enables sonodynamic therapy. Upon ultrasound activation, SonoMMT generates localized reactive oxygen species (ROS), efficiently eliminating captured pathogens and neutralizing residual toxins while preserving host cell integrity. In vitro assessments demonstrate robust antibacterial efficacy against bacteria. In vivo studies using a Salmonella typhimurium (S. typhimurium)-induced enteritis mouse model confirm that orally delivered SonoMMT significantly reduces bacterial loads, toxin levels, intestinal inflammation, and tissue damage. Moreover, gut microbiome analysis reveals beneficial shifts in microbial composition post-treatment, underscoring SonoMMT's dual action in pathogen clearance and microbiome restoration. Thus, SonoMMT represents a transformative advancement in bacterial enteritis management.},
}
RevDate: 2025-11-11
Dietary intervention with sourdough and high-fiber breads enhances metabolic and microbial homeostasis in mice.
Food research international (Ottawa, Ont.), 221(Pt 3):117433.
Sourdough (WBS) and high-fiber (HFB) breads are increasingly recognized for their metabolic health benefits. In this study, sourdough bread was prepared using lactic acid bacteria mixture (SPC Health Guard™), while Roman Meal whole grain bread served as the high-fiber bread variant. A 10-week mouse feeding experiment compared their physiological, immunological, and gut microbiome effects against conventional white bread (WB). Both WBS and HFB significantly reduced postprandial blood glucose levels and serum low-density lipoprotein (LDL) cholesterol. The incremental area under the curve (iAUC) of serum glucose was reduced by 61.7 % in WBS and 42.0 % in HFB groups. Notably, magnesium absorption was enhanced in the HFB group. Colonic cytokine analysis revealed decreased expression of pro-inflammatory markers (tumor necrosis factor-α; TNF-α, interleukin-6; IL-6) and increased anti-inflammatory interleukin-10 (IL-10) in both WBS and HFB groups, suggesting immune modulation through sourdough fermentation processes. Microbiome profiling showed HFB induced more extensive changes than WBS, enriching beneficial taxa including Eubacterium coprostanoligenes, Faecalibaculum, and Parasutterella, which are linked to lipid metabolism and anti-inflammatory effects. Metabolomic analysis identified shared elevations of DL-arginine and rhamnetin in both WBS and HFB groups, while HFB uniquely modulated amino acid and unsaturated fatty acid metabolism. Additionally, HFB-fed mice exhibited significantly higher levels of short-chain fatty acids (SCFAs), particularly acetate and propionate, reflecting enhanced microbial activity. Overall, both sourdough and high-fiber breads demonstrated metabolic and anti-inflammatory benefits. However, high-fiber bread showed broader effects on gut microbiota and metabolome remodeling, emphasizing the importance of dietary fiber in promoting host-microbe interactions and metabolic health.
Additional Links: PMID-41214943
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PubMed:
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@article {pmid41214943,
year = {2025},
author = {Kim, YT and Kwak, JE and Kwon, JG and Lee, DY and Kim, HB and Lee, JH},
title = {Dietary intervention with sourdough and high-fiber breads enhances metabolic and microbial homeostasis in mice.},
journal = {Food research international (Ottawa, Ont.)},
volume = {221},
number = {Pt 3},
pages = {117433},
doi = {10.1016/j.foodres.2025.117433},
pmid = {41214943},
issn = {1873-7145},
abstract = {Sourdough (WBS) and high-fiber (HFB) breads are increasingly recognized for their metabolic health benefits. In this study, sourdough bread was prepared using lactic acid bacteria mixture (SPC Health Guard™), while Roman Meal whole grain bread served as the high-fiber bread variant. A 10-week mouse feeding experiment compared their physiological, immunological, and gut microbiome effects against conventional white bread (WB). Both WBS and HFB significantly reduced postprandial blood glucose levels and serum low-density lipoprotein (LDL) cholesterol. The incremental area under the curve (iAUC) of serum glucose was reduced by 61.7 % in WBS and 42.0 % in HFB groups. Notably, magnesium absorption was enhanced in the HFB group. Colonic cytokine analysis revealed decreased expression of pro-inflammatory markers (tumor necrosis factor-α; TNF-α, interleukin-6; IL-6) and increased anti-inflammatory interleukin-10 (IL-10) in both WBS and HFB groups, suggesting immune modulation through sourdough fermentation processes. Microbiome profiling showed HFB induced more extensive changes than WBS, enriching beneficial taxa including Eubacterium coprostanoligenes, Faecalibaculum, and Parasutterella, which are linked to lipid metabolism and anti-inflammatory effects. Metabolomic analysis identified shared elevations of DL-arginine and rhamnetin in both WBS and HFB groups, while HFB uniquely modulated amino acid and unsaturated fatty acid metabolism. Additionally, HFB-fed mice exhibited significantly higher levels of short-chain fatty acids (SCFAs), particularly acetate and propionate, reflecting enhanced microbial activity. Overall, both sourdough and high-fiber breads demonstrated metabolic and anti-inflammatory benefits. However, high-fiber bread showed broader effects on gut microbiota and metabolome remodeling, emphasizing the importance of dietary fiber in promoting host-microbe interactions and metabolic health.},
}
RevDate: 2025-11-11
Coprophagy prevention interfered with intestinal barrier, lipid metabolism, and immune performance in rabbits via microbe-gut-liver axis.
Animal microbiome, 7(1):117.
Additional Links: PMID-41214843
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@article {pmid41214843,
year = {2025},
author = {Li, R and Li, F and Guo, H and Li, S and Wang, J and Wang, C},
title = {Coprophagy prevention interfered with intestinal barrier, lipid metabolism, and immune performance in rabbits via microbe-gut-liver axis.},
journal = {Animal microbiome},
volume = {7},
number = {1},
pages = {117},
pmid = {41214843},
issn = {2524-4671},
support = {SDAIT-21-10//Funds of Shandong Province Modern Agricultural Technology System Innovation Team Program/ ; ZR2023MC144//Natural Science Foundation of Shandong Province/ ; 3237306//National Natural Science Foundation of China/ ; },
}
RevDate: 2025-11-11
Probiotics to reduce ventilator-associated pneumonia in adults with acute non‑anoxic brain injury: Study Protocol for a Double-Blind Multicenter Randomized International Clinical Trial (PROACT).
Trials, 26(1):484.
BACKGROUND: Ventilator-associated pneumonia (VAP) remains a significant complication among critically ill patients, with associated mortality approaching 50%. Despite the implementation of established preventive strategies, additional interventions are urgently needed to further reduce the incidence of VAP. Probiotic therapy has emerged as a promising adjunctive approach; the benefits of probiotic therapy may be more pronounced in critically ill patients without pre-existing infections. The PROACT study will evaluate the prophylactic role of probiotics in a critically ill population with acute brain injury to reduce the VAP incidence, while also exploring microbiological endpoints and mortality to refine patient selection criteria.
METHODS: The PROACT study is a prospective, randomized, double-blind, placebo-controlled, multicenter trial designed to evaluate the efficacy of probiotic prophylaxis in adult critically ill patients requiring invasive mechanical ventilation following acute brain injury (e.g., head trauma, ischemic or hemorrhagic stroke). Patients with suspected pulmonary aspiration or pre-existing pulmonary infections at enrollment are excluded to reduce confounding. Participants are randomized in a 1:1 ratio to receive either a placebo (glucose polymer) or a probiotic formulation containing Lactobacillus acidophilus LA-5, Lactobacillus plantarum, Bifidobacterium lactis BB12, and Saccharomyces boulardii. The assigned intervention is administered twice daily via nasogastric tube and oropharyngeal application for up to 30 days or until intensive care unit (ICU) discharge. The primary endpoint is the incidence of VAP, as defined by current international guidelines, in the intention-to-treat (ITT) population. Secondary endpoints include the incidence of VAP in the modified intention-to-treat (mITT) population, catheter-related bloodstream infections, occurrence of sepsis and septic shock, 30-day all-cause mortality, ICU length of stay, and duration of mechanical ventilation. The study is powered at 80% (α = 0.05) to detect a clinically meaningful difference based on effect size estimates based on the PROVAP study, requiring a total sample size of 208 patients. All participating centers implement standard VAP prevention bundles as part of routine care.
DISCUSSION: By evaluating the efficacy of probiotic therapy in preventing VAP and the impact on mortality among critically ill brain-injured patients, this trial has the potential to generate high-quality evidence supporting the incorporation of probiotics into standard VAP prevention protocols. The findings may have significant implications for clinical practice guidelines and public health policy related to infection control and microbiome-targeted interventions in the intensive care setting.
TRIAL REGISTRATION: Registered at ClinicalTrials.gov (identifier: [NCT06092554]). Registered on 2023-10-15.
Additional Links: PMID-41214813
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@article {pmid41214813,
year = {2025},
author = {Corriero, A and Soloperto, R and Giglio, M and Salvagno, M and Trerotoli, P and Grasso, S and Ribezzi, M and Mosca, A and Petrillo, C and De Toma, N and Magnesa, G and Giacomucci, A and Accattoli, R and Gadaleta, RM and Florio, M and Cariello, M and Moschetta, A and Puntillo, F and Taccone, FS and Ranieri, VM},
title = {Probiotics to reduce ventilator-associated pneumonia in adults with acute non‑anoxic brain injury: Study Protocol for a Double-Blind Multicenter Randomized International Clinical Trial (PROACT).},
journal = {Trials},
volume = {26},
number = {1},
pages = {484},
pmid = {41214813},
issn = {1745-6215},
abstract = {BACKGROUND: Ventilator-associated pneumonia (VAP) remains a significant complication among critically ill patients, with associated mortality approaching 50%. Despite the implementation of established preventive strategies, additional interventions are urgently needed to further reduce the incidence of VAP. Probiotic therapy has emerged as a promising adjunctive approach; the benefits of probiotic therapy may be more pronounced in critically ill patients without pre-existing infections. The PROACT study will evaluate the prophylactic role of probiotics in a critically ill population with acute brain injury to reduce the VAP incidence, while also exploring microbiological endpoints and mortality to refine patient selection criteria.
METHODS: The PROACT study is a prospective, randomized, double-blind, placebo-controlled, multicenter trial designed to evaluate the efficacy of probiotic prophylaxis in adult critically ill patients requiring invasive mechanical ventilation following acute brain injury (e.g., head trauma, ischemic or hemorrhagic stroke). Patients with suspected pulmonary aspiration or pre-existing pulmonary infections at enrollment are excluded to reduce confounding. Participants are randomized in a 1:1 ratio to receive either a placebo (glucose polymer) or a probiotic formulation containing Lactobacillus acidophilus LA-5, Lactobacillus plantarum, Bifidobacterium lactis BB12, and Saccharomyces boulardii. The assigned intervention is administered twice daily via nasogastric tube and oropharyngeal application for up to 30 days or until intensive care unit (ICU) discharge. The primary endpoint is the incidence of VAP, as defined by current international guidelines, in the intention-to-treat (ITT) population. Secondary endpoints include the incidence of VAP in the modified intention-to-treat (mITT) population, catheter-related bloodstream infections, occurrence of sepsis and septic shock, 30-day all-cause mortality, ICU length of stay, and duration of mechanical ventilation. The study is powered at 80% (α = 0.05) to detect a clinically meaningful difference based on effect size estimates based on the PROVAP study, requiring a total sample size of 208 patients. All participating centers implement standard VAP prevention bundles as part of routine care.
DISCUSSION: By evaluating the efficacy of probiotic therapy in preventing VAP and the impact on mortality among critically ill brain-injured patients, this trial has the potential to generate high-quality evidence supporting the incorporation of probiotics into standard VAP prevention protocols. The findings may have significant implications for clinical practice guidelines and public health policy related to infection control and microbiome-targeted interventions in the intensive care setting.
