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ESP: PubMed Auto Bibliography 02 Jul 2025 at 01:48 Created:
Fecal Transplantation
Fecal Transplantion is a procedure in which fecal matter is collected from a tested donor, mixed with a saline or other solution, strained, and placed in a patient, by colonoscopy, endoscopy, sigmoidoscopy, or enema. The theory behind the procedure is that a normal gut microbial ecosystem is required for good health and that sometimes a benefucuial ecosystem can be destroyed, perhaps by antibiotics, allowing other bacteria, specifically Clostridium difficile to over-populate the colon, causing debilitating, sometimes fatal diarrhea. C. diff. is on the rise throughout the world. The CDC reports that approximately 347,000 people in the U.S. alone were diagnosed with this infection in 2012. Of those, at least 14,000 died. Fecal transplant has also had promising results with many other digestive or auto-immune diseases, including Irritable Bowel Syndrome, Crohn's Disease, and Ulcerative Colitis. It has also been used around the world to treat other conditions, although more research in other areas is needed. Fecal transplant was first documented in 4th century China, where the treatment was known as yellow soup.
Created with PubMed® Query: ( "(fecal OR faecal) (transplant OR transplantation)" OR "fecal microbiota transplant" ) NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2025-07-01
Fecal microbiota transplantation improves Sansui duck growth performance by balancing the cecal microbiome.
Scientific reports, 15(1):22403.
Improving growth performance is vital in poultry production. Although several studies have established associations between gut microbiota and growth, the direct impacts remain unclear. A total of 120 1-day-old Sansui ducks were randomly assigned to the FMT and CON groups. From the 1st day, ducks in the FMT group were orally administrated with 0.5 mL fecal microbiota suspension for three consecutive days, while sterile PBS solution was used as a substitute in the CON group. The results revealed that FMT improved average daily gain (ADG) (P < 0.001) and body weight (BW) (P < 0.001), with a tendency for a better feed conversion rate (FCR) (P = 0.062). LEfSe analysis indicated a significant increase in the abundance of the Lactobacillus (P < 0.001), Bifidobacterium (P = 0.006), Megamonas (P = 0.008), and Subdoligranulum (P = 0.005) in the FMT group. Similarly, the phyla Firmicutes/Bacteroidetes ratio was higher in the FMT group compared to the CON group. Additionally, the ACE, Chao, and Shannon indices were also significantly higher in the FMT group (P < 0.001). To sum up, FMT enhanced growth performance, which could be associated with reducing proinflammatory pathogen colonization in the duck cecum. This modulating effect likely results from increased microbial diversity and the enrichment of beneficial bacteria.
Additional Links: PMID-40593020
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@article {pmid40593020,
year = {2025},
author = {Yue, Y and Yao, B and Liao, F and He, Z and Sangsawad, P and Yang, S},
title = {Fecal microbiota transplantation improves Sansui duck growth performance by balancing the cecal microbiome.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {22403},
pmid = {40593020},
issn = {2045-2322},
support = {31960682//The National Nature Science Foundation of China/ ; 31960682//The National Nature Science Foundation of China/ ; 31960682//The National Nature Science Foundation of China/ ; 31960682//The National Nature Science Foundation of China/ ; 31960682//The National Nature Science Foundation of China/ ; },
abstract = {Improving growth performance is vital in poultry production. Although several studies have established associations between gut microbiota and growth, the direct impacts remain unclear. A total of 120 1-day-old Sansui ducks were randomly assigned to the FMT and CON groups. From the 1st day, ducks in the FMT group were orally administrated with 0.5 mL fecal microbiota suspension for three consecutive days, while sterile PBS solution was used as a substitute in the CON group. The results revealed that FMT improved average daily gain (ADG) (P < 0.001) and body weight (BW) (P < 0.001), with a tendency for a better feed conversion rate (FCR) (P = 0.062). LEfSe analysis indicated a significant increase in the abundance of the Lactobacillus (P < 0.001), Bifidobacterium (P = 0.006), Megamonas (P = 0.008), and Subdoligranulum (P = 0.005) in the FMT group. Similarly, the phyla Firmicutes/Bacteroidetes ratio was higher in the FMT group compared to the CON group. Additionally, the ACE, Chao, and Shannon indices were also significantly higher in the FMT group (P < 0.001). To sum up, FMT enhanced growth performance, which could be associated with reducing proinflammatory pathogen colonization in the duck cecum. This modulating effect likely results from increased microbial diversity and the enrichment of beneficial bacteria.},
}
RevDate: 2025-07-01
Fecal Microbiota Transplantation for Immune Regulation: Improving Ulcerative Colitis and Enhancing Cancer Immunotherapy.
International immunology pii:8180725 [Epub ahead of print].
The gut microbiota plays an integral role in maintaining health and regulating various host functions, including immune responses. Fecal microbiota transplantation (FMT) has emerged as a promising therapeutic approach to restore gut microbial balance. Although widely recognized for its efficacy in treating ulcerative colitis (UC), FMT is now being investigated as an adjuvant therapy to enhance the efficacy of immune checkpoint inhibitors (ICIs) in cancer treatment. This review summarizes the clinical applications of FMT in UC treatment and its potential role in cancer immunotherapy. FMT exhibits varying degrees of efficacy in the treatment of UC, with differences in outcomes attributed to variations in administration methods and donor selection. In cancer therapy, FMT has demonstrated the potential to improve ICI responses, particularly in patients with melanoma. However, its effects on other cancers remain unclear. Although FMT holds promise for UC and cancer immunotherapy, challenges such as inconsistent clinical outcomes and methodological variations persist. Standardized protocols and mechanistic studies are crucial to optimize FMT-based therapeutic strategies, and further research is required to establish its efficacy under diverse clinical conditions.
Additional Links: PMID-40592776
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@article {pmid40592776,
year = {2025},
author = {Zhang, X and Ishikawa, D and Nagahara, A},
title = {Fecal Microbiota Transplantation for Immune Regulation: Improving Ulcerative Colitis and Enhancing Cancer Immunotherapy.},
journal = {International immunology},
volume = {},
number = {},
pages = {},
doi = {10.1093/intimm/dxaf038},
pmid = {40592776},
issn = {1460-2377},
abstract = {The gut microbiota plays an integral role in maintaining health and regulating various host functions, including immune responses. Fecal microbiota transplantation (FMT) has emerged as a promising therapeutic approach to restore gut microbial balance. Although widely recognized for its efficacy in treating ulcerative colitis (UC), FMT is now being investigated as an adjuvant therapy to enhance the efficacy of immune checkpoint inhibitors (ICIs) in cancer treatment. This review summarizes the clinical applications of FMT in UC treatment and its potential role in cancer immunotherapy. FMT exhibits varying degrees of efficacy in the treatment of UC, with differences in outcomes attributed to variations in administration methods and donor selection. In cancer therapy, FMT has demonstrated the potential to improve ICI responses, particularly in patients with melanoma. However, its effects on other cancers remain unclear. Although FMT holds promise for UC and cancer immunotherapy, challenges such as inconsistent clinical outcomes and methodological variations persist. Standardized protocols and mechanistic studies are crucial to optimize FMT-based therapeutic strategies, and further research is required to establish its efficacy under diverse clinical conditions.},
}
RevDate: 2025-07-01
Reproducing in vitro artificial gut microbiota using glycerol stocks of fecal cultures combined with different prebiotic additives.
Journal of bioscience and bioengineering pii:S1389-1723(25)00136-7 [Epub ahead of print].
Artificial human microbiota can be produced in gut simulators from cryopreserved stocks. They are used for in vitro fermentation models and as alternative material for fecal microbiota transplantation therapy. However, current methods have limited information on microbial structure at the genus level and present challenges during cryopreservation. In this study, we used an edible glycerol stock of fecal batch culture instead of fresh feces to create artificial gut microbiota. Three glycerol stocks, generated through in vitro fecal fermentation with different prebiotic additives (such as fructooligosaccharide, xylan, pectin, and guar gum), were combined. Profiling via 16S rRNA gene amplicon sequencing revealed that the artificial gut microbiota derived from the combined glycerol stocks showed more amplicon sequence variants than those from a single glycerol stock. In the artificial microbiota, relative abundance values of common genera such as Bifidobacterium, Bacteroides, Prevotella, Faecalibacterium, and Escherichia were more than 10 % of those found in the original feces. Other commensal genera such as Collinsella, Anaerobutyricum hallii (formerly Eubacterium hallii) group, Anaerostipes, Blautia, Dorea, Lachnospiraceae UCG-004, and Oscillospiraceae UCG-003 were similarly maintained. Our data indicated that combining glycerol stocks of fecal cultures with different additives in a batch-type gut simulator is a useful option for producing artificial gut microbiota, the taxonomic compositions of which are comparable to those of the original feces.
Additional Links: PMID-40592615
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@article {pmid40592615,
year = {2025},
author = {Sasaki, K and Takeshima, Y and Fujino, A},
title = {Reproducing in vitro artificial gut microbiota using glycerol stocks of fecal cultures combined with different prebiotic additives.},
journal = {Journal of bioscience and bioengineering},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jbiosc.2025.06.002},
pmid = {40592615},
issn = {1347-4421},
abstract = {Artificial human microbiota can be produced in gut simulators from cryopreserved stocks. They are used for in vitro fermentation models and as alternative material for fecal microbiota transplantation therapy. However, current methods have limited information on microbial structure at the genus level and present challenges during cryopreservation. In this study, we used an edible glycerol stock of fecal batch culture instead of fresh feces to create artificial gut microbiota. Three glycerol stocks, generated through in vitro fecal fermentation with different prebiotic additives (such as fructooligosaccharide, xylan, pectin, and guar gum), were combined. Profiling via 16S rRNA gene amplicon sequencing revealed that the artificial gut microbiota derived from the combined glycerol stocks showed more amplicon sequence variants than those from a single glycerol stock. In the artificial microbiota, relative abundance values of common genera such as Bifidobacterium, Bacteroides, Prevotella, Faecalibacterium, and Escherichia were more than 10 % of those found in the original feces. Other commensal genera such as Collinsella, Anaerobutyricum hallii (formerly Eubacterium hallii) group, Anaerostipes, Blautia, Dorea, Lachnospiraceae UCG-004, and Oscillospiraceae UCG-003 were similarly maintained. Our data indicated that combining glycerol stocks of fecal cultures with different additives in a batch-type gut simulator is a useful option for producing artificial gut microbiota, the taxonomic compositions of which are comparable to those of the original feces.},
}
RevDate: 2025-07-01
CmpDate: 2025-07-01
Fecal microbiota transplantation: Current evidence and future directions.
Cleveland Clinic journal of medicine, 92(7):421-428 pii:92/7/421.
As we advance our understanding of the gut microbiota, the implications of dysbiosis are becoming increasingly apparent. Fecal microbiota transplantation (FMT), a well-established procedure, is recognized for effectively treating recurrent Clostridioides difficile infection, prompting further investigation into its other possible clinical applications. Donor selection and screening are essential to ensure safety and efficacy. Product development and standardization, such as the US Food and Drug Administration-approved live biotherapeutic products Rebyota and Vowst, are helping efforts to evaluate FMT for other gastrointestinal and extraintestinal diseases. However, additional clinical trials are needed to support its use beyond recurrent C difficile infection.
Additional Links: PMID-40592538
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@article {pmid40592538,
year = {2025},
author = {Cymbal, M and Chatterjee, A and Baggott, B},
title = {Fecal microbiota transplantation: Current evidence and future directions.},
journal = {Cleveland Clinic journal of medicine},
volume = {92},
number = {7},
pages = {421-428},
doi = {10.3949/ccjm.92a.24107},
pmid = {40592538},
issn = {1939-2869},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/trends ; *Clostridium Infections/therapy ; *Gastrointestinal Microbiome ; Clostridioides difficile ; Dysbiosis/therapy ; },
abstract = {As we advance our understanding of the gut microbiota, the implications of dysbiosis are becoming increasingly apparent. Fecal microbiota transplantation (FMT), a well-established procedure, is recognized for effectively treating recurrent Clostridioides difficile infection, prompting further investigation into its other possible clinical applications. Donor selection and screening are essential to ensure safety and efficacy. Product development and standardization, such as the US Food and Drug Administration-approved live biotherapeutic products Rebyota and Vowst, are helping efforts to evaluate FMT for other gastrointestinal and extraintestinal diseases. However, additional clinical trials are needed to support its use beyond recurrent C difficile infection.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Fecal Microbiota Transplantation/methods/trends
*Clostridium Infections/therapy
*Gastrointestinal Microbiome
Clostridioides difficile
Dysbiosis/therapy
RevDate: 2025-07-01
CmpDate: 2025-07-01
Immunomodulatory properties of the gut microbiome: diagnostic and therapeutic potential for rheumatoid arthritis.
Clinical and experimental medicine, 25(1):226.
Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent joint inflammation, synovial hyperplasia, and progressive joint destruction. Despite advancements in biologic disease-modifying antirheumatic drugs (bDMARDs) and TNF-α blockers, many RA patients still require more effective treatment options. Although genetic and environmental factors play a role in RA development, recent studies have emphasized the influence of the gut microbiota on disease onset and progression. Dysbiosis, or an imbalance in the gut microbial composition, has been linked to immune dysregulation, increased intestinal permeability, and systemic inflammation, all contributing to RA development. Research has revealed changes in the gut microbiome of RA patients, including an increased prevalence of Prevotella copri and a decreased presence of beneficial microbes such as Bifidobacterium, Bacteroides, and Lactobacillus. RA patients exhibit altered metabolite profiles, with reduced levels of short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate, which are linked to immune regulation and intestinal barrier function. Specific metabolites, such as L-arginine, phosphorylcholine, and arachidonic acid, have potential as RA biomarkers, with predictive value for diagnosis. Therapeutic approaches focusing on the microbiome, including probiotics, fecal microbiota transplantation, and traditional medicines, show promise in alleviating RA symptoms and regulating immune function. This review provides an updated overview of the immunomodulatory effects of the gut microbiome and explores its potential applications in the diagnosis and treatment of RA.
Additional Links: PMID-40591032
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Citation:
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@article {pmid40591032,
year = {2025},
author = {Abebaw, D and Akelew, Y and Adugna, A and Tegegne, BA and Teffera, ZH and Belayneh, M and Fenta, A and Selabat, B and Kindie, Y and Baylie, T and Mekuriaw, MG and Jemal, M and Atnaf, A},
title = {Immunomodulatory properties of the gut microbiome: diagnostic and therapeutic potential for rheumatoid arthritis.},
journal = {Clinical and experimental medicine},
volume = {25},
number = {1},
pages = {226},
pmid = {40591032},
issn = {1591-9528},
mesh = {Humans ; *Arthritis, Rheumatoid/therapy/diagnosis/immunology/microbiology ; *Gastrointestinal Microbiome/immunology ; Dysbiosis/immunology ; Probiotics/therapeutic use ; *Immunomodulation ; Fecal Microbiota Transplantation ; Biomarkers ; Animals ; },
abstract = {Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent joint inflammation, synovial hyperplasia, and progressive joint destruction. Despite advancements in biologic disease-modifying antirheumatic drugs (bDMARDs) and TNF-α blockers, many RA patients still require more effective treatment options. Although genetic and environmental factors play a role in RA development, recent studies have emphasized the influence of the gut microbiota on disease onset and progression. Dysbiosis, or an imbalance in the gut microbial composition, has been linked to immune dysregulation, increased intestinal permeability, and systemic inflammation, all contributing to RA development. Research has revealed changes in the gut microbiome of RA patients, including an increased prevalence of Prevotella copri and a decreased presence of beneficial microbes such as Bifidobacterium, Bacteroides, and Lactobacillus. RA patients exhibit altered metabolite profiles, with reduced levels of short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate, which are linked to immune regulation and intestinal barrier function. Specific metabolites, such as L-arginine, phosphorylcholine, and arachidonic acid, have potential as RA biomarkers, with predictive value for diagnosis. Therapeutic approaches focusing on the microbiome, including probiotics, fecal microbiota transplantation, and traditional medicines, show promise in alleviating RA symptoms and regulating immune function. This review provides an updated overview of the immunomodulatory effects of the gut microbiome and explores its potential applications in the diagnosis and treatment of RA.},
}
MeSH Terms:
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Humans
*Arthritis, Rheumatoid/therapy/diagnosis/immunology/microbiology
*Gastrointestinal Microbiome/immunology
Dysbiosis/immunology
Probiotics/therapeutic use
*Immunomodulation
Fecal Microbiota Transplantation
Biomarkers
Animals
RevDate: 2025-07-01
Targeting gut microbiota as a therapeutic approach for neurodegenerative diseases.
Neuroprotection, 3(2):120-130.
Recent evidence suggests a more important role of the gut microbiota in neurodegenerative diseases (NDDs) given its relationship through the microbiota-gut-brain as an active communication system aiding in maintaining homeostasis between the brain and the gut. This review focuses on how modulation of gut microbiota can serves as a therapeutic strategy for NDDs, emphasizing the neuroprotective effects of probiotics. Probiotics are live microorganisms that confer health benefits, and their interaction with gut-microbiota influences neurogenesis, neurotransmitter regulation, and neuroinflammation. Recent advancements, including germ-free animal models, fecal microbiota transplantation (FMT), and diverse probiotic strains, have revealed the underlying mechanisms linking gut health to brain function. Notably, several Lactobacillus and Bifidobacterium species have been shown to exert neuroprotective effects via the upregulation of neurotrophic factors such as brain-derived neurotrophic factor and enhancing mitochondrial function through reducing the impacts of oxidative stress. Interestingly, FMT has exhibited a degree of success in overcoming cognitive impairment and motor deficits in preclinical studies and clinical trials. However, further research is warranted to explore its therapeutic potential in humans. Overall, this review highlights the significant role of gut microbiota in NDDs and advocates for gut-targeted interventions as innovative approaches to mitigate these diseases.
Additional Links: PMID-40589476
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@article {pmid40589476,
year = {2025},
author = {Olajide, TS and Ijomone, OM},
title = {Targeting gut microbiota as a therapeutic approach for neurodegenerative diseases.},
journal = {Neuroprotection},
volume = {3},
number = {2},
pages = {120-130},
pmid = {40589476},
issn = {2770-730X},
abstract = {Recent evidence suggests a more important role of the gut microbiota in neurodegenerative diseases (NDDs) given its relationship through the microbiota-gut-brain as an active communication system aiding in maintaining homeostasis between the brain and the gut. This review focuses on how modulation of gut microbiota can serves as a therapeutic strategy for NDDs, emphasizing the neuroprotective effects of probiotics. Probiotics are live microorganisms that confer health benefits, and their interaction with gut-microbiota influences neurogenesis, neurotransmitter regulation, and neuroinflammation. Recent advancements, including germ-free animal models, fecal microbiota transplantation (FMT), and diverse probiotic strains, have revealed the underlying mechanisms linking gut health to brain function. Notably, several Lactobacillus and Bifidobacterium species have been shown to exert neuroprotective effects via the upregulation of neurotrophic factors such as brain-derived neurotrophic factor and enhancing mitochondrial function through reducing the impacts of oxidative stress. Interestingly, FMT has exhibited a degree of success in overcoming cognitive impairment and motor deficits in preclinical studies and clinical trials. However, further research is warranted to explore its therapeutic potential in humans. Overall, this review highlights the significant role of gut microbiota in NDDs and advocates for gut-targeted interventions as innovative approaches to mitigate these diseases.},
}
RevDate: 2025-07-01
CmpDate: 2025-07-01
Perspectives on Fecal Microbiota Transplantation: Uses and Modes of Administration.
Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology, 41:e20250014.
Fecal microbiota Transplantation (FMT), often referred to as stool transplantation, fecal transfusion, and fecal bacteria therapy, is considered one of the most medical innovations of the 20th century. Fecal microbiota Transplantation entails filtering and dilution of a healthy donor's feces before injecting it into the recipient's digestive system. In China, it was first administered orally in the fourth century for diarrhea and food poisoning under the name "Yellow Soup." It has recently been widely employed in a variety of clinical settings, including cases of Clostridium difficile infection that are recurring and resistant. By replacing the unhealthy intestinal microbiota with a healthy bacterial community, the FMT treatment aims to enhance the intestinal flora. It also looks at neurological conditions where alterations in gut microbiota are prevalent. We have discussed FMT in the context of its use in conditions affecting the nerve system, such as neurological and other conditions (multiple sclerosis, Parkinson's disease, Alzheimer's disease, stroke, epilepsy, Amyotrophic lateral sclerosis, Tourette syndrome, neuropathic pain, Huntington's diseases, etc.), as well as the role of gut microbiota in many neurological disorders.
Additional Links: PMID-40589142
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@article {pmid40589142,
year = {2025},
author = {Tiwari, R and Paswan, A and Tiwari, G and Reddy, VJS and Posa, MK},
title = {Perspectives on Fecal Microbiota Transplantation: Uses and Modes of Administration.},
journal = {Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology},
volume = {41},
number = {},
pages = {e20250014},
doi = {10.62958/j.cjap.2025.014},
pmid = {40589142},
issn = {1000-6834},
mesh = {*Fecal Microbiota Transplantation/methods ; Humans ; *Gastrointestinal Microbiome ; Feces/microbiology ; *Nervous System Diseases/therapy ; },
abstract = {Fecal microbiota Transplantation (FMT), often referred to as stool transplantation, fecal transfusion, and fecal bacteria therapy, is considered one of the most medical innovations of the 20th century. Fecal microbiota Transplantation entails filtering and dilution of a healthy donor's feces before injecting it into the recipient's digestive system. In China, it was first administered orally in the fourth century for diarrhea and food poisoning under the name "Yellow Soup." It has recently been widely employed in a variety of clinical settings, including cases of Clostridium difficile infection that are recurring and resistant. By replacing the unhealthy intestinal microbiota with a healthy bacterial community, the FMT treatment aims to enhance the intestinal flora. It also looks at neurological conditions where alterations in gut microbiota are prevalent. We have discussed FMT in the context of its use in conditions affecting the nerve system, such as neurological and other conditions (multiple sclerosis, Parkinson's disease, Alzheimer's disease, stroke, epilepsy, Amyotrophic lateral sclerosis, Tourette syndrome, neuropathic pain, Huntington's diseases, etc.), as well as the role of gut microbiota in many neurological disorders.},
}
MeSH Terms:
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*Fecal Microbiota Transplantation/methods
Humans
*Gastrointestinal Microbiome
Feces/microbiology
*Nervous System Diseases/therapy
RevDate: 2025-07-01
Circulating urobilinogen contributes to Inflammation, Intestinal Permeability and corticosteroid non-response in Severe Alcohol-associated Hepatitis.
Molecular therapy : the journal of the American Society of Gene Therapy pii:S1525-0016(25)00492-7 [Epub ahead of print].
Severe alcohol-associated hepatitis (SAH) is a life-threatening condition with high mortality rates and poor response to prednisolone therapy. Identifying reliable early predictors of therapy response and survival is critical. Plasma metabolomics was conducted on 70 SAH patients (50 responders, 20 non-responders) to identify biomarkers for non-response and early mortality. These findings were validated in a cohort of 153 patients and an independent cohort of 245 using high resolution mass spectrometry, machine learning, and severity indices. Temporal metabolic changes indicated interactions between the host and microbiome, with a focus on inflammation and intestinal permeability. Plasma metabolomics revealed that non-responders had significantly higher urobilinogen levels (3.6-fold change). Additionally, a decrease in alpha/beta diversity and temporal metabolic inactivity characterized non-responders. Plasma urobilinogen levels predicted non-response (AUC>0.97) and identified non-survivors (AUC=0.94) with a threshold of >0.07 mg/ml. Urobilinogen levels correlated with bacterial peptides belonging to Firmicutes and Proteobacteria, neutrophil activation, oxidative stress, and pro-inflammatory cytokine production. These changes contributed to non-response by increasing glucocorticoid receptor β expression and compromising intestinal permeability. Fecal microbiota transplantation decreased urobilinogen levels by reducing bilirubin reductase gene-containing microbiota. Plasma urobilinogen >0.07 mg/ml could predict early mortality, and modulation of the gut microbiome may improve outcomes in SAH patients.
Additional Links: PMID-40589086
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@article {pmid40589086,
year = {2025},
author = {Yadav, M and Gupta, A and Mathew, B and Tripathi, G and Dalal, N and Sharma, N and Yadav, P and Yadav, G and Singh, R and Bindal, V and Saif, R and Yadav, S and Sharma, N and Pandey, S and Bhat, SH and Singh, R and Kumar, J and Kushwaha, M and Khan, T and Sharma, NK and Bhaskar, A and Dwivedi, VP and Kumar, A and Kumar, N and Tripathi, DM and Trehanpati, N and Anupama Kumara, and Sharma, S and Sarin, SK and Maras, JS},
title = {Circulating urobilinogen contributes to Inflammation, Intestinal Permeability and corticosteroid non-response in Severe Alcohol-associated Hepatitis.},
journal = {Molecular therapy : the journal of the American Society of Gene Therapy},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ymthe.2025.06.041},
pmid = {40589086},
issn = {1525-0024},
abstract = {Severe alcohol-associated hepatitis (SAH) is a life-threatening condition with high mortality rates and poor response to prednisolone therapy. Identifying reliable early predictors of therapy response and survival is critical. Plasma metabolomics was conducted on 70 SAH patients (50 responders, 20 non-responders) to identify biomarkers for non-response and early mortality. These findings were validated in a cohort of 153 patients and an independent cohort of 245 using high resolution mass spectrometry, machine learning, and severity indices. Temporal metabolic changes indicated interactions between the host and microbiome, with a focus on inflammation and intestinal permeability. Plasma metabolomics revealed that non-responders had significantly higher urobilinogen levels (3.6-fold change). Additionally, a decrease in alpha/beta diversity and temporal metabolic inactivity characterized non-responders. Plasma urobilinogen levels predicted non-response (AUC>0.97) and identified non-survivors (AUC=0.94) with a threshold of >0.07 mg/ml. Urobilinogen levels correlated with bacterial peptides belonging to Firmicutes and Proteobacteria, neutrophil activation, oxidative stress, and pro-inflammatory cytokine production. These changes contributed to non-response by increasing glucocorticoid receptor β expression and compromising intestinal permeability. Fecal microbiota transplantation decreased urobilinogen levels by reducing bilirubin reductase gene-containing microbiota. Plasma urobilinogen >0.07 mg/ml could predict early mortality, and modulation of the gut microbiome may improve outcomes in SAH patients.},
}
RevDate: 2025-07-01
Leveraging gut microbiota for enhanced immune checkpoint blockade in solid tumor therapy.
Chinese medical journal [Epub ahead of print].
Gut microbiota can modulate antitumor immunity and influence immune checkpoint blockade (ICB) therapy efficacy and treatment-associated toxicity. Variations in the therapeutic effect of ICB among individuals are partially attributed to microbiota. This review summarizes current knowledge on how specific bacterial species enhance or hinder ICB outcomes by regulating immune cell activation, antigen presentation, and systemic inflammation. The review further outlines translational strategies to optimize ICB, including microbiota-targeted interventions (e.g., prebiotics, fecal microbiota transplantation, and metabolite therapies) to overcome resistance and mitigate treatment-related toxicities, focusing on immune-related colitis. Additionally, emerging microbial biomarkers in melanoma, lung cancer, and hepatobiliary cancers that predict ICB response are discussed, highlighting the gut microbiome as a potential target for personalized cancer immunotherapy. By integrating mechanistic insights with clinical evidence, this review underscores the potential of microbiota-centered approaches to improve patient outcomes in ICB-based treatments, emphasizing the pivotal role of the gut microbiota in modulating both therapeutic efficacy and immune-related adverse events.
Additional Links: PMID-40588803
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@article {pmid40588803,
year = {2025},
author = {Hu, J and Feng, T and Zhang, L and Zhou, Q and Zhu, L},
title = {Leveraging gut microbiota for enhanced immune checkpoint blockade in solid tumor therapy.},
journal = {Chinese medical journal},
volume = {},
number = {},
pages = {},
pmid = {40588803},
issn = {2542-5641},
abstract = {Gut microbiota can modulate antitumor immunity and influence immune checkpoint blockade (ICB) therapy efficacy and treatment-associated toxicity. Variations in the therapeutic effect of ICB among individuals are partially attributed to microbiota. This review summarizes current knowledge on how specific bacterial species enhance or hinder ICB outcomes by regulating immune cell activation, antigen presentation, and systemic inflammation. The review further outlines translational strategies to optimize ICB, including microbiota-targeted interventions (e.g., prebiotics, fecal microbiota transplantation, and metabolite therapies) to overcome resistance and mitigate treatment-related toxicities, focusing on immune-related colitis. Additionally, emerging microbial biomarkers in melanoma, lung cancer, and hepatobiliary cancers that predict ICB response are discussed, highlighting the gut microbiome as a potential target for personalized cancer immunotherapy. By integrating mechanistic insights with clinical evidence, this review underscores the potential of microbiota-centered approaches to improve patient outcomes in ICB-based treatments, emphasizing the pivotal role of the gut microbiota in modulating both therapeutic efficacy and immune-related adverse events.},
}
RevDate: 2025-06-30
Regulatory and Influencing Factors of Digestive Function in Elderly People: Roles of the Gut Microbiota and Nutritional Interventions.
Aging and disease pii:AD.2025.0565 [Epub ahead of print].
Aging is a natural and gradual biological process through which living organisms undergo physical, physiological, and sometimes psychological changes over time. Aging is commonly associated with a decline in gastrointestinal function, leading to various digestive disorders that impact the quality of life of older adults. The gut microbiota is a highly complex ecosystem that plays crucial roles in digestion, metabolic processes, immune functions, and overall health. However, emerging evidence indicates that many elderly individuals maintain relatively stable digestive health, suggesting the influence of modifiable regulatory factors. In this review, we describe the key physiological, microbial, and nutritional factors that regulate and influence digestive function in an aging population. Additionally, we explored the impact of age-associated alterations in the gut microbiota on digestive health challenges in older adults and emphasized the therapeutic potential of targeted nutritional intervention approaches, such as dietary modifications, prebiotics, probiotics, and symbiotic and fecal microbiota transplantation, which have shown promise in rebalancing the gut microbiome and reducing inflammation.
Additional Links: PMID-40586386
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@article {pmid40586386,
year = {2025},
author = {Li, K and Arbab, S and Du, Q and Zhou, J and Chen, Y and Tian, Y and Qijie, L and Ullah, H and Zhang, B},
title = {Regulatory and Influencing Factors of Digestive Function in Elderly People: Roles of the Gut Microbiota and Nutritional Interventions.},
journal = {Aging and disease},
volume = {},
number = {},
pages = {},
doi = {10.14336/AD.2025.0565},
pmid = {40586386},
issn = {2152-5250},
abstract = {Aging is a natural and gradual biological process through which living organisms undergo physical, physiological, and sometimes psychological changes over time. Aging is commonly associated with a decline in gastrointestinal function, leading to various digestive disorders that impact the quality of life of older adults. The gut microbiota is a highly complex ecosystem that plays crucial roles in digestion, metabolic processes, immune functions, and overall health. However, emerging evidence indicates that many elderly individuals maintain relatively stable digestive health, suggesting the influence of modifiable regulatory factors. In this review, we describe the key physiological, microbial, and nutritional factors that regulate and influence digestive function in an aging population. Additionally, we explored the impact of age-associated alterations in the gut microbiota on digestive health challenges in older adults and emphasized the therapeutic potential of targeted nutritional intervention approaches, such as dietary modifications, prebiotics, probiotics, and symbiotic and fecal microbiota transplantation, which have shown promise in rebalancing the gut microbiome and reducing inflammation.},
}
RevDate: 2025-06-30
Fecal Microbiota Transplantation (FMT) in Clostridium difficile Infection: A Paradigm Shift in Gastrointestinal Microbiome Modulation.
Cureus, 17(5):e85054.
Clostridium difficile (C. difficile) infection (CDI) poses a tremendous clinical challenge, especially in patients with recurrent disease and antibiotic resistance. Fecal microbiota transplantation (FMT) has become a new therapeutic strategy for restoring gut microbiota and decreasing CDI recurrence. The study aims to assess the clinical effectiveness of FMT in adult subjects with recurrent or refractory CDI, determine its effect on gut microbiome diversity, and track safety outcomes and rates of recurrence post-treatment. FMT was compared against standard antibiotic treatments to establish its efficacy in decreasing infection persistence and improving patients' quality of life. This study examines the efficacy, safety, and modulation of microbiota by FMT in an ensemble of 250 patients diagnosed with CDI, with equal gender distribution and a mean age of 55.61. Among the study participants, 131 (52.4%) underwent FMT by various routes of administration, including 66 (25.2%) through colonoscopy, 73 (29.2%) via a nasogastric tube, 60 (24.0%) via enema, and 54 (21.6%) through oral capsule administration. The success rate for FMT was reported as 88 (35.2%), partial success at 74 (29.6%), and treatment failure at 88 (35.2%). CDI recurrence was reported in 130 (52.0%) of patients after FMT. The gut microbiome enhanced diversity, measured in terms of the Shannon Diversity Index, increased significantly from 3.96 before FMT to 5.88 after FMT, thus indicating a favorable impact on gut microbial composition. Furthermore, 132 (52.8%) converted from C. difficile polymerase chain reaction (PCR) toxin positive to negative, corroborating successful pathogen clearance. On secondary outcomes, the quality of life in patients improved in 90 (36%), antibiotic dependence was reduced in 88 (35.2%), and hospitalization was lessened in 72 (28.8%). Inflammatory markers, such as white blood cell (WBC) counts and C-reactive protein (CRP), went downward but did not reach statistical significance. Logistic regression analysis identified age, severity of CDI, and prior exposure to antibiotics as the main predictors for the efficacy of FMT (p < 0.05). It is concluded that FMT is a promising alternative treatment for recurrent CDI through modulation of gut microbiota and decreasing the severity of infection. Future work is, however, required to establish treatment protocols with optimized results for long-term effectiveness and minimized recurrence risks.