TRIAL REGISTRATION: Registered at ClinicalTrials.gov (identifier: [NCT06092554]). Registered on 2023-10-15.},
}
RevDate: 2025-11-11
Decoding the microbial assembly and environmental drivers along the phyllosphere-rhizosphere continuum of leguminous green manure Astragalus sinicus.
Environmental microbiome, 20(1):140.
Green manure crops are increasingly recognized not only for their contributions to soil fertility but also for their role in shaping plant-associated microbiome. Astragalus sinicus, a widely used leguminous green manure in East Asian paddy fields, harbors distinct microbial assemblages across plant compartments, yet the ecological processes driving microbiome assembly along its phyllosphere-rhizosphere continuum remain unclear. In this study, we profiled microbiome composition across the rhizospheric, phyllospheric, and soil compartments of A. sinicus using 16S rRNA gene amplicon sequencing targeting the region south of the Yangtze River, analyzing 315 samples collected from seven rice-growing regions. We found that Proteobacteria predominated all sampled compartments, with Mesorhizobium (75.85-96.93%) constituting the predominant taxon in the root microbiome. The leaf microbiome showed higher variability, dominated by Vibrionimonas (0.31-46.6%), Pantoea (0.71-46.61%), Pseudomonas (0.07-24.6%) and Bradyrhizobium (0.06-8.45%). Co-occurrence networks revealed a distinct gradient, including expansive yet weakly connected soil networks, moderately sized and highly modular leaf networks, and compact, highly robust root consortia, delineating a shift from environmentally driven complexity to host-filtered stability. Root and leaf microbiome assembly was primarily governed by stochastic processes (- 2 < β-NTI < 2, NCM r[2] > 70%) and plant- mediated selection (DI = 0.01/0.02, DSI = 0.09/0.14), with soil nutrient conditions, particularly total nitrogen, organic carbon, available phosphorus, and available potassiu, playing significant roles in shaping microbiome composition (p < 0.05). These core plant-associated ASVs were selectively enriched by the plant from the soil in over 70% of the sampled regions. Among these, Mesorhizobium in roots and Methylobacterium-Methylorubrum in leaves were found to be critical for nitrogen fixation and nutrient cycling, as evidenced by previous studies. Our results highlight the intricate interactions between plants, microbes, and their environment, underscoring the importance of plant-mediated selection and soil nutrient conditions in shaping the microbiome of A. sinicus, with significant implications for sustainable agricultural practices.
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@article {pmid41214749,
year = {2025},
author = {Huang, Y and Dai, S and Ma, W and Sun, Y and Xu, Y and Wang, H and Meng, L and Huang, Y and He, C and Shen, R and Luo, Y and Teng, Y},
title = {Decoding the microbial assembly and environmental drivers along the phyllosphere-rhizosphere continuum of leguminous green manure Astragalus sinicus.},
journal = {Environmental microbiome},
volume = {20},
number = {1},
pages = {140},
pmid = {41214749},
issn = {2524-6372},
support = {42130718//National Natural Science Foundation of China/ ; SQ2022RA24910167//National Science and Technology Innovation Leading Talents Program/ ; },
abstract = {Green manure crops are increasingly recognized not only for their contributions to soil fertility but also for their role in shaping plant-associated microbiome. Astragalus sinicus, a widely used leguminous green manure in East Asian paddy fields, harbors distinct microbial assemblages across plant compartments, yet the ecological processes driving microbiome assembly along its phyllosphere-rhizosphere continuum remain unclear. In this study, we profiled microbiome composition across the rhizospheric, phyllospheric, and soil compartments of A. sinicus using 16S rRNA gene amplicon sequencing targeting the region south of the Yangtze River, analyzing 315 samples collected from seven rice-growing regions. We found that Proteobacteria predominated all sampled compartments, with Mesorhizobium (75.85-96.93%) constituting the predominant taxon in the root microbiome. The leaf microbiome showed higher variability, dominated by Vibrionimonas (0.31-46.6%), Pantoea (0.71-46.61%), Pseudomonas (0.07-24.6%) and Bradyrhizobium (0.06-8.45%). Co-occurrence networks revealed a distinct gradient, including expansive yet weakly connected soil networks, moderately sized and highly modular leaf networks, and compact, highly robust root consortia, delineating a shift from environmentally driven complexity to host-filtered stability. Root and leaf microbiome assembly was primarily governed by stochastic processes (- 2 < β-NTI < 2, NCM r[2] > 70%) and plant- mediated selection (DI = 0.01/0.02, DSI = 0.09/0.14), with soil nutrient conditions, particularly total nitrogen, organic carbon, available phosphorus, and available potassiu, playing significant roles in shaping microbiome composition (p < 0.05). These core plant-associated ASVs were selectively enriched by the plant from the soil in over 70% of the sampled regions. Among these, Mesorhizobium in roots and Methylobacterium-Methylorubrum in leaves were found to be critical for nitrogen fixation and nutrient cycling, as evidenced by previous studies. Our results highlight the intricate interactions between plants, microbes, and their environment, underscoring the importance of plant-mediated selection and soil nutrient conditions in shaping the microbiome of A. sinicus, with significant implications for sustainable agricultural practices.},
}
RevDate: 2025-11-11
Transport stress alters serum biochemistry and gut microbiota in Tibetan sheep (ovis aries): a 30-day recovery assessment.
BMC microbiology, 25(1):726.
BACKGROUND: Transport stress poses a major challenge to the livestock industry. Studies have shown that transportation stress can cause depression, elevated body temperature and dysbiosis of intestinal microbiota in meat goats, and in severe cases, even lead to death of the animals, which in turn affects the economic efficiency of the farming industry. However, the changes in blood biochemical indicators and flora of Tibetan sheep throughout the receiving period after long-distance transport remain unclear.
METHODS: In this study, six 7-month-old Tibetan sheep with similar body weights were selected for a 30-d transport trial, and blood and faecal samples were collected for blood biochemical indices and 16 S microbiome sequencing before transport (BT), and on day 1 (AT 1), day 16 (AT 16), and day 30 (AT 30) after the end of the transport, respectively.
RESULT: And a number of blood biochemical indices (creatine kinase (CK), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), aspartate aminotransferase (AST), cortisol (COR), and adrenocorticotropic hormone (ACTH)) were significantly elevated (P < 0.05). Combined analysis of physiological and biochemical indices with 16 S rDNA sequencing showed that Turicibacter, Romboutsia and Clostridium_sensu_stricto_1 were positively correlated with LDH, ALP, CK, AST, and ACTH, while Prevotellaceae_UCG_004 was negatively correlated. Furthermore, the observed recovery trends in vital signs after AT 16 suggest that Tibetan sheep may be able to adapt to the new environment within one month post-transport. The present study illustrated the effects of transport without measures on the vital signs, serum biochemical indicators and faecal microorganisms of Tibetan sheep throughout the receiving period, which is of great significance in guiding the transport of Tibetan sheep and solving the damage caused by transport stress on the economic benefits of the farming industry.
Additional Links: PMID-41214535
PubMed:
Citation:
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@article {pmid41214535,
year = {2025},
author = {Wang, R and Wang, M and Wang, J and Wang, P and Ou, J and Tang, W and Sun, G and Wang, Q and Cheng, X and Huang, Y and Chen, J and Zhang, Z and Ren, C},
title = {Transport stress alters serum biochemistry and gut microbiota in Tibetan sheep (ovis aries): a 30-day recovery assessment.},
journal = {BMC microbiology},
volume = {25},
number = {1},
pages = {726},
pmid = {41214535},
issn = {1471-2180},
support = {2022-NK-134//The Science and Technology Program of Qinghai Province/ ; 2023AH050981//The Scientific Research Project of Anhui Higher Education Institutions/ ; CARS-38//The National Modern Meat Sheep Industry Technology System/ ; },
abstract = {BACKGROUND: Transport stress poses a major challenge to the livestock industry. Studies have shown that transportation stress can cause depression, elevated body temperature and dysbiosis of intestinal microbiota in meat goats, and in severe cases, even lead to death of the animals, which in turn affects the economic efficiency of the farming industry. However, the changes in blood biochemical indicators and flora of Tibetan sheep throughout the receiving period after long-distance transport remain unclear.
METHODS: In this study, six 7-month-old Tibetan sheep with similar body weights were selected for a 30-d transport trial, and blood and faecal samples were collected for blood biochemical indices and 16 S microbiome sequencing before transport (BT), and on day 1 (AT 1), day 16 (AT 16), and day 30 (AT 30) after the end of the transport, respectively.
RESULT: And a number of blood biochemical indices (creatine kinase (CK), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), aspartate aminotransferase (AST), cortisol (COR), and adrenocorticotropic hormone (ACTH)) were significantly elevated (P < 0.05). Combined analysis of physiological and biochemical indices with 16 S rDNA sequencing showed that Turicibacter, Romboutsia and Clostridium_sensu_stricto_1 were positively correlated with LDH, ALP, CK, AST, and ACTH, while Prevotellaceae_UCG_004 was negatively correlated. Furthermore, the observed recovery trends in vital signs after AT 16 suggest that Tibetan sheep may be able to adapt to the new environment within one month post-transport. The present study illustrated the effects of transport without measures on the vital signs, serum biochemical indicators and faecal microorganisms of Tibetan sheep throughout the receiving period, which is of great significance in guiding the transport of Tibetan sheep and solving the damage caused by transport stress on the economic benefits of the farming industry.},
}
RevDate: 2025-11-11
Probiotics restore GABAergic neurons and attenuate postnatal seizures in periventricular leukomalacia.
Nutritional neuroscience [Epub ahead of print].
Objectives: Postnatal epilepsy often arises after periventricular leukomalacia (PVL) in preterm infants and resists to treatment. Its underlying mechanisms and potential preventive strategies remain unclear. Probiotics, known to alleviate microbial dysbiosis and reduce inflammation, may offer therapeutic benefits.Methods: PVL injure was conducted using a combination of hypoxia-ischemia and lipopolysaccharide treatment. The rats were evaluated for seizure susceptibility, neuroinflammation, GABAergic neurons, and gut microbiota composition before and after probiotic administration. The probiotic formulation included Lactobacillus rhamnosus, Lactobacillus casei, Bifidobacterium bifidum, Bifidobacterium lactis, Bifidobacterium longum and Bifidobacterium breve in galacto-oligosaccharide and Fructooligosaccharides.Results: PVL rats exhibited microgliosis, reduced density of premyelinating oligodendrocytes, and decreased myelin expression (all P < 0.05). At postnatal days 85-90, these rats showed a significantly higher frequency of electrographic seizures and longer total seizure duration (P < 0.05). A significant reduction in cortical GABAergic neurons, particularly somatostatin-positive interneurons, was also observed in PVL rats compared to controls (P < 0.01). Treatment with probiotics restored GABAergic neurons and significantly reduced seizure frequency and duration (P < 0.05). Additionally, probiotics modulated gut microbiota composition and increased levels of butyric acid in both fecal samples and cerebrospinal fluid (CSF) (P < 0.05). Probiotic treatment also reduced cortical microglial activation and lowered CSF levels of the proinflammatory cytokine TNF-α.Conclusion: Probiotic supplementation may reduce seizure activity following PVL brain injury by mitigating neuroinflammation and restoring GABAergic neurons via the gut-brain axis. These findings suggest that probiotics could serve as a promising adjuvant therapy for preventing epilepsy after PVL.
Additional Links: PMID-41214530
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@article {pmid41214530,
year = {2025},
author = {Chen, JS and Tu, MJ and Chang, YM and Tu, YF and Chiang, CW},
title = {Probiotics restore GABAergic neurons and attenuate postnatal seizures in periventricular leukomalacia.},
journal = {Nutritional neuroscience},
volume = {},
number = {},
pages = {1-14},
doi = {10.1080/1028415X.2025.2574964},
pmid = {41214530},
issn = {1476-8305},
abstract = {Objectives: Postnatal epilepsy often arises after periventricular leukomalacia (PVL) in preterm infants and resists to treatment. Its underlying mechanisms and potential preventive strategies remain unclear. Probiotics, known to alleviate microbial dysbiosis and reduce inflammation, may offer therapeutic benefits.Methods: PVL injure was conducted using a combination of hypoxia-ischemia and lipopolysaccharide treatment. The rats were evaluated for seizure susceptibility, neuroinflammation, GABAergic neurons, and gut microbiota composition before and after probiotic administration. The probiotic formulation included Lactobacillus rhamnosus, Lactobacillus casei, Bifidobacterium bifidum, Bifidobacterium lactis, Bifidobacterium longum and Bifidobacterium breve in galacto-oligosaccharide and Fructooligosaccharides.Results: PVL rats exhibited microgliosis, reduced density of premyelinating oligodendrocytes, and decreased myelin expression (all P < 0.05). At postnatal days 85-90, these rats showed a significantly higher frequency of electrographic seizures and longer total seizure duration (P < 0.05). A significant reduction in cortical GABAergic neurons, particularly somatostatin-positive interneurons, was also observed in PVL rats compared to controls (P < 0.01). Treatment with probiotics restored GABAergic neurons and significantly reduced seizure frequency and duration (P < 0.05). Additionally, probiotics modulated gut microbiota composition and increased levels of butyric acid in both fecal samples and cerebrospinal fluid (CSF) (P < 0.05). Probiotic treatment also reduced cortical microglial activation and lowered CSF levels of the proinflammatory cytokine TNF-α.Conclusion: Probiotic supplementation may reduce seizure activity following PVL brain injury by mitigating neuroinflammation and restoring GABAergic neurons via the gut-brain axis. These findings suggest that probiotics could serve as a promising adjuvant therapy for preventing epilepsy after PVL.},
}
RevDate: 2025-11-10
Metabolome-driven microbiome assembly in ginger (Zingiber officinale) enhances nutrient cycling and crop yield through keystone taxa.
Communications biology, 8(1):1547.
Plant microbiomes shape crop performance, but the mechanisms by which host-derived metabolites influence the recruitment and organisation of beneficial microbes-and how these affect crop yield-remain poorly understood. Few studies have linked multi-kingdom microbiome structure, metabolite profiles, and agronomic traits under field conditions. We integrated 16S rRNA and ITS amplicon sequencing with untargeted LC-MS/MS metabolomics across 36 samples from two Zingiber officinale (ginger) cultivars with contrasting yields. Bacterial communities were primarily shaped by stochastic processes (neutral model R[2] = 0.67-0.68), while fungal assembly was deterministic (βNTI < -2 in roots and rhizomes). The high-yield cultivar exhibited more complex co-occurrence networks (596 vs. 272 edges) and enrichment of keystone taxa, including Talaromyces and Devosia. Metabolomic profiling identified 586 unique compounds, with 24 enriched pathways in the high-yield cultivar, notably isoflavonoid biosynthesis and folate metabolism. Key host metabolites-Niazimin A and 1-oleoyl-lysophosphatidic acid-showed strong positive correlations (r > 0.75, P < 0.01) with nitrogen-fixing and growth-promoting microbes, whereas Oxindole correlated negatively. These findings suggest that host metabolic shifts and keystone microbes co-regulate microbiome structure and nutrient cycling. Our results provide mechanistic insight into microbiome-mediated yield differences and a basis for microbiome-informed crop design.
Additional Links: PMID-41214302
PubMed:
Citation:
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@article {pmid41214302,
year = {2025},
author = {Wang, W and He, W and Zhang, Y and Wang, X and Li, J and Zhang, X and Chu, B and Nie, Y and Portal-Gonzalez, N and Santos-Bermudez, R},
title = {Metabolome-driven microbiome assembly in ginger (Zingiber officinale) enhances nutrient cycling and crop yield through keystone taxa.},
journal = {Communications biology},
volume = {8},
number = {1},
pages = {1547},
pmid = {41214302},
issn = {2399-3642},
support = {32201546//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {Plant microbiomes shape crop performance, but the mechanisms by which host-derived metabolites influence the recruitment and organisation of beneficial microbes-and how these affect crop yield-remain poorly understood. Few studies have linked multi-kingdom microbiome structure, metabolite profiles, and agronomic traits under field conditions. We integrated 16S rRNA and ITS amplicon sequencing with untargeted LC-MS/MS metabolomics across 36 samples from two Zingiber officinale (ginger) cultivars with contrasting yields. Bacterial communities were primarily shaped by stochastic processes (neutral model R[2] = 0.67-0.68), while fungal assembly was deterministic (βNTI < -2 in roots and rhizomes). The high-yield cultivar exhibited more complex co-occurrence networks (596 vs. 272 edges) and enrichment of keystone taxa, including Talaromyces and Devosia. Metabolomic profiling identified 586 unique compounds, with 24 enriched pathways in the high-yield cultivar, notably isoflavonoid biosynthesis and folate metabolism. Key host metabolites-Niazimin A and 1-oleoyl-lysophosphatidic acid-showed strong positive correlations (r > 0.75, P < 0.01) with nitrogen-fixing and growth-promoting microbes, whereas Oxindole correlated negatively. These findings suggest that host metabolic shifts and keystone microbes co-regulate microbiome structure and nutrient cycling. Our results provide mechanistic insight into microbiome-mediated yield differences and a basis for microbiome-informed crop design.},
}
RevDate: 2025-11-10
A first examination of skin-transferred microbiota demonstrates the feasibility of utilizing microbes to determine the age of latent fingerprints: A proof-of-concept study.
Forensic science international, 378:112710 pii:S0379-0738(25)00354-8 [Epub ahead of print].
Friction ridge skin patterns, including latent fingerprints (LFs), have long been essential for human identification. However, traditional ridge examinations do not convey temporal information. The ability to estimate the Time-since-Deposition (TsDp) of LFs could provide valuable chronological context in criminal investigations, helping to reconstruct timelines and corroborate alibis. A recent study explored LF microbiota as potential biological "clocks" for TsDp estimations at the Phylum taxonomical rank. In that instance, it was revealed that the composition, relative abundance, and succession patterns of microorganisms varied over time. This dynamic nature made the transferred skin microbiome a promising candidate for investigating predictable temporal changes of LFs in semi-controlled environments, such as indoor locations. The present article further expands the taxonomic resolution of the original study by identifying time-dependent microbial taxa at the Family rank and suggesting specific temporal signatures through statistical analyses. The same experimental conditions were considered: three donors, hand washing conditions, and aging for 1, 7, 14, and 21 days. For this analysis, the relative abundance, presence, and temporal shifts were examined with a focus on time-variant taxa. The 16S rRNA gene (V4 region) sequencing revealed distinct temporal signatures across the observed time points and handwashing conditions. For example, in unwashed hands, the combined presence of Mycosphaerellaceae and Coxiellaceae indicated a freshly deposited LF. In contrast, under washed conditions, the presence of Ruminococcaceae and Beijerinckiaceae was associated with a recent deposition. These preliminary findings further demonstrate the potential of microbiome analysis as a forensic tool for estimating TsDp in LFs and are a feasibility study for further work.
Additional Links: PMID-41213205
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@article {pmid41213205,
year = {2025},
author = {De Alcaraz-Fossoul, J and Wang, Y and Marshall, PA and Liu, R and Broatch, J and Stasulli, NM and Cook, GD},
title = {A first examination of skin-transferred microbiota demonstrates the feasibility of utilizing microbes to determine the age of latent fingerprints: A proof-of-concept study.},
journal = {Forensic science international},
volume = {378},
number = {},
pages = {112710},
doi = {10.1016/j.forsciint.2025.112710},
pmid = {41213205},
issn = {1872-6283},
abstract = {Friction ridge skin patterns, including latent fingerprints (LFs), have long been essential for human identification. However, traditional ridge examinations do not convey temporal information. The ability to estimate the Time-since-Deposition (TsDp) of LFs could provide valuable chronological context in criminal investigations, helping to reconstruct timelines and corroborate alibis. A recent study explored LF microbiota as potential biological "clocks" for TsDp estimations at the Phylum taxonomical rank. In that instance, it was revealed that the composition, relative abundance, and succession patterns of microorganisms varied over time. This dynamic nature made the transferred skin microbiome a promising candidate for investigating predictable temporal changes of LFs in semi-controlled environments, such as indoor locations. The present article further expands the taxonomic resolution of the original study by identifying time-dependent microbial taxa at the Family rank and suggesting specific temporal signatures through statistical analyses. The same experimental conditions were considered: three donors, hand washing conditions, and aging for 1, 7, 14, and 21 days. For this analysis, the relative abundance, presence, and temporal shifts were examined with a focus on time-variant taxa. The 16S rRNA gene (V4 region) sequencing revealed distinct temporal signatures across the observed time points and handwashing conditions. For example, in unwashed hands, the combined presence of Mycosphaerellaceae and Coxiellaceae indicated a freshly deposited LF. In contrast, under washed conditions, the presence of Ruminococcaceae and Beijerinckiaceae was associated with a recent deposition. These preliminary findings further demonstrate the potential of microbiome analysis as a forensic tool for estimating TsDp in LFs and are a feasibility study for further work.},
}
RevDate: 2025-11-10
Periodontitis, Fusobacterium nucleatum, and Colorectal Carcinoma. A Review.
Neuro endocrinology letters, 46(4): pii:46042504 [Epub ahead of print].
Our review study addresses chronic periodontitis and its potential complications in the distal segments of the intestine and rectum. Subgingival colonization by gram-negative anaerobic bacteria such as Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Eikenella corrodens, and Fusobacterium nucleatum may, through haematogenous dissemination into non-oral tissues and organs, cause severe systemic diseases. In connection with colorectal carcinoma, the third most frequently diagnosed malignant tumor, special attention has been focused on the anaerobic rod Fusobacterium nucleatum, one of the key periodontal pathogens involved in periodontal pocket infections. A growing amount of direct and indirect evidence supports its role in the development, progression, and persistence of colorectal carcinoma in the distal colon and rectum. F. nucleatum possesses numerous virulence factors that underlie its remarkable infectious potential, not only within the oral cavity but also in the colonic environment, where they facilitate its integration into the dysbiotic microbiome and directly contribute to carcinogenesis in this region. Disruption of the physiological microbiota and colonization by F. nucleatum are now considered major drivers of malignant tumorigenesis in the distal colon. Several studies confirm the oral origin of F. nucleatum and its potential haematogenous spread into the intestinal microenvironment. Eradication of F. nucleatum from the colon is regarded as a crucial factor in achieving successful treatment outcomes for colorectal cancer (CRC). However, systemic administration of broad spectrum antibiotics adversely affects the composition of the normal gut microbiome, leading to microbial imbalance. For this reason, the elimination of F. nucleatum in the colon and rectum relies on a whole range of antibacterial agents that minimally disrupt the gut microbiota. Our eradication strategy for F. nucleatum emphasizes close cooperation between dentists or periodontologists and gastroenterologists or oncologists, targeting high-risk populations: patients with IBD, colorectal adenomas ≥1 cm, multiple polyps, or first-degree relatives with CRC diagnosed before age 60. These at risk patients undergo dental evaluation for periodontitis and gingivitis by collaborating dentists. Identified cases are treated using localized, comprehensive, and early eradication strategies targeting F. nucleatum and other periodontal pathogens within the periodontal pocket microenvironment. The primary objective of early interdisciplinary cooperation is to detect early stages of periodontitis with periodontal pocket depths of up to 4 mm. In such early forms of periodontitis, elimination of infection can be achieved through local approaches including scaling, deep scaling, and curettage, combined with the application of antibacterial solutions, varnishes, antimicrobial impregnated fibers, and, where appropriate, the use of periodontal lasers.