Additional Links: PMID-40585700
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@article {pmid40585700,
year = {2025},
author = {Hamza Saeed, M and Qamar, S and Ishtiaq, A and Umaira Khan, Q and Atta, A and Atta, M and Ishtiaq, H and Khan, M and Saeed, MR and Iqbal, A},
title = {Fecal Microbiota Transplantation (FMT) in Clostridium difficile Infection: A Paradigm Shift in Gastrointestinal Microbiome Modulation.},
journal = {Cureus},
volume = {17},
number = {5},
pages = {e85054},
doi = {10.7759/cureus.85054},
pmid = {40585700},
issn = {2168-8184},
abstract = {Clostridium difficile (C. difficile) infection (CDI) poses a tremendous clinical challenge, especially in patients with recurrent disease and antibiotic resistance. Fecal microbiota transplantation (FMT) has become a new therapeutic strategy for restoring gut microbiota and decreasing CDI recurrence. The study aims to assess the clinical effectiveness of FMT in adult subjects with recurrent or refractory CDI, determine its effect on gut microbiome diversity, and track safety outcomes and rates of recurrence post-treatment. FMT was compared against standard antibiotic treatments to establish its efficacy in decreasing infection persistence and improving patients' quality of life. This study examines the efficacy, safety, and modulation of microbiota by FMT in an ensemble of 250 patients diagnosed with CDI, with equal gender distribution and a mean age of 55.61. Among the study participants, 131 (52.4%) underwent FMT by various routes of administration, including 66 (25.2%) through colonoscopy, 73 (29.2%) via a nasogastric tube, 60 (24.0%) via enema, and 54 (21.6%) through oral capsule administration. The success rate for FMT was reported as 88 (35.2%), partial success at 74 (29.6%), and treatment failure at 88 (35.2%). CDI recurrence was reported in 130 (52.0%) of patients after FMT. The gut microbiome enhanced diversity, measured in terms of the Shannon Diversity Index, increased significantly from 3.96 before FMT to 5.88 after FMT, thus indicating a favorable impact on gut microbial composition. Furthermore, 132 (52.8%) converted from C. difficile polymerase chain reaction (PCR) toxin positive to negative, corroborating successful pathogen clearance. On secondary outcomes, the quality of life in patients improved in 90 (36%), antibiotic dependence was reduced in 88 (35.2%), and hospitalization was lessened in 72 (28.8%). Inflammatory markers, such as white blood cell (WBC) counts and C-reactive protein (CRP), went downward but did not reach statistical significance. Logistic regression analysis identified age, severity of CDI, and prior exposure to antibiotics as the main predictors for the efficacy of FMT (p < 0.05). It is concluded that FMT is a promising alternative treatment for recurrent CDI through modulation of gut microbiota and decreasing the severity of infection. Future work is, however, required to establish treatment protocols with optimized results for long-term effectiveness and minimized recurrence risks.},
}
RevDate: 2025-06-30
Gut microbiota from voluntary exercised mice protects the intestinal barrier by inhibiting neutrophil extracellular trap formation.
iScience, 28(6):112763 pii:S2589-0042(25)01024-7.
Ulcerative colitis is an inflammatory bowel disease characterized by impaired intestinal barrier function, dysregulated immune responses, and alterations in the gut microbiota. Excessive formation of neutrophil extracellular traps (NETs), driven by peptidyl arginine deiminase 4 (PAD4) activity, contributes to inflammation modulated by the gut microbiota. In this study, we used a mouse model of dextran sulfate sodium-induced colitis to investigate the effects of voluntary exercise and its underlying mechanisms. Exercise preconditioning attenuated colitis severity, maintained intestinal barrier integrity, normalized gut microbiota composition, and suppressed NET formation. PAD4 inhibition further enhanced these effects. By contrast, the depletion of the gut microbiota by antibiotics largely abolished the benefits of exercise. Additionally, fecal microbiota transplantation from exercised mice recapitulated these protective effects. These findings elucidate the interplay among exercise, gut microbiota, and PAD4-mediated NET formation. Targeting these pathways may offer promising therapeutic strategies for colitis.
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@article {pmid40585508,
year = {2025},
author = {Zhu, B and Wu, H and Zhang, H and Song, Q and Xiao, Y and Yu, B},
title = {Gut microbiota from voluntary exercised mice protects the intestinal barrier by inhibiting neutrophil extracellular trap formation.},
journal = {iScience},
volume = {28},
number = {6},
pages = {112763},
doi = {10.1016/j.isci.2025.112763},
pmid = {40585508},
issn = {2589-0042},
abstract = {Ulcerative colitis is an inflammatory bowel disease characterized by impaired intestinal barrier function, dysregulated immune responses, and alterations in the gut microbiota. Excessive formation of neutrophil extracellular traps (NETs), driven by peptidyl arginine deiminase 4 (PAD4) activity, contributes to inflammation modulated by the gut microbiota. In this study, we used a mouse model of dextran sulfate sodium-induced colitis to investigate the effects of voluntary exercise and its underlying mechanisms. Exercise preconditioning attenuated colitis severity, maintained intestinal barrier integrity, normalized gut microbiota composition, and suppressed NET formation. PAD4 inhibition further enhanced these effects. By contrast, the depletion of the gut microbiota by antibiotics largely abolished the benefits of exercise. Additionally, fecal microbiota transplantation from exercised mice recapitulated these protective effects. These findings elucidate the interplay among exercise, gut microbiota, and PAD4-mediated NET formation. Targeting these pathways may offer promising therapeutic strategies for colitis.},
}
RevDate: 2025-06-30
Exploring the role of gut microbiota in Parkinson's disease: insights from fecal microbiota transplantation.
Frontiers in neuroscience, 19:1574512.
As a common neurodegenerative disease, Parkinson's disease (PD) is typified by α-synuclein (α-syn) aggregation and progressive degeneration of dopaminergic neurons within the substantia nigra. Clinical manifestations encompass motor symptoms and non-motor aspects that severely impair quality of life. Existing treatments mainly address symptoms, with no effective disease-modifying therapies available. The gut microbiota refers to the community of microorganisms that colonize the intestinal tract. The gut microbiota, gut, and brain are all connected via a complicated, mutual communication pathway known as the "gut microbiota-gut-brain axis." Gut microbiota dysbiosis is strongly linked to the onset and course of PD, according to growing data. In individuals with PD, gut dysbiosis correlates with clinical phenotype, disease duration, severity, and progression rates. Mechanistically, gut dysbiosis contributes to PD through enhanced intestinal permeability, increased intestinal inflammation and neuroinflammation, abnormal α-syn aggregation, oxidative stress, and reduced neurotransmitter synthesis. Therefore, focusing on the gut microbiota is regarded as a potentially effective treatment strategy. Fecal microbiota transplantation (FMT) is an emerging approach to modulate gut microbiota, with the goal of recovering microbiota diversity and function by transferring functional intestinal flora from healthy individuals into patients' gastrointestinal tracts. FMT is expected to become a promising therapy of PD and has a broad research and application prospect. Evidence suggests that FMT may restore gut microbiota, ease clinical symptoms, and provide potential neuroprotective benefits. However, the precise therapeutic mechanisms of FMT in PD remain uncertain, necessitating further research to clarify its effectiveness. This review examines alterations in gut microbiota linked to PD, mechanisms through which gut dysbiosis influences the disease, and the latest advancements in FMT research for treating PD, setting the stage for its clinical application.
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@article {pmid40584885,
year = {2025},
author = {Guo, M and Gao, H and Wang, Y and Xiang, Y},
title = {Exploring the role of gut microbiota in Parkinson's disease: insights from fecal microbiota transplantation.},
journal = {Frontiers in neuroscience},
volume = {19},
number = {},
pages = {1574512},
doi = {10.3389/fnins.2025.1574512},
pmid = {40584885},
issn = {1662-4548},
abstract = {As a common neurodegenerative disease, Parkinson's disease (PD) is typified by α-synuclein (α-syn) aggregation and progressive degeneration of dopaminergic neurons within the substantia nigra. Clinical manifestations encompass motor symptoms and non-motor aspects that severely impair quality of life. Existing treatments mainly address symptoms, with no effective disease-modifying therapies available. The gut microbiota refers to the community of microorganisms that colonize the intestinal tract. The gut microbiota, gut, and brain are all connected via a complicated, mutual communication pathway known as the "gut microbiota-gut-brain axis." Gut microbiota dysbiosis is strongly linked to the onset and course of PD, according to growing data. In individuals with PD, gut dysbiosis correlates with clinical phenotype, disease duration, severity, and progression rates. Mechanistically, gut dysbiosis contributes to PD through enhanced intestinal permeability, increased intestinal inflammation and neuroinflammation, abnormal α-syn aggregation, oxidative stress, and reduced neurotransmitter synthesis. Therefore, focusing on the gut microbiota is regarded as a potentially effective treatment strategy. Fecal microbiota transplantation (FMT) is an emerging approach to modulate gut microbiota, with the goal of recovering microbiota diversity and function by transferring functional intestinal flora from healthy individuals into patients' gastrointestinal tracts. FMT is expected to become a promising therapy of PD and has a broad research and application prospect. Evidence suggests that FMT may restore gut microbiota, ease clinical symptoms, and provide potential neuroprotective benefits. However, the precise therapeutic mechanisms of FMT in PD remain uncertain, necessitating further research to clarify its effectiveness. This review examines alterations in gut microbiota linked to PD, mechanisms through which gut dysbiosis influences the disease, and the latest advancements in FMT research for treating PD, setting the stage for its clinical application.},
}
RevDate: 2025-06-30
Clinical effectiveness of fecal microbial transplantation for metabolic syndrome: Advances in clinical efficacy and multi-omics research.
Current research in microbial sciences, 9:100415 pii:S2666-5174(25)00077-X.
Even though metabolic syndrome (MetS) poses a serious risk to human health and life, existing treatment approaches are not very effective. The impact of gut bacteria on host metabolism has been the subject of numerous research, and fecal microbial transplantation (FMT) has demonstrated great promise in reducing insulin resistance and abdominal obesity in individuals with metabolic syndrome. These FMT investigations have connected alterations in the gut microbiota to clinical indicators of insulin resistance and obesity, in addition to using high-throughput methods to analyze the gut microbiome, metabolome, and epigenome of peripheral blood mononuclear cells in patients with MetS. It is still necessary to clarify and assess the clinical effectiveness and mode of action of FMT in the management of MetS. This review examines the connection between gut bacteria and MetS, the effectiveness of FMT as a treatment, and the changes in the gut microbiome, metabolome, epigenome, and other histones following the intervention. We also discuss the safety of FMT and suggest areas for further investigation.
Additional Links: PMID-40583967
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@article {pmid40583967,
year = {2025},
author = {Wang, H and Tian, J and Mi, J},
title = {Clinical effectiveness of fecal microbial transplantation for metabolic syndrome: Advances in clinical efficacy and multi-omics research.},
journal = {Current research in microbial sciences},
volume = {9},
number = {},
pages = {100415},
doi = {10.1016/j.crmicr.2025.100415},
pmid = {40583967},
issn = {2666-5174},
abstract = {Even though metabolic syndrome (MetS) poses a serious risk to human health and life, existing treatment approaches are not very effective. The impact of gut bacteria on host metabolism has been the subject of numerous research, and fecal microbial transplantation (FMT) has demonstrated great promise in reducing insulin resistance and abdominal obesity in individuals with metabolic syndrome. These FMT investigations have connected alterations in the gut microbiota to clinical indicators of insulin resistance and obesity, in addition to using high-throughput methods to analyze the gut microbiome, metabolome, and epigenome of peripheral blood mononuclear cells in patients with MetS. It is still necessary to clarify and assess the clinical effectiveness and mode of action of FMT in the management of MetS. This review examines the connection between gut bacteria and MetS, the effectiveness of FMT as a treatment, and the changes in the gut microbiome, metabolome, epigenome, and other histones following the intervention. We also discuss the safety of FMT and suggest areas for further investigation.},
}
RevDate: 2025-06-29
Yeast β-glucan ameliorated Salmonella-induced gut impairment in broiler chickens by modulating gut microbiome.
International journal of biological macromolecules pii:S0141-8130(25)06185-9 [Epub ahead of print].
Yeast β-glucan (YG) was reported to control Salmonella infection in poultry. Gut microbiota plays an important role in regulating immune functions and intestinal health. However, it is still unclear whether YG protects chickens from Salmonella infection by regulating gut microbiota. The impacts of YG on gut health of chickens infected with Salmonella enteritidis (SE) was investigated through histochemical and immunological methods, along with microbiomics. The role of gut microbiome induced by YG treatment in combating Salmonella infection was explored through FMT. Our findings showed that YG administration significantly ameliorated SE-induced gut impairment by decreasing gut permeability, enhancing intestinal barrier function, inhibiting intestinal inflammation, reducing Salmonella colonization, lowering g_Streptococcus and g_Ligilactobacillus but increasing g_Blautia, g_Bacillus and g_Faecalibacterium relative abundance. Transplantation fecal microbiota from YG-treated healthy donor chickens to antibiotic-treated recipient chicks significantly attenuated gut injury caused by SE infection through decreasing Salmonella colonization and invasion along with intestinal permeability, improving gut morphology, upregulating intestinal tight junction genes and proteins expression, downregulating pro-inflammatory cytokines expression. Additionally, FMT remarkably increased g_Bacteroides and g_Faecalibacterium relative abundances and butyric acid level, decreased g_Ruminococcus-torque-group relative abundance in the cecum.Collectively, we assume that yeast β-glucan alleviated Salmonella-induced gut impairment, a mechanism that is dependent on the gut commensal Bacteroides and Faecalibacterium.
Additional Links: PMID-40582671
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@article {pmid40582671,
year = {2025},
author = {Bi, R and Abbas, W and Li, J and Huang, J and Hu, J and Guo, F and Wang, Z},
title = {Yeast β-glucan ameliorated Salmonella-induced gut impairment in broiler chickens by modulating gut microbiome.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {145630},
doi = {10.1016/j.ijbiomac.2025.145630},
pmid = {40582671},
issn = {1879-0003},
abstract = {Yeast β-glucan (YG) was reported to control Salmonella infection in poultry. Gut microbiota plays an important role in regulating immune functions and intestinal health. However, it is still unclear whether YG protects chickens from Salmonella infection by regulating gut microbiota. The impacts of YG on gut health of chickens infected with Salmonella enteritidis (SE) was investigated through histochemical and immunological methods, along with microbiomics. The role of gut microbiome induced by YG treatment in combating Salmonella infection was explored through FMT. Our findings showed that YG administration significantly ameliorated SE-induced gut impairment by decreasing gut permeability, enhancing intestinal barrier function, inhibiting intestinal inflammation, reducing Salmonella colonization, lowering g_Streptococcus and g_Ligilactobacillus but increasing g_Blautia, g_Bacillus and g_Faecalibacterium relative abundance. Transplantation fecal microbiota from YG-treated healthy donor chickens to antibiotic-treated recipient chicks significantly attenuated gut injury caused by SE infection through decreasing Salmonella colonization and invasion along with intestinal permeability, improving gut morphology, upregulating intestinal tight junction genes and proteins expression, downregulating pro-inflammatory cytokines expression. Additionally, FMT remarkably increased g_Bacteroides and g_Faecalibacterium relative abundances and butyric acid level, decreased g_Ruminococcus-torque-group relative abundance in the cecum.Collectively, we assume that yeast β-glucan alleviated Salmonella-induced gut impairment, a mechanism that is dependent on the gut commensal Bacteroides and Faecalibacterium.},
}
RevDate: 2025-06-28
The gut microbiome and its resistome as predictors of clinical infections and phenotypic antibiotic resistance in hematopoietic stem cell transplant recipients.
The Journal of infectious diseases pii:8172082 [Epub ahead of print].
A relationship between the gut microbiome composition, its resistome, and risk of clinical infections may exist and was explored here using 663 shotgun-sequenced fecal samples from 276 stem cell transplant patients. E. faecium, E. coli, and E. faecalis were the three most prevalent causes of clinical infection, with vancomycin resistance in E. faecium as the most common antibiotic resistance feature. Associations between the gut microbiome, resistome, and clinical infections were tested, with significant findings (FDR<0.05) evaluated in multivariable analysis. A 10% increase in gut abundance of E. faecium was positively associated with subsequent clinical infection with E. faecium (OR=1.14, p=0.02). Additionally, a 1% increase in vanA gene abundance was positively associated with vancomycin-resistant E. faecium infection (OR=1.27, p<0.01). Here we used metagenomics to enhance the understanding of infectious sources and to identify patients at risk of clinical infection with antibiotic-resistant bacterial strains.
Additional Links: PMID-40581627
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@article {pmid40581627,
year = {2025},
author = {Nørgaard, JC and Marandi, RZ and Ilett, EE and Gulay, A and Paredes, R and Lundgren, JD and Jørgensen, M and Sengeløv, H},
title = {The gut microbiome and its resistome as predictors of clinical infections and phenotypic antibiotic resistance in hematopoietic stem cell transplant recipients.},
journal = {The Journal of infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/infdis/jiaf330},
pmid = {40581627},
issn = {1537-6613},
abstract = {A relationship between the gut microbiome composition, its resistome, and risk of clinical infections may exist and was explored here using 663 shotgun-sequenced fecal samples from 276 stem cell transplant patients. E. faecium, E. coli, and E. faecalis were the three most prevalent causes of clinical infection, with vancomycin resistance in E. faecium as the most common antibiotic resistance feature. Associations between the gut microbiome, resistome, and clinical infections were tested, with significant findings (FDR<0.05) evaluated in multivariable analysis. A 10% increase in gut abundance of E. faecium was positively associated with subsequent clinical infection with E. faecium (OR=1.14, p=0.02). Additionally, a 1% increase in vanA gene abundance was positively associated with vancomycin-resistant E. faecium infection (OR=1.27, p<0.01). Here we used metagenomics to enhance the understanding of infectious sources and to identify patients at risk of clinical infection with antibiotic-resistant bacterial strains.},
}
RevDate: 2025-06-28
CmpDate: 2025-06-28
Fecal Microbiome Transplantation for Recurrent CDI: Treatment Efficacy and Safety with Oral Capsules.
Journal of gastrointestinal and liver diseases : JGLD, 34(2):199-204.
BACKGROUND AND AIMS: Fecal microbiota transplantation is an effective treatment method for recurrent Clostridioides difficile infection. Widely used enteric tube and colonoscopy methods demonstrate excellent efficacy and safety results. Recent data suggest that new fecal microbiota transplantation methods using oral capsules may provide a less invasive approach. In this study, we aimed to compare primary fecal microbiota transplantation efficacy as well as short- and long-term safety of two different administration routes: oral capsules and enteric tube.
METHODS: This retrospective study included 60 consecutive patients who underwent fecal microbiota transplantation for recurrent Clostridioides difficile infection. Thirty participants received 50 oral capsules containing frozen material for a single day and 30 patients received fecal microbiota transplantation via nasoenteric tube. All patients received standard treatment with oral vancomycin 500 mg q.i.d. for at least five days before the procedure. After intervention, patients were followed up for at least six months. Data on Clostridioides difficile infection recurrences and health status were collected and analyzed.
RESULTS: The oral capsules group consisted of 30 patients. Among them, 22 (73.3%) participants experienced resolution of symptoms after a single fecal microbiota transplantation, while eight (26.7%) patients developed recurrent diarrhea within eight weeks. The other 30 patients received treatment via nasoenteric tube. Among them, 24 (80%) patients were cured after a single fecal microbiota transplantation, while six (20%) experienced recurrent disease within eight weeks. The primary efficacy did not show significant differences between the two groups (p=0.85). Throughout the follow-up period, no serious adverse events or fecal microbiota transplantation related deaths were reported in both groups.
CONCLUSIONS: Fecal microbiota transplantation with frozen oral capsules is a safe, less invasive method with comparable efficacy to nasoenteric administration route.
Additional Links: PMID-40580532
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@article {pmid40580532,
year = {2025},
author = {Urbonas, T and Petrauskas, D and Kiudelis, V and Jonaitis, L and Skieceviciene, J and Gedgaudas, R and Kiudeliene, E and Valantiene, I and Zykus, R and Varkalaite, G and Inciuraite, R and Trapenske, E and Kulokiene, U and Jonaitis, P and Ramonaite, R and Velickiene, J and Zvirbliene, A and Morkunas, E and Kuliaviene, I and Sumskiene, J and Adamonis, K and Macas, A and Kupcinskiene, K and Lukosiene, L and Janciauskas, D and Poskiene, L and Vitkauskiene, A and Ianiro, G and Gasbarrini, A and Kiudelis, G and Kupcinskas, J},
title = {Fecal Microbiome Transplantation for Recurrent CDI: Treatment Efficacy and Safety with Oral Capsules.},
journal = {Journal of gastrointestinal and liver diseases : JGLD},
volume = {34},
number = {2},
pages = {199-204},
doi = {10.15403/jgld-5990},
pmid = {40580532},
issn = {1842-1121},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/adverse effects ; Male ; Female ; Retrospective Studies ; Middle Aged ; Treatment Outcome ; Administration, Oral ; *Clostridium Infections/therapy/microbiology/diagnosis ; Aged ; Capsules ; Recurrence ; *Clostridioides difficile ; Adult ; Anti-Bacterial Agents/administration & dosage ; Time Factors ; Feces/microbiology ; },
abstract = {BACKGROUND AND AIMS: Fecal microbiota transplantation is an effective treatment method for recurrent Clostridioides difficile infection. Widely used enteric tube and colonoscopy methods demonstrate excellent efficacy and safety results. Recent data suggest that new fecal microbiota transplantation methods using oral capsules may provide a less invasive approach. In this study, we aimed to compare primary fecal microbiota transplantation efficacy as well as short- and long-term safety of two different administration routes: oral capsules and enteric tube.
METHODS: This retrospective study included 60 consecutive patients who underwent fecal microbiota transplantation for recurrent Clostridioides difficile infection. Thirty participants received 50 oral capsules containing frozen material for a single day and 30 patients received fecal microbiota transplantation via nasoenteric tube. All patients received standard treatment with oral vancomycin 500 mg q.i.d. for at least five days before the procedure. After intervention, patients were followed up for at least six months. Data on Clostridioides difficile infection recurrences and health status were collected and analyzed.
RESULTS: The oral capsules group consisted of 30 patients. Among them, 22 (73.3%) participants experienced resolution of symptoms after a single fecal microbiota transplantation, while eight (26.7%) patients developed recurrent diarrhea within eight weeks. The other 30 patients received treatment via nasoenteric tube. Among them, 24 (80%) patients were cured after a single fecal microbiota transplantation, while six (20%) experienced recurrent disease within eight weeks. The primary efficacy did not show significant differences between the two groups (p=0.85). Throughout the follow-up period, no serious adverse events or fecal microbiota transplantation related deaths were reported in both groups.
CONCLUSIONS: Fecal microbiota transplantation with frozen oral capsules is a safe, less invasive method with comparable efficacy to nasoenteric administration route.},
}
MeSH Terms:
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Humans
*Fecal Microbiota Transplantation/methods/adverse effects
Male
Female
Retrospective Studies
Middle Aged
Treatment Outcome
Administration, Oral
*Clostridium Infections/therapy/microbiology/diagnosis
Aged
Capsules
Recurrence
*Clostridioides difficile
Adult
Anti-Bacterial Agents/administration & dosage
Time Factors
Feces/microbiology
RevDate: 2025-06-30
CmpDate: 2025-06-27
[Pentosan polysulfate alleviates cyclophosphamide-induced interstitial cystitis/bladder pain syndrome in mice by modulating gut microbiota and bile acid metabolism].
Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 45(6):1270-1279.
OBJECTIVES: To investigate the therapeutic efficacy and mechanism of pentosan polysulfate (PPS) for cyclophosphamide (CYP)-induced interstitial cystitis/bladder pain syndrome (IC/BPS) in mice.
METHODS: Female C57BL/6 mice (6-8 weeks old) were randomized into control group, PPS treatment (25 mg/kg via gavage for 3 weeks) group, CYP treatment (3 separate intraperitoneal injections at 50 mg/kg in week 4), and CYP+PPS treatment group. Gut microbiota alterations of the mice were analyzed using 16S rDNA sequencing and non-targeted metabolomics. Fecal microbiota transplantation (FMT) was performed in CYP-treated recipient mice and those treated with both CYP and PPS. In the in vitro experiment, LPS-stimulated human bladder epithelial cells (SV-HUC-1) were used to assess the effects of deoxycholic acid (DCA) and TGR5 signaling inhibitor SBI-115 on barrier functions of bladder epithelial cells.
RESULTS: PPS treatment significantly improved the mechanical pain thresholds, restored the urodynamic parameters, and attenuated bladder inflammation and barrier dysfunction in CYP-treated mice. Mechanistically, PPS enriched the abundance of Eubacterium xylanophilum and increased DCA levels in the intestines of CYP-treated mice. FMT experiments confirmed microbiota-dependent therapeutic effects of PPS, shown by reduced bladder pathology in the recipient mice treated with both CYP and PPS. In SV-HUC-1 cells, DCA obviously alleviated LPS-induced inflammation and barrier disruption, and treatment with SBI-115 abolished these protective effects of DCA.
CONCLUSIONS: PPS ameliorates IC/BPS in mice by remodeling gut microbiota to enhance DCA production and activate TGR5 signaling, suggesting a novel microbiota-bile acid-TGR5 axis that mediates the therapeutic effect of PPS and a therapeutic strategy for IC/BPS by targeting gut-bladder crosstalk.
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@article {pmid40579140,
year = {2025},
author = {Zhu, Y and Zhu, Z and Wu, P},
title = {[Pentosan polysulfate alleviates cyclophosphamide-induced interstitial cystitis/bladder pain syndrome in mice by modulating gut microbiota and bile acid metabolism].},
journal = {Nan fang yi ke da xue xue bao = Journal of Southern Medical University},
volume = {45},
number = {6},
pages = {1270-1279},
pmid = {40579140},
issn = {1673-4254},
support = {82370782//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Cystitis, Interstitial/chemically induced/drug therapy ; *Gastrointestinal Microbiome/drug effects ; *Pentosan Sulfuric Polyester/pharmacology/therapeutic use ; Cyclophosphamide/adverse effects ; Mice, Inbred C57BL ; Female ; Mice ; *Bile Acids and Salts/metabolism ; Urinary Bladder ; Fecal Microbiota Transplantation ; Humans ; },
abstract = {OBJECTIVES: To investigate the therapeutic efficacy and mechanism of pentosan polysulfate (PPS) for cyclophosphamide (CYP)-induced interstitial cystitis/bladder pain syndrome (IC/BPS) in mice.
METHODS: Female C57BL/6 mice (6-8 weeks old) were randomized into control group, PPS treatment (25 mg/kg via gavage for 3 weeks) group, CYP treatment (3 separate intraperitoneal injections at 50 mg/kg in week 4), and CYP+PPS treatment group. Gut microbiota alterations of the mice were analyzed using 16S rDNA sequencing and non-targeted metabolomics. Fecal microbiota transplantation (FMT) was performed in CYP-treated recipient mice and those treated with both CYP and PPS. In the in vitro experiment, LPS-stimulated human bladder epithelial cells (SV-HUC-1) were used to assess the effects of deoxycholic acid (DCA) and TGR5 signaling inhibitor SBI-115 on barrier functions of bladder epithelial cells.
RESULTS: PPS treatment significantly improved the mechanical pain thresholds, restored the urodynamic parameters, and attenuated bladder inflammation and barrier dysfunction in CYP-treated mice. Mechanistically, PPS enriched the abundance of Eubacterium xylanophilum and increased DCA levels in the intestines of CYP-treated mice. FMT experiments confirmed microbiota-dependent therapeutic effects of PPS, shown by reduced bladder pathology in the recipient mice treated with both CYP and PPS. In SV-HUC-1 cells, DCA obviously alleviated LPS-induced inflammation and barrier disruption, and treatment with SBI-115 abolished these protective effects of DCA.
CONCLUSIONS: PPS ameliorates IC/BPS in mice by remodeling gut microbiota to enhance DCA production and activate TGR5 signaling, suggesting a novel microbiota-bile acid-TGR5 axis that mediates the therapeutic effect of PPS and a therapeutic strategy for IC/BPS by targeting gut-bladder crosstalk.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Cystitis, Interstitial/chemically induced/drug therapy
*Gastrointestinal Microbiome/drug effects
*Pentosan Sulfuric Polyester/pharmacology/therapeutic use
Cyclophosphamide/adverse effects
Mice, Inbred C57BL
Female
Mice
*Bile Acids and Salts/metabolism
Urinary Bladder
Fecal Microbiota Transplantation
Humans
RevDate: 2025-06-27
HDAC/NF-κB signaling pathway mediates gut microbiota dysbiosis in rheumatoid arthritis: Intervention mechanisms of Fengshining decoction.
Phytomedicine : international journal of phytotherapy and phytopharmacology, 145:156976 pii:S0944-7113(25)00614-2 [Epub ahead of print].
BACKGROUND: Gut microbiota dysbiosis has been associated with the development of rheumatoid arthritis (RA). Fengshining (FSN) is a traditional Chinese medicine decoction that can effectively alleviate RA. However, how FSN modulates the gut microbiota to mitigate RA has not been comprehensively studied. This study evaluated the gut microecological mechanisms underlying FSN's effects on RA, focusing on the impact of gut-derived short-chain fatty acids (SCFAs), specifically butyrate, in RA treatment.
METHODS: The pharmacological effects of FSN on type II collagen-induced arthritis (CIA) in mice were assessed via pathological indicators, metagenomics, and metabolomics analyses. Furthermore, the impact of FSN on gut microbiota and metabolic profiles was also evaluated. Moreover, a pseudo-germ-free CIA model was established to validate whether exogenous butyrate alleviates RA. This study also elucidated whether fecal microbiota transplantation (FMT) from FSN-treated mice could mitigate RA symptoms.
RESULTS: The data showed that FSN markedly alleviated CIA symptoms and reduced serum inflammatory cytokine levels. Metagenomic and metabolomic analyses revealed that FSN-enriched SCFA-producing bacteria, including Butyrivibrio, Faecalicatena, and Lacrimispora. Furthermore, FSN increased the activity of carbohydrate metabolism-related enzymes and upregulated the expression patterns of homologous protein families. Moreover, exogenous butyrate supplementation suppressed pro-inflammatory factors, modulating immune responses, and enhanced intestinal barrier function. Further, Western blot analysis validated that FSN inhibited the HDAC/NF-κB pathway.
CONCLUSION: This study indicated that the gut microecological mechanism of FSN might be associated with its herbal components, which regulate gut microbiota diversity, restore the intestinal barrier, and boost microbial metabolite production. Furthermore, butyrate was observed to modulate intestinal mucosa, inhibit inflammatory responses, repair the intestinal barrier, and mitigate joint damage, thus alleviating RA symptoms.
Additional Links: PMID-40578039
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PubMed:
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@article {pmid40578039,
year = {2025},
author = {Wen, Y and Li, M and Hao, Y and Peng, J and Wei, X and Zhang, Z and Liu, B and Wang, Y and Peng, T and Ma, Y},
title = {HDAC/NF-κB signaling pathway mediates gut microbiota dysbiosis in rheumatoid arthritis: Intervention mechanisms of Fengshining decoction.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {145},
number = {},
pages = {156976},
doi = {10.1016/j.phymed.2025.156976},
pmid = {40578039},
issn = {1618-095X},
abstract = {BACKGROUND: Gut microbiota dysbiosis has been associated with the development of rheumatoid arthritis (RA). Fengshining (FSN) is a traditional Chinese medicine decoction that can effectively alleviate RA. However, how FSN modulates the gut microbiota to mitigate RA has not been comprehensively studied. This study evaluated the gut microecological mechanisms underlying FSN's effects on RA, focusing on the impact of gut-derived short-chain fatty acids (SCFAs), specifically butyrate, in RA treatment.
METHODS: The pharmacological effects of FSN on type II collagen-induced arthritis (CIA) in mice were assessed via pathological indicators, metagenomics, and metabolomics analyses. Furthermore, the impact of FSN on gut microbiota and metabolic profiles was also evaluated. Moreover, a pseudo-germ-free CIA model was established to validate whether exogenous butyrate alleviates RA. This study also elucidated whether fecal microbiota transplantation (FMT) from FSN-treated mice could mitigate RA symptoms.
RESULTS: The data showed that FSN markedly alleviated CIA symptoms and reduced serum inflammatory cytokine levels. Metagenomic and metabolomic analyses revealed that FSN-enriched SCFA-producing bacteria, including Butyrivibrio, Faecalicatena, and Lacrimispora. Furthermore, FSN increased the activity of carbohydrate metabolism-related enzymes and upregulated the expression patterns of homologous protein families. Moreover, exogenous butyrate supplementation suppressed pro-inflammatory factors, modulating immune responses, and enhanced intestinal barrier function. Further, Western blot analysis validated that FSN inhibited the HDAC/NF-κB pathway.
CONCLUSION: This study indicated that the gut microecological mechanism of FSN might be associated with its herbal components, which regulate gut microbiota diversity, restore the intestinal barrier, and boost microbial metabolite production. Furthermore, butyrate was observed to modulate intestinal mucosa, inhibit inflammatory responses, repair the intestinal barrier, and mitigate joint damage, thus alleviating RA symptoms.},
}
RevDate: 2025-06-27
CmpDate: 2025-06-27
Is the gut microbiome of importance in fibromyalgia? A critical review of emerging evidence.
Clinical and experimental rheumatology, 43(6):990-998.
Fibromyalgia (FM) is a multifaceted chronic pain syndrome, predominantly affecting women, and characterised by a constellation of symptoms including diffuse musculoskeletal pain, fatigue, cognitive impairment and poor sleep quality. Its complex pathophysiology likely involves genetic, environmental and psychosocial factors. Recent studies have raised the possibility that the gut microbiome may influence FM symptoms via the gut-brain axis, although this hypothesis remains unconfirmed. This review aims to explore potential associations between gut microbiome alterations, nutrition, and FM, with particular attention to the limitations of current evidence. While certain studies have reported differences in the gut microbiota composition of patients with FM, these findings are preliminary and often derive from small, heterogeneous cohorts. Likewise, faecal microbiota transplantation studies in animals and limited human trials suggest a possible link to pain sensitivity, but further validation is needed.Nutritional interventions, including prebiotics, probiotics and specific dietary strategies, have shown early promise in modulating gut microbiota and alleviating FM symptoms. Nutrients such as magnesium, selenium and omega-3 fatty acids, as well as antioxidant compounds, may influence pain and inflammation pathways, but definitive clinical recommendations are lacking. Given the emerging nature of this field, larger and better-controlled studies are required to clarify the role of the gut microbiome and nutrition in FM. A multidisciplinary management strategy, integrating nutritional approaches cautiously and based on individual profiles, may offer benefits, although no standard therapeutic guidelines currently exist.
Additional Links: PMID-40576702
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PubMed:
Citation:
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@article {pmid40576702,
year = {2025},
author = {Shtrozberg, S and Bazzichi, L and Sarzi-Puttini, P and Aloush, V and Ablin, JN},
title = {Is the gut microbiome of importance in fibromyalgia? A critical review of emerging evidence.},
journal = {Clinical and experimental rheumatology},
volume = {43},
number = {6},
pages = {990-998},
doi = {10.55563/clinexprheumatol/pmajsv},
pmid = {40576702},
issn = {0392-856X},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Fibromyalgia/microbiology/physiopathology/therapy/diagnosis ; Animals ; Probiotics/therapeutic use ; Nutritional Status ; Dysbiosis ; Prebiotics ; Fecal Microbiota Transplantation ; },
abstract = {Fibromyalgia (FM) is a multifaceted chronic pain syndrome, predominantly affecting women, and characterised by a constellation of symptoms including diffuse musculoskeletal pain, fatigue, cognitive impairment and poor sleep quality. Its complex pathophysiology likely involves genetic, environmental and psychosocial factors. Recent studies have raised the possibility that the gut microbiome may influence FM symptoms via the gut-brain axis, although this hypothesis remains unconfirmed. This review aims to explore potential associations between gut microbiome alterations, nutrition, and FM, with particular attention to the limitations of current evidence. While certain studies have reported differences in the gut microbiota composition of patients with FM, these findings are preliminary and often derive from small, heterogeneous cohorts. Likewise, faecal microbiota transplantation studies in animals and limited human trials suggest a possible link to pain sensitivity, but further validation is needed.Nutritional interventions, including prebiotics, probiotics and specific dietary strategies, have shown early promise in modulating gut microbiota and alleviating FM symptoms. Nutrients such as magnesium, selenium and omega-3 fatty acids, as well as antioxidant compounds, may influence pain and inflammation pathways, but definitive clinical recommendations are lacking. Given the emerging nature of this field, larger and better-controlled studies are required to clarify the role of the gut microbiome and nutrition in FM. A multidisciplinary management strategy, integrating nutritional approaches cautiously and based on individual profiles, may offer benefits, although no standard therapeutic guidelines currently exist.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome
*Fibromyalgia/microbiology/physiopathology/therapy/diagnosis
Animals
Probiotics/therapeutic use
Nutritional Status
Dysbiosis
Prebiotics
Fecal Microbiota Transplantation
RevDate: 2025-06-27
Short- and long-term development of gut microbiota in children after liver transplantation - a prospective observational trial.
Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society pii:01445473-990000000-00648 [Epub ahead of print].
In children, little is known on gut microbiota (GM) in end-stage liver disease and its association with graft function after pediatric liver transplantation (pLT). We analyzed GM composition and function in children before pLT, longitudinally post-pLT and in long-term survivors (LT-pLT) in order to assess the impact of disease severity, treatment and pLT on GM and delineate associations with graft and patient health. Fecal samples (FS) of 29 children (17f, age 2.6 [0.2-15.7] years) awaiting pLT were included with longitudinal follow-ups until 12M post-transplant in 18, and compared with 38 LT-pLT (21f, age 11 [2.7-17.7] years, 7.8 [1.0-17.0] years post-pLT) and 94 healthy controls (HC). Samples were analyzed using quantitative 16S rRNA gene analyses combined with shotgun metagenomics (subset of samples). Pre-pLT patients showed reduced alpha-diversities and altered GM composition compared with LT-pLT and HC, associated with disease severity and anti-pruritic treatment with Rifampicin. Dysbiosis increased after pLT and started to recover after 3M. Although bacterial concentrations, alpha diversity and gene richness increased post-pLT, levels remained below those of HC. Abundances of key functions, e.g. the capacity to synthesize butyrate, also remained reduced. Quantitative analyses revealed true extent of differences between patients and HC that were underestimated using relative abundance data. GM diversity and functional capacities correlated negatively with transaminase levels mid- and long-term after pLT. Random Forest analyses based on GM were able to predict hepatocellular damage at high accuracy (AUC: 0.89). We provide comprehensive, quantitative insights into GM composition and function before and after pLT. A link between GM alterations with (long-term) graft health was uncovered providing possible targets to modulate GM function in order to increase graft and patient health.
Additional Links: PMID-40576662
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PubMed:
Citation:
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@article {pmid40576662,
year = {2025},
author = {Goldschmidt, I and Kramer, M and Junge, N and Ouro-Djobo, N and Poets, A and Rathert, M and Geffers, R and Baumann, U and Hartleben, B and Schulze, KD and Woltemate, S and Vital, M},
title = {Short- and long-term development of gut microbiota in children after liver transplantation - a prospective observational trial.},
journal = {Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society},
volume = {},
number = {},
pages = {},
doi = {10.1097/LVT.0000000000000659},
pmid = {40576662},
issn = {1527-6473},
abstract = {In children, little is known on gut microbiota (GM) in end-stage liver disease and its association with graft function after pediatric liver transplantation (pLT). We analyzed GM composition and function in children before pLT, longitudinally post-pLT and in long-term survivors (LT-pLT) in order to assess the impact of disease severity, treatment and pLT on GM and delineate associations with graft and patient health. Fecal samples (FS) of 29 children (17f, age 2.6 [0.2-15.7] years) awaiting pLT were included with longitudinal follow-ups until 12M post-transplant in 18, and compared with 38 LT-pLT (21f, age 11 [2.7-17.7] years, 7.8 [1.0-17.0] years post-pLT) and 94 healthy controls (HC). Samples were analyzed using quantitative 16S rRNA gene analyses combined with shotgun metagenomics (subset of samples). Pre-pLT patients showed reduced alpha-diversities and altered GM composition compared with LT-pLT and HC, associated with disease severity and anti-pruritic treatment with Rifampicin. Dysbiosis increased after pLT and started to recover after 3M. Although bacterial concentrations, alpha diversity and gene richness increased post-pLT, levels remained below those of HC. Abundances of key functions, e.g. the capacity to synthesize butyrate, also remained reduced. Quantitative analyses revealed true extent of differences between patients and HC that were underestimated using relative abundance data. GM diversity and functional capacities correlated negatively with transaminase levels mid- and long-term after pLT. Random Forest analyses based on GM were able to predict hepatocellular damage at high accuracy (AUC: 0.89). We provide comprehensive, quantitative insights into GM composition and function before and after pLT. A link between GM alterations with (long-term) graft health was uncovered providing possible targets to modulate GM function in order to increase graft and patient health.},
}
RevDate: 2025-06-27
Fecal Microbiota Transplantation Modulates Th17/Treg Balance via JAK/STAT Pathway in ARDS Rats.
Advanced biology [Epub ahead of print].
This study evaluated the therapeutic effects of fecal microbiota transplantation (FMT) on lipopolysaccharide (LPS)-induced acute respiratory distress syndrome (ARDS) in rats. The study focused on the balance of T-helper 17 (Th17) and regulatory T (Treg) cells, as well as the modulation of the JAK/STAT pathway. This study established a rat ARDS model using intranasal LPS instillation, administering interventions such as FMT, Treg cell depletion, and JAK inhibitors. Assessments included histopathological examination of lung and intestinal tissues, flow cytometry for Th17 and Treg cell proportions, qPCR and Western blot for gene and protein expression, ELISA for inflammatory cytokines, and correlation analysis using Spearman's method for cytokine-immune cell interactions. Results indicated that FMT and JAK inhibitors significantly reduce lung damage induced by LPS, reduced alveolar destruction and inflammation, restored Th17/Treg balance, and inhibited JAK/STAT pathway activity. Notably, FMT decreased pro-inflammatory cytokines (IL-2, IL-6, IL-8, IL-17A, IL-23, TGF-β1) and increased anti-inflammatory cytokines (IL-10, IL-35) in serum. Spearman correlation analysis indicated that FMT restored immune balance by modulating the interactions between cytokines and immune cells. In conclusion, FMT effectively alleviates lung and intestinal injury in LPS-induced ARDS rat models by modulating Th17/Treg balance and inhibiting JAK/STAT pathway activity, demonstrating promising therapeutic potential for ARDS treatment.
Additional Links: PMID-40575995
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PubMed:
Citation:
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@article {pmid40575995,
year = {2025},
author = {Zhang, D and Dong, B and Chen, J and Zhang, Z and Zeng, W and Liao, L and Xiong, X and Qin, X and Fan, X},
title = {Fecal Microbiota Transplantation Modulates Th17/Treg Balance via JAK/STAT Pathway in ARDS Rats.},
journal = {Advanced biology},
volume = {},
number = {},
pages = {e00028},
doi = {10.1002/adbi.202500028},
pmid = {40575995},
issn = {2701-0198},
support = {2022NSFSC0046//Natural Science Foundation of Sichuan Province of China/ ; 2022QN074//Southwest Medical University School-Level Project/ ; 2023JYJ049//Luzhou City Science and Technology Program Project/ ; LRYGCC202120//Guangxi Key Specialty Construction Project Funding, Liuzhou City People's Hospital High-Level Talent Research Startup Fund/ ; lry202408//Liuzhou People's Hospital In-house Project Funding/ ; lry202409//Liuzhou People's Hospital In-house Project Funding/ ; lry202411//Liuzhou People's Hospital In-house Project Funding/ ; GXZYB20240601//Guangxi Autonomous Region Traditional Chinese Medicine Self-Funded Project/ ; 2024YB0103B003//Liuzhou City Science and Technology Program Project/ ; },
abstract = {This study evaluated the therapeutic effects of fecal microbiota transplantation (FMT) on lipopolysaccharide (LPS)-induced acute respiratory distress syndrome (ARDS) in rats. The study focused on the balance of T-helper 17 (Th17) and regulatory T (Treg) cells, as well as the modulation of the JAK/STAT pathway. This study established a rat ARDS model using intranasal LPS instillation, administering interventions such as FMT, Treg cell depletion, and JAK inhibitors. Assessments included histopathological examination of lung and intestinal tissues, flow cytometry for Th17 and Treg cell proportions, qPCR and Western blot for gene and protein expression, ELISA for inflammatory cytokines, and correlation analysis using Spearman's method for cytokine-immune cell interactions. Results indicated that FMT and JAK inhibitors significantly reduce lung damage induced by LPS, reduced alveolar destruction and inflammation, restored Th17/Treg balance, and inhibited JAK/STAT pathway activity. Notably, FMT decreased pro-inflammatory cytokines (IL-2, IL-6, IL-8, IL-17A, IL-23, TGF-β1) and increased anti-inflammatory cytokines (IL-10, IL-35) in serum. Spearman correlation analysis indicated that FMT restored immune balance by modulating the interactions between cytokines and immune cells. In conclusion, FMT effectively alleviates lung and intestinal injury in LPS-induced ARDS rat models by modulating Th17/Treg balance and inhibiting JAK/STAT pathway activity, demonstrating promising therapeutic potential for ARDS treatment.},
}
RevDate: 2025-06-27
Microbiome, dysbiosis and use of probiotics in various diseases.
World journal of virology, 14(2):99574.
The community of microorganisms that colonize certain areas of the human body is called microbiota. Microorganisms such as bacteria, fungi and viruses make up the microbiota. The sum of the genomes of these microorganisms and microorganisms refers to the microbiome. It has been shown that microbiota has important effects such as protecting the organ from pathogens, contributing to metabolic functions (such as vitamin synthesis, carbohydrate digestion) and providing immunoregulation. Dysbiosis refers to compositional and functional changes in the microbiota. At the beginning of the 21[st] century, numerous studies have investigated the human microbiota and its imbalance in relation to various diseases and found that dysbiosis is associated with many diseases. The aim of this mini-review article is to provide brief information about dysbiosis and its care and to raise awareness.
Additional Links: PMID-40575647
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@article {pmid40575647,
year = {2025},
author = {Tüsüz Önata, E and Özdemir, Ö},
title = {Microbiome, dysbiosis and use of probiotics in various diseases.},
journal = {World journal of virology},
volume = {14},
number = {2},
pages = {99574},
pmid = {40575647},
issn = {2220-3249},
abstract = {The community of microorganisms that colonize certain areas of the human body is called microbiota. Microorganisms such as bacteria, fungi and viruses make up the microbiota. The sum of the genomes of these microorganisms and microorganisms refers to the microbiome. It has been shown that microbiota has important effects such as protecting the organ from pathogens, contributing to metabolic functions (such as vitamin synthesis, carbohydrate digestion) and providing immunoregulation. Dysbiosis refers to compositional and functional changes in the microbiota. At the beginning of the 21[st] century, numerous studies have investigated the human microbiota and its imbalance in relation to various diseases and found that dysbiosis is associated with many diseases. The aim of this mini-review article is to provide brief information about dysbiosis and its care and to raise awareness.},
}
RevDate: 2025-06-27
Exploring the gut microbiome's influence on cancer-associated anemia: Mechanisms, clinical challenges, and innovative therapies.
World journal of gastrointestinal pharmacology and therapeutics, 16(2):105375.
BACKGROUND: Anemia is a prevalent and challenging complication in patients with hematologic and solid malignancies, which stems from the direct effects of malignancy, treatment-induced toxicities, and systemic inflammation. It affects patients' survival, functional status, and quality of life profoundly. Recent literature has highlighted the emerging role of the gut microbiome in the pathogenesis of cancer-associated anemia. The gut microbiota, through its intricate interplay with iron metabolism, inflammatory pathways, and immune modulation, may either exacerbate or ameliorate anemia depending on its composition, and functional integrity. Dysbiosis, characterized by disruption in the gut microbial ecosystem, is very common in cancer patients. This microbial imbalance is implicated in anemia causation through diminished iron absorption, persistent low-grade inflammation, and suppression of erythropoiesis.
AIM: To consolidate current evidence regarding the interplay between gut microbiome and anemia in the setting of malignancies. It aims to provide a detailed exploration of the mechanistic links between dysbiosis and anemia, identifies unique challenges associated with various cancer types, and evaluates the efficacy of microbiome-focused therapies. Through this integrative approach, the review seeks to establish a foundation for innovative clinical strategies aimed at mitigating anemia and improving patient outcomes in oncology.
METHODS: A literature search was performed using multiple databases, including Google Scholar, PubMed, Scopus, and Web of Science, using a combination of keywords and Boolean operators to refine results. Keywords included "cancer-associated anemia", "gut microbiome", "intestinal microbiota", "iron metabolism", "gut dysbiosis", "short-chain fatty acids", "hematopoiesis", "probiotics", "prebiotics", and "fecal microbiota transplantation". Articles published in English between 2000 and December 2024 were included, with a focus on contemporary and relevant findings.
RESULTS: Therapeutic strategies aimed at restoration of gut microbial homeostasis, such as probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation (FMT), can inhibit anemia-causing pathways by enhancing microbial diversity, suppressing detrimental flora, reducing systemic inflammation and optimizing nutrient absorption.
CONCLUSION: Gut dysbiosis causes anemia and impairs response to chemotherapy in cancer patients. Microbiome-centered interventions, such as probiotics, prebiotics, dietary modifications, and FMT, have shown efficacy in restoring microbial balance, reducing inflammation, and enhancing nutrient bioavailability. Emerging approaches, including engineered probiotics and bacteriophage therapies, are promising precision-based, customizable solutions for various microbiome compositions and imbalances. Future research should focus on integrating microbiome-targeted strategies with established anemia therapies.
Additional Links: PMID-40575364
PubMed:
Citation:
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@article {pmid40575364,
year = {2025},
author = {Bangolo, A and Amoozgar, B and Habibi, M and Simms, E and Nagesh, VK and Wadhwani, S and Wadhwani, N and Auda, A and Elias, D and Mansour, C and Abbott, R and Jebara, N and Zhang, L and Gill, S and Ahmed, K and Ip, A and Goy, A and Cho, C},
title = {Exploring the gut microbiome's influence on cancer-associated anemia: Mechanisms, clinical challenges, and innovative therapies.},
journal = {World journal of gastrointestinal pharmacology and therapeutics},
volume = {16},
number = {2},
pages = {105375},
pmid = {40575364},
issn = {2150-5349},
abstract = {BACKGROUND: Anemia is a prevalent and challenging complication in patients with hematologic and solid malignancies, which stems from the direct effects of malignancy, treatment-induced toxicities, and systemic inflammation. It affects patients' survival, functional status, and quality of life profoundly. Recent literature has highlighted the emerging role of the gut microbiome in the pathogenesis of cancer-associated anemia. The gut microbiota, through its intricate interplay with iron metabolism, inflammatory pathways, and immune modulation, may either exacerbate or ameliorate anemia depending on its composition, and functional integrity. Dysbiosis, characterized by disruption in the gut microbial ecosystem, is very common in cancer patients. This microbial imbalance is implicated in anemia causation through diminished iron absorption, persistent low-grade inflammation, and suppression of erythropoiesis.
AIM: To consolidate current evidence regarding the interplay between gut microbiome and anemia in the setting of malignancies. It aims to provide a detailed exploration of the mechanistic links between dysbiosis and anemia, identifies unique challenges associated with various cancer types, and evaluates the efficacy of microbiome-focused therapies. Through this integrative approach, the review seeks to establish a foundation for innovative clinical strategies aimed at mitigating anemia and improving patient outcomes in oncology.
METHODS: A literature search was performed using multiple databases, including Google Scholar, PubMed, Scopus, and Web of Science, using a combination of keywords and Boolean operators to refine results. Keywords included "cancer-associated anemia", "gut microbiome", "intestinal microbiota", "iron metabolism", "gut dysbiosis", "short-chain fatty acids", "hematopoiesis", "probiotics", "prebiotics", and "fecal microbiota transplantation". Articles published in English between 2000 and December 2024 were included, with a focus on contemporary and relevant findings.
RESULTS: Therapeutic strategies aimed at restoration of gut microbial homeostasis, such as probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation (FMT), can inhibit anemia-causing pathways by enhancing microbial diversity, suppressing detrimental flora, reducing systemic inflammation and optimizing nutrient absorption.
CONCLUSION: Gut dysbiosis causes anemia and impairs response to chemotherapy in cancer patients. Microbiome-centered interventions, such as probiotics, prebiotics, dietary modifications, and FMT, have shown efficacy in restoring microbial balance, reducing inflammation, and enhancing nutrient bioavailability. Emerging approaches, including engineered probiotics and bacteriophage therapies, are promising precision-based, customizable solutions for various microbiome compositions and imbalances. Future research should focus on integrating microbiome-targeted strategies with established anemia therapies.},
}
RevDate: 2025-06-27
Fecal Butyrate and Deoxycholic Acid Concentrations Correlate With Mortality in Patients With Liver Disease.
Gastro hep advances, 4(8):100695.
BACKGROUND AND AIMS: The intestinal microbiome produces metabolites, including short chain fatty acids (SCFAs) and secondary bile acids (BAs), that impact host physiology. Loss of intestinal microbiome diversity is associated with cirrhosis progression, but the impact of microbiome-associated metabolites on liver disease remains largely undefined. We aimed to correlate fecal metabolite concentrations with the severity and progression of liver disease.
METHODS: In this cross-sectional study, fecal samples from patients hospitalized with liver disease were analyzed by shotgun metagenomic sequencing to determine microbiome compositions and targeted mass spectrometry to quantify SCFAs and BAs. Random survival forest and logistic regression models identified clinical, metagenomic, and metabolomic features associated with rehospitalization and survival.
RESULTS: This cross-sectional study included 24 chronic liver disease, 18 compensated cirrhosis, 225 decompensated cirrhosis and 40 acute-on-chronic liver failure patients and 27 control fecal donors. Microbiome sequencing and metabolite profiling correlated microbial diversity and SCFA and BA concentrations with liver disease severity. Butyrate and deoxycholic acid (DCA) were more important features than individual microbial species in random survival forest models predicting 30-day transplant-free survival, and low butyrate and DCA were associated with 30-day mortality (P < .0001). After controlling for model for end stage liver disease (MELD)-sodium score, disease stage, age and gender, low fecal concentrations of butyrate and DCA remained significant risk factors for death (Cox 1.38, P = .027). Bacterial species associated with butyrate and DCA concentrations included Bifidobacterium spp. and F. prausnitzii.
CONCLUSION: Mass spectrometry rapidly identifies patients with low fecal butyrate and DCA concentrations who are at increased risk of 30-day mortality. These findings set the stage for clinical trials of microbiome reconstitution with butyrate and DCA-producing bacterial species.
Additional Links: PMID-40574876
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Citation:
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@article {pmid40574876,
year = {2025},
author = {Odenwald, MA and Ramaswamy, R and Lin, H and Lehmann, C and Moran, A and Mullowney, MW and Sidebottom, AM and Hernandez, A and McMillin, M and Rose, A and Moran, D and Little, J and Sulakhe, D and D'Souza, M and Woodson, C and Tanveer, T and de Porto, A and Dylla, N and Sundararajan, A and Burgo, V and Cantoral, J and Jadczak, C and Adler, E and Aronsohn, A and Pamer, EG and Rinella, ME},
title = {Fecal Butyrate and Deoxycholic Acid Concentrations Correlate With Mortality in Patients With Liver Disease.},
journal = {Gastro hep advances},
volume = {4},
number = {8},
pages = {100695},
pmid = {40574876},
issn = {2772-5723},
abstract = {BACKGROUND AND AIMS: The intestinal microbiome produces metabolites, including short chain fatty acids (SCFAs) and secondary bile acids (BAs), that impact host physiology. Loss of intestinal microbiome diversity is associated with cirrhosis progression, but the impact of microbiome-associated metabolites on liver disease remains largely undefined. We aimed to correlate fecal metabolite concentrations with the severity and progression of liver disease.
METHODS: In this cross-sectional study, fecal samples from patients hospitalized with liver disease were analyzed by shotgun metagenomic sequencing to determine microbiome compositions and targeted mass spectrometry to quantify SCFAs and BAs. Random survival forest and logistic regression models identified clinical, metagenomic, and metabolomic features associated with rehospitalization and survival.
RESULTS: This cross-sectional study included 24 chronic liver disease, 18 compensated cirrhosis, 225 decompensated cirrhosis and 40 acute-on-chronic liver failure patients and 27 control fecal donors. Microbiome sequencing and metabolite profiling correlated microbial diversity and SCFA and BA concentrations with liver disease severity. Butyrate and deoxycholic acid (DCA) were more important features than individual microbial species in random survival forest models predicting 30-day transplant-free survival, and low butyrate and DCA were associated with 30-day mortality (P < .0001). After controlling for model for end stage liver disease (MELD)-sodium score, disease stage, age and gender, low fecal concentrations of butyrate and DCA remained significant risk factors for death (Cox 1.38, P = .027). Bacterial species associated with butyrate and DCA concentrations included Bifidobacterium spp. and F. prausnitzii.
CONCLUSION: Mass spectrometry rapidly identifies patients with low fecal butyrate and DCA concentrations who are at increased risk of 30-day mortality. These findings set the stage for clinical trials of microbiome reconstitution with butyrate and DCA-producing bacterial species.},
}
RevDate: 2025-06-27
CmpDate: 2025-06-27
The gut-immune axis in primary immune thrombocytopenia (ITP): a paradigm shifts in treatment approaches.
Frontiers in immunology, 16:1595977.
Primary immune thrombocytopenia (ITP) is an autoimmune disorder characterized by platelet destruction and impaired production, leading to bleeding risk. While immunosuppressive therapies are standard, many patients experience relapses or refractory disease, highlighting the need for novel approaches. Emerging evidence suggests the gut microbiota plays a role in immune regulation, yet its impact on ITP remains unclear. Dysbiosis has been linked to immune dysfunction in other autoimmune diseases, but whether it drives or results from immune dysregulation in ITP is debated. This review explores the gut-immune axis in ITP, focusing on microbiota-driven immune modulation, cytokine signaling, and platelet homeostasis. We assess microbiota-targeted interventions, including fecal microbiota transplantation (FMT), probiotics, and dietary modifications, while addressing key controversies and knowledge gaps. Advances in microbiome sequencing and artificial intelligence may facilitate personalized interventions. Standardizing microbiota-based diagnostics and validating their efficacy in clinical trials are crucial for their integration into ITP management. Bridging these gaps may lead to microbiota-driven strategies that enhance immune regulation and improve patient outcomes.
Additional Links: PMID-40574831
PubMed:
Citation:
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@article {pmid40574831,
year = {2025},
author = {Guo, X and Wang, K and Liu, Q and Baran, N and Ma, W},
title = {The gut-immune axis in primary immune thrombocytopenia (ITP): a paradigm shifts in treatment approaches.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1595977},
pmid = {40574831},
issn = {1664-3224},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Purpura, Thrombocytopenic, Idiopathic/therapy/immunology/microbiology ; Dysbiosis/immunology ; Fecal Microbiota Transplantation ; Animals ; Blood Platelets/immunology ; Probiotics/therapeutic use ; },
abstract = {Primary immune thrombocytopenia (ITP) is an autoimmune disorder characterized by platelet destruction and impaired production, leading to bleeding risk. While immunosuppressive therapies are standard, many patients experience relapses or refractory disease, highlighting the need for novel approaches. Emerging evidence suggests the gut microbiota plays a role in immune regulation, yet its impact on ITP remains unclear. Dysbiosis has been linked to immune dysfunction in other autoimmune diseases, but whether it drives or results from immune dysregulation in ITP is debated. This review explores the gut-immune axis in ITP, focusing on microbiota-driven immune modulation, cytokine signaling, and platelet homeostasis. We assess microbiota-targeted interventions, including fecal microbiota transplantation (FMT), probiotics, and dietary modifications, while addressing key controversies and knowledge gaps. Advances in microbiome sequencing and artificial intelligence may facilitate personalized interventions. Standardizing microbiota-based diagnostics and validating their efficacy in clinical trials are crucial for their integration into ITP management. Bridging these gaps may lead to microbiota-driven strategies that enhance immune regulation and improve patient outcomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/immunology
*Purpura, Thrombocytopenic, Idiopathic/therapy/immunology/microbiology
Dysbiosis/immunology
Fecal Microbiota Transplantation
Animals
Blood Platelets/immunology
Probiotics/therapeutic use
RevDate: 2025-06-27
Fecal Microbiota Transplantation from Noni Fruit Phenolic-Rich Extract Intervention Mouse Donors Ameliorates Lipid Metabolism Disorder by Regulating the FXR-FGF15 Pathway in a Gut Microbiota-Dependent Manner.
Journal of agricultural and food chemistry [Epub ahead of print].
Noni fruit phenolic-rich extract (NFE) has been confirmed to alleviate lipid metabolism disturbance, with emerging evidence implicating bile acids (BAs) metabolism in a gut microbiota-dependent manner in mediating the effect. The effect and potential mechanism of fecal microbiota transplantation from NFE intervention mouse donors (FMT-NFE) on lipid metabolism disorder were investigated. The results reveal FMT-NFE intervention regulated the body weight, lipid profile levels, and liver damage. FMT-NFE intervention upgraded the abundance of bile salt hydrolase (BSH)-expressing bacteria and short-chain fatty acid (SCFA)-producing bacteria in feces, which is accompanied by changes of BSH activity and BAs profile as well as elevation of the SCFA level. Moreover, western blotting and immunofluorescence results confirmed the intestinal FXR-FGF15 pathway was activated by FMT-NFE intervention, which was accompanied by activation of the liver FXR and inhibition of CYP7A1 expression to control cholesterol-to-BAs conversion. These findings underscore the mechanisms behind maintaining BAs and lipid metabolism homeostasis of NFE.
Additional Links: PMID-40574570
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PubMed:
Citation:
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@article {pmid40574570,
year = {2025},
author = {Yang, D and Yang, X and Zhou, Y and Wang, H and Wang, R},
title = {Fecal Microbiota Transplantation from Noni Fruit Phenolic-Rich Extract Intervention Mouse Donors Ameliorates Lipid Metabolism Disorder by Regulating the FXR-FGF15 Pathway in a Gut Microbiota-Dependent Manner.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c05184},
pmid = {40574570},
issn = {1520-5118},
abstract = {Noni fruit phenolic-rich extract (NFE) has been confirmed to alleviate lipid metabolism disturbance, with emerging evidence implicating bile acids (BAs) metabolism in a gut microbiota-dependent manner in mediating the effect. The effect and potential mechanism of fecal microbiota transplantation from NFE intervention mouse donors (FMT-NFE) on lipid metabolism disorder were investigated. The results reveal FMT-NFE intervention regulated the body weight, lipid profile levels, and liver damage. FMT-NFE intervention upgraded the abundance of bile salt hydrolase (BSH)-expressing bacteria and short-chain fatty acid (SCFA)-producing bacteria in feces, which is accompanied by changes of BSH activity and BAs profile as well as elevation of the SCFA level. Moreover, western blotting and immunofluorescence results confirmed the intestinal FXR-FGF15 pathway was activated by FMT-NFE intervention, which was accompanied by activation of the liver FXR and inhibition of CYP7A1 expression to control cholesterol-to-BAs conversion. These findings underscore the mechanisms behind maintaining BAs and lipid metabolism homeostasis of NFE.},
}
RevDate: 2025-06-27
CmpDate: 2025-06-27
Ten Previously Unassigned Human Cosavirus Genotypes Detected in Feces of Children with Non-Polio Acute Flaccid Paralysis in Nigeria in 2020.
Viruses, 17(6): pii:v17060844.
Since its discovery via metagenomics in 2008, human cosavirus (HCoSV) has been detected in the cerebrospinal fluid (CSF) and feces of humans with meningitis, acute flaccid paralysis (AFP), and acute gastroenteritis. To date, 34 HCoSV genotypes have been documented by the Picornaviridae study group. However, the documented genetic diversity of HCoSV in Nigeria is limited. Here we describe the genetic diversity of HCoSV in Nigeria using a metagenomics approach. Archived and anonymized fecal specimens from children (under 15 years old) diagnosed with non-polio AFP from five states in Nigeria were analyzed. Virus-like particles were purified from 55 pools (made from 254 samples) using the NetoVIR protocol. Pools were subjected to nucleic acid extraction and metagenomic sequencing. Reads were trimmed and assembled, and contigs classified as HCoSV were subjected to phylogenetic, pairwise identity, recombination analysis, and, when necessary, immuno-informatics and capsid structure prediction. Fifteen pools yielded 23 genomes of HCoSV. Phylogenetic and pairwise identity analysis showed that all belonged to four species (eleven, three, three, and six members of Cosavirus asiani, Cosavirus bepakis, Cosavirus depakis, and Cosavirus eaustrali, respectively) and seventeen genotypes. Ten genomes belong to seven (HCoSV-A3/A10, A15, A17, A19, A24, D3, and E1) previously assigned genotypes, while the remaining thirteen genomes belonged to ten newly proposed genotypes across the four HCoSV species, based on the near-complete VP1 region (VP1*) of the cosavirus genome. Our analysis suggests the existence of at least seven and eight Cosavirus bepakis and Cosavirus eaustrali genotypes, respectively (including those described here). We report the first near-complete genomes of Cosavirus bepakis and Cosavirus depakis from Nigeria, which contributes to the increasing knowledge of the diversity of HCoSV, raising the number of tentative genotypes from 34 to over 40. Our findings suggest that the genetic diversity of HCoSV might be broader than is currently documented, highlighting the need for enhanced surveillance.
Additional Links: PMID-40573435
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PubMed:
Citation:
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@article {pmid40573435,
year = {2025},
author = {Ajileye, TG and Akinleye, TE and Faleye, TOC and De Coninck, L and George, UE and Onoja, AB and Agbaje, ST and Ifeorah, IM and Olayinka, OA and Oni, EI and Oragwa, AO and Popoola, BO and Olayinka, OT and Osasona, OG and George, OA and Ajayi, PG and Suleiman, AA and Muhammad, AI and Komolafe, I and Adeniji, AJ and Matthijnssens, J and Adewumi, MO},
title = {Ten Previously Unassigned Human Cosavirus Genotypes Detected in Feces of Children with Non-Polio Acute Flaccid Paralysis in Nigeria in 2020.},
journal = {Viruses},
volume = {17},
number = {6},
pages = {},
doi = {10.3390/v17060844},
pmid = {40573435},
issn = {1999-4915},
mesh = {Humans ; *Feces/virology ; Nigeria/epidemiology ; Phylogeny ; *Genotype ; Child ; Child, Preschool ; *Picornaviridae/genetics/classification/isolation & purification ; Genome, Viral ; Infant ; *Picornaviridae Infections/virology/epidemiology ; Genetic Variation ; Adolescent ; Female ; Male ; Metagenomics ; *Paralysis/virology ; },
abstract = {Since its discovery via metagenomics in 2008, human cosavirus (HCoSV) has been detected in the cerebrospinal fluid (CSF) and feces of humans with meningitis, acute flaccid paralysis (AFP), and acute gastroenteritis. To date, 34 HCoSV genotypes have been documented by the Picornaviridae study group. However, the documented genetic diversity of HCoSV in Nigeria is limited. Here we describe the genetic diversity of HCoSV in Nigeria using a metagenomics approach. Archived and anonymized fecal specimens from children (under 15 years old) diagnosed with non-polio AFP from five states in Nigeria were analyzed. Virus-like particles were purified from 55 pools (made from 254 samples) using the NetoVIR protocol. Pools were subjected to nucleic acid extraction and metagenomic sequencing. Reads were trimmed and assembled, and contigs classified as HCoSV were subjected to phylogenetic, pairwise identity, recombination analysis, and, when necessary, immuno-informatics and capsid structure prediction. Fifteen pools yielded 23 genomes of HCoSV. Phylogenetic and pairwise identity analysis showed that all belonged to four species (eleven, three, three, and six members of Cosavirus asiani, Cosavirus bepakis, Cosavirus depakis, and Cosavirus eaustrali, respectively) and seventeen genotypes. Ten genomes belong to seven (HCoSV-A3/A10, A15, A17, A19, A24, D3, and E1) previously assigned genotypes, while the remaining thirteen genomes belonged to ten newly proposed genotypes across the four HCoSV species, based on the near-complete VP1 region (VP1*) of the cosavirus genome. Our analysis suggests the existence of at least seven and eight Cosavirus bepakis and Cosavirus eaustrali genotypes, respectively (including those described here). We report the first near-complete genomes of Cosavirus bepakis and Cosavirus depakis from Nigeria, which contributes to the increasing knowledge of the diversity of HCoSV, raising the number of tentative genotypes from 34 to over 40. Our findings suggest that the genetic diversity of HCoSV might be broader than is currently documented, highlighting the need for enhanced surveillance.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Feces/virology
Nigeria/epidemiology
Phylogeny
*Genotype
Child
Child, Preschool
*Picornaviridae/genetics/classification/isolation & purification
Genome, Viral
Infant
*Picornaviridae Infections/virology/epidemiology
Genetic Variation
Adolescent
Female
Male
Metagenomics
*Paralysis/virology
RevDate: 2025-06-27
CmpDate: 2025-06-27
Inhibition of Bovine Enterovirus Infection by Magnolol via Modulating the Gut Microbiota in Mice.
Viruses, 17(6): pii:v17060750.