Additional Links: PMID-41213144
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@article {pmid41213144,
year = {2025},
author = {Straka, M and Borecová, P and Straka, M},
title = {Periodontitis, Fusobacterium nucleatum, and Colorectal Carcinoma. A Review.},
journal = {Neuro endocrinology letters},
volume = {46},
number = {4},
pages = {},
pmid = {41213144},
issn = {2354-4716},
abstract = {Our review study addresses chronic periodontitis and its potential complications in the distal segments of the intestine and rectum. Subgingival colonization by gram-negative anaerobic bacteria such as Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Eikenella corrodens, and Fusobacterium nucleatum may, through haematogenous dissemination into non-oral tissues and organs, cause severe systemic diseases. In connection with colorectal carcinoma, the third most frequently diagnosed malignant tumor, special attention has been focused on the anaerobic rod Fusobacterium nucleatum, one of the key periodontal pathogens involved in periodontal pocket infections. A growing amount of direct and indirect evidence supports its role in the development, progression, and persistence of colorectal carcinoma in the distal colon and rectum. F. nucleatum possesses numerous virulence factors that underlie its remarkable infectious potential, not only within the oral cavity but also in the colonic environment, where they facilitate its integration into the dysbiotic microbiome and directly contribute to carcinogenesis in this region. Disruption of the physiological microbiota and colonization by F. nucleatum are now considered major drivers of malignant tumorigenesis in the distal colon. Several studies confirm the oral origin of F. nucleatum and its potential haematogenous spread into the intestinal microenvironment. Eradication of F. nucleatum from the colon is regarded as a crucial factor in achieving successful treatment outcomes for colorectal cancer (CRC). However, systemic administration of broad spectrum antibiotics adversely affects the composition of the normal gut microbiome, leading to microbial imbalance. For this reason, the elimination of F. nucleatum in the colon and rectum relies on a whole range of antibacterial agents that minimally disrupt the gut microbiota. Our eradication strategy for F. nucleatum emphasizes close cooperation between dentists or periodontologists and gastroenterologists or oncologists, targeting high-risk populations: patients with IBD, colorectal adenomas ≥1 cm, multiple polyps, or first-degree relatives with CRC diagnosed before age 60. These at risk patients undergo dental evaluation for periodontitis and gingivitis by collaborating dentists. Identified cases are treated using localized, comprehensive, and early eradication strategies targeting F. nucleatum and other periodontal pathogens within the periodontal pocket microenvironment. The primary objective of early interdisciplinary cooperation is to detect early stages of periodontitis with periodontal pocket depths of up to 4 mm. In such early forms of periodontitis, elimination of infection can be achieved through local approaches including scaling, deep scaling, and curettage, combined with the application of antibacterial solutions, varnishes, antimicrobial impregnated fibers, and, where appropriate, the use of periodontal lasers.},
}
RevDate: 2025-11-10
Bacillus proteolyticus Enhances the Biocontrol of Needle Cast in Cathaya argyrophylla by Modulating Physiological Pathways and the Phyllosphere Microbiome.
Phytopathology [Epub ahead of print].
Cathaya argyrophylla, a relict species endemic to China in the Pinaceae family, is classified as endangered on the IUCN Red List of Threatened Species. Needle cast caused by the fungal pathogen Neofusicoccum parvum is one of the most prevalent diseases affecting C. argyrophylla, leading to needle discoloration and necrosis, which poses a serious threat to its growth. Currently, there is a lack of effective biological control methods for this disease. In this study, we isolated an endophytic bacterium, Bacillus proteolyticus X6-1, from healthy needles of C. argyrophylla. This strain demonstrated a 65.5% inhibition of N. parvum in vitro. The pot experiment demonstrated that after inoculation with B. proteolyticus X6-1, the disease incidence and index of needle cast in C. argyrophylla were reduced by 42% and 20.3% respectively. Given its potential efficacy against needle cast in C. argyrophylla, we employed co-culture techniques alongside transcriptomics and high-throughput sequencing to elucidate the biological control mechanisms of strain X6-1. Furthermore, X6-1 enhanced the photosynthetic activity and antioxidant enzyme levels of C. argyrophylla. Inoculation with the B. proteolyticus strain further altered the phyllosphere microbiome by promoting the enrichment of beneficial microorganisms while decreasing the abundance of Neofusicoccum spp. Transcriptomic analysis revealed that B. proteolyticus regulates key biological pathways associated with growth in C. argyrophylla. Moreover, strain X6-1 produces protease and β-glucanase enzymes, which which may contribute to its antifungal activity. Collectively, these findings suggest that B. proteolyticus may serve as an effective biocontrol agent for managing needle cast in C. argyrophylla.
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@article {pmid41213120,
year = {2025},
author = {Wei, HJ and Lei, JJ and Wei, XL and Gou, W and Han, JH and Yu, C},
title = {Bacillus proteolyticus Enhances the Biocontrol of Needle Cast in Cathaya argyrophylla by Modulating Physiological Pathways and the Phyllosphere Microbiome.},
journal = {Phytopathology},
volume = {},
number = {},
pages = {},
doi = {10.1094/PHYTO-11-24-0346-R},
pmid = {41213120},
issn = {0031-949X},
abstract = {Cathaya argyrophylla, a relict species endemic to China in the Pinaceae family, is classified as endangered on the IUCN Red List of Threatened Species. Needle cast caused by the fungal pathogen Neofusicoccum parvum is one of the most prevalent diseases affecting C. argyrophylla, leading to needle discoloration and necrosis, which poses a serious threat to its growth. Currently, there is a lack of effective biological control methods for this disease. In this study, we isolated an endophytic bacterium, Bacillus proteolyticus X6-1, from healthy needles of C. argyrophylla. This strain demonstrated a 65.5% inhibition of N. parvum in vitro. The pot experiment demonstrated that after inoculation with B. proteolyticus X6-1, the disease incidence and index of needle cast in C. argyrophylla were reduced by 42% and 20.3% respectively. Given its potential efficacy against needle cast in C. argyrophylla, we employed co-culture techniques alongside transcriptomics and high-throughput sequencing to elucidate the biological control mechanisms of strain X6-1. Furthermore, X6-1 enhanced the photosynthetic activity and antioxidant enzyme levels of C. argyrophylla. Inoculation with the B. proteolyticus strain further altered the phyllosphere microbiome by promoting the enrichment of beneficial microorganisms while decreasing the abundance of Neofusicoccum spp. Transcriptomic analysis revealed that B. proteolyticus regulates key biological pathways associated with growth in C. argyrophylla. Moreover, strain X6-1 produces protease and β-glucanase enzymes, which which may contribute to its antifungal activity. Collectively, these findings suggest that B. proteolyticus may serve as an effective biocontrol agent for managing needle cast in C. argyrophylla.},
}
RevDate: 2025-11-10
Multi-Omics Advances in Major Depressive Disorder for Molecular Insights, Biomarker Discovery, and Therapeutic Development.
Aging and disease pii:AD.2025.1075 [Epub ahead of print].
Major depressive disorder (MDD) affects hundreds of millions worldwide and remains a major unmet clinical need because conventional monoaminergic agents achieve remission in fewer than half of patients and leave a substantial treatment-resistant subgroup. To address this gap, integrative multi-omics approaches, combined with computational systems biology, are being used to dissect its multifactorial etiology. Here, we review key findings from large Genome-wide association studies (GWAS), single-cell and spatial transcriptomics, proteomics, and metabolomics that converge on disrupted neuroplasticity, immune-inflammatory signaling, HPA-axis dysregulation, mitochondrial metabolism, and gut-brain interactions. We describe how AI-driven network modeling and structure-based drug design (SBDD) are translating multi-omics signals into candidate biomarkers and mechanism-based therapeutics, for example, N-methyl-D-aspartate/glutamatergic modulators, kappa opioid antagonists, anti-inflammatory agents, and epigenetic modulators. We highlighted the clinical implications, specifically molecularly stratified biomarkers for patient selection, trial enrichment, and structure-guided optimization of rapid-acting antidepressants and microbiome-based interventions. Finally, we discuss the limitations and immediate translational priorities that emphasize the trajectory from multi-omics discovery to precision psychiatry for MDD.
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@article {pmid41213078,
year = {2025},
author = {Elasbali, AM and Adnan, M and Ali, AS and Shamsi, A and Hassan, MI},
title = {Multi-Omics Advances in Major Depressive Disorder for Molecular Insights, Biomarker Discovery, and Therapeutic Development.},
journal = {Aging and disease},
volume = {},
number = {},
pages = {},
doi = {10.14336/AD.2025.1075},
pmid = {41213078},
issn = {2152-5250},
abstract = {Major depressive disorder (MDD) affects hundreds of millions worldwide and remains a major unmet clinical need because conventional monoaminergic agents achieve remission in fewer than half of patients and leave a substantial treatment-resistant subgroup. To address this gap, integrative multi-omics approaches, combined with computational systems biology, are being used to dissect its multifactorial etiology. Here, we review key findings from large Genome-wide association studies (GWAS), single-cell and spatial transcriptomics, proteomics, and metabolomics that converge on disrupted neuroplasticity, immune-inflammatory signaling, HPA-axis dysregulation, mitochondrial metabolism, and gut-brain interactions. We describe how AI-driven network modeling and structure-based drug design (SBDD) are translating multi-omics signals into candidate biomarkers and mechanism-based therapeutics, for example, N-methyl-D-aspartate/glutamatergic modulators, kappa opioid antagonists, anti-inflammatory agents, and epigenetic modulators. We highlighted the clinical implications, specifically molecularly stratified biomarkers for patient selection, trial enrichment, and structure-guided optimization of rapid-acting antidepressants and microbiome-based interventions. Finally, we discuss the limitations and immediate translational priorities that emphasize the trajectory from multi-omics discovery to precision psychiatry for MDD.},
}
RevDate: 2025-11-10
Thermophilic microbiome acclimation for enhanced anaerobic digestion of food waste: Optimization and performance evaluation.
PloS one, 20(11):e0336355.
Thermophilic anaerobic digestion (TAD) represents a promising approach for food waste (FW) treatment, offering significant advantages including accelerated reaction rates and increased volumetric biogas yield. However, the practical application of TAD is hindered by both the limited availability of thermophilic methanogenic consortia and heightened sensitivity to organic loading rate (OLR) fluctuations. In this study, a two-stage temperature shift strategy from mesophilic to thermophilic was implemented to establish a stable methanogenic community. The results showed that daily biogas yield increased steadily with rising fermentation temperature, reaching to a peak of 671.2 ml at 55 °C, which were 60.8% higher than that of mesophilic digestion. Microbial community analysis revealed that TAD increased the abundance of dominant hydrolytic bacteria (e.g., Defluviitoga) and hydrogenotrophic methanogen (e.g., Methanoculleus), consequently enhancing biogas production efficiency. Moreover, gradually increasing the OLR from 1.5 to 4 g VS/(L·d) significantly enhanced both biogas production and CH4 content, achieving a peak daily biogas yield of 2264.8 ml with sustained CH4 concentration stability (72-76%).