Bovine enterovirus (BEV) infection is one of the important infectious diseases that cause digestive and respiratory symptoms in cattle, posing a significant threat to the cattle industry. Currently, no vaccines or therapeutic drugs are available for this disease. In our study, we utilized a mouse model to investigate the effects of BEV infection on the gut microbiota and examine the therapeutic potential of magnolol (Mag), a polyphenolic bioactive substance, in terms of BEV infection. BEV infection significantly altered the microbiota composition, where the abundance of some beneficial bacteria, such as Lactobacillaceae and Lactobacillus, was markedly reduced. Mag effectively inhibited BEV infection in vivo. Upon BEV infection, Mag treatment reduced the α-diversity of the microbiota, with statistically significant differences on day 3 post-infection compared to the Mag-untreated group. More interestingly, Mag treatment significantly reversed the effect of BEV infection on the Lactobacillaceae and Lactobacillus abundance, indicating that Mag positively regulates beneficial bacteria. The fecal microbiota transplantation (FMT) experiment demonstrated that feces from Mag-treated mice significantly decreased the virus loads in the small intestine samples of BEV-infected mice. These findings demonstrate the interaction between BEV infection and the gut microbiota and highlight the important regulatory role of the gut microbiota in Mag's anti-BEV effects, opening up a new avenue for preventing and controlling BEV infection via targeted modulation of the gut microbiota.
Additional Links: PMID-40573341
Publisher:
PubMed:
Citation:
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@article {pmid40573341,
year = {2025},
author = {Hu, J and Zhang, Q and Liu, D and Cui, X and Wang, Q and Gong, W and Wang, X},
title = {Inhibition of Bovine Enterovirus Infection by Magnolol via Modulating the Gut Microbiota in Mice.},
journal = {Viruses},
volume = {17},
number = {6},
pages = {},
doi = {10.3390/v17060750},
pmid = {40573341},
issn = {1999-4915},
support = {2016YFD0500904 and 2017YFD0500104//National Key Research & Development Program/ ; },
mesh = {Animals ; *Lignans/pharmacology/therapeutic use ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Biphenyl Compounds/pharmacology/therapeutic use ; *Enterovirus Infections/drug therapy/virology/veterinary/microbiology ; Cattle ; Disease Models, Animal ; Feces/microbiology ; Fecal Microbiota Transplantation ; *Antiviral Agents/pharmacology ; Viral Load/drug effects ; Enterovirus/drug effects ; },
abstract = {Bovine enterovirus (BEV) infection is one of the important infectious diseases that cause digestive and respiratory symptoms in cattle, posing a significant threat to the cattle industry. Currently, no vaccines or therapeutic drugs are available for this disease. In our study, we utilized a mouse model to investigate the effects of BEV infection on the gut microbiota and examine the therapeutic potential of magnolol (Mag), a polyphenolic bioactive substance, in terms of BEV infection. BEV infection significantly altered the microbiota composition, where the abundance of some beneficial bacteria, such as Lactobacillaceae and Lactobacillus, was markedly reduced. Mag effectively inhibited BEV infection in vivo. Upon BEV infection, Mag treatment reduced the α-diversity of the microbiota, with statistically significant differences on day 3 post-infection compared to the Mag-untreated group. More interestingly, Mag treatment significantly reversed the effect of BEV infection on the Lactobacillaceae and Lactobacillus abundance, indicating that Mag positively regulates beneficial bacteria. The fecal microbiota transplantation (FMT) experiment demonstrated that feces from Mag-treated mice significantly decreased the virus loads in the small intestine samples of BEV-infected mice. These findings demonstrate the interaction between BEV infection and the gut microbiota and highlight the important regulatory role of the gut microbiota in Mag's anti-BEV effects, opening up a new avenue for preventing and controlling BEV infection via targeted modulation of the gut microbiota.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Lignans/pharmacology/therapeutic use
*Gastrointestinal Microbiome/drug effects
Mice
*Biphenyl Compounds/pharmacology/therapeutic use
*Enterovirus Infections/drug therapy/virology/veterinary/microbiology
Cattle
Disease Models, Animal
Feces/microbiology
Fecal Microbiota Transplantation
*Antiviral Agents/pharmacology
Viral Load/drug effects
Enterovirus/drug effects
RevDate: 2025-06-27
CmpDate: 2025-06-27
Kidney-Gut Axis in Chronic Kidney Disease: Therapeutic Perspectives from Microbiota Modulation and Nutrition.
Nutrients, 17(12): pii:nu17121961.
Chronic kidney disease (CKD) has a high prevalence worldwide, with an increasing incidence. One of the mechanisms of CKD progression involves a disordered inter-organ relationship between the kidneys and the intestine, known as the kidney-gut axis. In CKD, two pathological gut conditions-disturbed gut microbiota composition called uremic dysbiosis and leaky gut-contribute to the progression of CKD. Dysbiosis is associated with the increased production of gut-derived uremic toxins, leaky gut, and chronic systemic inflammation, leading to worsening uremia, which in turn aggravates the gut condition. This vicious cycle should be a target of the therapeutic strategy against CKD. The modulation of uremic dysbiosis, including prebiotics, probiotics, and synbiotics, has been a typical treatment approach, although clinical evidence for their efficacy has been insufficient. Some non-antibiotic drugs have an impact on human gut bacteria that are believed to play a role in their clinical efficacy on kidney function. Nutrition therapies, including a low-protein diet, dietary fiber, a Mediterranean diet, and whole grains, positively influence gut microbiota composition and have been linked to a decreased risk of CKD. Novel strategies are currently being explored, involving the use of postbiotics, microbiome sequencing techniques, and fecal microbiota transplantation, although clinical application remains to be tested. Human trials investigating the above-mentioned interventions remain inconclusive due to several limitations, including dietary variability and genetic factors. Future research should focus on the development of more effective probiotics, prebiotics, and microbial metabolism-modifying drugs, not only for CKD but for other systemic diseases as well.
Additional Links: PMID-40573072
Publisher:
PubMed:
Citation:
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@article {pmid40573072,
year = {2025},
author = {Wakino, S and Hasegawa, K and Tamaki, M and Minato, M and Inagaki, T},
title = {Kidney-Gut Axis in Chronic Kidney Disease: Therapeutic Perspectives from Microbiota Modulation and Nutrition.},
journal = {Nutrients},
volume = {17},
number = {12},
pages = {},
doi = {10.3390/nu17121961},
pmid = {40573072},
issn = {2072-6643},
mesh = {Humans ; *Renal Insufficiency, Chronic/microbiology/therapy/physiopathology ; *Gastrointestinal Microbiome/physiology ; *Dysbiosis/therapy/microbiology ; Probiotics/therapeutic use ; Prebiotics/administration & dosage ; *Kidney/physiopathology ; Synbiotics/administration & dosage ; Fecal Microbiota Transplantation ; Uremia/microbiology ; *Nutrition Therapy/methods ; },
abstract = {Chronic kidney disease (CKD) has a high prevalence worldwide, with an increasing incidence. One of the mechanisms of CKD progression involves a disordered inter-organ relationship between the kidneys and the intestine, known as the kidney-gut axis. In CKD, two pathological gut conditions-disturbed gut microbiota composition called uremic dysbiosis and leaky gut-contribute to the progression of CKD. Dysbiosis is associated with the increased production of gut-derived uremic toxins, leaky gut, and chronic systemic inflammation, leading to worsening uremia, which in turn aggravates the gut condition. This vicious cycle should be a target of the therapeutic strategy against CKD. The modulation of uremic dysbiosis, including prebiotics, probiotics, and synbiotics, has been a typical treatment approach, although clinical evidence for their efficacy has been insufficient. Some non-antibiotic drugs have an impact on human gut bacteria that are believed to play a role in their clinical efficacy on kidney function. Nutrition therapies, including a low-protein diet, dietary fiber, a Mediterranean diet, and whole grains, positively influence gut microbiota composition and have been linked to a decreased risk of CKD. Novel strategies are currently being explored, involving the use of postbiotics, microbiome sequencing techniques, and fecal microbiota transplantation, although clinical application remains to be tested. Human trials investigating the above-mentioned interventions remain inconclusive due to several limitations, including dietary variability and genetic factors. Future research should focus on the development of more effective probiotics, prebiotics, and microbial metabolism-modifying drugs, not only for CKD but for other systemic diseases as well.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Renal Insufficiency, Chronic/microbiology/therapy/physiopathology
*Gastrointestinal Microbiome/physiology
*Dysbiosis/therapy/microbiology
Probiotics/therapeutic use
Prebiotics/administration & dosage
*Kidney/physiopathology
Synbiotics/administration & dosage
Fecal Microbiota Transplantation
Uremia/microbiology
*Nutrition Therapy/methods
RevDate: 2025-06-27
The Interplay Between the Gut Microbiota and Colorectal Cancer: A Review of the Literature.
Microorganisms, 13(6):.
Lifestyle, diet, and genetics are established risk factors for developing colorectal cancer (CRC). In recent years, the role of the gut microbiota (GM) has been increasingly highlighted in several studies, suggesting an effect on both the disease's pathogenesis and the efficacy and tolerability of treatments. We conducted a search on Medline, aiming to identify published studies exploring the role of the GM in the development and treatment of CRC. Dysbiosis, an imbalance in GM, is common in CRC patients and is associated with precancerous lesions, aggressive tumors, and varied therapy outcomes. Restoring GM balance can reduce treatment complications and may improve prognosis. The review details how GM influences CRC through metabolite production, inflammation modulation, and immune response alteration. Diet significantly impacts GM composition, with processed meats and high-fat diets increasing CRC risk, while fiber-rich diets are protective. The role of the GM in CRC treatments like surgery, chemotherapy, radiotherapy, and immunotherapy is also explored, noting its influence on complications, chemoresistance, and treatment efficacy. Future strategies involving GM modulation through diet, probiotics, and fecal microbiota transplantation (FMT) show promise for CRC prevention and treatment, warranting further research.
Additional Links: PMID-40572299
PubMed:
Citation:
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@article {pmid40572299,
year = {2025},
author = {Cintoni, M and Palombaro, M and Zoli, E and D'Agostino, G and Pulcini, G and Leonardi, E and Raoul, P and Rinninella, E and De Maio, F and Capristo, E and Gasbarrini, A and Mele, MC},
title = {The Interplay Between the Gut Microbiota and Colorectal Cancer: A Review of the Literature.},
journal = {Microorganisms},
volume = {13},
number = {6},
pages = {},
pmid = {40572299},
issn = {2076-2607},
abstract = {Lifestyle, diet, and genetics are established risk factors for developing colorectal cancer (CRC). In recent years, the role of the gut microbiota (GM) has been increasingly highlighted in several studies, suggesting an effect on both the disease's pathogenesis and the efficacy and tolerability of treatments. We conducted a search on Medline, aiming to identify published studies exploring the role of the GM in the development and treatment of CRC. Dysbiosis, an imbalance in GM, is common in CRC patients and is associated with precancerous lesions, aggressive tumors, and varied therapy outcomes. Restoring GM balance can reduce treatment complications and may improve prognosis. The review details how GM influences CRC through metabolite production, inflammation modulation, and immune response alteration. Diet significantly impacts GM composition, with processed meats and high-fat diets increasing CRC risk, while fiber-rich diets are protective. The role of the GM in CRC treatments like surgery, chemotherapy, radiotherapy, and immunotherapy is also explored, noting its influence on complications, chemoresistance, and treatment efficacy. Future strategies involving GM modulation through diet, probiotics, and fecal microbiota transplantation (FMT) show promise for CRC prevention and treatment, warranting further research.},
}
RevDate: 2025-06-27
Modulating the Gut-Muscle Axis: Increasing SCFA-Producing Gut Microbiota Commensals and Decreasing Endotoxin Production to Mitigate Cancer Cachexia.
Microorganisms, 13(6):.
Cancer cachexia is a multi-organ and multifactorial syndrome characterized by muscle wasting (with or without adipose tissue loss) and systemic inflammation in patients with advanced malignancies. Gut microbiota dysbiosis, particularly the depletion of short-chain fatty acid (SCFA)-producing bacteria, may contribute to the progression of cancer cachexia. Studies in both murine models and humans consistently associate cachexia with a decline in SCFA-producing gut microbiota commensals and an overgrowth of pro-inflammatory pathobionts. These microbial imbalances may lead to reduced levels of SCFAs and branched-chain amino acids (BCAAs) and alter the normal bile acid profile. BCAAs and the maintenance of a normal bile acid profile are associated with muscle synthesis and decreased breakdown. While SCFAs (acetate, propionate, and butyrate), contribute to intestinal barrier integrity and immune regulation. SCFA depletion may increase gut permeability, allowing bacterial endotoxins, such as lipopolysaccharide (LPS), to enter the bloodstream. This may lead to chronic inflammation, muscle catabolism, and impairment of anabolic pathways. Interventions targeting gut microbiota in preclinical models have mitigated inflammation and muscle loss. While clinical data are limited, it suggests an improvement in immune functions and better tolerance to anticancer therapies. Current evidence is predominantly derived from cross-sectional studies suggesting associations without causality. Thus, future longitudinal studies are needed to identify biomarkers and optimize personalized therapy.
Additional Links: PMID-40572244
PubMed:
Citation:
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@article {pmid40572244,
year = {2025},
author = {Roy, S and Alizadeh Bahmani, AH and Davids, M and Herrema, H and Nieuwdorp, M},
title = {Modulating the Gut-Muscle Axis: Increasing SCFA-Producing Gut Microbiota Commensals and Decreasing Endotoxin Production to Mitigate Cancer Cachexia.},
journal = {Microorganisms},
volume = {13},
number = {6},
pages = {},
pmid = {40572244},
issn = {2076-2607},
abstract = {Cancer cachexia is a multi-organ and multifactorial syndrome characterized by muscle wasting (with or without adipose tissue loss) and systemic inflammation in patients with advanced malignancies. Gut microbiota dysbiosis, particularly the depletion of short-chain fatty acid (SCFA)-producing bacteria, may contribute to the progression of cancer cachexia. Studies in both murine models and humans consistently associate cachexia with a decline in SCFA-producing gut microbiota commensals and an overgrowth of pro-inflammatory pathobionts. These microbial imbalances may lead to reduced levels of SCFAs and branched-chain amino acids (BCAAs) and alter the normal bile acid profile. BCAAs and the maintenance of a normal bile acid profile are associated with muscle synthesis and decreased breakdown. While SCFAs (acetate, propionate, and butyrate), contribute to intestinal barrier integrity and immune regulation. SCFA depletion may increase gut permeability, allowing bacterial endotoxins, such as lipopolysaccharide (LPS), to enter the bloodstream. This may lead to chronic inflammation, muscle catabolism, and impairment of anabolic pathways. Interventions targeting gut microbiota in preclinical models have mitigated inflammation and muscle loss. While clinical data are limited, it suggests an improvement in immune functions and better tolerance to anticancer therapies. Current evidence is predominantly derived from cross-sectional studies suggesting associations without causality. Thus, future longitudinal studies are needed to identify biomarkers and optimize personalized therapy.},
}
RevDate: 2025-06-27
The Effects of Fecal Microbial Transplantation on the Symptoms in Autism Spectrum Disorder, Gut Microbiota and Metabolites: A Scoping Review.
Microorganisms, 13(6):.
The bilateral interaction between the brain and the gut has recently been on the spectrum of researchers' interests, including complex neural, endocrinological, and immunological signaling pathways. The first case reports and clinical studies have already reported that delivering microbes through fecal microbial transplantation (FMT) may alleviate symptoms of psychiatric disorders. Therefore, modifying the gut microbiota through FMT holds promise as a potential treatment for psychiatric diseases. This scoping review assessed studies from PubMed related to FMT in autism spectrum disorder and attention deficit hyperactivity disorder. The evaluation included nine clinical studies and case reports. The beneficial and persistent effect on the autism spectrum disorder (ASD) symptoms has been reported. Also, an increased microflora diversity and altered levels of neurometabolites in serum were identified, albeit with a tendency to return to baseline over time. The microbiome-gut-brain axis could provide new targets for preventing and treating psychiatric disorders. However, a recent large randomized clinical trial has shed light on the previously collected data and suggested a possible contribution of the placebo effect. This highlights the necessity of large randomized double-blind studies to reliably assess the effect of FMT in ASD.
Additional Links: PMID-40572178
PubMed:
Citation:
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@article {pmid40572178,
year = {2025},
author = {Maniscalco, I and Bartochowski, P and Priori, V and Iancau, SP and De Francesco, M and Innamorati, M and Jagodzinska, N and Giupponi, G and Masucci, L and Conca, A and Mroczek, M},
title = {The Effects of Fecal Microbial Transplantation on the Symptoms in Autism Spectrum Disorder, Gut Microbiota and Metabolites: A Scoping Review.},
journal = {Microorganisms},
volume = {13},
number = {6},
pages = {},
pmid = {40572178},
issn = {2076-2607},
abstract = {The bilateral interaction between the brain and the gut has recently been on the spectrum of researchers' interests, including complex neural, endocrinological, and immunological signaling pathways. The first case reports and clinical studies have already reported that delivering microbes through fecal microbial transplantation (FMT) may alleviate symptoms of psychiatric disorders. Therefore, modifying the gut microbiota through FMT holds promise as a potential treatment for psychiatric diseases. This scoping review assessed studies from PubMed related to FMT in autism spectrum disorder and attention deficit hyperactivity disorder. The evaluation included nine clinical studies and case reports. The beneficial and persistent effect on the autism spectrum disorder (ASD) symptoms has been reported. Also, an increased microflora diversity and altered levels of neurometabolites in serum were identified, albeit with a tendency to return to baseline over time. The microbiome-gut-brain axis could provide new targets for preventing and treating psychiatric disorders. However, a recent large randomized clinical trial has shed light on the previously collected data and suggested a possible contribution of the placebo effect. This highlights the necessity of large randomized double-blind studies to reliably assess the effect of FMT in ASD.},
}
RevDate: 2025-06-26
Gut microbial dysbiosis aggravated Parkinson-like pathology induced by MPTP/probenecid.
Physiology & behavior pii:S0031-9384(25)00209-4 [Epub ahead of print].
Parkinson's disease (PD) is a common neurodegenerative disorder, characterized by resting tremor, bradykinesia, rigidity and postural instability. Recent studies have proved that gut microbiota (GM) dysbiosis exists in PD patients. However, the causal relationship between gut microbial dysbiosis and pathogenesis of PD remains unexplored. Here, using MPTP/probenecid-induced PD mouse model and an antibiotic cocktail (ABX)-induced pseudo-germ-free status, we observed that GM diversity and abundance significantly decreased in feces of ABX-treated PD mice by 16S rRNA sequencing. Remarkably, gut microbial dysbiosis induced by ABX aggravated GI dysfunction and motor deficits in PD mice. Moreover, ABX treatment caused more severe inflammation, and dopaminergic (DAergic) neuronal loss in both the gut and brain. Further study showed that fecal microbiota transplantation (FMT) corrected gut microbial dysbiosis, along with increased short-chain fatty acids (SCFAs). Additionally, GI and motor dysfunctions were improved, peripheral and central inflammation were also attenuated when PD mice were treated with FMT. These findings revealed that gut microbial dysbiosis could aggravate PD pathological damages, and highlighted that gut microbial dysbiosis might be an important factor that impacts PD pathogenesis through the microbiota-gut-brain axis.
Additional Links: PMID-40571138
Publisher:
PubMed:
Citation:
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@article {pmid40571138,
year = {2025},
author = {Chen, QZ and Shang, JM and Jiang, YQ and Yang, Y and Zang, CX and Ma, JW and Dong, YR and Wang, JR and Zhou, N and Yang, X and Li, FF and Bao, XQ and Zhang, D},
title = {Gut microbial dysbiosis aggravated Parkinson-like pathology induced by MPTP/probenecid.},
journal = {Physiology & behavior},
volume = {},
number = {},
pages = {115008},
doi = {10.1016/j.physbeh.2025.115008},
pmid = {40571138},
issn = {1873-507X},
abstract = {Parkinson's disease (PD) is a common neurodegenerative disorder, characterized by resting tremor, bradykinesia, rigidity and postural instability. Recent studies have proved that gut microbiota (GM) dysbiosis exists in PD patients. However, the causal relationship between gut microbial dysbiosis and pathogenesis of PD remains unexplored. Here, using MPTP/probenecid-induced PD mouse model and an antibiotic cocktail (ABX)-induced pseudo-germ-free status, we observed that GM diversity and abundance significantly decreased in feces of ABX-treated PD mice by 16S rRNA sequencing. Remarkably, gut microbial dysbiosis induced by ABX aggravated GI dysfunction and motor deficits in PD mice. Moreover, ABX treatment caused more severe inflammation, and dopaminergic (DAergic) neuronal loss in both the gut and brain. Further study showed that fecal microbiota transplantation (FMT) corrected gut microbial dysbiosis, along with increased short-chain fatty acids (SCFAs). Additionally, GI and motor dysfunctions were improved, peripheral and central inflammation were also attenuated when PD mice were treated with FMT. These findings revealed that gut microbial dysbiosis could aggravate PD pathological damages, and highlighted that gut microbial dysbiosis might be an important factor that impacts PD pathogenesis through the microbiota-gut-brain axis.},
}
RevDate: 2025-06-26
Are we there yet? Gut microbiota for cancer diagnosis, prognosis and treatment.
Seminars in oncology, 52(4):152376 pii:S0093-7754(25)00068-5 [Epub ahead of print].
Cancer remains as one of the leading causes of death worldwide, emphasizing the need for innovative diagnostic and therapeutic tools. The gut microbiota has emerged as a factor that influences cancer progression, prognosis, and treatment outcomes. This review analyzes observational and interventional studies conducted with human subjects over the past 5 years, highlighting significant advancements in gut microbiota research for cancer management. Observational studies consistently demonstrated differences in gut microbial composition between cancer patients and healthy controls. Moreover, microbial diversity, particularly at the species and strain level, correlated significantly with clinical outcomes. Interventional studies showed the potential of probiotics and fecal microbiota transplantation (FMT) as adjuncts in cancer therapy by restoring microbial diversity, reducing inflammation, and alleviating chemotherapy-induced complications. Collectively, these findings suggest the gut microbiota's potential as a tool for cancer care. Future research should focus on standardizing taxonomic-level analyses, optimizing probiotic formulations, and validating FMT/AFMT clinical protocols to fully harness the gut microbiota's diagnostic and therapeutic capabilities in oncology.
Additional Links: PMID-40570572
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PubMed:
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@article {pmid40570572,
year = {2025},
author = {Ordóñez, C and Zurita, S and Ramírez, G and Cordeiro, F and Garcia-Matamoros, K and Huaman-Garaicoa, F and Orellana-Manzano, A and Sandoya-Onofre, L and Pogo, J and Carvajal-Aldaz, D},
title = {Are we there yet? Gut microbiota for cancer diagnosis, prognosis and treatment.},
journal = {Seminars in oncology},
volume = {52},
number = {4},
pages = {152376},
doi = {10.1016/j.seminoncol.2025.152376},
pmid = {40570572},
issn = {1532-8708},
abstract = {Cancer remains as one of the leading causes of death worldwide, emphasizing the need for innovative diagnostic and therapeutic tools. The gut microbiota has emerged as a factor that influences cancer progression, prognosis, and treatment outcomes. This review analyzes observational and interventional studies conducted with human subjects over the past 5 years, highlighting significant advancements in gut microbiota research for cancer management. Observational studies consistently demonstrated differences in gut microbial composition between cancer patients and healthy controls. Moreover, microbial diversity, particularly at the species and strain level, correlated significantly with clinical outcomes. Interventional studies showed the potential of probiotics and fecal microbiota transplantation (FMT) as adjuncts in cancer therapy by restoring microbial diversity, reducing inflammation, and alleviating chemotherapy-induced complications. Collectively, these findings suggest the gut microbiota's potential as a tool for cancer care. Future research should focus on standardizing taxonomic-level analyses, optimizing probiotic formulations, and validating FMT/AFMT clinical protocols to fully harness the gut microbiota's diagnostic and therapeutic capabilities in oncology.},
}
RevDate: 2025-06-26
CmpDate: 2025-06-26
The effect of fecal microbiota transplantation on levels of tryptophan metabolites in intestine and serum of gnotobiotic mice.
Biomeditsinskaia khimiia, 71(3):209-216.
Gut microbiota is one of the key suppliers of tryptophan metabolites, which perform various functions in the host organism, including their role as signaling molecules. Fecal microbiota transplantation (FMT) is widely used as a method for determining the contribution of microorganisms to the content of various metabolites in the holoorganism. In this regard, the aim of our study was to investigate the effect of FMT on the level of tryptophan metabolites in feces and blood in gnotobiotic mice. It was found that both before and after FMT, indole-3-lactate, and quinolinic acid were the dominant tryptophan metabolites in the intestine. FMT increased the content of both indoles (indole-3-acetate, indole-3-acrylate, indole-3-butyrate, indole-3-lactate) and kynurenines (anthranilic and xanthurenic acids) in the intestine. In serum of mice after FMT, indole metabolites (indole-3-butyrate, indole-3-carboxaldehyde, indole-3-lactate, indole-3-propionate) predominantly increased; however, tryptamine and xanthurenic acid also demonstrated a clear increase. The use of FMT demonstrates that the intestinal microbiota is a source of not only indole derivatives of tryptophan, but also metabolites of the kynurenine pathway.
Additional Links: PMID-40570072
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@article {pmid40570072,
year = {2025},
author = {Shatova, OP and Shestopalov, AV and Zlatnik, EY and Novikova, IA and Goncharova, AS and Maksimov, AY},
title = {The effect of fecal microbiota transplantation on levels of tryptophan metabolites in intestine and serum of gnotobiotic mice.},
journal = {Biomeditsinskaia khimiia},
volume = {71},
number = {3},
pages = {209-216},
doi = {10.18097/PBMCR1554},
pmid = {40570072},
issn = {2310-6972},
mesh = {Animals ; *Tryptophan/metabolism/blood ; Mice ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; Germ-Free Life ; Indoles/metabolism/blood ; *Intestines/microbiology ; Feces/microbiology ; Male ; Kynurenine/blood/metabolism ; Quinolinic Acid/metabolism/blood ; },
abstract = {Gut microbiota is one of the key suppliers of tryptophan metabolites, which perform various functions in the host organism, including their role as signaling molecules. Fecal microbiota transplantation (FMT) is widely used as a method for determining the contribution of microorganisms to the content of various metabolites in the holoorganism. In this regard, the aim of our study was to investigate the effect of FMT on the level of tryptophan metabolites in feces and blood in gnotobiotic mice. It was found that both before and after FMT, indole-3-lactate, and quinolinic acid were the dominant tryptophan metabolites in the intestine. FMT increased the content of both indoles (indole-3-acetate, indole-3-acrylate, indole-3-butyrate, indole-3-lactate) and kynurenines (anthranilic and xanthurenic acids) in the intestine. In serum of mice after FMT, indole metabolites (indole-3-butyrate, indole-3-carboxaldehyde, indole-3-lactate, indole-3-propionate) predominantly increased; however, tryptamine and xanthurenic acid also demonstrated a clear increase. The use of FMT demonstrates that the intestinal microbiota is a source of not only indole derivatives of tryptophan, but also metabolites of the kynurenine pathway.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Tryptophan/metabolism/blood
Mice
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
Germ-Free Life
Indoles/metabolism/blood
*Intestines/microbiology
Feces/microbiology
Male
Kynurenine/blood/metabolism
Quinolinic Acid/metabolism/blood
RevDate: 2025-06-26
Microbiota interaction with Tregs: a target for colitis.
Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico [Epub ahead of print].
Gut-resident microbiota associate with host immune system to promote homeostasis, and regulatory T cells (Tregs) are critical in the maintenance of immune balance. Tregs have immunosuppressive activity, and their presence hampers the development of inflammatory diseases. This review aims to unravel microbiome impact on Tregs in bowel inflammation and harnessing such interaction to combat colitis as a separate disease or a consequence of immune checkpoint inhibitor (ICI) therapy of cancer. Short-chain fatty acids (SCFAs) are microbial-derived metabolites associated positively with Treg generation and maintenance and being effective for hampering bowel inflammation. Treg induction shapes gut microbiota profile and support microorganism colonization in their niche and protect the host from inflammation, while suppression of Treg differentiation and activity directs microbiota-induced Th17 expansion and inducing inflammation. Thus, balancing Treg representation with Th17 cells and Treg reprogramming through manipulation of gut microbiota can offer therapy. Microbiota epithelial attachment/detachment and interaction with antigen-presenting cells (APCs) are important for the final fate of T cell signature. Fecal microbial transplantation (FMT) is a strategy for promoting normobiosis and represents a navel approach to targeting colitis. FMT with appropriate microbiota from healthy donors can reinforce microbial diversity, density and persistence to enrich their environment with transforming growth factor (TGF)-β, induce IL-10 producing APCs and reinforce gut barrier, with all these being effective for recovering Tregs, restoring intestinal homeostasis and hampering colitis. ICI therapy of cancer may predispose subjects to colitis due to the impact on microbiome and reducing Treg population. FMT promotes local Treg reorchestration, being advantageous in cancer patients.
Additional Links: PMID-40569502
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Citation:
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@article {pmid40569502,
year = {2025},
author = {Mortezaee, K},
title = {Microbiota interaction with Tregs: a target for colitis.},
journal = {Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico},
volume = {},
number = {},
pages = {},
pmid = {40569502},
issn = {1699-3055},
abstract = {Gut-resident microbiota associate with host immune system to promote homeostasis, and regulatory T cells (Tregs) are critical in the maintenance of immune balance. Tregs have immunosuppressive activity, and their presence hampers the development of inflammatory diseases. This review aims to unravel microbiome impact on Tregs in bowel inflammation and harnessing such interaction to combat colitis as a separate disease or a consequence of immune checkpoint inhibitor (ICI) therapy of cancer. Short-chain fatty acids (SCFAs) are microbial-derived metabolites associated positively with Treg generation and maintenance and being effective for hampering bowel inflammation. Treg induction shapes gut microbiota profile and support microorganism colonization in their niche and protect the host from inflammation, while suppression of Treg differentiation and activity directs microbiota-induced Th17 expansion and inducing inflammation. Thus, balancing Treg representation with Th17 cells and Treg reprogramming through manipulation of gut microbiota can offer therapy. Microbiota epithelial attachment/detachment and interaction with antigen-presenting cells (APCs) are important for the final fate of T cell signature. Fecal microbial transplantation (FMT) is a strategy for promoting normobiosis and represents a navel approach to targeting colitis. FMT with appropriate microbiota from healthy donors can reinforce microbial diversity, density and persistence to enrich their environment with transforming growth factor (TGF)-β, induce IL-10 producing APCs and reinforce gut barrier, with all these being effective for recovering Tregs, restoring intestinal homeostasis and hampering colitis. ICI therapy of cancer may predispose subjects to colitis due to the impact on microbiome and reducing Treg population. FMT promotes local Treg reorchestration, being advantageous in cancer patients.},
}
RevDate: 2025-06-26
Fecal microbiota transplantation for decolonization from multidrug-resistant bacteria in pediatric allogeneic hematopoietic stem cell transplantation recipients: a retrospective real-word data study.
Haematologica [Epub ahead of print].
Not available.
Additional Links: PMID-40568731
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PubMed:
Citation:
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@article {pmid40568731,
year = {2025},
author = {Masetti, R and Barbara, G and Muratore, E and Marasco, G and Cremon, C and Marangoni, A and Brigidi, P and Putignani, L and Angelino, G and Quagliarella, F and Galaverna, F and Leardini, D and Lazzarotto, T and Gabelli, M and Savarino, E and Zecca, M and Faraci, M and Prete, A and Biffi, A and Locatelli, F and Merli, P},
title = {Fecal microbiota transplantation for decolonization from multidrug-resistant bacteria in pediatric allogeneic hematopoietic stem cell transplantation recipients: a retrospective real-word data study.},
journal = {Haematologica},
volume = {},
number = {},
pages = {},
doi = {10.3324/haematol.2025.288067},
pmid = {40568731},
issn = {1592-8721},
abstract = {Not available.},
}
RevDate: 2025-06-26
Deciphering the contributions of fecal microbiota from patients with high-grade glioma to tumor development in a humanized microbiome mouse model of glioma.
Neuro-oncology advances, 7(1):vdaf085.
BACKGROUND: Recent studies have revealed associations between gut microbiota and glioma. However, the underlying mechanisms remain poorly understood. This study primarily aims to elucidate the impact of altered gut microbiota on tumor progression in glioma-bearing mice.
METHODS: Fecal samples were collected from glioma patients and healthy controls to compare the effects of human-derived gut microbiota on glioma development in mice. We also analyzed the associations between these microbiota profiles and plasma metabolites.
RESULTS: Significant differences were observed in both the composition and diversity of the gut microbiota between glioma patients and healthy controls. Mice transplanted with gut microbiota from high-grade glioma patients (HGG-FMT) exhibited accelerated glioma progression compared to those transplanted with microbiota from healthy individuals (HC-FMT). Specifically, Eisenbergiella, Mailhella, and Merdimonas were significantly enriched in HGG-FMT mice, while Limosilactobacillus and Anaerospora increased in HC-FMT mice. Furthermore, Merdimonas showed a positive correlation with sphingosine, sphingosine 1-phosphate, and D-sphingosine in HGG-FMT mice. Conversely, Limosilactobacillus was positively correlated with stearidonic acid and eicosapentaenoic acid in HC-FMT mice.
CONCLUSIONS: Our findings demonstrate that gut microbiota from high-grade glioma patients can promote glioma progression in mice, potentially through mechanisms involving sphingosine 1-phosphate. This metabolite may enter the bloodstream and accelerate glioma growth, offering novel insights into glioma pathogenesis and potential treatment options.
Additional Links: PMID-40568683
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Citation:
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@article {pmid40568683,
year = {2025},
author = {Wang, C and Fan, Y and Zhang, L and Zhao, Z and Luo, F and Sun, K and Zeng, M and Tian, H and Peng, M and Luo, Y and Zhao, H and He, S and Sun, H},
title = {Deciphering the contributions of fecal microbiota from patients with high-grade glioma to tumor development in a humanized microbiome mouse model of glioma.},
journal = {Neuro-oncology advances},
volume = {7},
number = {1},
pages = {vdaf085},
pmid = {40568683},
issn = {2632-2498},
abstract = {BACKGROUND: Recent studies have revealed associations between gut microbiota and glioma. However, the underlying mechanisms remain poorly understood. This study primarily aims to elucidate the impact of altered gut microbiota on tumor progression in glioma-bearing mice.
METHODS: Fecal samples were collected from glioma patients and healthy controls to compare the effects of human-derived gut microbiota on glioma development in mice. We also analyzed the associations between these microbiota profiles and plasma metabolites.