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@article {pmid41212895,
year = {2025},
author = {Shao, H and Yuan, C and Qiang, J and Hua, W and Cheng, Y and Wang, W},
title = {Thermophilic microbiome acclimation for enhanced anaerobic digestion of food waste: Optimization and performance evaluation.},
journal = {PloS one},
volume = {20},
number = {11},
pages = {e0336355},
pmid = {41212895},
issn = {1932-6203},
abstract = {Thermophilic anaerobic digestion (TAD) represents a promising approach for food waste (FW) treatment, offering significant advantages including accelerated reaction rates and increased volumetric biogas yield. However, the practical application of TAD is hindered by both the limited availability of thermophilic methanogenic consortia and heightened sensitivity to organic loading rate (OLR) fluctuations. In this study, a two-stage temperature shift strategy from mesophilic to thermophilic was implemented to establish a stable methanogenic community. The results showed that daily biogas yield increased steadily with rising fermentation temperature, reaching to a peak of 671.2 ml at 55 °C, which were 60.8% higher than that of mesophilic digestion. Microbial community analysis revealed that TAD increased the abundance of dominant hydrolytic bacteria (e.g., Defluviitoga) and hydrogenotrophic methanogen (e.g., Methanoculleus), consequently enhancing biogas production efficiency. Moreover, gradually increasing the OLR from 1.5 to 4 g VS/(L·d) significantly enhanced both biogas production and CH4 content, achieving a peak daily biogas yield of 2264.8 ml with sustained CH4 concentration stability (72-76%).},
}
RevDate: 2025-11-10
Salivary microbiome dysbiosis in patients with Alzheimer's disease.
Journal of Alzheimer's disease : JAD [Epub ahead of print].
BackgroundInvestigating human oral microbiota is now of great interest, being clinically significant for general and oral health. Many research studies have started to focus on the link between oral microbial dysbiosis and Alzheimer's disease. However, little is known about North African populations.ObjectiveWe aimed to distinguish the dissimilarity in the structure of microbial oral flora between the Alzheimer's disease patients and healthy controls in a Tunisian population.MethodsWe investigated the salivary microbiota using next-generation shotgun sequencing.ResultsThe overall structure of the oral microbial community of the Alzheimer's disease patient group was obviously different from the healthy control group. Significantly higher levels of Haemophilus (25.26%) were noticed in the AD group. However, Neisseria (10.17%) showed lower levels compared to the HC group. Considering the disease severity, Selenomonas and Aggregatibacter showed gradually higher levels as the disease progressed. Porphyromonas showed the highest levels in the mild stage of the disease, while Treponema, Selenomonas, and Peptostreptococcus were associated with severe stage. The presence of key taxa, Aggregatibacter and Selenomonas may constitute a dysbiosis signature in individuals with AD.ConclusionsThese findings may be of high relevance for orienting further studies on evaluating the physio-pathological process, confirming the implication of oral microbiota in AD and opening diagnostic and therapeutic avenues.
Additional Links: PMID-41212647
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PubMed:
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@article {pmid41212647,
year = {2025},
author = {Hamdi, A and Stathopoulou, P and Gharbi, A and Saadouli, I and Najjari, A and Kacem, I and Ouzari, HI and Bel Mokhtar, N and Tsiamis, G and Gouider, R and Klibi, N},
title = {Salivary microbiome dysbiosis in patients with Alzheimer's disease.},
journal = {Journal of Alzheimer's disease : JAD},
volume = {},
number = {},
pages = {13872877251393229},
doi = {10.1177/13872877251393229},
pmid = {41212647},
issn = {1875-8908},
abstract = {BackgroundInvestigating human oral microbiota is now of great interest, being clinically significant for general and oral health. Many research studies have started to focus on the link between oral microbial dysbiosis and Alzheimer's disease. However, little is known about North African populations.ObjectiveWe aimed to distinguish the dissimilarity in the structure of microbial oral flora between the Alzheimer's disease patients and healthy controls in a Tunisian population.MethodsWe investigated the salivary microbiota using next-generation shotgun sequencing.ResultsThe overall structure of the oral microbial community of the Alzheimer's disease patient group was obviously different from the healthy control group. Significantly higher levels of Haemophilus (25.26%) were noticed in the AD group. However, Neisseria (10.17%) showed lower levels compared to the HC group. Considering the disease severity, Selenomonas and Aggregatibacter showed gradually higher levels as the disease progressed. Porphyromonas showed the highest levels in the mild stage of the disease, while Treponema, Selenomonas, and Peptostreptococcus were associated with severe stage. The presence of key taxa, Aggregatibacter and Selenomonas may constitute a dysbiosis signature in individuals with AD.ConclusionsThese findings may be of high relevance for orienting further studies on evaluating the physio-pathological process, confirming the implication of oral microbiota in AD and opening diagnostic and therapeutic avenues.},
}
RevDate: 2025-11-10
Postbiotics: Novel Modulators of Gut Health, Metabolism, and Their Mechanisms of Action.
Probiotics and antimicrobial proteins [Epub ahead of print].
Postbiotics, defined as non-viable microbial cells, structural components, or metabolites, have recently emerged as promising modulators of gut health and metabolism. Unlike probiotics, they circumvent safety concerns associated with live microorganisms, including potential translocation, antibiotic resistance transfer, and viability loss during storage. Postbiotics encompass diverse bioactive compounds such as short-chain fatty acids (SCFAs), exopolysaccharides, bacteriocins, antioxidant enzymes, surface layer proteins, and bacterial lysates, each exerting distinct biological effects. Mechanistically, they enhance epithelial barrier function, regulate innate and adaptive immune responses, and modulate host gene expression through pattern recognition receptors and epigenetic modifications. SCFAs, particularly butyrate and propionate, improve intestinal homeostasis, insulin sensitivity, and anti-inflammatory signaling, while bacteriocins and EPSs display antibacterial, antiviral, anticancer, and immunomodulatory properties. Postbiotics also interfere with viral replication, inhibit pathogen adhesion, and attenuate inflammatory pathways, highlighting their multifunctional roles. Compared to probiotics and prebiotics, they offer superior safety, chemical stability, and clinical applicability, especially in vulnerable populations such as infants, elderly individuals, and immunocompromised patients. Preclinical and in vitro studies provide compelling evidence for their therapeutic potential in metabolic disorders, infections, cancer, and immune-mediated diseases; however, clinical data remain limited. Further research is required to establish standardized definitions, optimal formulations, dosing strategies, and regulatory frameworks to support their integration into functional nutrition and precision medicine. Collectively, postbiotics represent a next-generation approach to microbiota-targeted interventions, offering novel opportunities for disease prevention, adjunctive therapy, and the advancement of microbiome-based therapeutics.
Additional Links: PMID-41212512
PubMed:
Citation:
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@article {pmid41212512,
year = {2025},
author = {Eraghieh Farahani, H and Pourhajibagher, M and Asgharzadeh, S and Bahador, A},
title = {Postbiotics: Novel Modulators of Gut Health, Metabolism, and Their Mechanisms of Action.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {41212512},
issn = {1867-1314},
abstract = {Postbiotics, defined as non-viable microbial cells, structural components, or metabolites, have recently emerged as promising modulators of gut health and metabolism. Unlike probiotics, they circumvent safety concerns associated with live microorganisms, including potential translocation, antibiotic resistance transfer, and viability loss during storage. Postbiotics encompass diverse bioactive compounds such as short-chain fatty acids (SCFAs), exopolysaccharides, bacteriocins, antioxidant enzymes, surface layer proteins, and bacterial lysates, each exerting distinct biological effects. Mechanistically, they enhance epithelial barrier function, regulate innate and adaptive immune responses, and modulate host gene expression through pattern recognition receptors and epigenetic modifications. SCFAs, particularly butyrate and propionate, improve intestinal homeostasis, insulin sensitivity, and anti-inflammatory signaling, while bacteriocins and EPSs display antibacterial, antiviral, anticancer, and immunomodulatory properties. Postbiotics also interfere with viral replication, inhibit pathogen adhesion, and attenuate inflammatory pathways, highlighting their multifunctional roles. Compared to probiotics and prebiotics, they offer superior safety, chemical stability, and clinical applicability, especially in vulnerable populations such as infants, elderly individuals, and immunocompromised patients. Preclinical and in vitro studies provide compelling evidence for their therapeutic potential in metabolic disorders, infections, cancer, and immune-mediated diseases; however, clinical data remain limited. Further research is required to establish standardized definitions, optimal formulations, dosing strategies, and regulatory frameworks to support their integration into functional nutrition and precision medicine. Collectively, postbiotics represent a next-generation approach to microbiota-targeted interventions, offering novel opportunities for disease prevention, adjunctive therapy, and the advancement of microbiome-based therapeutics.},
}
RevDate: 2025-11-10
Mechanisms of Innate Immune Modulation by High-Fat Diet: Implications for Obesity and Asthma.
Current allergy and asthma reports, 25(1):51.
PURPOSE OF THE REVIEW: The innate immune system plays a critical role in mediating many of the physiological consequences of high-fat diet consumption. Dietary lipids, and specifically saturated fatty acids like palmitate and stearate, directly activate innate immune cells and alter the composition of the gut microbiome. Moreover, long-term high-fat diet feeding can induce chronic inflammation, adipose expansion, and the development of obesity. High-fat diet consumption and obesity also worsen the risk for chronic diseases like asthma.
RECENT FINDINGS: It is well known that high-fat diet feeding activates innate immune cells and alters the gut microbiome. However, emerging research provides new insight into the mechanisms by which high-fat diet feeding and obesity affect innate immunity and further disease development. These emerging mechanisms include the induction of lipid-associated macrophages (LAMs), innate immune memory, and innate-adaptive crosstalk leading to T cell exhaustion and granzyme K production. These novel mechanisms help us better understand the effect of high-fat diets on innate immunity, and future studies in these areas may help us better identify new therapeutic strategies for managing obesity and asthma.
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@article {pmid41212444,
year = {2025},
author = {Caslin, HL and Williams, JW},
title = {Mechanisms of Innate Immune Modulation by High-Fat Diet: Implications for Obesity and Asthma.},
journal = {Current allergy and asthma reports},
volume = {25},
number = {1},
pages = {51},
pmid = {41212444},
issn = {1534-6315},
support = {25TPA1471583//American Heart Association/ ; 25TPA1471583//American Heart Association/ ; },
abstract = {PURPOSE OF THE REVIEW: The innate immune system plays a critical role in mediating many of the physiological consequences of high-fat diet consumption. Dietary lipids, and specifically saturated fatty acids like palmitate and stearate, directly activate innate immune cells and alter the composition of the gut microbiome. Moreover, long-term high-fat diet feeding can induce chronic inflammation, adipose expansion, and the development of obesity. High-fat diet consumption and obesity also worsen the risk for chronic diseases like asthma.
RECENT FINDINGS: It is well known that high-fat diet feeding activates innate immune cells and alters the gut microbiome. However, emerging research provides new insight into the mechanisms by which high-fat diet feeding and obesity affect innate immunity and further disease development. These emerging mechanisms include the induction of lipid-associated macrophages (LAMs), innate immune memory, and innate-adaptive crosstalk leading to T cell exhaustion and granzyme K production. These novel mechanisms help us better understand the effect of high-fat diets on innate immunity, and future studies in these areas may help us better identify new therapeutic strategies for managing obesity and asthma.},
}
RevDate: 2025-11-10
Climate Change, Air Pollution and the Global Obesity Syndemic: a Review of Current Evidence.
Current obesity reports, 14(1):78.
PURPOSE OF REVIEW: Climate change and obesity are two converging global crises with complex and interrelated pathways. This review aims to synthesize recent evidence linking climate-related exposures, including rising ambient temperatures, air pollution, and urbanization to the pathogenesis of obesity. It also explores how obesity itself increases vulnerability to heat injury and environmental stress, highlighting the bidirectional nature of this syndemic.
RECENT FINDINGS: Epidemiologic evidence has supported associations between air pollution and increased body mass index, central adiposity, and metabolic dysfunction across the lifespan. Mechanistic research implicates impaired thermogenesis, chronic inflammation and oxidative stress, endocrine disruption, hypothalamic inflammation, and microbiome dysbiosis as key pathways linking environmental exposures to adiposity. Obesity further amplifies the physiological burden of climate-related stressors, such as heatwaves, due to reduced heat dissipation and altered hormonal responses. Anti-obesity medications may exacerbate heat-related risks via dehydration and gastrointestinal side effects. Urban greenness appears to offer a partial protective effect, modulating the obesogenic impact of air pollution and heat, particularly in low-income settings. Obesity and climate change share common socioeconomic, behavioral, and environmental drivers. Addressing this dual burden requires integrated strategies that promote environmental sustainability and metabolic health. These include green infrastructure, active transportation, climate-adapted clinical care, and public health strategies that reflect planetary health principles. Recognizing obesity not only as a medical condition but also as an environmentally influenced disorder is essential for effective, future-oriented prevention and intervention efforts.
Additional Links: PMID-41212427
PubMed:
Citation:
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@article {pmid41212427,
year = {2025},
author = {Vallianou, NG and Kounatidis, DC and Geladari, EV and Evangelopoulos, A and Kaldis, V and Stratigou, T and Evangelopoulos, AA and Karampela, I and Dalamaga, M},
title = {Climate Change, Air Pollution and the Global Obesity Syndemic: a Review of Current Evidence.},
journal = {Current obesity reports},
volume = {14},
number = {1},
pages = {78},
pmid = {41212427},
issn = {2162-4968},
abstract = {PURPOSE OF REVIEW: Climate change and obesity are two converging global crises with complex and interrelated pathways. This review aims to synthesize recent evidence linking climate-related exposures, including rising ambient temperatures, air pollution, and urbanization to the pathogenesis of obesity. It also explores how obesity itself increases vulnerability to heat injury and environmental stress, highlighting the bidirectional nature of this syndemic.
RECENT FINDINGS: Epidemiologic evidence has supported associations between air pollution and increased body mass index, central adiposity, and metabolic dysfunction across the lifespan. Mechanistic research implicates impaired thermogenesis, chronic inflammation and oxidative stress, endocrine disruption, hypothalamic inflammation, and microbiome dysbiosis as key pathways linking environmental exposures to adiposity. Obesity further amplifies the physiological burden of climate-related stressors, such as heatwaves, due to reduced heat dissipation and altered hormonal responses. Anti-obesity medications may exacerbate heat-related risks via dehydration and gastrointestinal side effects. Urban greenness appears to offer a partial protective effect, modulating the obesogenic impact of air pollution and heat, particularly in low-income settings. Obesity and climate change share common socioeconomic, behavioral, and environmental drivers. Addressing this dual burden requires integrated strategies that promote environmental sustainability and metabolic health. These include green infrastructure, active transportation, climate-adapted clinical care, and public health strategies that reflect planetary health principles. Recognizing obesity not only as a medical condition but also as an environmentally influenced disorder is essential for effective, future-oriented prevention and intervention efforts.},
}
RevDate: 2025-11-10
Erianin is a therapeutic candidate for addressing neuroinflammation triggered by intracerebral hemorrhage.
Langenbeck's archives of surgery, 411(1):10.
BACKGROUND: Neuroinflammation is a common consequence of intracerebral hemorrhage (ICH), leading to neurological impairments. Research indicates that the gut microbiome can influence neuroinflammatory responses. Erianin, is a potential therapeutic agent in the treatment of inflammation. Yet, the specific impact of erianin on ICH-induced inflammation and its interaction with the gut microbiome remain areas of ongoing investigation.
METHODS: ICH mouse model was established and treated with erianin. Neurobehavioral tests, brain water content, immunofluorescence, western blotting, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were performed to measure the neurological defects and neuroinflammation and neuron apoptosis. Immunofluorescent staining and western blotting assay were performed to assess the activation states of microglia and inflammation. The quantitative real-time polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), and FITC-dextran assays were utilized to measure the intestinal barrier integrity. The composition of the gut microbiota was analyzed by sequencing the 16 S rRNA extracted from fecal samples.
RESULTS: Administration of Erianin notably decreased inflammation in the brain and improved neurological function in ICH mice by inhibiting the proinflammatory activation of microglia. Additionally, Erianin bolstered intestinal barrier integrity, evidenced by decreased levels of lipopolysaccharide-binding protein. Furthermore, treatment with Erianin led to observable shifts in the gut microbiota. Notably, the activation of the ERK signaling pathway was found to counteract the neuroprotective effects of Erianin following ICH.
CONCLUSIONS: Erianin is a therapeutic candidate for addressing neuroinflammation triggered by ICH, with its mechanisms of action likely involving the modulation of ERK signaling and the gut microbiome.
Additional Links: PMID-41212347
PubMed:
Citation:
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@article {pmid41212347,
year = {2025},
author = {Li, SW and Wang, HC and Chen, MS},
title = {Erianin is a therapeutic candidate for addressing neuroinflammation triggered by intracerebral hemorrhage.},
journal = {Langenbeck's archives of surgery},
volume = {411},
number = {1},
pages = {10},
pmid = {41212347},
issn = {1435-2451},
abstract = {BACKGROUND: Neuroinflammation is a common consequence of intracerebral hemorrhage (ICH), leading to neurological impairments. Research indicates that the gut microbiome can influence neuroinflammatory responses. Erianin, is a potential therapeutic agent in the treatment of inflammation. Yet, the specific impact of erianin on ICH-induced inflammation and its interaction with the gut microbiome remain areas of ongoing investigation.
METHODS: ICH mouse model was established and treated with erianin. Neurobehavioral tests, brain water content, immunofluorescence, western blotting, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were performed to measure the neurological defects and neuroinflammation and neuron apoptosis. Immunofluorescent staining and western blotting assay were performed to assess the activation states of microglia and inflammation. The quantitative real-time polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), and FITC-dextran assays were utilized to measure the intestinal barrier integrity. The composition of the gut microbiota was analyzed by sequencing the 16 S rRNA extracted from fecal samples.
RESULTS: Administration of Erianin notably decreased inflammation in the brain and improved neurological function in ICH mice by inhibiting the proinflammatory activation of microglia. Additionally, Erianin bolstered intestinal barrier integrity, evidenced by decreased levels of lipopolysaccharide-binding protein. Furthermore, treatment with Erianin led to observable shifts in the gut microbiota. Notably, the activation of the ERK signaling pathway was found to counteract the neuroprotective effects of Erianin following ICH.
CONCLUSIONS: Erianin is a therapeutic candidate for addressing neuroinflammation triggered by ICH, with its mechanisms of action likely involving the modulation of ERK signaling and the gut microbiome.},
}
RevDate: 2025-11-10
Transcriptomic and functional responses of the cystic fibrosis airway epithelium to CFTR modulator therapy.
JCI insight, 10(21): pii:196018.
Elexacaftor/tezacaftor/ivacaftor (ETI) cystic fibrosis transmembrane conductance regulator (CFTR) modulator therapy has led to rapid and substantial improvements in cystic fibrosis (CF) airway disease. Underlying molecular and cellular mechanisms, long-term efficacy, and ability to reverse airway epithelial remodeling in established disease remain unclear. Longitudinal nasal brushes from an adult CF cohort were used to evaluate gene expression, cellular composition, stem cell function, and microbiome changes at baseline and at 6 months and 2 years after ETI. The baseline to 6 month span showed a massive downregulation of extensive neutrophilic inflammatory gene expression programs that correlated with increased pulmonary function and decreased sinusitis. Primary airway epithelial stem cell cultures from matched donor samples showed partially improved differentiation and barrier capacity at 6 months. Although clinical outcomes remained stable during the 6 month to 2 year span, transcriptional changes revealed a resurgence of baseline inflammatory programs. The time course of gene expression was consistent with ongoing normalization of epithelial remodeling. Relative abundance of Pseudomonas also decreased during the time course. These data suggest that ETI rectifies inflammation, epithelial remodeling, and bacterial infection in the airways, but resurgence of inflammatory gene expression may indicate ongoing inflammation, potentially presaging disease progression with long-term therapy.
Additional Links: PMID-41212059
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PubMed:
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@article {pmid41212059,
year = {2025},
author = {Vladar, EK and Gillen, AE and Yadav, S and Murphree, MR and Baraghoshi, D and Harris, JK and Pruesse, E and Niemiec, SS and Wilson, AW and Hisert, KB and Humphries, SM and Strand, M and Lynch, DA and Seibold, MA and Beswick, DM and Taylor-Cousar, JL},
title = {Transcriptomic and functional responses of the cystic fibrosis airway epithelium to CFTR modulator therapy.},
journal = {JCI insight},
volume = {10},
number = {21},
pages = {},
doi = {10.1172/jci.insight.196018},
pmid = {41212059},
issn = {2379-3708},
abstract = {Elexacaftor/tezacaftor/ivacaftor (ETI) cystic fibrosis transmembrane conductance regulator (CFTR) modulator therapy has led to rapid and substantial improvements in cystic fibrosis (CF) airway disease. Underlying molecular and cellular mechanisms, long-term efficacy, and ability to reverse airway epithelial remodeling in established disease remain unclear. Longitudinal nasal brushes from an adult CF cohort were used to evaluate gene expression, cellular composition, stem cell function, and microbiome changes at baseline and at 6 months and 2 years after ETI. The baseline to 6 month span showed a massive downregulation of extensive neutrophilic inflammatory gene expression programs that correlated with increased pulmonary function and decreased sinusitis. Primary airway epithelial stem cell cultures from matched donor samples showed partially improved differentiation and barrier capacity at 6 months. Although clinical outcomes remained stable during the 6 month to 2 year span, transcriptional changes revealed a resurgence of baseline inflammatory programs. The time course of gene expression was consistent with ongoing normalization of epithelial remodeling. Relative abundance of Pseudomonas also decreased during the time course. These data suggest that ETI rectifies inflammation, epithelial remodeling, and bacterial infection in the airways, but resurgence of inflammatory gene expression may indicate ongoing inflammation, potentially presaging disease progression with long-term therapy.},
}
RevDate: 2025-11-10
[Thematic priorities in oncology: analytical overview of publication trends and vectors of translational growth].
Problemy sotsial'noi gigieny, zdravookhraneniia i istorii meditsiny, 33(0):1069-1074.
Amid the rapid expansion of biomedical publications and the increasing complexity of the oncology research landscape, there is a growing need for a systematic analysis of thematic priorities that define global and national trajectories of scientific advancement. Oncology, as a field at the forefront of interdisciplinary innovation, spans domains from immune and cellular technologies to molecular imaging and epigenetic targets. Identifying frontier research areas that combine high scientific intensity, sustained international relevance, and translational potential is becoming a key tool for science policy and strategic planning. This study aims to map the most prominent oncology-related topics that emerged between 2021 and 2025, using data from the SciVal platform. A content-bibliometric analysis was conducted on the twenty leading thematic clusters in global oncology, followed by a comparative assessment of their representation in the Russian publication landscape. Metrics analyzed included publication output, field-weighted citation impact (FWCI), engagement dynamics, and institutional distribution. The results indicate that Russian research is contributing to several key topics, exhibiting high citation performance in niche areas such as exosomes, CAR-T therapy, radiomics, and immunotherapy for non-small cell lung cancer. However, many globally significant topics remain underrepresented in the Russian agenda, reflecting structural and human resource gaps in areas such as epigenetics, microbiome studies, precision immunomodulation, and regulated cell death mechanisms. These findings highlight both thematic gaps and institutional growth zones that require targeted support. Identifying advanced research areas positioned at the interface of scientific innovation and clinical applicability may inform the modernization of research infrastructure, the prioritization of national grant programs, and the integration of Russian research centers into global scientific consortia.