RESULTS: Significant differences were observed in both the composition and diversity of the gut microbiota between glioma patients and healthy controls. Mice transplanted with gut microbiota from high-grade glioma patients (HGG-FMT) exhibited accelerated glioma progression compared to those transplanted with microbiota from healthy individuals (HC-FMT). Specifically, Eisenbergiella, Mailhella, and Merdimonas were significantly enriched in HGG-FMT mice, while Limosilactobacillus and Anaerospora increased in HC-FMT mice. Furthermore, Merdimonas showed a positive correlation with sphingosine, sphingosine 1-phosphate, and D-sphingosine in HGG-FMT mice. Conversely, Limosilactobacillus was positively correlated with stearidonic acid and eicosapentaenoic acid in HC-FMT mice.
CONCLUSIONS: Our findings demonstrate that gut microbiota from high-grade glioma patients can promote glioma progression in mice, potentially through mechanisms involving sphingosine 1-phosphate. This metabolite may enter the bloodstream and accelerate glioma growth, offering novel insights into glioma pathogenesis and potential treatment options.},
}
RevDate: 2025-06-26
CmpDate: 2025-06-26
Fecal Microbiota Transplantation from Mice Receiving Magnetic Mitohormesis Treatment Reverses High-Fat Diet-Induced Metabolic and Osteogenic Dysfunction.
International journal of molecular sciences, 26(12): pii:ijms26125450.
This study compared the metabolic consequences of fecal microbiota transplantation (FMT) from donor mice that had been either administered pulsed electromagnetic field (PEMF) therapy or exercised to recipient mice fed a high-fat diet (HFD). Eight weeks of PEMF treatment (10 min/week) enhanced PGC-1α-associated mitochondrial and metabolic gene expression in white and brown adipose to a greater degree than eight weeks of exercise (30-40 min/week). FMT from PEMF-treated donor mice recapitulated these adipogenic adaptations in HFD-fed recipient mice more faithfully than FMT from exercised donors. Direct PEMF treatment altered hepatic phospholipid composition, reducing long-chain ceramides (C16:0) and increasing very long-chain ceramides (C24:0), which could be transferred to PEMF-FMT recipient mice. FMT from PEMF-treated mice was also more effective at recovering glucose tolerance than FMT from exercised mice. PEMF treatment also enhanced bone density in both donor and HFD recipient mice. The gut Firmicutes/Bacteroidetes (F/B) ratio was lowest in both the directly PEMF-exposed and PEMF-FMT recipient mouse groups, consistent with a leaner phenotype. PEMF treatment, either directly applied or via FMT, enhanced adipose thermogenesis, ceramide levels, bone density, hepatic lipids, F/B ratio, and inflammatory blood biomarkers more than exercise. PEMF therapy may represent a non-invasive and non-strenuous method to ameliorate metabolic disorders.
Additional Links: PMID-40564914
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PubMed:
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@article {pmid40564914,
year = {2025},
author = {Wong, JKC and Patel, BK and Tai, YK and Tan, TZ and Khine, WWT and Chen, WC and Kukumberg, M and Ching, J and Lee, LS and Chua, KV and Tan, TY and Wu, KY and Bai, X and Iversen, JN and Purnamawati, K and Abdul Jalil, R and Kumar, AP and Lee, YK and Moochhala, SM and Franco-Obregón, A},
title = {Fecal Microbiota Transplantation from Mice Receiving Magnetic Mitohormesis Treatment Reverses High-Fat Diet-Induced Metabolic and Osteogenic Dysfunction.},
journal = {International journal of molecular sciences},
volume = {26},
number = {12},
pages = {},
doi = {10.3390/ijms26125450},
pmid = {40564914},
issn = {1422-0067},
support = {A-0001177-01-00//iHealthtech Microbiome in Health, Disease and Aging 2018 Joint Research Grant/ ; MOE-T2EP30120-0016//Ministry of Education/ ; NUHSRO/2023/039/RO5+6/Seed-Mar/04//National University Health System/ ; },
mesh = {Animals ; *Diet, High-Fat/adverse effects ; Mice ; *Fecal Microbiota Transplantation/methods ; Male ; *Osteogenesis ; Mice, Inbred C57BL ; Ceramides/metabolism ; Gastrointestinal Microbiome ; *Magnetic Field Therapy/methods ; Liver/metabolism ; *Metabolic Diseases/therapy/etiology/metabolism ; Bone Density ; },
abstract = {This study compared the metabolic consequences of fecal microbiota transplantation (FMT) from donor mice that had been either administered pulsed electromagnetic field (PEMF) therapy or exercised to recipient mice fed a high-fat diet (HFD). Eight weeks of PEMF treatment (10 min/week) enhanced PGC-1α-associated mitochondrial and metabolic gene expression in white and brown adipose to a greater degree than eight weeks of exercise (30-40 min/week). FMT from PEMF-treated donor mice recapitulated these adipogenic adaptations in HFD-fed recipient mice more faithfully than FMT from exercised donors. Direct PEMF treatment altered hepatic phospholipid composition, reducing long-chain ceramides (C16:0) and increasing very long-chain ceramides (C24:0), which could be transferred to PEMF-FMT recipient mice. FMT from PEMF-treated mice was also more effective at recovering glucose tolerance than FMT from exercised mice. PEMF treatment also enhanced bone density in both donor and HFD recipient mice. The gut Firmicutes/Bacteroidetes (F/B) ratio was lowest in both the directly PEMF-exposed and PEMF-FMT recipient mouse groups, consistent with a leaner phenotype. PEMF treatment, either directly applied or via FMT, enhanced adipose thermogenesis, ceramide levels, bone density, hepatic lipids, F/B ratio, and inflammatory blood biomarkers more than exercise. PEMF therapy may represent a non-invasive and non-strenuous method to ameliorate metabolic disorders.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Diet, High-Fat/adverse effects
Mice
*Fecal Microbiota Transplantation/methods
Male
*Osteogenesis
Mice, Inbred C57BL
Ceramides/metabolism
Gastrointestinal Microbiome
*Magnetic Field Therapy/methods
Liver/metabolism
*Metabolic Diseases/therapy/etiology/metabolism
Bone Density
RevDate: 2025-06-26
CmpDate: 2025-06-26
Prolonged Intestinal Ethanol Absorption and Oxidative Stress: Revisiting the Gut-Liver Axis in Alcohol-Associated Disease.
International journal of molecular sciences, 26(12): pii:ijms26125442.
Chronic alcohol consumption induces oxidative stress not only in the liver but also in the gastrointestinal tract, where prolonged intestinal ethanol absorption plays a pivotal and underrecognized role. This review reframes ethanol pharmacokinetics to emphasize sustained jejunal and ileal uptake, which maintains elevated blood alcohol levels and perpetuates redox imbalance across the gut-liver axis. We integrate recent findings on ethanol-induced barrier dysfunction, CYP2E1-mediated ROS production, microbial dysbiosis, and mitochondrial disruption, proposing that the intestine is an active site of injury and a driver of systemic inflammation. Key mechanistic insights reveal that gut-derived endotoxins, compromised epithelial integrity, and microbiome-mitochondria interactions converge to exacerbate hepatic and extrahepatic damage. We further explore emerging therapeutic strategies-ranging from NAD[+] repletion and probiotics to fecal microbiota transplantation-that target this upstream pathology. Recognizing prolonged intestinal ethanol absorption as a clinically meaningful phase offers new directions for early intervention and redox-based treatment in alcohol-associated disease.
Additional Links: PMID-40564903
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@article {pmid40564903,
year = {2025},
author = {Chung, BS and Yang, K and Park, C and Ryu, T},
title = {Prolonged Intestinal Ethanol Absorption and Oxidative Stress: Revisiting the Gut-Liver Axis in Alcohol-Associated Disease.},
journal = {International journal of molecular sciences},
volume = {26},
number = {12},
pages = {},
doi = {10.3390/ijms26125442},
pmid = {40564903},
issn = {1422-0067},
support = {RS-2023-00238039//National Research Foundation of Korea/ ; },
mesh = {Humans ; *Oxidative Stress/drug effects ; *Ethanol/pharmacokinetics/metabolism ; *Intestinal Absorption ; Animals ; *Liver/metabolism/drug effects ; Gastrointestinal Microbiome ; *Liver Diseases, Alcoholic/metabolism ; Intestinal Mucosa/metabolism ; *Alcoholism/metabolism ; Dysbiosis ; },
abstract = {Chronic alcohol consumption induces oxidative stress not only in the liver but also in the gastrointestinal tract, where prolonged intestinal ethanol absorption plays a pivotal and underrecognized role. This review reframes ethanol pharmacokinetics to emphasize sustained jejunal and ileal uptake, which maintains elevated blood alcohol levels and perpetuates redox imbalance across the gut-liver axis. We integrate recent findings on ethanol-induced barrier dysfunction, CYP2E1-mediated ROS production, microbial dysbiosis, and mitochondrial disruption, proposing that the intestine is an active site of injury and a driver of systemic inflammation. Key mechanistic insights reveal that gut-derived endotoxins, compromised epithelial integrity, and microbiome-mitochondria interactions converge to exacerbate hepatic and extrahepatic damage. We further explore emerging therapeutic strategies-ranging from NAD[+] repletion and probiotics to fecal microbiota transplantation-that target this upstream pathology. Recognizing prolonged intestinal ethanol absorption as a clinically meaningful phase offers new directions for early intervention and redox-based treatment in alcohol-associated disease.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Oxidative Stress/drug effects
*Ethanol/pharmacokinetics/metabolism
*Intestinal Absorption
Animals
*Liver/metabolism/drug effects
Gastrointestinal Microbiome
*Liver Diseases, Alcoholic/metabolism
Intestinal Mucosa/metabolism
*Alcoholism/metabolism
Dysbiosis
RevDate: 2025-06-26
Possible Applications of Fecal Microbiota Transplantation in the Pediatric Population: A Systematic Review.
Biomedicines, 13(6): pii:biomedicines13061393.
Background: The potential therapeutic role of fecal microbiota transplantation (FMT) in various diseases has been thoroughly studied over the last few decades. However, the majority of studies focus on the adult population, therefore, conclusions regarding the application of FMT in the pediatric population are much less clear. This systematic review aims to summarize the research conducted so far on the efficacy and safety of FMT in the pediatric population, assess the quality of the evidence of its effectiveness, and outline the most promising areas for future research. Methods: We performed a systematic literature search from the index date to 8 June 2024 on the Embase, PubMed, and Web of Science databases. One author screened the resulting 121 articles. Eventually, 35 eligible studies that reported FMT use in seven different diseases were identified. Results: All of the studies assessed FMT as a safe procedure without many serious adverse effects. The best-documented application, which is the only one recommended in official guidelines, is recurrent Clostridioides difficile infection. Other disease entities in which the use of FMT has been studied with good clinical effects are inflammatory bowel disease, allergic colitis, autism, Tourette syndrome, and colonization with multi-drug-resistant organisms. However, it should be noted that the majority of studies are cohort and case-control studies, without randomization, which translates into low evidence quality. In one randomized, controlled trial focusing on the effect of FMT on weight loss in obese individuals, a lack of effect was found. Conclusions: While FMT and subsequent iterations of gut microbiota-targeted interventions hold promising therapeutic potential for various disease entities in the pediatric population, the current evidence behind this conclusion is of low quality. Based on current studies, these methods appear to be both effective and safe. However, further randomized clinical trials are necessary, especially within the pediatric population, for which such studies remain scarce.
Additional Links: PMID-40564111
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PubMed:
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@article {pmid40564111,
year = {2025},
author = {Bieganska, EA and Kosinski, P and Wolski, M},
title = {Possible Applications of Fecal Microbiota Transplantation in the Pediatric Population: A Systematic Review.},
journal = {Biomedicines},
volume = {13},
number = {6},
pages = {},
doi = {10.3390/biomedicines13061393},
pmid = {40564111},
issn = {2227-9059},
abstract = {Background: The potential therapeutic role of fecal microbiota transplantation (FMT) in various diseases has been thoroughly studied over the last few decades. However, the majority of studies focus on the adult population, therefore, conclusions regarding the application of FMT in the pediatric population are much less clear. This systematic review aims to summarize the research conducted so far on the efficacy and safety of FMT in the pediatric population, assess the quality of the evidence of its effectiveness, and outline the most promising areas for future research. Methods: We performed a systematic literature search from the index date to 8 June 2024 on the Embase, PubMed, and Web of Science databases. One author screened the resulting 121 articles. Eventually, 35 eligible studies that reported FMT use in seven different diseases were identified. Results: All of the studies assessed FMT as a safe procedure without many serious adverse effects. The best-documented application, which is the only one recommended in official guidelines, is recurrent Clostridioides difficile infection. Other disease entities in which the use of FMT has been studied with good clinical effects are inflammatory bowel disease, allergic colitis, autism, Tourette syndrome, and colonization with multi-drug-resistant organisms. However, it should be noted that the majority of studies are cohort and case-control studies, without randomization, which translates into low evidence quality. In one randomized, controlled trial focusing on the effect of FMT on weight loss in obese individuals, a lack of effect was found. Conclusions: While FMT and subsequent iterations of gut microbiota-targeted interventions hold promising therapeutic potential for various disease entities in the pediatric population, the current evidence behind this conclusion is of low quality. Based on current studies, these methods appear to be both effective and safe. However, further randomized clinical trials are necessary, especially within the pediatric population, for which such studies remain scarce.},
}
RevDate: 2025-06-26
The Multi-Faceted Role of Gut Microbiota in Alopecia Areata.
Biomedicines, 13(6): pii:biomedicines13061379.
Alopecia areata (AA) is a complex autoimmune disorder with multifactorial pathogenesis. Recent research highlights the gut microbiota as a possible key player in AA pathogenesis through the gut-skin axis: gut dysbiosis may disrupt intestinal barrier integrity and immune tolerance by affecting T regulatory cells, potentially contributing to disease onset and progression. The purpose of this review is to analyze the current evidence on the correlation between gut microbiota and AA, dissecting both the pathogenetic role of its alterations in the onset and progression of disease and its potential role as a therapeutic target.
Additional Links: PMID-40564097
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@article {pmid40564097,
year = {2025},
author = {Severino, A and Porcari, S and Rondinella, D and Capuano, E and Rozera, T and Kaitsas, F and Gasbarrini, A and Cammarota, G and Ianiro, G},
title = {The Multi-Faceted Role of Gut Microbiota in Alopecia Areata.},
journal = {Biomedicines},
volume = {13},
number = {6},
pages = {},
doi = {10.3390/biomedicines13061379},
pmid = {40564097},
issn = {2227-9059},
abstract = {Alopecia areata (AA) is a complex autoimmune disorder with multifactorial pathogenesis. Recent research highlights the gut microbiota as a possible key player in AA pathogenesis through the gut-skin axis: gut dysbiosis may disrupt intestinal barrier integrity and immune tolerance by affecting T regulatory cells, potentially contributing to disease onset and progression. The purpose of this review is to analyze the current evidence on the correlation between gut microbiota and AA, dissecting both the pathogenetic role of its alterations in the onset and progression of disease and its potential role as a therapeutic target.},
}
RevDate: 2025-06-25
CmpDate: 2025-06-26
Gut microbiota implication in diabetic kidney disease: mechanisms and novel therapeutic strategies.
Renal failure, 47(1):2517402.
Diabetic kidney disease (DKD) is one of the leading causes of chronic kidney disease and end-stage renal disease worldwide, predominantly driven by the rise in type 2 diabetes mellitus. Recent evidence highlights the crucial role of gut microbiota dysbiosis in the development and progression of DKD. Dysbiosis, characterized by a reduction in beneficial short-chain fatty acid-producing bacteria and an increase in pathogenic species such as Proteobacteria and Bacteroides, exacerbates systemic inflammation, insulin resistance, and kidney damage through mechanisms like increased intestinal permeability and the production of pro-inflammatory metabolites like lipopolysaccharides. This review explores the impact of specific bacterial taxa on DKD risk and progression, such as Alistipes, Subdoligranulum, and their interactions with metabolic pathways. Furthermore, we discuss novel therapeutic strategies targeting gut microbiota, including probiotics, prebiotics, synbiotics, and fecal microbiota transplantation, which have shown promise in ameliorating DKD symptoms. However, the heterogeneity of gut microbiota across individuals and the challenges in treatment standardization call for personalized approaches and further research into the gut-kidney axis.
Additional Links: PMID-40563141
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PubMed:
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@article {pmid40563141,
year = {2025},
author = {Zhang, Y and Qing, J and Saed, YA and Li, Y},
title = {Gut microbiota implication in diabetic kidney disease: mechanisms and novel therapeutic strategies.},
journal = {Renal failure},
volume = {47},
number = {1},
pages = {2517402},
doi = {10.1080/0886022X.2025.2517402},
pmid = {40563141},
issn = {1525-6049},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Dysbiosis/complications/microbiology/therapy ; *Diabetic Nephropathies/microbiology/therapy/etiology ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Prebiotics/administration & dosage ; *Diabetes Mellitus, Type 2/complications ; Synbiotics/administration & dosage ; Disease Progression ; },
abstract = {Diabetic kidney disease (DKD) is one of the leading causes of chronic kidney disease and end-stage renal disease worldwide, predominantly driven by the rise in type 2 diabetes mellitus. Recent evidence highlights the crucial role of gut microbiota dysbiosis in the development and progression of DKD. Dysbiosis, characterized by a reduction in beneficial short-chain fatty acid-producing bacteria and an increase in pathogenic species such as Proteobacteria and Bacteroides, exacerbates systemic inflammation, insulin resistance, and kidney damage through mechanisms like increased intestinal permeability and the production of pro-inflammatory metabolites like lipopolysaccharides. This review explores the impact of specific bacterial taxa on DKD risk and progression, such as Alistipes, Subdoligranulum, and their interactions with metabolic pathways. Furthermore, we discuss novel therapeutic strategies targeting gut microbiota, including probiotics, prebiotics, synbiotics, and fecal microbiota transplantation, which have shown promise in ameliorating DKD symptoms. However, the heterogeneity of gut microbiota across individuals and the challenges in treatment standardization call for personalized approaches and further research into the gut-kidney axis.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology
*Dysbiosis/complications/microbiology/therapy
*Diabetic Nephropathies/microbiology/therapy/etiology
Probiotics/therapeutic use
Fecal Microbiota Transplantation
Prebiotics/administration & dosage
*Diabetes Mellitus, Type 2/complications
Synbiotics/administration & dosage
Disease Progression
RevDate: 2025-06-25
Stunting is associated with persistent and transferable alterations in the gut microbiome.
Gut pathogens, 17(1):49.
As robust animal models to study the pathophysiology of stunting are absent, we have comparatively characterized the gut microbiota of malnourished/stunted vs. clinically healthy/normal Kenyan toddlers (12-24 months old) and established a gnotobiotic (Gn) pig fecal transplant model to gain understanding of microbial community structure associated with stunting. As expected, the bacterial composition between the two toddler groups was distinct: Actinobacteria was most prevalent in healthy toddlers, whereas Proteobacteria dominated in stunted toddlers. Although the diversity indices showed no significant differences, unique bacterial genera were found in each toddler group: three genera unique to stunted toddlers and ten unique to healthy toddlers, with eight genera shared between the groups. We observed a higher number of enriched bacterial virulence genes in healthy vs. stunted toddlers suggesting that the microbiome plasticity and functional characteristics of the healthy toddlers allow for the pathogen/pathobiont control. In contrast, we noted the presence of more genes associated with antimicrobial-resistance (AMR) bacteria in stunted toddlers, possibly due to early-life antibiotic treatments. Of interest, functional analysis showed that CAZymes associated with carbohydrate biosynthesis, and a few metabolic pathways related to protein/amino acid, carbohydrate and fat catabolism were enriched in stunted toddlers. In contrast carbohydrate degradation CAZymes and numerous anabolic pathways were prevalent in healthy toddlers. These patterns were also evident in the Gn pigs transplanted with stunted/healthy human fecal microbiota (HFM). Overall, our findings suggest that the microbiota transplanted Gn pigs represent a valuable model for studying the infant microbial community structure and the impacts of stunting on the child gut microbiota. Additionally, this is the first study to demonstrate that the healthy vs. stunted microbiota composition and function remained different in the Gn pigs throughout the study. This information and the Gn pig model are vital for developing and testing targeted interventions for malnourished/stunted populations, consequently advancing microbiome-based diagnosis and personalized medicine.
Additional Links: PMID-40563092
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Citation:
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@article {pmid40563092,
year = {2025},
author = {Amimo, JO and Kunyanga, CN and Raev, SA and Kick, M and Micheal, H and Saif, LJ and Vlasova, AN},
title = {Stunting is associated with persistent and transferable alterations in the gut microbiome.},
journal = {Gut pathogens},
volume = {17},
number = {1},
pages = {49},
pmid = {40563092},
issn = {1757-4749},
support = {OPP1117467//Bill and Melinda Gates Foundation/ ; R01A1099451//National Institute of Allergy and Infectious Diseases/ ; },
abstract = {As robust animal models to study the pathophysiology of stunting are absent, we have comparatively characterized the gut microbiota of malnourished/stunted vs. clinically healthy/normal Kenyan toddlers (12-24 months old) and established a gnotobiotic (Gn) pig fecal transplant model to gain understanding of microbial community structure associated with stunting. As expected, the bacterial composition between the two toddler groups was distinct: Actinobacteria was most prevalent in healthy toddlers, whereas Proteobacteria dominated in stunted toddlers. Although the diversity indices showed no significant differences, unique bacterial genera were found in each toddler group: three genera unique to stunted toddlers and ten unique to healthy toddlers, with eight genera shared between the groups. We observed a higher number of enriched bacterial virulence genes in healthy vs. stunted toddlers suggesting that the microbiome plasticity and functional characteristics of the healthy toddlers allow for the pathogen/pathobiont control. In contrast, we noted the presence of more genes associated with antimicrobial-resistance (AMR) bacteria in stunted toddlers, possibly due to early-life antibiotic treatments. Of interest, functional analysis showed that CAZymes associated with carbohydrate biosynthesis, and a few metabolic pathways related to protein/amino acid, carbohydrate and fat catabolism were enriched in stunted toddlers. In contrast carbohydrate degradation CAZymes and numerous anabolic pathways were prevalent in healthy toddlers. These patterns were also evident in the Gn pigs transplanted with stunted/healthy human fecal microbiota (HFM). Overall, our findings suggest that the microbiota transplanted Gn pigs represent a valuable model for studying the infant microbial community structure and the impacts of stunting on the child gut microbiota. Additionally, this is the first study to demonstrate that the healthy vs. stunted microbiota composition and function remained different in the Gn pigs throughout the study. This information and the Gn pig model are vital for developing and testing targeted interventions for malnourished/stunted populations, consequently advancing microbiome-based diagnosis and personalized medicine.},
}
RevDate: 2025-06-25
CmpDate: 2025-06-25
Review Article: Fecal Microbiota Transplantation in Melanoma: Mechanisms-Mediated Enhancement of Anti-Tumor Immunotherapy.
Critical reviews in oncogenesis, 30(2):23-35.
The gut microbiota is integral to human health, influencing nutrition, metabolism, and immunity. Dysbiosis has been implicated in cancer development and resistance to therapies, highlighting the potential of microbiota modulation as a therapeutic strategy. Melanoma, while comprising only 1% of skin cancer diagnoses, accounts for over 80% of skin cancer related deaths, emphasizing the need for innovative approaches to enhance treatment efficacy. Although immune checkpoint inhibitors (ICIs) such as anti-programmed cell death protein (PD-1) and cytotoxic T-lymphocyte associated protein 4 (CTLA-4) blockade therapies have significantly improved survival for some melanoma patients, the majority fails to achieve durable responses and often develops long-term resistance to these treatments. Fecal microbiota transplantation (FMT) is emerging as a promising intervention to restore microbial balance and enhance treatment efficacy. This review explores the historical evolution and current applications of FMT in oncology, with a focus on its ability to modulate the gut microbiome, augment antitumor immunity, and overcome resistance to checkpoint blockade therapy in melanoma. Despite its promise, significant challenges remain, including ensuring the safety of the procedure, selecting suitable donors, and addressing regulatory hurdles. Future research aimed at optimizing FMT protocols, identifying key microbial strains, and understanding the mechanisms underlying microbiota-immune interactions will be essential to fully harness the potential of FMT as a transformative adjunct in cancer treatment.
Additional Links: PMID-40561430
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PubMed:
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@article {pmid40561430,
year = {2025},
author = {Ung, W and Bonavida, B},
title = {Review Article: Fecal Microbiota Transplantation in Melanoma: Mechanisms-Mediated Enhancement of Anti-Tumor Immunotherapy.},
journal = {Critical reviews in oncogenesis},
volume = {30},
number = {2},
pages = {23-35},
doi = {10.1615/CritRevOncog.2025058249},
pmid = {40561430},
issn = {0893-9675},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Melanoma/therapy/immunology/microbiology/etiology ; *Immunotherapy/methods ; *Gastrointestinal Microbiome/immunology ; Immune Checkpoint Inhibitors/therapeutic use ; Animals ; *Skin Neoplasms/therapy/immunology/microbiology ; },
abstract = {The gut microbiota is integral to human health, influencing nutrition, metabolism, and immunity. Dysbiosis has been implicated in cancer development and resistance to therapies, highlighting the potential of microbiota modulation as a therapeutic strategy. Melanoma, while comprising only 1% of skin cancer diagnoses, accounts for over 80% of skin cancer related deaths, emphasizing the need for innovative approaches to enhance treatment efficacy. Although immune checkpoint inhibitors (ICIs) such as anti-programmed cell death protein (PD-1) and cytotoxic T-lymphocyte associated protein 4 (CTLA-4) blockade therapies have significantly improved survival for some melanoma patients, the majority fails to achieve durable responses and often develops long-term resistance to these treatments. Fecal microbiota transplantation (FMT) is emerging as a promising intervention to restore microbial balance and enhance treatment efficacy. This review explores the historical evolution and current applications of FMT in oncology, with a focus on its ability to modulate the gut microbiome, augment antitumor immunity, and overcome resistance to checkpoint blockade therapy in melanoma. Despite its promise, significant challenges remain, including ensuring the safety of the procedure, selecting suitable donors, and addressing regulatory hurdles. Future research aimed at optimizing FMT protocols, identifying key microbial strains, and understanding the mechanisms underlying microbiota-immune interactions will be essential to fully harness the potential of FMT as a transformative adjunct in cancer treatment.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Fecal Microbiota Transplantation/methods
*Melanoma/therapy/immunology/microbiology/etiology
*Immunotherapy/methods
*Gastrointestinal Microbiome/immunology
Immune Checkpoint Inhibitors/therapeutic use
Animals
*Skin Neoplasms/therapy/immunology/microbiology
RevDate: 2025-06-25
Faecal Microbiota Transplantation as an Adjuvant Treatment for Extraintestinal Disorders: Translating Insights from Human Medicine to Veterinary Practice.
Veterinary sciences, 12(6): pii:vetsci12060541.
Faecal microbiota transplantation (FMT) has emerged as a transformative therapy in human medicine, particularly for managing recurrent Clostridioides difficile infections and other gastrointestinal (GI) disorders. Beyond the GI tract, FMT has shown potential in addressing extraintestinal conditions in people, including metabolic, immune-mediated, dermatological, neurological, and infectious diseases. Research in people has highlighted its efficacy in decolonising multidrug-resistant organisms in infection, mitigating autoimmune diseases, and improving outcomes in metabolic disorders such as obesity and diabetes. Furthermore, FMT has also been linked to enhanced responses to immunotherapy in cancer and improved management of hepatic and renal conditions. These findings underscore the intricate connections between the gut microbiome and systemic health, opening novel therapeutic avenues. In veterinary medicine, while FMT has demonstrated benefits for GI disorders, its application in extraintestinal diseases remains largely unexplored. Emerging evidence suggests that conditions such as atopic dermatitis, chronic kidney disease, immune-mediated diseases, and behavioural disorders in companion animals could benefit from microbiome-targeted therapies. However, significant gaps in knowledge persist, particularly regarding the long-term safety and efficacy for veterinary applications. This review synthesises findings from human medicine to assess their relevance for veterinary applications and future research.
Additional Links: PMID-40559778
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PubMed:
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@article {pmid40559778,
year = {2025},
author = {Nishigaki, A and Marchesi, JR and Previdelli, RL},
title = {Faecal Microbiota Transplantation as an Adjuvant Treatment for Extraintestinal Disorders: Translating Insights from Human Medicine to Veterinary Practice.},
journal = {Veterinary sciences},
volume = {12},
number = {6},
pages = {},
doi = {10.3390/vetsci12060541},
pmid = {40559778},
issn = {2306-7381},
abstract = {Faecal microbiota transplantation (FMT) has emerged as a transformative therapy in human medicine, particularly for managing recurrent Clostridioides difficile infections and other gastrointestinal (GI) disorders. Beyond the GI tract, FMT has shown potential in addressing extraintestinal conditions in people, including metabolic, immune-mediated, dermatological, neurological, and infectious diseases. Research in people has highlighted its efficacy in decolonising multidrug-resistant organisms in infection, mitigating autoimmune diseases, and improving outcomes in metabolic disorders such as obesity and diabetes. Furthermore, FMT has also been linked to enhanced responses to immunotherapy in cancer and improved management of hepatic and renal conditions. These findings underscore the intricate connections between the gut microbiome and systemic health, opening novel therapeutic avenues. In veterinary medicine, while FMT has demonstrated benefits for GI disorders, its application in extraintestinal diseases remains largely unexplored. Emerging evidence suggests that conditions such as atopic dermatitis, chronic kidney disease, immune-mediated diseases, and behavioural disorders in companion animals could benefit from microbiome-targeted therapies. However, significant gaps in knowledge persist, particularly regarding the long-term safety and efficacy for veterinary applications. This review synthesises findings from human medicine to assess their relevance for veterinary applications and future research.},
}
RevDate: 2025-06-25
CmpDate: 2025-06-25
EmsB Microsatellite Analysis of Echinococcus multilocularis Specimens Isolated from Belgian Patients with Alveolar Echinococcosis and from Animal Hosts.
Pathogens (Basel, Switzerland), 14(6): pii:pathogens14060584.
Alveolar echinococcosis (AE), caused by Echinococcus multilocularis (E. multilocularis), is a severe parasitic zoonosis that is potentially fatal for humans. The parasite is primarily transmitted by wildlife, with red foxes acting as definitive hosts and rodents as intermediate hosts, while humans can become accidental but dead-end hosts. The aim of this study is to use EmsB typing on E. multilocularis isolates from human AE cases and local animals such as foxes and rodents. In this study, retrospective EmsB typing was performed on 39 samples, including 11 tissue samples from 10 patients, 18 fecal swabs from foxes, and 10 tissue samples from rodents. A dendrogram was created to determine the EmsB profiles present. The results showed that all the rodent samples were associated with the EmsB P1 profile (10/10), while the human and fox samples shared the EmsB profile P1 (5/11 humans and 8/18 foxes), a profile near P4 (2/11 humans and 3 foxes), and a profile near P8 (1/11 humans and 1/18 foxes). The study demonstrates that the same EmsB profiles circulate among humans and animals, confirming that wildlife reservoirs play a key role in transmission.
Additional Links: PMID-40559592
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PubMed:
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@article {pmid40559592,
year = {2025},
author = {Egrek, S and Knapp, J and Sacheli, R and El Moussaoui, K and Léonard, P and Larranaga Lapique, E and Millon, L and Engelskirchen, S and Detry, O and Linden, A and Hayette, MP},
title = {EmsB Microsatellite Analysis of Echinococcus multilocularis Specimens Isolated from Belgian Patients with Alveolar Echinococcosis and from Animal Hosts.},
journal = {Pathogens (Basel, Switzerland)},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/pathogens14060584},
pmid = {40559592},
issn = {2076-0817},
mesh = {Animals ; *Echinococcus multilocularis/genetics/isolation & purification/classification ; Humans ; Foxes/parasitology ; *Microsatellite Repeats ; Belgium/epidemiology ; *Echinococcosis/parasitology ; Retrospective Studies ; Zoonoses/parasitology ; *Echinococcosis, Hepatic/parasitology ; Genotype ; Rodentia/parasitology ; Feces/parasitology ; },
abstract = {Alveolar echinococcosis (AE), caused by Echinococcus multilocularis (E. multilocularis), is a severe parasitic zoonosis that is potentially fatal for humans. The parasite is primarily transmitted by wildlife, with red foxes acting as definitive hosts and rodents as intermediate hosts, while humans can become accidental but dead-end hosts. The aim of this study is to use EmsB typing on E. multilocularis isolates from human AE cases and local animals such as foxes and rodents. In this study, retrospective EmsB typing was performed on 39 samples, including 11 tissue samples from 10 patients, 18 fecal swabs from foxes, and 10 tissue samples from rodents. A dendrogram was created to determine the EmsB profiles present. The results showed that all the rodent samples were associated with the EmsB P1 profile (10/10), while the human and fox samples shared the EmsB profile P1 (5/11 humans and 8/18 foxes), a profile near P4 (2/11 humans and 3 foxes), and a profile near P8 (1/11 humans and 1/18 foxes). The study demonstrates that the same EmsB profiles circulate among humans and animals, confirming that wildlife reservoirs play a key role in transmission.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Echinococcus multilocularis/genetics/isolation & purification/classification
Humans
Foxes/parasitology
*Microsatellite Repeats
Belgium/epidemiology
*Echinococcosis/parasitology
Retrospective Studies
Zoonoses/parasitology
*Echinococcosis, Hepatic/parasitology
Genotype
Rodentia/parasitology
Feces/parasitology
RevDate: 2025-06-25
Gut-Microbiome Signatures Predicting Response to Neoadjuvant Chemoradiotherapy in Locally Advanced Rectal Cancer: A Systematic Review.
Metabolites, 15(6): pii:metabo15060412.
BACKGROUND AND OBJECTIVES: Rectal cancer management increasingly relies on watch-and-wait strategies after neoadjuvant chemoradiotherapy (nCRT). Accurate, non-invasive prediction of pathological complete response (pCR) remains elusive. Emerging evidence suggests that gut-microbiome composition modulates radio-chemosensitivity. We systematically reviewed primary studies that correlated baseline or on-treatment gut-microbiome features with nCRT response in locally advanced rectal cancer (LARC).
METHODS: MEDLINE, Embase and PubMed were searched from inception to 30 April 2025. Eligibility required (i) prospective or retrospective human studies of LARC, (ii) faecal or mucosal microbiome profiling by 16S, metagenomics, or metatranscriptomics, and (iii) response assessment using tumour-regression grade or pCR. Narrative synthesis and random-effects proportion meta-analysis were performed where data were homogeneous.
RESULTS: Twelve studies (n = 1354 unique patients, median sample = 73, range 22-735) met inclusion. Four independent machine-learning models achieved an Area Under the Receiver Operating Characteristic curve AUROC ≥ 0.85 for pCR prediction. Consistently enriched taxa in responders included Lachnospiraceae bacterium, Blautia wexlerae, Roseburia spp., and Intestinimonas butyriciproducens. Non-responders showed over-representation of Fusobacterium nucleatum, Bacteroides fragilis, and Prevotella spp. Two studies linked butyrate-producing modules to radiosensitivity, whereas nucleotide-biosynthesis pathways conferred resistance. Pooled pCR rate in patients with a "butyrate-rich" baseline profile was 44% (95% CI 35-54) versus 21% (95% CI 15-29) in controls (I[2] = 18%).
CONCLUSIONS: Despite heterogeneity, convergent functional and taxonomic signals underpin a microbiome-based radiosensitivity axis in LARC. Multi-centre validation cohorts and intervention trials manipulating these taxa, such as prebiotics or live-biotherapeutics, are warranted before clinical deployment.
Additional Links: PMID-40559436
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PubMed:
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@article {pmid40559436,
year = {2025},
author = {Domilescu, I and Miutescu, B and Horhat, FG and Popescu, A and Nica, C and Ghiuchici, AM and Gadour, E and Sîrbu, I and Hutanu, D},
title = {Gut-Microbiome Signatures Predicting Response to Neoadjuvant Chemoradiotherapy in Locally Advanced Rectal Cancer: A Systematic Review.},
journal = {Metabolites},
volume = {15},
number = {6},
pages = {},
doi = {10.3390/metabo15060412},
pmid = {40559436},
issn = {2218-1989},
abstract = {BACKGROUND AND OBJECTIVES: Rectal cancer management increasingly relies on watch-and-wait strategies after neoadjuvant chemoradiotherapy (nCRT). Accurate, non-invasive prediction of pathological complete response (pCR) remains elusive. Emerging evidence suggests that gut-microbiome composition modulates radio-chemosensitivity. We systematically reviewed primary studies that correlated baseline or on-treatment gut-microbiome features with nCRT response in locally advanced rectal cancer (LARC).
METHODS: MEDLINE, Embase and PubMed were searched from inception to 30 April 2025. Eligibility required (i) prospective or retrospective human studies of LARC, (ii) faecal or mucosal microbiome profiling by 16S, metagenomics, or metatranscriptomics, and (iii) response assessment using tumour-regression grade or pCR. Narrative synthesis and random-effects proportion meta-analysis were performed where data were homogeneous.
RESULTS: Twelve studies (n = 1354 unique patients, median sample = 73, range 22-735) met inclusion. Four independent machine-learning models achieved an Area Under the Receiver Operating Characteristic curve AUROC ≥ 0.85 for pCR prediction. Consistently enriched taxa in responders included Lachnospiraceae bacterium, Blautia wexlerae, Roseburia spp., and Intestinimonas butyriciproducens. Non-responders showed over-representation of Fusobacterium nucleatum, Bacteroides fragilis, and Prevotella spp. Two studies linked butyrate-producing modules to radiosensitivity, whereas nucleotide-biosynthesis pathways conferred resistance. Pooled pCR rate in patients with a "butyrate-rich" baseline profile was 44% (95% CI 35-54) versus 21% (95% CI 15-29) in controls (I[2] = 18%).
CONCLUSIONS: Despite heterogeneity, convergent functional and taxonomic signals underpin a microbiome-based radiosensitivity axis in LARC. Multi-centre validation cohorts and intervention trials manipulating these taxa, such as prebiotics or live-biotherapeutics, are warranted before clinical deployment.},
}
RevDate: 2025-06-25
IgA Dysfunction Induced by Early-Lifetime Low-Dose Antibiotics Exposure Aggravates Diet-Induced Metabolic Syndrome.
Antibiotics (Basel, Switzerland), 14(6): pii:antibiotics14060574.
Background: Low-dose antibiotic contamination in animal feed is a persistent global food safety challenge. Transient early-life exposure to low-dose penicillin (LDP) is known to induce metabolic syndrome (MetS) in adult mice, but the underlying mechanisms are unclear. Introduction: This study investigated the role of gut microbiota (GM) and intestinal immunity in mediating the long-term metabolic effects of early-life LDP exposure. Methods: Mice were exposed to LDP transiently during early life. GM composition was analyzed. Intestinal IgA responses were quantified. Bacterial encroachment, systemic and adipose tissue inflammation, and diet-induced MetS were assessed. Germ-free (GF) mice received GM transplants from LDP-exposed or control mice to test causality and persistence. Results: Early-life LDP exposure significantly disrupted GM composition, particularly in the ileum, in 30-day-old mice. These GM alterations caused persistent suppression of intestinal IgA responses, evidenced by reduced IgA-producing cells and sIgA levels. This suppression was constrained to early-life exposure: transferring LDP-modified GM to GF mice produced only a transient reduction in fecal sIgA. The LDP-induced sIgA reduction decreased IgA binding of bacteria, leading to increased bacterial encroachment and systemic and adipose tissue inflammation. These pathological changes exacerbated diet-induced MetS. Discussion: Our findings demonstrate that early-life LDP exposure induces persistent intestinal IgA deficiency through lasting GM alterations initiated in early development. This deficiency drives bacterial encroachment, inflammation, and ultimately exacerbates MetS. Conclusions: The exacerbation of diet-induced metabolic syndrome by early-life LDP exposure occurs through an intestinal sIgA-dependent pathway triggered by persistent GM disruption. This highlights a critical mechanism linking early-life antibiotic exposure, gut immune dysfunction, and long-term metabolic health, with significant implications for food safety.
Additional Links: PMID-40558164
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PubMed:
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@article {pmid40558164,
year = {2025},
author = {Han, X and Qin, Y and Guo, J and Huang, W and You, Y and Zhan, J and Yin, Y},
title = {IgA Dysfunction Induced by Early-Lifetime Low-Dose Antibiotics Exposure Aggravates Diet-Induced Metabolic Syndrome.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/antibiotics14060574},
pmid = {40558164},
issn = {2079-6382},
support = {82330017 and 82270610//National Natural Science Foundation/ ; },
abstract = {Background: Low-dose antibiotic contamination in animal feed is a persistent global food safety challenge. Transient early-life exposure to low-dose penicillin (LDP) is known to induce metabolic syndrome (MetS) in adult mice, but the underlying mechanisms are unclear. Introduction: This study investigated the role of gut microbiota (GM) and intestinal immunity in mediating the long-term metabolic effects of early-life LDP exposure. Methods: Mice were exposed to LDP transiently during early life. GM composition was analyzed. Intestinal IgA responses were quantified. Bacterial encroachment, systemic and adipose tissue inflammation, and diet-induced MetS were assessed. Germ-free (GF) mice received GM transplants from LDP-exposed or control mice to test causality and persistence. Results: Early-life LDP exposure significantly disrupted GM composition, particularly in the ileum, in 30-day-old mice. These GM alterations caused persistent suppression of intestinal IgA responses, evidenced by reduced IgA-producing cells and sIgA levels. This suppression was constrained to early-life exposure: transferring LDP-modified GM to GF mice produced only a transient reduction in fecal sIgA. The LDP-induced sIgA reduction decreased IgA binding of bacteria, leading to increased bacterial encroachment and systemic and adipose tissue inflammation. These pathological changes exacerbated diet-induced MetS. Discussion: Our findings demonstrate that early-life LDP exposure induces persistent intestinal IgA deficiency through lasting GM alterations initiated in early development. This deficiency drives bacterial encroachment, inflammation, and ultimately exacerbates MetS. Conclusions: The exacerbation of diet-induced metabolic syndrome by early-life LDP exposure occurs through an intestinal sIgA-dependent pathway triggered by persistent GM disruption. This highlights a critical mechanism linking early-life antibiotic exposure, gut immune dysfunction, and long-term metabolic health, with significant implications for food safety.},
}
RevDate: 2025-06-24
Xiaoer Huanglong pellets remodels the periphery microenvironment to improve attention deficit hyperactivity disorder based on the microbiota-gut-brain axis.
Phytomedicine : international journal of phytotherapy and phytopharmacology, 145:157007 pii:S0944-7113(25)00646-4 [Epub ahead of print].
BACKGROUND: Recently, research interest in attention deficit hyperactivity disorder (ADHD) has grown significantly, driven by its increasing incidence and substantial societal impact. Among the various pathogenic mechanisms under investigation, the microbiota-gut-brain axis has emerged as a crucial area of focus. In the context of ADHD treatment, Xiaoer Huanglong Pellets (XRHLP), a traditional Chinese herbal formulation, have demonstrated therapeutic efficacy, although the underlying mechanisms remain partially understood.
PURPOSE: This study aimed to analyze and compare the therapeutic effects and underlying mechanisms of XRHLP, including gastric release (WR_HL), enteric release (CR_HL), and colon release (JCR_HL) pellets, for ADHD treatment.
METHODS: This study employed a multi-modal approach to investigate the effects of XRHLP on ADHD. Behavioral assessments combined with Enzyme-linked immunosorbent assay and Western-blot analyses were conducted to evaluate the therapeutic outcomes in model rats with ADHD. Comprehensive profiling of the gut-brain axis was performed using 16S ribosomal RNA sequencing and untargeted and targeted metabolomic analyses. The causal role of the gut microbiota was further validated using fecal microbiota transplantation (FMT).
RESULTS: WR_HL, CR_HL, and JCR_HL improved ADHD-like behaviors and neurotransmission dysfunction, with JCR_HL exhibiting superior intervention effects compared to WR_HL and CR_HL. These therapeutic effects are mediated through multiple pathways, including the restoration of gut microbial homeostasis, attenuation of inflammatory cascades, and repair of compromised intestinal and blood-brain barrier. The intervention also corrected systemic metabolic imbalances by specifically addressing the abnormalities in amino acid metabolism, neurotransmitter regulation, and short-chain fatty acid production. FMT experiments further confirmed the critical role of microbial modulation in mediating the behavioral and microbial regulatory effects of XRHLP.
CONCLUSION: In summary, XRHLP exerts anti-ADHD effects by improving the microbiota-gut-brain axis and correcting amino acid metabolic disorders, providing new insights into the molecular mechanisms by which traditional Chinese medicine influences ADHD and offers potential avenues for drug development.
Additional Links: PMID-40554893
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@article {pmid40554893,
year = {2025},
author = {You, L and Peng, H and Liu, J and Sai, N and Zhao, W and Li, X and Yang, C and Guo, P and Ni, J},
title = {Xiaoer Huanglong pellets remodels the periphery microenvironment to improve attention deficit hyperactivity disorder based on the microbiota-gut-brain axis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {145},
number = {},
pages = {157007},
doi = {10.1016/j.phymed.2025.157007},
pmid = {40554893},
issn = {1618-095X},
abstract = {BACKGROUND: Recently, research interest in attention deficit hyperactivity disorder (ADHD) has grown significantly, driven by its increasing incidence and substantial societal impact. Among the various pathogenic mechanisms under investigation, the microbiota-gut-brain axis has emerged as a crucial area of focus. In the context of ADHD treatment, Xiaoer Huanglong Pellets (XRHLP), a traditional Chinese herbal formulation, have demonstrated therapeutic efficacy, although the underlying mechanisms remain partially understood.
PURPOSE: This study aimed to analyze and compare the therapeutic effects and underlying mechanisms of XRHLP, including gastric release (WR_HL), enteric release (CR_HL), and colon release (JCR_HL) pellets, for ADHD treatment.
METHODS: This study employed a multi-modal approach to investigate the effects of XRHLP on ADHD. Behavioral assessments combined with Enzyme-linked immunosorbent assay and Western-blot analyses were conducted to evaluate the therapeutic outcomes in model rats with ADHD. Comprehensive profiling of the gut-brain axis was performed using 16S ribosomal RNA sequencing and untargeted and targeted metabolomic analyses. The causal role of the gut microbiota was further validated using fecal microbiota transplantation (FMT).
RESULTS: WR_HL, CR_HL, and JCR_HL improved ADHD-like behaviors and neurotransmission dysfunction, with JCR_HL exhibiting superior intervention effects compared to WR_HL and CR_HL. These therapeutic effects are mediated through multiple pathways, including the restoration of gut microbial homeostasis, attenuation of inflammatory cascades, and repair of compromised intestinal and blood-brain barrier. The intervention also corrected systemic metabolic imbalances by specifically addressing the abnormalities in amino acid metabolism, neurotransmitter regulation, and short-chain fatty acid production. FMT experiments further confirmed the critical role of microbial modulation in mediating the behavioral and microbial regulatory effects of XRHLP.
CONCLUSION: In summary, XRHLP exerts anti-ADHD effects by improving the microbiota-gut-brain axis and correcting amino acid metabolic disorders, providing new insights into the molecular mechanisms by which traditional Chinese medicine influences ADHD and offers potential avenues for drug development.},
}
RevDate: 2025-06-24
Perfluorooctane sulfonic acid impairs spermatogenesis via the liver-gut microbiota-testis axis: a central role of chenodeoxycholic acid metabolism.
Journal of advanced research pii:S2090-1232(25)00446-1 [Epub ahead of print].
INTRODUCTION: Perfluorooctane sulfonic acid (PFOS) as a global contaminant is ubiquitously presented in the environmental media and human body. The association between PFOS exposure and reduced male fertility has been recently discovered. However, the relevant mechanism remains unexplored.
OBJECTIVES: Our study aimed to investigate the effect and mechanism of PFOS exposure on male reproductive function.
METHODS: In a murine PFOS exposure model, single-nucleus transcriptome sequencing was performed to delineate the transcriptomic landscape of mouse testes at the single-cell resolution. We examined the serum metabolomic profile and conducted in-depth analysis of hepatic transcriptome datasets to explore the metabolic connections between liver and testis under PFOS exposure. Through integrating chenodeoxycholic acid intervention, fecal microbiota transplantation (FMT), metagenomic sequencing, testicular metabolome, Ligilactobacillus murinus (L. murinus) metabolome, and administration of L. murinus, we confirmed the role of the liver-gut microbiota-testis axis and screened the critical gut microbiota involved in PFOS-mediated spermatogenic disorders.
RESULTS: The results showed that PFOS exposure led to spermatogenic arrest and abnormal spermatogenic microenvironment in the mouse testis. The PFOS-repressed hepatic chenodeoxycholic acid (CDCA) synthesis contributed to the reduced serum/testicular levels of essential fatty acid (linoleic acid) and lipid-soluble vitamins (retinol, vitamin D3), which was responsible for the spermatogenic arrest. Beyond this, PFOS-mediated impaired CDCA production decreased the abundance of gut L. murinus, which affected spermatogenesis through the potential involvement of aspartic acid metabolism. For the first time to our knowledge, we comprehensively assessed the effects of PFOS exposure on the spermatogenic process and elucidated the unrecognized role of liver-gut microbiota-testis axis in PFOS-induced abnormal spermatogenesis.
CONCLUSIONS: The unveiled organ crosstalks provide new insights into the metabolism-disrupting properties, hepatotoxicity, and reproductive toxicity of PFOS, which may facilitate the development of molecule-, metabolite-, and microbe-based strategies for PFOS-induced metabolic diseases and reproductive disorders.
Additional Links: PMID-40554061
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PubMed:
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@article {pmid40554061,
year = {2025},
author = {Yang, W and Zou, P and He, S and Cui, H and Yang, Z and An, H and Chen, Q and Huang, W and Guo, H and Liu, J and Ling, X and Cao, J and Ao, L},
title = {Perfluorooctane sulfonic acid impairs spermatogenesis via the liver-gut microbiota-testis axis: a central role of chenodeoxycholic acid metabolism.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2025.06.037},
pmid = {40554061},
issn = {2090-1224},
abstract = {INTRODUCTION: Perfluorooctane sulfonic acid (PFOS) as a global contaminant is ubiquitously presented in the environmental media and human body. The association between PFOS exposure and reduced male fertility has been recently discovered. However, the relevant mechanism remains unexplored.
OBJECTIVES: Our study aimed to investigate the effect and mechanism of PFOS exposure on male reproductive function.
METHODS: In a murine PFOS exposure model, single-nucleus transcriptome sequencing was performed to delineate the transcriptomic landscape of mouse testes at the single-cell resolution. We examined the serum metabolomic profile and conducted in-depth analysis of hepatic transcriptome datasets to explore the metabolic connections between liver and testis under PFOS exposure. Through integrating chenodeoxycholic acid intervention, fecal microbiota transplantation (FMT), metagenomic sequencing, testicular metabolome, Ligilactobacillus murinus (L. murinus) metabolome, and administration of L. murinus, we confirmed the role of the liver-gut microbiota-testis axis and screened the critical gut microbiota involved in PFOS-mediated spermatogenic disorders.
RESULTS: The results showed that PFOS exposure led to spermatogenic arrest and abnormal spermatogenic microenvironment in the mouse testis. The PFOS-repressed hepatic chenodeoxycholic acid (CDCA) synthesis contributed to the reduced serum/testicular levels of essential fatty acid (linoleic acid) and lipid-soluble vitamins (retinol, vitamin D3), which was responsible for the spermatogenic arrest. Beyond this, PFOS-mediated impaired CDCA production decreased the abundance of gut L. murinus, which affected spermatogenesis through the potential involvement of aspartic acid metabolism. For the first time to our knowledge, we comprehensively assessed the effects of PFOS exposure on the spermatogenic process and elucidated the unrecognized role of liver-gut microbiota-testis axis in PFOS-induced abnormal spermatogenesis.
CONCLUSIONS: The unveiled organ crosstalks provide new insights into the metabolism-disrupting properties, hepatotoxicity, and reproductive toxicity of PFOS, which may facilitate the development of molecule-, metabolite-, and microbe-based strategies for PFOS-induced metabolic diseases and reproductive disorders.},
}
RevDate: 2025-06-24
Whole food diet induces remission in children and young adults with mild-moderate Crohn's disease and is more tolerable than exclusive enteral nutrition: a randomized controlled trial.
Gastroenterology pii:S0016-5085(25)00896-0 [Epub ahead of print].
BACKGROUND: Tasty&Healthy (T&H) is a whole-food diet for Crohn's disease (CD), which excludes processed food, gluten, red meat, and dairy, without requiring formula or mandatory ingredients. TASTI-MM was a clinician-blinded, randomized-controlled trial comparing tolerability and effectiveness of T&H vs. exclusive enteral nutrition (EEN).
METHODS: Patients with biologic-naive mild-moderate CD aged 6-25 years were randomized to either T&H or EEN for 8 weeks, receiving weekly dietary support. Tolerability was evaluated by weekly interviews, questionnaires and intake diaries. Other outcomes included symptomatic remission, Mucosal-Inflammation Non-Invasive (MINI) index, calprotectin, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Fecal microbiome was analyzed by metagenomics at baseline, week-4 and week-8. Data were analyzed by the intention-to-treat approach unless specified otherwise.
RESULTS: Among 83 included patients (41 T&H, 42 EEN; mean age 14.5±3.7 years), 88% tolerated T&H vs. 52% for EEN (aOR 7.7 [95%CI 2.4-25]; p<0.001). Calprotectin, CRP and ESR decreased significantly in both groups, with no between-group differences. Symptomatic remission was achieved in 56% of T&H group vs. 38% of the EEN group (aOR 2.5 [0.98-6.3], p=0.1; per-protocol: 67% vs. 76%; p=0.47). Calprotectin <250μg/g was achieved in 34% vs. 33% (aOR 0.97 [0.37-2.6], p=0.84) and MINI<8 in 44% vs. 31% (aOR 1.8 [0.7-4.5]; p=0.33). Microbiome α-diversity improved in the T&H arm and declined in the EEN arm, showing superior species richness at both week-4 and week-8. Species associated with bowel inflammation, such as Ruminococcus gnavus, decreased in T&H and increased in EEN (q<0.001).
CONCLUSIONS: T&H demonstrated better tolerability than EEN for inducing remission in mild-to-moderate CD, while positively affecting the microbiome (TASTI-MM, NCT#04239248).
Additional Links: PMID-40553742
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@article {pmid40553742,
year = {2025},
author = {Frutkoff, YA and Plotkin, L and Pollak, D and Livovsky, J and Focht, G and Lev-Tzion, R and Ledder, O and Assa, A and Yogev, D and Orlanski-Meyer, E and Broide, E and Kierkuś, J and Kang, B and Weiss, B and Aloi, M and Schwerd, T and Shouval, DS and Bramuzzo, M and Griffiths, AM and Yassour, M and Turner, D},
title = {Whole food diet induces remission in children and young adults with mild-moderate Crohn's disease and is more tolerable than exclusive enteral nutrition: a randomized controlled trial.},
journal = {Gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1053/j.gastro.2025.06.011},
pmid = {40553742},
issn = {1528-0012},
abstract = {BACKGROUND: Tasty&Healthy (T&H) is a whole-food diet for Crohn's disease (CD), which excludes processed food, gluten, red meat, and dairy, without requiring formula or mandatory ingredients. TASTI-MM was a clinician-blinded, randomized-controlled trial comparing tolerability and effectiveness of T&H vs. exclusive enteral nutrition (EEN).
METHODS: Patients with biologic-naive mild-moderate CD aged 6-25 years were randomized to either T&H or EEN for 8 weeks, receiving weekly dietary support. Tolerability was evaluated by weekly interviews, questionnaires and intake diaries. Other outcomes included symptomatic remission, Mucosal-Inflammation Non-Invasive (MINI) index, calprotectin, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Fecal microbiome was analyzed by metagenomics at baseline, week-4 and week-8. Data were analyzed by the intention-to-treat approach unless specified otherwise.
RESULTS: Among 83 included patients (41 T&H, 42 EEN; mean age 14.5±3.7 years), 88% tolerated T&H vs. 52% for EEN (aOR 7.7 [95%CI 2.4-25]; p<0.001). Calprotectin, CRP and ESR decreased significantly in both groups, with no between-group differences. Symptomatic remission was achieved in 56% of T&H group vs. 38% of the EEN group (aOR 2.5 [0.98-6.3], p=0.1; per-protocol: 67% vs. 76%; p=0.47). Calprotectin <250μg/g was achieved in 34% vs. 33% (aOR 0.97 [0.37-2.6], p=0.84) and MINI<8 in 44% vs. 31% (aOR 1.8 [0.7-4.5]; p=0.33). Microbiome α-diversity improved in the T&H arm and declined in the EEN arm, showing superior species richness at both week-4 and week-8. Species associated with bowel inflammation, such as Ruminococcus gnavus, decreased in T&H and increased in EEN (q<0.001).
CONCLUSIONS: T&H demonstrated better tolerability than EEN for inducing remission in mild-to-moderate CD, while positively affecting the microbiome (TASTI-MM, NCT#04239248).},
}
RevDate: 2025-06-24
Narrative review of the association between gut microbiota and peripheral artery disease.
Vascular medicine (London, England) [Epub ahead of print].
It has been posited that the inflammatory process seen in atherosclerosis is underpinned by gut dysbiosis. Dysbiosis refers to alterations in the function, composition, and diversity of the human gut microbiota, all of which are influenced by endogenous and exogenous stimuli. Currently there is limited literature describing the association between gut microbiota and peripheral artery disease (PAD). This review summarizes the evidence surrounding the role of gut microbiota in the initiation of atherosclerosis (through direct infection of atherosclerotic plaque or systemic immune response to bacterial products and metabolites) and how dysbiosis may influence the various treatment modalities for PAD, including medical therapy (pharmacotherapy, lifestyle changes, and supervised exercise training) and surgery (endovascular and open revascularization). In particular, the role of short chain fatty acids (SCFAs), the effects of exercise on SCFA-producing and lactic acid bacteria (LAB) and, consequently, the lack of targeted research into dietary interventions and supplementation are highlighted in this review. This review highlights the potential for gut microbiota as not only a therapeutic target in patients with PAD, but also as a diagnostic and screening tool. It is imperative that the focus of future research is on the potential for personalized treatment which targets the gut microbiota (such as synbiotics, postbiotics, nicotinamide adenine dinucleotide (NAD) supplementation, selective antibiotics, resistance exercise, senolytics, and fecal microbial transplantation [FMT]) to be utilized as adjuncts to already existing treatment options for PAD. This review also highlights the potential role of biobanks and analysis of atherosclerotic plaques in further advancing knowledge and research in this area.
Additional Links: PMID-40552988
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Citation:
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@article {pmid40552988,
year = {2025},
author = {Park, JM and Beckman, I and Delaney, CL},
title = {Narrative review of the association between gut microbiota and peripheral artery disease.},
journal = {Vascular medicine (London, England)},
volume = {},
number = {},
pages = {1358863X251346062},
doi = {10.1177/1358863X251346062},
pmid = {40552988},
issn = {1477-0377},
abstract = {It has been posited that the inflammatory process seen in atherosclerosis is underpinned by gut dysbiosis. Dysbiosis refers to alterations in the function, composition, and diversity of the human gut microbiota, all of which are influenced by endogenous and exogenous stimuli. Currently there is limited literature describing the association between gut microbiota and peripheral artery disease (PAD). This review summarizes the evidence surrounding the role of gut microbiota in the initiation of atherosclerosis (through direct infection of atherosclerotic plaque or systemic immune response to bacterial products and metabolites) and how dysbiosis may influence the various treatment modalities for PAD, including medical therapy (pharmacotherapy, lifestyle changes, and supervised exercise training) and surgery (endovascular and open revascularization). In particular, the role of short chain fatty acids (SCFAs), the effects of exercise on SCFA-producing and lactic acid bacteria (LAB) and, consequently, the lack of targeted research into dietary interventions and supplementation are highlighted in this review. This review highlights the potential for gut microbiota as not only a therapeutic target in patients with PAD, but also as a diagnostic and screening tool. It is imperative that the focus of future research is on the potential for personalized treatment which targets the gut microbiota (such as synbiotics, postbiotics, nicotinamide adenine dinucleotide (NAD) supplementation, selective antibiotics, resistance exercise, senolytics, and fecal microbial transplantation [FMT]) to be utilized as adjuncts to already existing treatment options for PAD. This review also highlights the potential role of biobanks and analysis of atherosclerotic plaques in further advancing knowledge and research in this area.},
}
RevDate: 2025-06-24
Epigallocatechin-3-Gallate Attenuates Benign Prostatic Hyperplasia Development via Regulating Firmicutes to Inhibit Gastric Secretion of Insulin-Like Growth Factor-1.
Cell biology international [Epub ahead of print].
Benign prostatic hyperplasia (BPH), a prevalent age-related condition in men, is increasingly linked to metabolic syndrome (MetS) and gut microbiota dysbiosis. This study reveals how Firmicutes-dominant microbial imbalance drives BPH progression via IGF-1 signaling and identifies the green tea polyphenol epigallocatechin-3-gallate (EGCG) as a dual-action therapeutic. Using MetS-BPH mouse models and human prostate cell lines, we demonstrated that BPH-associated gut microbiota-particularly elevated Firmicutes and an increased Firmicutes/Bacteroidetes ratio-promotes prostate hyperplasia by upregulating IGF-1. Both BPH mice and recipient mice transplanted with BPH microbiota showed elevated serum and prostate IGF-1 levels, mirroring findings in human BPH patients. Mechanistically, IGF-1 stimulated prostate cell proliferation (RWPE-1/WPMY-1) and suppressed apoptosis via PI3K/AKT/mTOR activation, while the IGF-1 antagonist Linsitinib reversed these effects. EGCG emerged as a potent modulator of this gut-prostate axis: it selectively reduced Firmicutes overgrowth in BPH mice, normalized IGF-1 levels, and inhibited downstream PI3K/AKT/mTOR signaling. In fecal microbiota transplantation experiments, EGCG counteracted IGF-1-driven prostate enlargement and microbial dysbiosis, underscoring its dual role in rebalancing gut flora and blocking growth factor pathways. Our findings position EGCG as a promising intervention for MetS-associated BPH, simultaneously targeting microbial dysbiosis and IGF-1 signaling. This study not only elucidates the Firmicutes-IGF-1 axis in BPH pathogenesis but also highlights the therapeutic potential of dietary polyphenols in metabolic urological disorders.
Additional Links: PMID-40552775
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PubMed:
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@article {pmid40552775,
year = {2025},
author = {Yang, T and Shao, Y and Wang, Z and Liu, C and Gu, M},
title = {Epigallocatechin-3-Gallate Attenuates Benign Prostatic Hyperplasia Development via Regulating Firmicutes to Inhibit Gastric Secretion of Insulin-Like Growth Factor-1.},
journal = {Cell biology international},
volume = {},
number = {},
pages = {},
doi = {10.1002/cbin.70032},
pmid = {40552775},
issn = {1095-8355},
support = {//The work was sponsored by the Interdisciplinary Program of Shanghai Jiao Tong University (Project Number YG2024QNB17) and the National Natural Science Foundation of China (Grant Nos. 82170788 and 81900687)./ ; },
abstract = {Benign prostatic hyperplasia (BPH), a prevalent age-related condition in men, is increasingly linked to metabolic syndrome (MetS) and gut microbiota dysbiosis. This study reveals how Firmicutes-dominant microbial imbalance drives BPH progression via IGF-1 signaling and identifies the green tea polyphenol epigallocatechin-3-gallate (EGCG) as a dual-action therapeutic. Using MetS-BPH mouse models and human prostate cell lines, we demonstrated that BPH-associated gut microbiota-particularly elevated Firmicutes and an increased Firmicutes/Bacteroidetes ratio-promotes prostate hyperplasia by upregulating IGF-1. Both BPH mice and recipient mice transplanted with BPH microbiota showed elevated serum and prostate IGF-1 levels, mirroring findings in human BPH patients. Mechanistically, IGF-1 stimulated prostate cell proliferation (RWPE-1/WPMY-1) and suppressed apoptosis via PI3K/AKT/mTOR activation, while the IGF-1 antagonist Linsitinib reversed these effects. EGCG emerged as a potent modulator of this gut-prostate axis: it selectively reduced Firmicutes overgrowth in BPH mice, normalized IGF-1 levels, and inhibited downstream PI3K/AKT/mTOR signaling. In fecal microbiota transplantation experiments, EGCG counteracted IGF-1-driven prostate enlargement and microbial dysbiosis, underscoring its dual role in rebalancing gut flora and blocking growth factor pathways. Our findings position EGCG as a promising intervention for MetS-associated BPH, simultaneously targeting microbial dysbiosis and IGF-1 signaling. This study not only elucidates the Firmicutes-IGF-1 axis in BPH pathogenesis but also highlights the therapeutic potential of dietary polyphenols in metabolic urological disorders.},
}
RevDate: 2025-06-24
CmpDate: 2025-06-24
Microbiome compositional changes and clonal engraftment in a phase 3 trial of fecal microbiota, live-jslm for recurrent Clostridioides difficile infection.
Gut microbes, 17(1):2520412.
Live microbiota therapies have shown promise in many gastrointestinal diseases, including in the prevention of recurrent Clostridioides difficile infections (rCDI); however, frameworks for their pharmacokinetic and pharmacodynamic analysis are not fully established. Fecal microbiota, live-jslm (RBL) is the first microbiota-based product approved by the US Food and Drug Administration for the prevention of rCDI and was superior to placebo in the PUNCH™ CD3 phase 3 clinical trial (NCT03244644). In this analysis, deep shotgun metagenomic sequencing was used to assess changes in gut microbiome compositions of participants and engraftment of bacterial clonal populations (i.e. strains) from RBL to recipients. Among RBL responders, gut microbiota shifted toward compositions that resembled healthy donors as early as 1 week after RBL administration; the resulting microbiota compositions included clonal populations that engrafted from RBL to recipients. Engraftment was higher in RBL responders compared with non-responders, and many clonally engrafted populations persisted for ≥ 6 months. Bacteroidia species were among the most effectively engrafted species from RBL. This study utilizes data from a large clinical trial to establish a method with high specificity for exploring clonal engraftment from microbiota-based treatments to facilitate future pharmacokinetic and pharmacodynamic analyses.Clinicaltrials Registration: NCT03244644.
Additional Links: PMID-40552763
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@article {pmid40552763,
year = {2025},
author = {Claypool, J and Lindved, G and Myers, PN and Ward, T and Nielsen, HB and Blount, KF},
title = {Microbiome compositional changes and clonal engraftment in a phase 3 trial of fecal microbiota, live-jslm for recurrent Clostridioides difficile infection.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2520412},
doi = {10.1080/19490976.2025.2520412},
pmid = {40552763},
issn = {1949-0984},
mesh = {Humans ; *Clostridium Infections/therapy/microbiology ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; *Feces/microbiology ; Male ; *Clostridioides difficile/physiology ; Female ; Middle Aged ; *Bacteria/classification/genetics/isolation & purification ; Adult ; Recurrence ; Aged ; },
abstract = {Live microbiota therapies have shown promise in many gastrointestinal diseases, including in the prevention of recurrent Clostridioides difficile infections (rCDI); however, frameworks for their pharmacokinetic and pharmacodynamic analysis are not fully established. Fecal microbiota, live-jslm (RBL) is the first microbiota-based product approved by the US Food and Drug Administration for the prevention of rCDI and was superior to placebo in the PUNCH™ CD3 phase 3 clinical trial (NCT03244644). In this analysis, deep shotgun metagenomic sequencing was used to assess changes in gut microbiome compositions of participants and engraftment of bacterial clonal populations (i.e. strains) from RBL to recipients. Among RBL responders, gut microbiota shifted toward compositions that resembled healthy donors as early as 1 week after RBL administration; the resulting microbiota compositions included clonal populations that engrafted from RBL to recipients. Engraftment was higher in RBL responders compared with non-responders, and many clonally engrafted populations persisted for ≥ 6 months. Bacteroidia species were among the most effectively engrafted species from RBL. This study utilizes data from a large clinical trial to establish a method with high specificity for exploring clonal engraftment from microbiota-based treatments to facilitate future pharmacokinetic and pharmacodynamic analyses.Clinicaltrials Registration: NCT03244644.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Clostridium Infections/therapy/microbiology
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
*Feces/microbiology
Male
*Clostridioides difficile/physiology
Female
Middle Aged
*Bacteria/classification/genetics/isolation & purification
Adult
Recurrence
Aged
RevDate: 2025-06-24
Effects of semaglutide on metabolism and gut microbiota in high-fat diet-induced obese mice.
Frontiers in pharmacology, 16:1562896.
BACKGROUND: The purpose of this study was to explore how semaglutide, a GLP-1RA, regulates serum metabolism and gut microbiota to improve obesity in mice and whether fecal microbiota transplantation (FMT) can transmit the beneficial effects of semaglutide to recipient mice.
METHODS: Male C57BL/6J mice were given standard diet (ND), high-fat diet (HFD), or high-fat diet with semaglutide (SHF, 100 μg/kg). Fecal microbiota transplantation was used to transplant the fecal suspension supernatant (MT) and bacteria (FMT) from SHF group mice to antibiotic-induced pseudo-germ-free mice.