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@article {pmid41212006,
year = {2025},
author = {Alshevskaya, AA and Aksenova, EI and Khasanov, RY},
title = {[Thematic priorities in oncology: analytical overview of publication trends and vectors of translational growth].},
journal = {Problemy sotsial'noi gigieny, zdravookhraneniia i istorii meditsiny},
volume = {33},
number = {0},
pages = {1069-1074},
doi = {10.32687/0869-866X-2025-33-s2-1069-1074},
pmid = {41212006},
issn = {0869-866X},
abstract = {Amid the rapid expansion of biomedical publications and the increasing complexity of the oncology research landscape, there is a growing need for a systematic analysis of thematic priorities that define global and national trajectories of scientific advancement. Oncology, as a field at the forefront of interdisciplinary innovation, spans domains from immune and cellular technologies to molecular imaging and epigenetic targets. Identifying frontier research areas that combine high scientific intensity, sustained international relevance, and translational potential is becoming a key tool for science policy and strategic planning. This study aims to map the most prominent oncology-related topics that emerged between 2021 and 2025, using data from the SciVal platform. A content-bibliometric analysis was conducted on the twenty leading thematic clusters in global oncology, followed by a comparative assessment of their representation in the Russian publication landscape. Metrics analyzed included publication output, field-weighted citation impact (FWCI), engagement dynamics, and institutional distribution. The results indicate that Russian research is contributing to several key topics, exhibiting high citation performance in niche areas such as exosomes, CAR-T therapy, radiomics, and immunotherapy for non-small cell lung cancer. However, many globally significant topics remain underrepresented in the Russian agenda, reflecting structural and human resource gaps in areas such as epigenetics, microbiome studies, precision immunomodulation, and regulated cell death mechanisms. These findings highlight both thematic gaps and institutional growth zones that require targeted support. Identifying advanced research areas positioned at the interface of scientific innovation and clinical applicability may inform the modernization of research infrastructure, the prioritization of national grant programs, and the integration of Russian research centers into global scientific consortia.},
}
RevDate: 2025-11-10
Identification and characterization of a novel plaque-invisible lytic single-stranded RNA phage.
Journal of virology [Epub ahead of print].
The RNA phages offer promising applications in biotechnology, including vaccine development and drug delivery. However, their potential remains underexplored due to the limited number of known RNA phages, partly because conventional methods fail to identify plaque-invisible lytic phages that do not form plaques. Here, we introduced a novel method that combines RNA-inclusive metagenomic studies and quantitative reverse transcription-PCR (RMS-RT-qPCR) to identify and characterize active RNA phages from environmental samples. This study led to the discovery of a new active Qbeta-like phage, named Cute. Genomic analysis revealed that Cute is a new member of the Qubevirus genus. Although Cute does not form plaques, it can be observed to continuously release into the supernatant when co-cultured with the host by RT-qPCR detection. This discovery underscores the potential diversity of RNA phages in nature and the limitations of traditional culture-dependent techniques. Our findings suggest that RMS-RT-qPCR could aid in the discovery of active RNA phages with significant biotechnological applications.IMPORTANCEThe discovery and characterization of RNA phages might be historically constrained by traditional culture-based methods. Our study provides a powerful tool for identifying active RNA phages by combining RNA-inclusive metagenomic analysis with RT-qPCR. This method expands our understanding of the diversity and ecological roles of RNA phages, which are often overlooked in microbiome studies. This research highlights the importance of RNA phages in natural ecosystems and their potential applications in biotechnology and medicine, such as antimicrobial therapies and vaccine development. By expanding our understanding of RNA phage diversity, this study opens new avenues for their utilization in various fields, emphasizing the need for continued exploration of these versatile biological entities.
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PubMed:
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@article {pmid41211992,
year = {2025},
author = {Wang, Y and Tian, F and Zhang, J and Xu, S and Li, M and Tong, Y},
title = {Identification and characterization of a novel plaque-invisible lytic single-stranded RNA phage.},
journal = {Journal of virology},
volume = {},
number = {},
pages = {e0163724},
doi = {10.1128/jvi.01637-24},
pmid = {41211992},
issn = {1098-5514},
abstract = {The RNA phages offer promising applications in biotechnology, including vaccine development and drug delivery. However, their potential remains underexplored due to the limited number of known RNA phages, partly because conventional methods fail to identify plaque-invisible lytic phages that do not form plaques. Here, we introduced a novel method that combines RNA-inclusive metagenomic studies and quantitative reverse transcription-PCR (RMS-RT-qPCR) to identify and characterize active RNA phages from environmental samples. This study led to the discovery of a new active Qbeta-like phage, named Cute. Genomic analysis revealed that Cute is a new member of the Qubevirus genus. Although Cute does not form plaques, it can be observed to continuously release into the supernatant when co-cultured with the host by RT-qPCR detection. This discovery underscores the potential diversity of RNA phages in nature and the limitations of traditional culture-dependent techniques. Our findings suggest that RMS-RT-qPCR could aid in the discovery of active RNA phages with significant biotechnological applications.IMPORTANCEThe discovery and characterization of RNA phages might be historically constrained by traditional culture-based methods. Our study provides a powerful tool for identifying active RNA phages by combining RNA-inclusive metagenomic analysis with RT-qPCR. This method expands our understanding of the diversity and ecological roles of RNA phages, which are often overlooked in microbiome studies. This research highlights the importance of RNA phages in natural ecosystems and their potential applications in biotechnology and medicine, such as antimicrobial therapies and vaccine development. By expanding our understanding of RNA phage diversity, this study opens new avenues for their utilization in various fields, emphasizing the need for continued exploration of these versatile biological entities.},
}
RevDate: 2025-11-10
Impact of oral Chlamydia vaccination on host gut microbiome and metabolite composition.
mSystems [Epub ahead of print].
Chlamydia trachomatis, an intracellular pathogen, is recognized as the most common sexually transmitted bacterial infection among women worldwide. Chlamydia infections can lead to undesirable clinical outcomes, including pelvic inflammatory disease and infertility. Recently, the gut has been identified as a niche for Chlamydia colonization in human gut-derived organoids. However, despite the biological impact on the host remaining under investigation, oral inoculation of Chlamydia as a whole-organism vaccine has been reported as a promising strategy for preventing genital Chlamydia infections in mice. Few studies have evaluated the impact of oral Chlamydia vaccination on the gut microbiome and metabolite changes. In this study, we assessed time-series alterations in the gut microbiome and metabolites following oral Chlamydia muridarum inoculation in a mice model, and we analyzed the composition and correlation between serum immune parameters and the sequencing profiles in the host. We identified 129 microbial changes and 186 differentially abundant metabolites in the gut across various vaccination approaches during the 30-day immunization process. Additionally, we discussed the potential influence of live Chlamydia on gut epithelium and the biomarkers of effective immunization based on correlation analysis.IMPORTANCEChlamydia infections primarily lead to morbidity rather than mortality. Consequently, in developing and implementing a Chlamydia vaccine, the utmost priority is evaluation of safety. As a promising yet controversial approach, live oral vaccination for Chlamydia raises concerns regarding its impact on the host's gut environment. Our study not only investigates changes in the gut microbiome and metabolites during vaccination but also identifies changes in gut epithelium during vaccination and potential biomarkers during immunization. These findings are crucial for the development of whole-organism oral Chlamydia vaccines and provide valuable insights into the long-term colonization of Chlamydia in the gut.
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@article {pmid41211986,
year = {2025},
author = {Huang, Y and Wan, J and Shu, C and Yan, X and Ma, J and Zhang, T and He, J and Wan, Z and Li, G and Zhang, Q and Zhou, Z and Sun, X and Zhao, J and Zhang, P and Wang, L and Zhang, T and Tian, Q},
title = {Impact of oral Chlamydia vaccination on host gut microbiome and metabolite composition.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0128525},
doi = {10.1128/msystems.01285-25},
pmid = {41211986},
issn = {2379-5077},
abstract = {Chlamydia trachomatis, an intracellular pathogen, is recognized as the most common sexually transmitted bacterial infection among women worldwide. Chlamydia infections can lead to undesirable clinical outcomes, including pelvic inflammatory disease and infertility. Recently, the gut has been identified as a niche for Chlamydia colonization in human gut-derived organoids. However, despite the biological impact on the host remaining under investigation, oral inoculation of Chlamydia as a whole-organism vaccine has been reported as a promising strategy for preventing genital Chlamydia infections in mice. Few studies have evaluated the impact of oral Chlamydia vaccination on the gut microbiome and metabolite changes. In this study, we assessed time-series alterations in the gut microbiome and metabolites following oral Chlamydia muridarum inoculation in a mice model, and we analyzed the composition and correlation between serum immune parameters and the sequencing profiles in the host. We identified 129 microbial changes and 186 differentially abundant metabolites in the gut across various vaccination approaches during the 30-day immunization process. Additionally, we discussed the potential influence of live Chlamydia on gut epithelium and the biomarkers of effective immunization based on correlation analysis.IMPORTANCEChlamydia infections primarily lead to morbidity rather than mortality. Consequently, in developing and implementing a Chlamydia vaccine, the utmost priority is evaluation of safety. As a promising yet controversial approach, live oral vaccination for Chlamydia raises concerns regarding its impact on the host's gut environment. Our study not only investigates changes in the gut microbiome and metabolites during vaccination but also identifies changes in gut epithelium during vaccination and potential biomarkers during immunization. These findings are crucial for the development of whole-organism oral Chlamydia vaccines and provide valuable insights into the long-term colonization of Chlamydia in the gut.},
}
RevDate: 2025-11-10
Dynamic but constrained: repeated acquisitions of nutritional symbionts in bed bugs (Heteroptera: Cimicidae) from a narrow taxonomic pool.
mSystems [Epub ahead of print].
Bed bugs (Heteroptera: Cimicidae) harbor obligate bacterial symbionts that supplement their blood diet with missing nutrients, especially B vitamins. The primary symbiont, transovarially transmitted Wolbachia, is notable for a horizontally acquired biotin operon. Additional maternally inherited bacteria, including Symbiopectobacterium and Tisiphia, have been detected but are considered facultative and nonessential. However, nearly all current knowledge is derived from the human-associated Cimex lectularius, leaving symbiont diversity across more than 100 bed bug species largely unknown. Using amplicon and metagenomic data, we identified Wolbachia, Symbiopectobacterium, Sodalis, Serratia, and Tisiphia as candidate symbionts, with at least 16 independent acquisition events across the cimicid species, sometimes involving multiple strains per host. Phylogenetic comparisons indicated that some of these origins were followed by cospeciation. Wolbachia was present in most hosts except Cacodminae, where Symbiopectobacterium occurred as the sole symbiont, suggesting its obligate role. Analysis of 23 draft genomes revealed heterogeneity in size and gene content, consistent with varying stages of symbiotic reduction. Most lineages lost many biosynthetic pathways; only riboflavin and lipoic acid synthesis remained universally conserved. Our survey reveals a dynamic evolution of bed bug symbioses, with repeated symbiont acquisitions, cospeciation, and frequent coinfections. Despite independent origins, most symbionts belong to Wolbachia, Symbiopectobacterium, or Sodalis, implying unknown mechanisms shaping host specificity. Two points merit further study. First, Symbiopectobacterium as the sole obligate symbiont in Cacodminae suggests broader sampling may uncover greater symbiotic diversity. Second, uncertainties in biotin synthesis function call for deeper investigation into the evolution of this pathway in symbiotic bacteria.IMPORTANCEBed bugs are obligate blood-feeding insects that depend on bacterial partners to supply nutrients missing from their diet. Most previous research has focused on the human-associated species Cimex lectularius, leaving little known about symbiont diversity across other species. By surveying a broad phylogenetic range, we found that bed bugs have repeatedly acquired different bacteria as symbionts, including lineages not previously recognized as essential. Notably, finding Symbiopectobacterium as the sole symbiont in one subfamily shows that the nutritional partnerships in bed bugs are more dynamic than previously thought. At the same time, the majority of the 16 independent acquisitions involve only four bacterial genera, suggesting efficient mechanisms that constrain and shape bed bug-symbiont specificity.
Additional Links: PMID-41211985
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41211985,
year = {2025},
author = {Hypša, V and Martinů, J and Mahmood, S and Gupta, S and Nováková, E and Roth, S and Balvín, O},
title = {Dynamic but constrained: repeated acquisitions of nutritional symbionts in bed bugs (Heteroptera: Cimicidae) from a narrow taxonomic pool.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0124725},
doi = {10.1128/msystems.01247-25},
pmid = {41211985},
issn = {2379-5077},
abstract = {Bed bugs (Heteroptera: Cimicidae) harbor obligate bacterial symbionts that supplement their blood diet with missing nutrients, especially B vitamins. The primary symbiont, transovarially transmitted Wolbachia, is notable for a horizontally acquired biotin operon. Additional maternally inherited bacteria, including Symbiopectobacterium and Tisiphia, have been detected but are considered facultative and nonessential. However, nearly all current knowledge is derived from the human-associated Cimex lectularius, leaving symbiont diversity across more than 100 bed bug species largely unknown. Using amplicon and metagenomic data, we identified Wolbachia, Symbiopectobacterium, Sodalis, Serratia, and Tisiphia as candidate symbionts, with at least 16 independent acquisition events across the cimicid species, sometimes involving multiple strains per host. Phylogenetic comparisons indicated that some of these origins were followed by cospeciation. Wolbachia was present in most hosts except Cacodminae, where Symbiopectobacterium occurred as the sole symbiont, suggesting its obligate role. Analysis of 23 draft genomes revealed heterogeneity in size and gene content, consistent with varying stages of symbiotic reduction. Most lineages lost many biosynthetic pathways; only riboflavin and lipoic acid synthesis remained universally conserved. Our survey reveals a dynamic evolution of bed bug symbioses, with repeated symbiont acquisitions, cospeciation, and frequent coinfections. Despite independent origins, most symbionts belong to Wolbachia, Symbiopectobacterium, or Sodalis, implying unknown mechanisms shaping host specificity. Two points merit further study. First, Symbiopectobacterium as the sole obligate symbiont in Cacodminae suggests broader sampling may uncover greater symbiotic diversity. Second, uncertainties in biotin synthesis function call for deeper investigation into the evolution of this pathway in symbiotic bacteria.IMPORTANCEBed bugs are obligate blood-feeding insects that depend on bacterial partners to supply nutrients missing from their diet. Most previous research has focused on the human-associated species Cimex lectularius, leaving little known about symbiont diversity across other species. By surveying a broad phylogenetic range, we found that bed bugs have repeatedly acquired different bacteria as symbionts, including lineages not previously recognized as essential. Notably, finding Symbiopectobacterium as the sole symbiont in one subfamily shows that the nutritional partnerships in bed bugs are more dynamic than previously thought. At the same time, the majority of the 16 independent acquisitions involve only four bacterial genera, suggesting efficient mechanisms that constrain and shape bed bug-symbiont specificity.},
}
RevDate: 2025-11-10
Gut microbiota-derived tryptophan indole metabolites ameliorate collagen-induced arthritis in mice via aryl hydrocarbon receptor activation in T cells and intestinal epithelial cells.
Arthritis & rheumatology (Hoboken, N.J.) [Epub ahead of print].
OBJECTIVE: To investigate the specific role of tryptophan metabolism, especially that of microbiome-derived metabolites, in the development of rheumatoid arthritis (RA).
METHODS: We employed metabolomics to profile metabolites in 53 high-risk for RA individuals (PreRAs), 30 established RA patients and 38 healthy individuals. Fecal microbiota transplantation (FMT) and collagen-induced arthritis (CIA) mouse models were used to investigate the impact of gut microbiome on arthritis severity, gut barrier function, and metabolic change. Treg cell differentiation and epithelial cells' barrier function were assessed by flow cytometry, immunofluoresence staining and western blotting. Co-immunoprecipitation and luciferase were applied for molecular mechanism studies.
RESULTS: Dysregulated tryptophan metabolism exists in RA and PreRA individuals, as well as in FMT mice, characterized by a shift toward the kynurenine pathway and reduced activity of serotonin and indole pathways. Indole-3-lactic acid (ILA) and indole-3-acetic acid (IAA) significantly alleviated arthritis in CIA mice by expanding Treg cells via the classical aryl hydrocarbon receptor (AhR)-aryl hydrocarbon receptor nuclear translocator (ARNT)-xenobiotic response element (XRE) signaling pathway. Moreover, ILA repaired the leaking gut by increasing Zo-1 and occludin expression in Caco-2 cells, which was blocked by AhR antagonist CH223191. Moreover, CH223191 treatment could significantly reverse the improving effects of ILA and IAA on arthritis in mice.
CONCLUSION: These findings indicate that Trp indole metabolites may play a negative regulatory role in the progression of RA by affecting Treg cell development and intestinal gut barrier function.
Additional Links: PMID-41211636
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41211636,
year = {2025},
author = {Wu, L and Zhang, Q and Tang, Z and Li, Y and Wu, T and Chen, L and Tan, C and Zhang, L and Ji, X and Zhang, S and Wu, Y and Bozec, A and Zaiss, MM and Luo, Y},
title = {Gut microbiota-derived tryptophan indole metabolites ameliorate collagen-induced arthritis in mice via aryl hydrocarbon receptor activation in T cells and intestinal epithelial cells.},
journal = {Arthritis & rheumatology (Hoboken, N.J.)},
volume = {},
number = {},
pages = {},
doi = {10.1002/art.43430},
pmid = {41211636},
issn = {2326-5205},
abstract = {OBJECTIVE: To investigate the specific role of tryptophan metabolism, especially that of microbiome-derived metabolites, in the development of rheumatoid arthritis (RA).
METHODS: We employed metabolomics to profile metabolites in 53 high-risk for RA individuals (PreRAs), 30 established RA patients and 38 healthy individuals. Fecal microbiota transplantation (FMT) and collagen-induced arthritis (CIA) mouse models were used to investigate the impact of gut microbiome on arthritis severity, gut barrier function, and metabolic change. Treg cell differentiation and epithelial cells' barrier function were assessed by flow cytometry, immunofluoresence staining and western blotting. Co-immunoprecipitation and luciferase were applied for molecular mechanism studies.
RESULTS: Dysregulated tryptophan metabolism exists in RA and PreRA individuals, as well as in FMT mice, characterized by a shift toward the kynurenine pathway and reduced activity of serotonin and indole pathways. Indole-3-lactic acid (ILA) and indole-3-acetic acid (IAA) significantly alleviated arthritis in CIA mice by expanding Treg cells via the classical aryl hydrocarbon receptor (AhR)-aryl hydrocarbon receptor nuclear translocator (ARNT)-xenobiotic response element (XRE) signaling pathway. Moreover, ILA repaired the leaking gut by increasing Zo-1 and occludin expression in Caco-2 cells, which was blocked by AhR antagonist CH223191. Moreover, CH223191 treatment could significantly reverse the improving effects of ILA and IAA on arthritis in mice.
CONCLUSION: These findings indicate that Trp indole metabolites may play a negative regulatory role in the progression of RA by affecting Treg cell development and intestinal gut barrier function.},
}
RevDate: 2025-11-10
Polypharmacy, anticholinergic burden and oral microbiome among U.S. middle-aged and older adults: a representative national survey.
Journal of oral microbiology, 17(1):2580559.
OBJECTIVES: Polypharmacy has been linked to alterations in gut microbiota, but its effects on the oral microbiome remain underexplored. This study aimed to examine the association of polypharmacy and anticholinergic burden with oral microbiome diversity and composition.
METHODS: We conducted a cross-sectional analysis using data from NHANES 2009-2012, including participants aged 55-69 years who reported at least one prescription medication. Polypharmacy was defined as the concurrent use of five or more medications. Anticholinergic burden was quantified by the Anticholinergic Cognitive Burden scale and the Anticholinergic Drug Scale. Oral microbiome profiling comprised alpha diversity, beta diversity, and taxonomic composition at multiple phylogenetic levels. Associations were analyzed via weighted multivariable linear regression, principal coordinate analysis (PCoA), and multivariate analysis of variance.
RESULTS: Among 1,596 participants, 29.2% reported polypharmacy, which correlated with higher anticholinergic burden. Both polypharmacy and anticholinergic burden were inversely associated with alpha diversity across multiple measures. Taxonomic analyses showed heterogeneous associations, with Porphyromonadaceae negatively linked to both exposures. PCoA indicated significant differences in community structure by polypharmacy status (Bray-Curtis: R² = 0.35%, P < .001).
CONCLUSIONS: Among middle-aged and older U.S. adults, both polypharmacy and anticholinergic burden were inversely associated with oral microbiome diversity and linked to distinct microbiome composition.
Additional Links: PMID-41211602
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41211602,
year = {2025},
author = {Wei, K and Yang, Y and Chen, C and Yang, Y and Hu, K and Chen, Q},
title = {Polypharmacy, anticholinergic burden and oral microbiome among U.S. middle-aged and older adults: a representative national survey.},
journal = {Journal of oral microbiology},
volume = {17},
number = {1},
pages = {2580559},
pmid = {41211602},
issn = {2000-2297},
abstract = {OBJECTIVES: Polypharmacy has been linked to alterations in gut microbiota, but its effects on the oral microbiome remain underexplored. This study aimed to examine the association of polypharmacy and anticholinergic burden with oral microbiome diversity and composition.
METHODS: We conducted a cross-sectional analysis using data from NHANES 2009-2012, including participants aged 55-69 years who reported at least one prescription medication. Polypharmacy was defined as the concurrent use of five or more medications. Anticholinergic burden was quantified by the Anticholinergic Cognitive Burden scale and the Anticholinergic Drug Scale. Oral microbiome profiling comprised alpha diversity, beta diversity, and taxonomic composition at multiple phylogenetic levels. Associations were analyzed via weighted multivariable linear regression, principal coordinate analysis (PCoA), and multivariate analysis of variance.
RESULTS: Among 1,596 participants, 29.2% reported polypharmacy, which correlated with higher anticholinergic burden. Both polypharmacy and anticholinergic burden were inversely associated with alpha diversity across multiple measures. Taxonomic analyses showed heterogeneous associations, with Porphyromonadaceae negatively linked to both exposures. PCoA indicated significant differences in community structure by polypharmacy status (Bray-Curtis: R² = 0.35%, P < .001).
CONCLUSIONS: Among middle-aged and older U.S. adults, both polypharmacy and anticholinergic burden were inversely associated with oral microbiome diversity and linked to distinct microbiome composition.},
}
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