RESULTS: Results showed that semaglutide significantly reduced the body weight, body fat, FBG, and insulin levels induced by high-fat diet, and improved insulin resistance and sensitivity damage (p < 0.05). This was achieved by regulating the expression of genes related to lipid metabolism such as Pparα, Pparγ, Cpt1a, and Pgc1α in the liver and adipose tissue, as well as the appetite-related genes Leptin, Agrp, Npy, and Pomc in the hypothalamus. After stopping semaglutide intervention 4 weeks, the body weight of the mice rebounded significantly. Fecal microbiota transplantation could transmit the beneficial effects of semaglutide to recipient mice. Semaglutide and fecal microbiota transplantation affected metabolic pathways such as serum amino acid metabolism and pyrimidine metabolism in obese mice, and reshaped the composition and proportion of fecal gut microbiota in obese mice.
CONCLUSION: In summary, semaglutide could inhibit food intake and improve obesity, regulate serum metabolism and the composition of gut microbiota in mice. Bacterial transplantation is key to transmitting the improvement brought about by fecal microbiota transplantation of semaglutide to recipient mice.
Additional Links: PMID-40552153
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@article {pmid40552153,
year = {2025},
author = {Sun, L and Shang, B and Lv, S and Liu, G and Wu, Q and Geng, Y},
title = {Effects of semaglutide on metabolism and gut microbiota in high-fat diet-induced obese mice.},
journal = {Frontiers in pharmacology},
volume = {16},
number = {},
pages = {1562896},
pmid = {40552153},
issn = {1663-9812},
abstract = {BACKGROUND: The purpose of this study was to explore how semaglutide, a GLP-1RA, regulates serum metabolism and gut microbiota to improve obesity in mice and whether fecal microbiota transplantation (FMT) can transmit the beneficial effects of semaglutide to recipient mice.
METHODS: Male C57BL/6J mice were given standard diet (ND), high-fat diet (HFD), or high-fat diet with semaglutide (SHF, 100 μg/kg). Fecal microbiota transplantation was used to transplant the fecal suspension supernatant (MT) and bacteria (FMT) from SHF group mice to antibiotic-induced pseudo-germ-free mice.
RESULTS: Results showed that semaglutide significantly reduced the body weight, body fat, FBG, and insulin levels induced by high-fat diet, and improved insulin resistance and sensitivity damage (p < 0.05). This was achieved by regulating the expression of genes related to lipid metabolism such as Pparα, Pparγ, Cpt1a, and Pgc1α in the liver and adipose tissue, as well as the appetite-related genes Leptin, Agrp, Npy, and Pomc in the hypothalamus. After stopping semaglutide intervention 4 weeks, the body weight of the mice rebounded significantly. Fecal microbiota transplantation could transmit the beneficial effects of semaglutide to recipient mice. Semaglutide and fecal microbiota transplantation affected metabolic pathways such as serum amino acid metabolism and pyrimidine metabolism in obese mice, and reshaped the composition and proportion of fecal gut microbiota in obese mice.
CONCLUSION: In summary, semaglutide could inhibit food intake and improve obesity, regulate serum metabolism and the composition of gut microbiota in mice. Bacterial transplantation is key to transmitting the improvement brought about by fecal microbiota transplantation of semaglutide to recipient mice.},
}
RevDate: 2025-06-24
CmpDate: 2025-06-24
Lactobacillus regulate muscle fiber type conversion in Chinese native pigs via tryptophan metabolism.
NPJ biofilms and microbiomes, 11(1):114.
Identifying potential gut microbes and metabolites that can influence muscle fiber type is gaining interest in meat quality research. In this study, muscle fiber characteristics, muscle metabolite profiles, and gut microbiota and metabolome were compared among three pig breeds (Taoyuan black, TB; Xiangcun black, XB; and Duroc pigs). The results showed that the slow-twitch fiber percentage was higher (P < 0.05) in native pigs (TB and XB pigs) compared to Duroc pigs. The differences were mainly regulated by Lactobacillus abundance and tryptophan metabolism. Further, fecal microbiota transplantation from XB pigs transferred a higher slow-twitch fiber percentage, Lactobacillus abundance, kynurenic acid level, and AMPK/PGC-1α expression to mice. These findings suggest that Lactobacillus in the colon of TB and XB pigs, through kynurenic acid production, may promote slow-twitch fiber formation via the AMPK/PGC-1α signaling pathway.
Additional Links: PMID-40550813
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Citation:
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@article {pmid40550813,
year = {2025},
author = {Song, B and Azad, MAK and Zhu, Q and Cheng, Y and Ding, S and Yao, K and Kong, X},
title = {Lactobacillus regulate muscle fiber type conversion in Chinese native pigs via tryptophan metabolism.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {114},
pmid = {40550813},
issn = {2055-5008},
support = {32350410424//National Natural Science Foundation of China/ ; 2022JJ30643//Hunan Province Natural Science Foundation/ ; 092GJHZ2022044FN//Future Partner Special Network Fund of Chinese Academy of Sciences/ ; 2023YFD1301305//National Key Research and Development Project/ ; },
mesh = {Animals ; *Tryptophan/metabolism ; Swine/microbiology ; *Lactobacillus/metabolism/physiology ; Mice ; Gastrointestinal Microbiome ; Kynurenic Acid/metabolism ; *Muscle Fibers, Slow-Twitch/metabolism ; Feces/microbiology ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism/genetics ; AMP-Activated Protein Kinases/metabolism ; *Muscle Fibers, Skeletal/metabolism ; Metabolome ; },
abstract = {Identifying potential gut microbes and metabolites that can influence muscle fiber type is gaining interest in meat quality research. In this study, muscle fiber characteristics, muscle metabolite profiles, and gut microbiota and metabolome were compared among three pig breeds (Taoyuan black, TB; Xiangcun black, XB; and Duroc pigs). The results showed that the slow-twitch fiber percentage was higher (P < 0.05) in native pigs (TB and XB pigs) compared to Duroc pigs. The differences were mainly regulated by Lactobacillus abundance and tryptophan metabolism. Further, fecal microbiota transplantation from XB pigs transferred a higher slow-twitch fiber percentage, Lactobacillus abundance, kynurenic acid level, and AMPK/PGC-1α expression to mice. These findings suggest that Lactobacillus in the colon of TB and XB pigs, through kynurenic acid production, may promote slow-twitch fiber formation via the AMPK/PGC-1α signaling pathway.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Tryptophan/metabolism
Swine/microbiology
*Lactobacillus/metabolism/physiology
Mice
Gastrointestinal Microbiome
Kynurenic Acid/metabolism
*Muscle Fibers, Slow-Twitch/metabolism
Feces/microbiology
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism/genetics
AMP-Activated Protein Kinases/metabolism
*Muscle Fibers, Skeletal/metabolism
Metabolome
RevDate: 2025-06-24
CmpDate: 2025-06-24
[Association between gut microbiota and hyperuricemia: insights into innovative therapeutic strategies].
Sheng wu gong cheng xue bao = Chinese journal of biotechnology, 41(6):2290-2309.
Uric acid (UA) is the final metabolite of purines in the human body. An imbalance in UA production and excretion that disrupts homeostasis leads to elevated blood UA levels and the development of hyperuricemia (HUA). Approximately one-third of UA is excreted through the intestinal tract. As a crucial component of the intestinal microenvironment, the gut microbiota plays a pivotal role in regulating blood UA levels. Alterations or imbalances in gut microbiota composition are linked to the onset of HUA, which implies the potential of gut microbiota as a novel target for the prevention and treatment of HUA. This review introduces the occurrence mechanism and damage of hyperuricemia, examines the association between HUA and the gut microbiota and their metabolites, and explores the molecular mechanisms underlying gut microbiota-targeted therapies for HUA. Furthermore, it discusses the potential applications of probiotics, prebiotics, and traditional Chinese medicine (including both single herbs and compound formulas) with UA-lowering effects, along with cutting-edge technologies such as fecal microbiota transplantation and machine learning in HUA treatment. This review provides valuable perspectives and strategies for improving the prevention and treatment of HUA.
Additional Links: PMID-40550671
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@article {pmid40550671,
year = {2025},
author = {Zhang, S and Liu, X and Zhong, Y and Fu, Y},
title = {[Association between gut microbiota and hyperuricemia: insights into innovative therapeutic strategies].},
journal = {Sheng wu gong cheng xue bao = Chinese journal of biotechnology},
volume = {41},
number = {6},
pages = {2290-2309},
doi = {10.13345/j.cjb.250060},
pmid = {40550671},
issn = {1872-2075},
mesh = {*Hyperuricemia/therapy/microbiology ; Humans ; *Gastrointestinal Microbiome/physiology ; Probiotics/therapeutic use ; Uric Acid/metabolism/blood ; Fecal Microbiota Transplantation ; Prebiotics ; Medicine, Chinese Traditional ; },
abstract = {Uric acid (UA) is the final metabolite of purines in the human body. An imbalance in UA production and excretion that disrupts homeostasis leads to elevated blood UA levels and the development of hyperuricemia (HUA). Approximately one-third of UA is excreted through the intestinal tract. As a crucial component of the intestinal microenvironment, the gut microbiota plays a pivotal role in regulating blood UA levels. Alterations or imbalances in gut microbiota composition are linked to the onset of HUA, which implies the potential of gut microbiota as a novel target for the prevention and treatment of HUA. This review introduces the occurrence mechanism and damage of hyperuricemia, examines the association between HUA and the gut microbiota and their metabolites, and explores the molecular mechanisms underlying gut microbiota-targeted therapies for HUA. Furthermore, it discusses the potential applications of probiotics, prebiotics, and traditional Chinese medicine (including both single herbs and compound formulas) with UA-lowering effects, along with cutting-edge technologies such as fecal microbiota transplantation and machine learning in HUA treatment. This review provides valuable perspectives and strategies for improving the prevention and treatment of HUA.},
}
MeSH Terms:
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*Hyperuricemia/therapy/microbiology
Humans
*Gastrointestinal Microbiome/physiology
Probiotics/therapeutic use
Uric Acid/metabolism/blood
Fecal Microbiota Transplantation
Prebiotics
Medicine, Chinese Traditional
RevDate: 2025-06-24
CmpDate: 2025-06-24
[Pathogenesis and progress in diagnosis and treatment of diversion colitis after colorectal cancer surgery].
Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery, 28(6):627-632.
Diversion colitis (DC) is a non-specific inflammation caused by the lack of fecal flow stimulation in the distal intestine after intestinal diversion surgery. It is mainly related to factors such as intestinal flora imbalance, deficiency of short-chain fatty acid (SCFA) and immune abnormalities. The clinical manifestations of diversion colitis include abdominal pain, mucus and bloody stools, diarrhea and other symptoms, but most patients may have no obvious symptoms. Diagnosis mainly relies on endoscopic examination and pathological characteristics. Common endoscopic findings include mucosal congestion, edema, and increased fragility, and the histological manifestation is mainly lymphoid follicle hyperplasia. Other intestinal inflammatory diseases need to be excluded. The treatment options include surgical and conservative medical therapies, among which stoma reversal is the most effective treatment to restore intestinal continuity. Conservative treatments such as SCFA, 5-aminosalicylic acid (5-ASA), steroid or cellulose solution enema, leukocyte removal therapy and fecal microbiota transplantation (FMT) can be used for those who cannot undergo surgery, combined with diet and lifestyle support to improve symptoms. This article summarized the pathogenesis, status, clinical features, diagnostic strategy and treatment progress of DC, hoping to provide reference for the diagnosis and treatment of DC.
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@article {pmid40550654,
year = {2025},
author = {Zhang, ZW and Ye, YJ and Shen, ZL},
title = {[Pathogenesis and progress in diagnosis and treatment of diversion colitis after colorectal cancer surgery].},
journal = {Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery},
volume = {28},
number = {6},
pages = {627-632},
doi = {10.3760/cma.j.cn441530-20250326-00125},
pmid = {40550654},
issn = {1671-0274},
support = {82272841//National Natural Science Foundation of China/ ; },
mesh = {Humans ; *Colorectal Neoplasms/surgery ; *Colitis/diagnosis/therapy/etiology ; *Postoperative Complications/therapy/diagnosis/etiology ; Fecal Microbiota Transplantation ; },
abstract = {Diversion colitis (DC) is a non-specific inflammation caused by the lack of fecal flow stimulation in the distal intestine after intestinal diversion surgery. It is mainly related to factors such as intestinal flora imbalance, deficiency of short-chain fatty acid (SCFA) and immune abnormalities. The clinical manifestations of diversion colitis include abdominal pain, mucus and bloody stools, diarrhea and other symptoms, but most patients may have no obvious symptoms. Diagnosis mainly relies on endoscopic examination and pathological characteristics. Common endoscopic findings include mucosal congestion, edema, and increased fragility, and the histological manifestation is mainly lymphoid follicle hyperplasia. Other intestinal inflammatory diseases need to be excluded. The treatment options include surgical and conservative medical therapies, among which stoma reversal is the most effective treatment to restore intestinal continuity. Conservative treatments such as SCFA, 5-aminosalicylic acid (5-ASA), steroid or cellulose solution enema, leukocyte removal therapy and fecal microbiota transplantation (FMT) can be used for those who cannot undergo surgery, combined with diet and lifestyle support to improve symptoms. This article summarized the pathogenesis, status, clinical features, diagnostic strategy and treatment progress of DC, hoping to provide reference for the diagnosis and treatment of DC.},
}
MeSH Terms:
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Humans
*Colorectal Neoplasms/surgery
*Colitis/diagnosis/therapy/etiology
*Postoperative Complications/therapy/diagnosis/etiology
Fecal Microbiota Transplantation
RevDate: 2025-06-23
Impact of Gut Microbiota Alterations on Mitochondrial Bioenergetics in Cortical Astrocytes and Sensorimotor Impairment in a Rat Model of Lipopolysaccharide-Associated Encephalopathy.
Shock (Augusta, Ga.) pii:00024382-990000000-00677 [Epub ahead of print].
PURPOSE: Brain dysfunction is a significant complication of sepsis, commonly referred to as sepsis-associated encephalopathy (SAE). Alterations in gut microbiota during sepsis may contribute to development of SAE through the gut-brain axis. This study investigated effects of fecal transplantation from healthy or endotoxemic individuals on gut microbiota and brain function in a rat model of lipopolysaccharide (LPS)-associated encephalopathy.
METHODS: Following LPS induction, rats received daily oral gavage of fecal microbiota transplants for three days. Sensory and motor functions were assessed daily throughout the seven-day study period after LPS exposure. On day seven post-LPS, the study examined gut microbiota structure and composition, serum and fecal short-chain fatty acids (SCFAs) levels, ileal villus length, intestinal permeability, neuronal and glial ultrastructure, cytokine concentrations (pro-inflammatory and anti-inflammatory), and mitochondrial bioenergetics.
RESULTS: Administration of healthy donor feces preserved gut microbial structure and composition, maintained ileal villus length, and improved intestinal permeability following LPS treatment. Additionally, it increased SCFA levels, reduced pro-inflammatory cytokines, enhanced anti-inflammatory cytokine release, and restored sensitivity to mechanical and thermal stimuli, as well as motor function. Rats treated with healthy donor feces also exhibited reduced neuronal necrosis and a decreased density of mitochondria in cortical astrocytes. Notably, mitochondrial metabolism in LPS-treated rats returned to near-normal levels following treatment with healthy donor feces. In contrast, administration of endotoxemic donor feces exacerbated these effects in LPS-treated rats.
CONCLUSION: Ameliorating gut dysbiosis prevents mitochondrial dysfunction in astrocytes by promoting SCFA production and enhancing anti-inflammatory cytokine release. This process preserves neuronal integrity and mitigates the severity of encephalopathy.
Additional Links: PMID-40550557
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@article {pmid40550557,
year = {2025},
author = {Huang, CT and Wang, YC and Lin, SC and Lai, YC and Chen, SH and Feng, ST and Tsai, YJ},
title = {Impact of Gut Microbiota Alterations on Mitochondrial Bioenergetics in Cortical Astrocytes and Sensorimotor Impairment in a Rat Model of Lipopolysaccharide-Associated Encephalopathy.},
journal = {Shock (Augusta, Ga.)},
volume = {},
number = {},
pages = {},
doi = {10.1097/SHK.0000000000002637},
pmid = {40550557},
issn = {1540-0514},
abstract = {PURPOSE: Brain dysfunction is a significant complication of sepsis, commonly referred to as sepsis-associated encephalopathy (SAE). Alterations in gut microbiota during sepsis may contribute to development of SAE through the gut-brain axis. This study investigated effects of fecal transplantation from healthy or endotoxemic individuals on gut microbiota and brain function in a rat model of lipopolysaccharide (LPS)-associated encephalopathy.
METHODS: Following LPS induction, rats received daily oral gavage of fecal microbiota transplants for three days. Sensory and motor functions were assessed daily throughout the seven-day study period after LPS exposure. On day seven post-LPS, the study examined gut microbiota structure and composition, serum and fecal short-chain fatty acids (SCFAs) levels, ileal villus length, intestinal permeability, neuronal and glial ultrastructure, cytokine concentrations (pro-inflammatory and anti-inflammatory), and mitochondrial bioenergetics.
RESULTS: Administration of healthy donor feces preserved gut microbial structure and composition, maintained ileal villus length, and improved intestinal permeability following LPS treatment. Additionally, it increased SCFA levels, reduced pro-inflammatory cytokines, enhanced anti-inflammatory cytokine release, and restored sensitivity to mechanical and thermal stimuli, as well as motor function. Rats treated with healthy donor feces also exhibited reduced neuronal necrosis and a decreased density of mitochondria in cortical astrocytes. Notably, mitochondrial metabolism in LPS-treated rats returned to near-normal levels following treatment with healthy donor feces. In contrast, administration of endotoxemic donor feces exacerbated these effects in LPS-treated rats.
CONCLUSION: Ameliorating gut dysbiosis prevents mitochondrial dysfunction in astrocytes by promoting SCFA production and enhancing anti-inflammatory cytokine release. This process preserves neuronal integrity and mitigates the severity of encephalopathy.},
}
RevDate: 2025-06-23
Fecal microbiota transplant (FMT) is associated with the resolution of recurrent urinary tract infections (UTIs).
Urology pii:S0090-4295(25)00607-7 [Epub ahead of print].
Additional Links: PMID-40550284
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PubMed:
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@article {pmid40550284,
year = {2025},
author = {Biggs, GAY},
title = {Fecal microbiota transplant (FMT) is associated with the resolution of recurrent urinary tract infections (UTIs).},
journal = {Urology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.urology.2025.06.040},
pmid = {40550284},
issn = {1527-9995},
}
RevDate: 2025-06-23
Recent Insights About Probiotics Related Pharmabiotics in Pharmacology: Prevention and Management of Diseases.
Probiotics and antimicrobial proteins [Epub ahead of print].
The science of pharmacology investigates the effects of drugs on living organisms and vice versa. The frequency of side effects of some drugs used in traditional pharmacological treatment approaches and/or their inability to provide adequate treatment has led to the importance of new drug research and development (R&D) studies. Recently, due to the discovery that some diseases are associated with an imbalanced microbiota (dysbiosis), there has been a surge of interest in therapeutic approaches that can restore balance (biosis) to the microbiota. This review discusses the current status of the pharmabiotic potential of probiotics, prebiotics, synbiotics, paraprobiotics, postbiotics, metabiotics, next-generation probiotics, and fecal microbiota transplantation; describes their pharmacological functions from gastrointestinal disorders to neurodegenerative diseases; and also discusses the developments in pharmaceutical applications of probiotics and their derivatives.
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@article {pmid40549339,
year = {2025},
author = {Bulut, SD and Döndaş, HA and Celebioglu, HU and Sansano, JM and Döndaş, NY},
title = {Recent Insights About Probiotics Related Pharmabiotics in Pharmacology: Prevention and Management of Diseases.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {40549339},
issn = {1867-1314},
abstract = {The science of pharmacology investigates the effects of drugs on living organisms and vice versa. The frequency of side effects of some drugs used in traditional pharmacological treatment approaches and/or their inability to provide adequate treatment has led to the importance of new drug research and development (R&D) studies. Recently, due to the discovery that some diseases are associated with an imbalanced microbiota (dysbiosis), there has been a surge of interest in therapeutic approaches that can restore balance (biosis) to the microbiota. This review discusses the current status of the pharmabiotic potential of probiotics, prebiotics, synbiotics, paraprobiotics, postbiotics, metabiotics, next-generation probiotics, and fecal microbiota transplantation; describes their pharmacological functions from gastrointestinal disorders to neurodegenerative diseases; and also discusses the developments in pharmaceutical applications of probiotics and their derivatives.},
}
RevDate: 2025-06-24
Fecal microbiota transplantation in allergic diseases.
World journal of methodology, 15(2):101430.
Microorganisms such as bacteria, fungi, viruses, parasites living in the human intestine constitute the human intestinal microbiota. Dysbiosis refers to compositional and quantitative changes that negatively affect healthy gut microbiota. In recent years, with the demonstration that many diseases are associated with dysbiosis, treatment strategies targeting the correction of dysbiosis in the treatment of these diseases have begun to be investigated. Faecal microbiota transplantation (FMT) is the process of transferring faeces from a healthy donor to another recipient in order to restore the gut microbiota and provide a therapeutic benefit. FMT studies have gained popularity after probiotic, prebiotic, symbiotic studies in the treatment of dysbiosis and related diseases. FMT has emerged as a potential new therapy in the treatment of allergic diseases as it is associated with the maintenance of intestinal microbiota and immunological balance (T helper 1/T helper 2 cells) and thus suppression of allergic responses. In this article, the definition, application, safety and use of FMT in allergic diseases will be discussed with current data.
Additional Links: PMID-40548224
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Citation:
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@article {pmid40548224,
year = {2025},
author = {Tüsüz Önata, E and Özdemir, Ö},
title = {Fecal microbiota transplantation in allergic diseases.},
journal = {World journal of methodology},
volume = {15},
number = {2},
pages = {101430},
pmid = {40548224},
issn = {2222-0682},
abstract = {Microorganisms such as bacteria, fungi, viruses, parasites living in the human intestine constitute the human intestinal microbiota. Dysbiosis refers to compositional and quantitative changes that negatively affect healthy gut microbiota. In recent years, with the demonstration that many diseases are associated with dysbiosis, treatment strategies targeting the correction of dysbiosis in the treatment of these diseases have begun to be investigated. Faecal microbiota transplantation (FMT) is the process of transferring faeces from a healthy donor to another recipient in order to restore the gut microbiota and provide a therapeutic benefit. FMT studies have gained popularity after probiotic, prebiotic, symbiotic studies in the treatment of dysbiosis and related diseases. FMT has emerged as a potential new therapy in the treatment of allergic diseases as it is associated with the maintenance of intestinal microbiota and immunological balance (T helper 1/T helper 2 cells) and thus suppression of allergic responses. In this article, the definition, application, safety and use of FMT in allergic diseases will be discussed with current data.},
}
RevDate: 2025-06-24
Dietary convergence induces individual responses in faecal microbiome composition.
eGastroenterology, 3(2):e100161.
BACKGROUND: Dietary variation has been identified as a key contributor to microbiome diversification. However, assessing its true impact in a cross-sectional setting is complicated by biological confounders and methodological hurdles. We aimed to estimate the impact of a reduction of dietary variation (dietary convergence) on faecal microbiota composition among individuals consuming a Western-type diet.
METHODS: 18 healthy volunteers recruited in the region of Flanders (Belgium) were followed up for 21 days. Participants were allowed to consume their habitual diet during a baseline and follow-up period (7 and 8 days, respectively), intersected by a 6-day intervention during which dietary options were restricted to oat flakes, whole milk and still water. Faecal samples were collected on a daily basis. Quantitative microbiome profiles were constructed, combining 16S rRNA gene amplicon sequencing with flow cytometry cell counting. Blood samples were taken at the beginning and end of each study week.
RESULTS: While the intervention did not affect transit time (as assessed through the analysis of stool moisture), consumption of the restricted diet resulted in an increased prevalence of the Bacteroides2 microbiome community type. Microbial load and Faecalibacterium abundance decreased markedly. Despite dietary restrictions, no convergence of microbial communities (reduction of interindividual and intraindividual variation) was observed. The effect size (ES) of the intervention on genus-level microbiome community differentiation was estimated as 3.4%, but substantial interindividual variation was observed (1.67%-16.42%).
CONCLUSION: The impact of dietary variation on microbiome composition in a Western population is significant but limited in ES, with notable individual exceptions. Dietary convergence does not invariably translate into interindividual convergence of faecal microbial communities.
Additional Links: PMID-40548146
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Citation:
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@article {pmid40548146,
year = {2025},
author = {Vermeulen, A and Bootsma, E and Proost, S and Vieira-Silva, S and Kathagen, G and Vázquez-Castellanos, JF and Tito, RY and Sabino, J and Vermeire, S and Matthys, C and Raes, J and Falony, G},
title = {Dietary convergence induces individual responses in faecal microbiome composition.},
journal = {eGastroenterology},
volume = {3},
number = {2},
pages = {e100161},
pmid = {40548146},
issn = {2976-7296},
abstract = {BACKGROUND: Dietary variation has been identified as a key contributor to microbiome diversification. However, assessing its true impact in a cross-sectional setting is complicated by biological confounders and methodological hurdles. We aimed to estimate the impact of a reduction of dietary variation (dietary convergence) on faecal microbiota composition among individuals consuming a Western-type diet.
METHODS: 18 healthy volunteers recruited in the region of Flanders (Belgium) were followed up for 21 days. Participants were allowed to consume their habitual diet during a baseline and follow-up period (7 and 8 days, respectively), intersected by a 6-day intervention during which dietary options were restricted to oat flakes, whole milk and still water. Faecal samples were collected on a daily basis. Quantitative microbiome profiles were constructed, combining 16S rRNA gene amplicon sequencing with flow cytometry cell counting. Blood samples were taken at the beginning and end of each study week.
RESULTS: While the intervention did not affect transit time (as assessed through the analysis of stool moisture), consumption of the restricted diet resulted in an increased prevalence of the Bacteroides2 microbiome community type. Microbial load and Faecalibacterium abundance decreased markedly. Despite dietary restrictions, no convergence of microbial communities (reduction of interindividual and intraindividual variation) was observed. The effect size (ES) of the intervention on genus-level microbiome community differentiation was estimated as 3.4%, but substantial interindividual variation was observed (1.67%-16.42%).
CONCLUSION: The impact of dietary variation on microbiome composition in a Western population is significant but limited in ES, with notable individual exceptions. Dietary convergence does not invariably translate into interindividual convergence of faecal microbial communities.},
}
RevDate: 2025-06-24
Integrative review of the gut microbiome's role in pain management for orthopaedic conditions.
World journal of experimental medicine, 15(2):102969.
The gut microbiome, a complex ecosystem of microorganisms, has a significant role in modulating pain, particularly within orthopaedic conditions. Its impact on immune and neurological functions is underscored by the gut-brain axis, which influences inflammation, pain perception, and systemic immune responses. This integrative review examines current research on how gut dysbiosis is associated with various pain pathways, notably nociceptive and neuroinflammatory mechanisms linked to central sensitization. We highlight advancements in meta-omics technologies, such as metagenomics and metaproteomics, which deepen our understanding of microbiome-host interactions and their implications in pain. Recent studies emphasize that gut-derived short-chain fatty acids and microbial metabolites play roles in modulating neuroinflammation and nociception, contributing to pain management. Probiotics, prebiotics, synbiotics, and faecal microbiome transplants are explored as potential therapeutic strategies to alleviate pain through gut microbiome modulation, offering an adjunct or alternative to opioids. However, variability in individual microbiomes poses challenges to standardizing these treatments, necessitating further rigorous clinical trials. A multidisciplinary approach combining microbiology, immunology, neurology, and orthopaedics is essential to develop innovative, personalized pain management strategies rooted in gut health, with potential to transform orthopaedic pain care.
Additional Links: PMID-40546666
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@article {pmid40546666,
year = {2025},
author = {Jeyaraman, N and Jeyaraman, M and Dhanpal, P and Ramasubramanian, S and Nallakumarasamy, A and Muthu, S and Santos, GS and da Fonseca, LF and Lana, JF},
title = {Integrative review of the gut microbiome's role in pain management for orthopaedic conditions.},
journal = {World journal of experimental medicine},
volume = {15},
number = {2},
pages = {102969},
pmid = {40546666},
issn = {2220-315X},
abstract = {The gut microbiome, a complex ecosystem of microorganisms, has a significant role in modulating pain, particularly within orthopaedic conditions. Its impact on immune and neurological functions is underscored by the gut-brain axis, which influences inflammation, pain perception, and systemic immune responses. This integrative review examines current research on how gut dysbiosis is associated with various pain pathways, notably nociceptive and neuroinflammatory mechanisms linked to central sensitization. We highlight advancements in meta-omics technologies, such as metagenomics and metaproteomics, which deepen our understanding of microbiome-host interactions and their implications in pain. Recent studies emphasize that gut-derived short-chain fatty acids and microbial metabolites play roles in modulating neuroinflammation and nociception, contributing to pain management. Probiotics, prebiotics, synbiotics, and faecal microbiome transplants are explored as potential therapeutic strategies to alleviate pain through gut microbiome modulation, offering an adjunct or alternative to opioids. However, variability in individual microbiomes poses challenges to standardizing these treatments, necessitating further rigorous clinical trials. A multidisciplinary approach combining microbiology, immunology, neurology, and orthopaedics is essential to develop innovative, personalized pain management strategies rooted in gut health, with potential to transform orthopaedic pain care.},
}
RevDate: 2025-06-23
Gut Microbiota as a Key Modulator of Chronic Disease: Implications for Diabetes, Autoimmunity, and Cancer.
Cureus, 17(5):e84687.
The gut microbiota (GM) represents an intricate, dynamic, and complex ecosystem. It plays a key role in health and disease. The GM interacts with the host and modulates various physiological functions, including metabolism, immune regulation, and neurological function. This narrative review comprehensively analyses the role of the GM in the development and progression of three major chronic conditions, namely diabetes, autoimmune disorders, and cancer. Using a structured literature search strategy across databases such as Google Scholar, PubMed, Scopus, and Web of Science, relevant studies published between 2000 and 2025 were identified and analysed. This review highlights that dysbiosis contributes significantly to the pathogenesis of these chronic conditions. In type 2 diabetes mellitus (T2DM), alterations in the GM are associated with systemic inflammation, insulin resistance, and decreased microbial diversity. Similarly, in autoimmune disorders such as rheumatoid arthritis (RA), multiple sclerosis (MS), and inflammatory bowel disease (IBD), dysbiosis disrupts immune homeostasis, which in turn causes sustained inflammation and aberrant immune responses. Lastly, dysbiosis has been linked to the onset and progression of various gastrointestinal cancers through mechanisms including chronic inflammation and the production of carcinogenic metabolites. Fecal microbiota transplantation (FMT), probiotics, prebiotics, and dietary modifications are being explored for their potential to restore microbial balance and improve clinical outcomes. In conclusion, this review highlights the GM's pivotal role in the pathogenesis of chronic diseases and its potential as a therapeutic target.
Additional Links: PMID-40546462
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@article {pmid40546462,
year = {2025},
author = {Inayat, N and Zahir, A and Hashmat, AJ and Khan, A and Ahmad, A and Sikander, M and Zakir, S and Ahmad, S and Awan, SK and Raza, SS and Varrassi, G},
title = {Gut Microbiota as a Key Modulator of Chronic Disease: Implications for Diabetes, Autoimmunity, and Cancer.},
journal = {Cureus},
volume = {17},
number = {5},
pages = {e84687},
doi = {10.7759/cureus.84687},
pmid = {40546462},
issn = {2168-8184},
abstract = {The gut microbiota (GM) represents an intricate, dynamic, and complex ecosystem. It plays a key role in health and disease. The GM interacts with the host and modulates various physiological functions, including metabolism, immune regulation, and neurological function. This narrative review comprehensively analyses the role of the GM in the development and progression of three major chronic conditions, namely diabetes, autoimmune disorders, and cancer. Using a structured literature search strategy across databases such as Google Scholar, PubMed, Scopus, and Web of Science, relevant studies published between 2000 and 2025 were identified and analysed. This review highlights that dysbiosis contributes significantly to the pathogenesis of these chronic conditions. In type 2 diabetes mellitus (T2DM), alterations in the GM are associated with systemic inflammation, insulin resistance, and decreased microbial diversity. Similarly, in autoimmune disorders such as rheumatoid arthritis (RA), multiple sclerosis (MS), and inflammatory bowel disease (IBD), dysbiosis disrupts immune homeostasis, which in turn causes sustained inflammation and aberrant immune responses. Lastly, dysbiosis has been linked to the onset and progression of various gastrointestinal cancers through mechanisms including chronic inflammation and the production of carcinogenic metabolites. Fecal microbiota transplantation (FMT), probiotics, prebiotics, and dietary modifications are being explored for their potential to restore microbial balance and improve clinical outcomes. In conclusion, this review highlights the GM's pivotal role in the pathogenesis of chronic diseases and its potential as a therapeutic target.},
}
RevDate: 2025-06-23
How is the human microbiome linked to kidney stones?.
Frontiers in cellular and infection microbiology, 15:1602413.
In recent years, the incidence of kidney stones has continued to rise worldwide, and conventional treatments have limited efficacy in treating stones associated with recurrent or metabolic abnormalities. The microbiome, as the 'second genome' of the host, is involved in the development of kidney stones through metabolic regulation, immune homeostasis and inflammatory response. Studies have shown that the urinary microbiome of healthy people is dominated by commensal bacteria such as Lactobacillus and Streptococcus, which maintain microenvironmental homeostasis, whereas patients with renal stones have a significantly reduced diversity of intestinal and urinary microbiomes, with a reduced abundance of oxalic acid-degrading bacteria (e.g., Bifidobacterium oxalicum, Bifidobacterium bifidum), and a possible concentration of pathogenic bacteria (e.g., Proteus mirabilis). The microbiome regulates stone formation through mechanisms such as metabolites (e.g., short-chain fatty acids), changes in urine physicochemical properties (e.g., elevated pH), and imbalances in the inflammatory and immune microenvironments. For example, urease-producing bacteria promote magnesium ammonium phosphate stone formation through the breakdown of urea, whereas dysbiosis of the intestinal flora increases urinary oxalic acid excretion and exacerbates the risk of calcium oxalate stones. Microbiome-based diagnostic markers (e.g., elevated abundance of Aspergillus phylum) and targeted intervention strategies (e.g., probiotic supplementation, faecal bacteria transplantation) show potential for clinical application. However, technical bottlenecks (e.g., sequencing bias in low-biomass samples), mechanistic complexity (e.g., multistrain synergism), and individual heterogeneity remain major challenges for future research. Integration of multi-omics data, development of personalised therapies and interdisciplinary research will be the core directions to decipher the relationship between microbiome and kidney stones.
Additional Links: PMID-40546285
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@article {pmid40546285,
year = {2025},
author = {Pei, X and Liu, M and Yu, S},
title = {How is the human microbiome linked to kidney stones?.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1602413},
doi = {10.3389/fcimb.2025.1602413},
pmid = {40546285},
issn = {2235-2988},
abstract = {In recent years, the incidence of kidney stones has continued to rise worldwide, and conventional treatments have limited efficacy in treating stones associated with recurrent or metabolic abnormalities. The microbiome, as the 'second genome' of the host, is involved in the development of kidney stones through metabolic regulation, immune homeostasis and inflammatory response. Studies have shown that the urinary microbiome of healthy people is dominated by commensal bacteria such as Lactobacillus and Streptococcus, which maintain microenvironmental homeostasis, whereas patients with renal stones have a significantly reduced diversity of intestinal and urinary microbiomes, with a reduced abundance of oxalic acid-degrading bacteria (e.g., Bifidobacterium oxalicum, Bifidobacterium bifidum), and a possible concentration of pathogenic bacteria (e.g., Proteus mirabilis). The microbiome regulates stone formation through mechanisms such as metabolites (e.g., short-chain fatty acids), changes in urine physicochemical properties (e.g., elevated pH), and imbalances in the inflammatory and immune microenvironments. For example, urease-producing bacteria promote magnesium ammonium phosphate stone formation through the breakdown of urea, whereas dysbiosis of the intestinal flora increases urinary oxalic acid excretion and exacerbates the risk of calcium oxalate stones. Microbiome-based diagnostic markers (e.g., elevated abundance of Aspergillus phylum) and targeted intervention strategies (e.g., probiotic supplementation, faecal bacteria transplantation) show potential for clinical application. However, technical bottlenecks (e.g., sequencing bias in low-biomass samples), mechanistic complexity (e.g., multistrain synergism), and individual heterogeneity remain major challenges for future research. Integration of multi-omics data, development of personalised therapies and interdisciplinary research will be the core directions to decipher the relationship between microbiome and kidney stones.},
}
RevDate: 2025-06-23
Buyang Huanwu Decoction Modulates the Gut Microbiota-C/EBPβ/AEP Axis to Ameliorate Cognitive Impairment in Alzheimer's Disease Mice.
CNS neuroscience & therapeutics, 31(6):e70480.
BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and behavioral disturbances. Buyang Huanwu Decoction (BYHWD), a traditional Chinese herbal formulation, has demonstrated potential neuroprotective effects. This study aims to evaluate the therapeutic impact of BYHWD on cognitive impairments in 3×Tg mice and to investigate its underlying mechanism through modulation of the gut microbiota-C/EBPβ/AEP signaling pathway.
METHODS: In two independent experiments, we assessed the effects of BYHWD and its derived fecal microbiota transplantation (FMT-BYHWD) on behavioral performance, neuropathological alterations, and signaling pathways in 3×Tg mice.
RESULTS: Treatment with BYHWD significantly improved cognitive function in 3×Tg mice and mitigated AD-like pathological changes. By suppressing the C/EBPβ/AEP signaling pathway, BYHWD reduced pathological Aβ plaque deposition, diminished tau hyperphosphorylation, and inhibited the release of pro-inflammatory cytokines. Further analysis revealed that BYHWD restored gut microbiota balance and suppressed the activation of the C/EBPβ/AEP pathway in the hippocampus. Moreover, transplanting FMT-BYHWD from BYHWD-treated mice to germ-free 3×Tg mice also ameliorated their cognitive deficits and AD-like pathology, suggesting that the anti-AD effects of BYHWD are mediated through the gut-brain axis by regulating the interplay between gut microbiota and the C/EBPβ/AEP signaling pathway.
CONCLUSION: This study uncovers the mechanism by which BYHWD improves cognitive deficits and neuropathological changes in 3×Tg mice via the gut-brain axis, mediated by the modulation of the gut microbiota-C/EBPβ/AEP signaling pathway, providing a novel therapeutic strategy for AD.
Additional Links: PMID-40546239
Publisher:
PubMed:
Citation:
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@article {pmid40546239,
year = {2025},
author = {Liang, J and Dong, X and Yang, J and Hu, N and Luo, X and Cong, S and Chen, J and Zhao, W and Liu, B},
title = {Buyang Huanwu Decoction Modulates the Gut Microbiota-C/EBPβ/AEP Axis to Ameliorate Cognitive Impairment in Alzheimer's Disease Mice.},
journal = {CNS neuroscience & therapeutics},
volume = {31},
number = {6},
pages = {e70480},
doi = {10.1111/cns.70480},
pmid = {40546239},
issn = {1755-5949},
support = {2024yjscx013//Innovative Research Project for Postgraduate Students of Heilongjiang University of Traditional Chinese Medicine/ ; LH2022H059//Natural Science Foundation of Heilongjiang Province of China/ ; LH2023H073//Natural Science Foundation of Heilongjiang Province of China/ ; },
abstract = {BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and behavioral disturbances. Buyang Huanwu Decoction (BYHWD), a traditional Chinese herbal formulation, has demonstrated potential neuroprotective effects. This study aims to evaluate the therapeutic impact of BYHWD on cognitive impairments in 3×Tg mice and to investigate its underlying mechanism through modulation of the gut microbiota-C/EBPβ/AEP signaling pathway.
METHODS: In two independent experiments, we assessed the effects of BYHWD and its derived fecal microbiota transplantation (FMT-BYHWD) on behavioral performance, neuropathological alterations, and signaling pathways in 3×Tg mice.
RESULTS: Treatment with BYHWD significantly improved cognitive function in 3×Tg mice and mitigated AD-like pathological changes. By suppressing the C/EBPβ/AEP signaling pathway, BYHWD reduced pathological Aβ plaque deposition, diminished tau hyperphosphorylation, and inhibited the release of pro-inflammatory cytokines. Further analysis revealed that BYHWD restored gut microbiota balance and suppressed the activation of the C/EBPβ/AEP pathway in the hippocampus. Moreover, transplanting FMT-BYHWD from BYHWD-treated mice to germ-free 3×Tg mice also ameliorated their cognitive deficits and AD-like pathology, suggesting that the anti-AD effects of BYHWD are mediated through the gut-brain axis by regulating the interplay between gut microbiota and the C/EBPβ/AEP signaling pathway.
CONCLUSION: This study uncovers the mechanism by which BYHWD improves cognitive deficits and neuropathological changes in 3×Tg mice via the gut-brain axis, mediated by the modulation of the gut microbiota-C/EBPβ/AEP signaling pathway, providing a novel therapeutic strategy for AD.},
}
RevDate: 2025-06-21
Bloodstream infection by Lactobacillus rhamnosus in a haematology patient: why metagenomics can make the difference.
Gut pathogens, 17(1):47.
BACKGROUND: Bloodstream infections (BSIs) pose a persistent threat to hospitalized patients, particularly those who are immunocompromised and susceptible to infections caused by anaerobic or facultative anaerobic bacteria. Alterations in gut microbiota composition can predispose individuals to intestinal domination by one or more pathobionts, increasing the risk of bacterial translocation into the bloodstream and subsequent bacteremia.
CASE PRESENTATION: We report the case of a 20-year-old female with multiple relapsed/refractory Philadelphia-negative B-cell acute lymphoblastic leukemia, initially referred to our hematology center for CAR-T cell therapy. The patient ultimately underwent allogeneic hematopoietic stem cell transplantation, which was complicated by infections, moderate-to-severe graft-versus-host disease, hepatic sinusoidal obstruction syndrome, and transplant-associated thrombotic microangiopathy, all contributing to a fatal outcome. Blood cultures obtained in the final week before the patient succumbed to multi-organ toxicity grew Lactobacillus rhamnosus. A fecal sample collected concurrently for intestinal microbiota characterization revealed a marked predominance of Bacillota (98.5%), with Lacticaseibacillus dominating at 47.9%, followed by Pediococcus (18.59%) and Staphylococcus (3.5%) at the genus level. We performed genomic comparison between the L. rhamnosus isolated from blood cultures and the best-matched strain detected in the intestinal microbiota.
CONCLUSIONS: We report the isolation of L. rhamnosus from blood cultures in a patient post hematopoietic cell transplantation, with genomic similarity to a gut-dominant L. rhamnosus strain. This case highlights the potential link between intestinal domination and subsequent bloodstream infection, supporting the value of gut microbiota profiling as an adjunctive tool for monitoring high-risk patients, such as hematopoietic cell transplant recipients.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13099-025-00722-3.
Additional Links: PMID-40544256
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Citation:
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@article {pmid40544256,
year = {2025},
author = {Mannavola, CM and De Maio, F and Marra, J and Fiori, B and Santarelli, G and Posteraro, B and Sica, S and D'Inzeo, T and Sanguinetti, M},
title = {Bloodstream infection by Lactobacillus rhamnosus in a haematology patient: why metagenomics can make the difference.},
journal = {Gut pathogens},
volume = {17},
number = {1},
pages = {47},
pmid = {40544256},
issn = {1757-4749},
support = {PE00000007, INF-ACT//EU funding for the MUR PNRR Extended Partnership initiative on Emerging Infectious Diseases/ ; },
abstract = {BACKGROUND: Bloodstream infections (BSIs) pose a persistent threat to hospitalized patients, particularly those who are immunocompromised and susceptible to infections caused by anaerobic or facultative anaerobic bacteria. Alterations in gut microbiota composition can predispose individuals to intestinal domination by one or more pathobionts, increasing the risk of bacterial translocation into the bloodstream and subsequent bacteremia.
CASE PRESENTATION: We report the case of a 20-year-old female with multiple relapsed/refractory Philadelphia-negative B-cell acute lymphoblastic leukemia, initially referred to our hematology center for CAR-T cell therapy. The patient ultimately underwent allogeneic hematopoietic stem cell transplantation, which was complicated by infections, moderate-to-severe graft-versus-host disease, hepatic sinusoidal obstruction syndrome, and transplant-associated thrombotic microangiopathy, all contributing to a fatal outcome. Blood cultures obtained in the final week before the patient succumbed to multi-organ toxicity grew Lactobacillus rhamnosus. A fecal sample collected concurrently for intestinal microbiota characterization revealed a marked predominance of Bacillota (98.5%), with Lacticaseibacillus dominating at 47.9%, followed by Pediococcus (18.59%) and Staphylococcus (3.5%) at the genus level. We performed genomic comparison between the L. rhamnosus isolated from blood cultures and the best-matched strain detected in the intestinal microbiota.
CONCLUSIONS: We report the isolation of L. rhamnosus from blood cultures in a patient post hematopoietic cell transplantation, with genomic similarity to a gut-dominant L. rhamnosus strain. This case highlights the potential link between intestinal domination and subsequent bloodstream infection, supporting the value of gut microbiota profiling as an adjunctive tool for monitoring high-risk patients, such as hematopoietic cell transplant recipients.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13099-025-00722-3.},
}
RevDate: 2025-06-21
Role of the intestinal flora-immunity axis in the pathogenesis of rheumatoid arthritis-mechanisms regulating short-chain fatty acids and Th17/Treg homeostasis.
Molecular biology reports, 52(1):617.
BACKGROUND: The pathogenesis of rheumatoid arthritis (RA), a chronic systemic autoimmune disease, is closely linked to the interactions between intestinal flora and metabolites. Recent research has shown that the "gut-joint axis" is an important regulator of immune homeostasis, gut microbiota dysbiosis not only causes pro-inflammatory bacteria to proliferate abnormally, but it also decreases the biosynthesis of short-chain fatty acids (SCFAs). This dual imbalance ultimately exacerbates synovial inflammation and encourages bone destruction by upsetting the balance of Th17/Treg cells, that is, the over-activation of Th17 cells and the impaired function of regulatory T cells (Treg).
OBJECTIVE: To clarify the molecular mechanism by which intestinal flora-derived SCFAs alter the pathogenic process of RA by controlling Th17/Treg balance, and to establish a theoretical foundation for targeted treatments.
METHODS: We integrated multidisciplinary evidence to create a "flora-SCFAs-immunity-joints" by conducting a systematic search of domestic and international literature in PubMed, Web of Science, and other databases over the past ten years, with a focus on intestinal flora composition, SCFA biosynthesis, Th17/Treg immunoregulation, and RA animal model research. We create a "flora-SCFAs-immunity-joint" network by integrating information from many disciplines.
OUTCOMES: Dietary fiber is broken down by intestinal flora to produce SCFAs (acetic, propionic, and butyric acids), which control Th17/Treg balance in two ways: (1) Encourage Treg differentiation: propionic acid activates the GPR43-cAMP/PKA-CREB pathway, which promotes Treg expansion and secretion of IL-10/TGF-β; (2) Inhibit Th17 polarization, SCFAs inhibited Th17 cell differentiation, down-regulated IL-23 secretion from dendritic cells, and blocked IL-6/STAT3 and RORγt signaling. Butyric acid also inhibits histone deacetylase (HDAC) activity, Foxp3 expression, and epigenetic stability. In a collagen-induced arthritis (CIA) paradigm, animal studies shown that fecal transplantation or SCFA supplementation dramatically decreased bone degradation and joint inflammatory scores. Its therapeutic translational potential was suggested by the negative correlation found between the Th17/Treg ratio and the amount of SCFAs in the gut of RA patients.
CONCLUSION: Through multi-target control of Th17/Treg balance, SCFAs show distinct benefits over conventional immunosuppression in the treatment of RA. Verification is still required for the pharmacokinetic constraints of SCFAs, variations in individual flora, and causative processes. To support the specific immune intervention in RA, it will be important in the future to integrate multi-omics technology to evaluate the trans-organ regulatory network of the "gut-joint axis" and to create nano-delivery methods or modified bacterial tactics to increase the targeting of SCFAs.
Additional Links: PMID-40544212
PubMed:
Citation:
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@article {pmid40544212,
year = {2025},
author = {Lv, J and Hao, P and Zhou, Y and Liu, T and Wang, L and Song, C and Wang, Z and Liu, Z and Liu, Y},
title = {Role of the intestinal flora-immunity axis in the pathogenesis of rheumatoid arthritis-mechanisms regulating short-chain fatty acids and Th17/Treg homeostasis.},
journal = {Molecular biology reports},
volume = {52},
number = {1},
pages = {617},
pmid = {40544212},
issn = {1573-4978},
support = {2024ZKZ009//Southwest Medical University (SWMU) School-level Scientific Research Program/ ; },
abstract = {BACKGROUND: The pathogenesis of rheumatoid arthritis (RA), a chronic systemic autoimmune disease, is closely linked to the interactions between intestinal flora and metabolites. Recent research has shown that the "gut-joint axis" is an important regulator of immune homeostasis, gut microbiota dysbiosis not only causes pro-inflammatory bacteria to proliferate abnormally, but it also decreases the biosynthesis of short-chain fatty acids (SCFAs). This dual imbalance ultimately exacerbates synovial inflammation and encourages bone destruction by upsetting the balance of Th17/Treg cells, that is, the over-activation of Th17 cells and the impaired function of regulatory T cells (Treg).
OBJECTIVE: To clarify the molecular mechanism by which intestinal flora-derived SCFAs alter the pathogenic process of RA by controlling Th17/Treg balance, and to establish a theoretical foundation for targeted treatments.
METHODS: We integrated multidisciplinary evidence to create a "flora-SCFAs-immunity-joints" by conducting a systematic search of domestic and international literature in PubMed, Web of Science, and other databases over the past ten years, with a focus on intestinal flora composition, SCFA biosynthesis, Th17/Treg immunoregulation, and RA animal model research. We create a "flora-SCFAs-immunity-joint" network by integrating information from many disciplines.
OUTCOMES: Dietary fiber is broken down by intestinal flora to produce SCFAs (acetic, propionic, and butyric acids), which control Th17/Treg balance in two ways: (1) Encourage Treg differentiation: propionic acid activates the GPR43-cAMP/PKA-CREB pathway, which promotes Treg expansion and secretion of IL-10/TGF-β; (2) Inhibit Th17 polarization, SCFAs inhibited Th17 cell differentiation, down-regulated IL-23 secretion from dendritic cells, and blocked IL-6/STAT3 and RORγt signaling. Butyric acid also inhibits histone deacetylase (HDAC) activity, Foxp3 expression, and epigenetic stability. In a collagen-induced arthritis (CIA) paradigm, animal studies shown that fecal transplantation or SCFA supplementation dramatically decreased bone degradation and joint inflammatory scores. Its therapeutic translational potential was suggested by the negative correlation found between the Th17/Treg ratio and the amount of SCFAs in the gut of RA patients.
CONCLUSION: Through multi-target control of Th17/Treg balance, SCFAs show distinct benefits over conventional immunosuppression in the treatment of RA. Verification is still required for the pharmacokinetic constraints of SCFAs, variations in individual flora, and causative processes. To support the specific immune intervention in RA, it will be important in the future to integrate multi-omics technology to evaluate the trans-organ regulatory network of the "gut-joint axis" and to create nano-delivery methods or modified bacterial tactics to increase the targeting of SCFAs.},
}
RevDate: 2025-06-22
Engrafting gut bacteriophages have potential to modulate microbial metabolism in fecal microbiota transplantation.
Microbiome, 13(1):149.
BACKGROUND: Fecal microbiota transplantation (FMT) is widely used to treat severe infections and investigated for the treatment of complex diseases. The therapeutic efficacy of FMT is related to the successful engraftment of bacteriophages from healthy donors to recipients. However, gut bacteriophage contributions to FMT engraftment and treatment outcomes remain unclear.
METHODS: The gut phageome from previously published metagenomes of donors and recipients across 23 FMT studies was assembled and functionally annotated for a meta-analysis.
RESULTS: Gut phageome profiles of FMT recipients, especially those with recurrent Clostridioides difficile infection (rCDI), shifted toward donor phageomes, accompanied by increased phageome alpha diversity. Engraftment of donor phages varied between recipient conditions with the highest engraftment rate, overrepresented by putative temperate phage, in patients with rCDI. Consistently, a higher proportion of auxiliary metabolic genes (AMGs), with the potential to support and modulate bacterial metabolism, were annotated on putative temperate phages.
CONCLUSIONS: FMT leads to significant taxonomic, functional, and lifestyle shifts in recipient phageome composition. Future FMT studies should include gut phageome characterization and consider it as a potential factor in microbial community shifts and treatment outcomes. Video Abstract.
Additional Links: PMID-40542451
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Citation:
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@article {pmid40542451,
year = {2025},
author = {Ji, S and Ahmad, F and Peng, B and Yang, Y and Su, M and Zhao, X and Vatanen, T},
title = {Engrafting gut bacteriophages have potential to modulate microbial metabolism in fecal microbiota transplantation.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {149},
pmid = {40542451},
issn = {2049-2618},
support = {U22A20365//Joint Funds of National Natural Science Foundation of China/ ; T2341019//National Natural Science Foundation of China/ ; 2023A1515012429//Natural Science Foundation of Guangdong Province/ ; 2024B03J1343//Guangzhou Science and Technology Plan Project/ ; },
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) is widely used to treat severe infections and investigated for the treatment of complex diseases. The therapeutic efficacy of FMT is related to the successful engraftment of bacteriophages from healthy donors to recipients. However, gut bacteriophage contributions to FMT engraftment and treatment outcomes remain unclear.
METHODS: The gut phageome from previously published metagenomes of donors and recipients across 23 FMT studies was assembled and functionally annotated for a meta-analysis.
RESULTS: Gut phageome profiles of FMT recipients, especially those with recurrent Clostridioides difficile infection (rCDI), shifted toward donor phageomes, accompanied by increased phageome alpha diversity. Engraftment of donor phages varied between recipient conditions with the highest engraftment rate, overrepresented by putative temperate phage, in patients with rCDI. Consistently, a higher proportion of auxiliary metabolic genes (AMGs), with the potential to support and modulate bacterial metabolism, were annotated on putative temperate phages.
CONCLUSIONS: FMT leads to significant taxonomic, functional, and lifestyle shifts in recipient phageome composition. Future FMT studies should include gut phageome characterization and consider it as a potential factor in microbial community shifts and treatment outcomes. Video Abstract.},
}
RevDate: 2025-06-20
Curing inflammatory bowel diseases: breaking the barriers of current therapies- emerging strategies for a definitive treatment.
Current opinion in immunology, 95:102593 pii:S0952-7915(25)00069-X [Epub ahead of print].
Chronic intestinal inflammation in inflammatory bowel diseases (IBD) reflects the interplay of genetic predisposition, immune dysregulation, microbial imbalance, and epithelial barrier defects. Current therapies for IBD primarily focus on controlling inflammation necessitating lifelong treatment and face a 'therapeutic ceiling' due to primary and secondary loss of efficacy over time. Immune-mediated approaches do not address additional pathogenic mechanisms, such as impairment of epithelial barrier and gut microbial ecology. Thus, innovative strategies are required to foster the field closer to a definitive cure. This review discusses novel strategies to overcome current therapeutic limitations, including immune reset via hematopoietic stem cell transplantation and B cell-targeted therapies, antigen-specific interventions such as chimeric antigen receptor T cells and tolerogenic vaccines, and intestinal epithelial barrier restoration. We also explore microbiota-based strategies - ranging from fecal microbiota transplantation to engineered consortia and bacteriophages - and discuss the adjunctive role of diet. Together, we outline a potential research roadmap toward a potential cure for IBD.
Additional Links: PMID-40540980
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@article {pmid40540980,
year = {2025},
author = {Noviello, D and Amoroso, C and Vecchi, M and Facciotti, F and Caprioli, F},
title = {Curing inflammatory bowel diseases: breaking the barriers of current therapies- emerging strategies for a definitive treatment.},
journal = {Current opinion in immunology},
volume = {95},
number = {},
pages = {102593},
doi = {10.1016/j.coi.2025.102593},
pmid = {40540980},
issn = {1879-0372},
abstract = {Chronic intestinal inflammation in inflammatory bowel diseases (IBD) reflects the interplay of genetic predisposition, immune dysregulation, microbial imbalance, and epithelial barrier defects. Current therapies for IBD primarily focus on controlling inflammation necessitating lifelong treatment and face a 'therapeutic ceiling' due to primary and secondary loss of efficacy over time. Immune-mediated approaches do not address additional pathogenic mechanisms, such as impairment of epithelial barrier and gut microbial ecology. Thus, innovative strategies are required to foster the field closer to a definitive cure. This review discusses novel strategies to overcome current therapeutic limitations, including immune reset via hematopoietic stem cell transplantation and B cell-targeted therapies, antigen-specific interventions such as chimeric antigen receptor T cells and tolerogenic vaccines, and intestinal epithelial barrier restoration. We also explore microbiota-based strategies - ranging from fecal microbiota transplantation to engineered consortia and bacteriophages - and discuss the adjunctive role of diet. Together, we outline a potential research roadmap toward a potential cure for IBD.},
}
RevDate: 2025-06-20
The gut virome and human health: From diversity to personalized medicine.
Engineering microbiology, 5(1):100191.
The human gut virome plays a crucial role in the gut and overall health; its diversity and regulatory functions influence bacterial populations, metabolism, and immune responses. Bacteriophages (phages) and eukaryotic viruses within the gut microbiome contribute to these processes, and recent advancements in sequencing technologies and bioinformatics have greatly expanded our understanding of the gut virome. These advances have led to the development of phage-based therapeutics, diagnostics, and artificial intelligence-driven precision medicine. The emerging field of phageomics shows promise for delivering personalized phage therapies that combat antimicrobial resistance by specifically targeting pathogenic bacteria while preserving beneficial microbes. Moreover, CRISPR-Cas systems delivered via phages have shown success in selectively targeting antibiotic resistance genes and enhancing treatment effectiveness. Phage-based diagnostics are highly sensitive in detecting bacterial pathogens, offering significant benefits for human health and zoonotic disease surveillance. This synthesis of the current knowledge highlights the pivotal role of the gut virome in regulating microbial communities and its transformative potential in personalized medicine, emphasizing its importance in advancing therapeutic and diagnostic strategies for improving health outcomes.
Additional Links: PMID-40538711
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Citation:
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@article {pmid40538711,
year = {2025},
author = {Lathakumari, RH and Vajravelu, LK and Gopinathan, A and Vimala, PB and Panneerselvam, V and Ravi, SSS and Thulukanam, J},
title = {The gut virome and human health: From diversity to personalized medicine.},
journal = {Engineering microbiology},
volume = {5},
number = {1},
pages = {100191},
pmid = {40538711},
issn = {2667-3703},
abstract = {The human gut virome plays a crucial role in the gut and overall health; its diversity and regulatory functions influence bacterial populations, metabolism, and immune responses. Bacteriophages (phages) and eukaryotic viruses within the gut microbiome contribute to these processes, and recent advancements in sequencing technologies and bioinformatics have greatly expanded our understanding of the gut virome. These advances have led to the development of phage-based therapeutics, diagnostics, and artificial intelligence-driven precision medicine. The emerging field of phageomics shows promise for delivering personalized phage therapies that combat antimicrobial resistance by specifically targeting pathogenic bacteria while preserving beneficial microbes. Moreover, CRISPR-Cas systems delivered via phages have shown success in selectively targeting antibiotic resistance genes and enhancing treatment effectiveness. Phage-based diagnostics are highly sensitive in detecting bacterial pathogens, offering significant benefits for human health and zoonotic disease surveillance. This synthesis of the current knowledge highlights the pivotal role of the gut virome in regulating microbial communities and its transformative potential in personalized medicine, emphasizing its importance in advancing therapeutic and diagnostic strategies for improving health outcomes.},
}
RevDate: 2025-06-20
Radiation-induced injury and the gut microbiota: insights from a microbial perspective.
Therapeutic advances in gastroenterology, 18:17562848251347347.
Although radiotherapy is the second most effective cancer treatment, radiation injuries limit its use. About 80% of abdominal-pelvic radiotherapy patients develop acute radiation enteritis, with 20% discontinuing radiotherapy. The lack of effective mitigation measures restricts its clinical application. Recent studies have proposed gut microbiota as a potential biomarker for radiation injuries. However, the interaction between gut microbiota and radiation injuries remains poorly understood. This review summarizes two forms of interaction between gut microbiota and radiation injuries based on the location of the radiation field. One type of interaction, referred to as "direct interaction," involves changes in the diversity and composition of gut microbiota, alterations in microbiota-derived metabolites, disruption of the intestinal barrier, activation of inflammatory responses within the intestine, and involvement of the host's immune system. The second form, called "indirect interaction," includes the influence of the gut microbiota on various body systems, such as gut microbiota-brain axis, gut microbiota-cardiopulmonary axis, and gut microbiota-oral axis. Additionally, we examine promising interventions aimed at reshaping the gut microbiota, including the use of probiotics, prebiotics, and fecal microbiota transplantation. The interaction between radiation injuries and gut microbiota is more complex than previously understood. Therefore, further clarification of the underlying mechanisms will facilitate the application of gut microbiota in preventing and alleviating radiation injuries.
Additional Links: PMID-40535532
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Citation:
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@article {pmid40535532,
year = {2025},
author = {Wang, Q and Xu, G and Yan, O and Wang, S and Wang, X},
title = {Radiation-induced injury and the gut microbiota: insights from a microbial perspective.},
journal = {Therapeutic advances in gastroenterology},
volume = {18},
number = {},
pages = {17562848251347347},
pmid = {40535532},
issn = {1756-283X},
abstract = {Although radiotherapy is the second most effective cancer treatment, radiation injuries limit its use. About 80% of abdominal-pelvic radiotherapy patients develop acute radiation enteritis, with 20% discontinuing radiotherapy. The lack of effective mitigation measures restricts its clinical application. Recent studies have proposed gut microbiota as a potential biomarker for radiation injuries. However, the interaction between gut microbiota and radiation injuries remains poorly understood. This review summarizes two forms of interaction between gut microbiota and radiation injuries based on the location of the radiation field. One type of interaction, referred to as "direct interaction," involves changes in the diversity and composition of gut microbiota, alterations in microbiota-derived metabolites, disruption of the intestinal barrier, activation of inflammatory responses within the intestine, and involvement of the host's immune system. The second form, called "indirect interaction," includes the influence of the gut microbiota on various body systems, such as gut microbiota-brain axis, gut microbiota-cardiopulmonary axis, and gut microbiota-oral axis. Additionally, we examine promising interventions aimed at reshaping the gut microbiota, including the use of probiotics, prebiotics, and fecal microbiota transplantation. The interaction between radiation injuries and gut microbiota is more complex than previously understood. Therefore, further clarification of the underlying mechanisms will facilitate the application of gut microbiota in preventing and alleviating radiation injuries.},
}
RevDate: 2025-06-19
Relationship between high-fat diet, gut microbiota, and precocious puberty: mechanisms and implications.
Frontiers in microbiology, 16:1564902.
Precocious puberty (PP) is the second most common pediatric endocrine disorder globally and poses a growing public health concern, particularly among girls. While the exact biological mechanisms underlying PP remain unclear, unhealthy dietary patterns, particularly the consumption of a high-fat diet (HFD), are recognized as significant modifiable risk factors. The gut microbiota (GM) is an environmental factor that is disrupted by HFD and may modulate the onset and progression of PP. This review explored the intricate relationship between HFD, GM, and PP, and elucidated the potential mechanisms by which HFD may promote PP development by summarizing evidence from preclinical to clinical research, focusing on the role of GM and its derived metabolites, including short-chain fatty acids, bile acids, lipopolysaccharides, and neurotransmitters. Mechanistic exploration provides novel insights for developing microbiota-targeted therapeutic strategies, such as dietary and lifestyle interventions, fecal microbiota transplantation, probiotics, and traditional Chinese medicine, paving the way for promising approaches to prevent and manage PP.
Additional Links: PMID-40535011
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Citation:
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@article {pmid40535011,
year = {2025},
author = {Wu, N and Ning, K and Liu, Y and Wang, Q and Li, N and Zhang, L},
title = {Relationship between high-fat diet, gut microbiota, and precocious puberty: mechanisms and implications.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1564902},
pmid = {40535011},
issn = {1664-302X},
abstract = {Precocious puberty (PP) is the second most common pediatric endocrine disorder globally and poses a growing public health concern, particularly among girls. While the exact biological mechanisms underlying PP remain unclear, unhealthy dietary patterns, particularly the consumption of a high-fat diet (HFD), are recognized as significant modifiable risk factors. The gut microbiota (GM) is an environmental factor that is disrupted by HFD and may modulate the onset and progression of PP. This review explored the intricate relationship between HFD, GM, and PP, and elucidated the potential mechanisms by which HFD may promote PP development by summarizing evidence from preclinical to clinical research, focusing on the role of GM and its derived metabolites, including short-chain fatty acids, bile acids, lipopolysaccharides, and neurotransmitters. Mechanistic exploration provides novel insights for developing microbiota-targeted therapeutic strategies, such as dietary and lifestyle interventions, fecal microbiota transplantation, probiotics, and traditional Chinese medicine, paving the way for promising approaches to prevent and manage PP.},
}
RevDate: 2025-06-19
Gut microbiota in liver diseases: initiation, development and therapy.
Frontiers in medicine, 12:1615839.
The gut microbiota plays a pivotal role in the pathogenesis and progression of various liver diseases, including viral hepatitis, alcoholic fatty liver disease, metabolic dysfunction-associated steatotic liver disease, drug-induced hepatitis, liver cirrhosis, hepatocellular carcinoma, and other hepatic disorders. Research indicates that dysbiosis of the gut microbiota can disrupt the integrity of the intestinal barrier and interfere with the immune functions of the gut-liver axis, thereby mediating the progression of liver diseases. Analysis of microbial composition and metabolites in fecal samples can assess the diversity of gut microbiota and the abundance of specific microbial populations, providing auxiliary diagnostic information for liver diseases. Furthermore, interventions such as fecal microbiota transplantation, probiotics, prebiotics, bacteriophages, and necessary antibiotic treatments offer multiple approaches to modulate the gut microbiota, presenting promising new strategies for the prevention and treatment of liver diseases. This review summarizes the latest research advances on the role of gut microbiota in liver diseases, offering novel theoretical foundations and practical directions for the diagnosis and treatment of hepatic disorders.
Additional Links: PMID-40534699
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Citation:
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@article {pmid40534699,
year = {2025},
author = {Yu, JX and Wu, J and Chen, X and Zang, SG and Li, XB and Wu, LP and Xuan, SH},
title = {Gut microbiota in liver diseases: initiation, development and therapy.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1615839},
pmid = {40534699},
issn = {2296-858X},
abstract = {The gut microbiota plays a pivotal role in the pathogenesis and progression of various liver diseases, including viral hepatitis, alcoholic fatty liver disease, metabolic dysfunction-associated steatotic liver disease, drug-induced hepatitis, liver cirrhosis, hepatocellular carcinoma, and other hepatic disorders. Research indicates that dysbiosis of the gut microbiota can disrupt the integrity of the intestinal barrier and interfere with the immune functions of the gut-liver axis, thereby mediating the progression of liver diseases. Analysis of microbial composition and metabolites in fecal samples can assess the diversity of gut microbiota and the abundance of specific microbial populations, providing auxiliary diagnostic information for liver diseases. Furthermore, interventions such as fecal microbiota transplantation, probiotics, prebiotics, bacteriophages, and necessary antibiotic treatments offer multiple approaches to modulate the gut microbiota, presenting promising new strategies for the prevention and treatment of liver diseases. This review summarizes the latest research advances on the role of gut microbiota in liver diseases, offering novel theoretical foundations and practical directions for the diagnosis and treatment of hepatic disorders.},
}
RevDate: 2025-06-18
CmpDate: 2025-06-18
Maternal intestinal L. vaginalis facilitates embryo implantation and survival through enhancing uterine receptivity in sows.
Microbiome, 13(1):145.
BACKGROUND: The embryo implantation quality during early pregnancy is the predominant factor for embryo survival and litter performance in sows. Gut microbiota is demonstrated to show a correlation to pregnancy outcomes by participating in regulating maternal metabolism. However, the specific functional microbiota and its mechanical effects on regulating embryo implantation and survival remain unclear. The objective of this study was to clarify whether embryo implantation and litter performance were affected by maternal intestinal microbiota, and to identify specific microbial communities and its mechanism in regulating embryo implantation.
RESULTS: In this study, we first conducted 16S rRNA sequencing and metabolomic analysis revealing the intestinal microbiota and metabolism of 42 sows with different litter size to select the potential functional microbiota that may contribute to embryo survival. Then, we explored the effects of that microbiota on embryo implantation and litter performance through microbiota transplantation in mice and sows. We found that maternal intestinal L. vaginalis exhibits enrichment in sows with higher litter size, which could facilitate embryo implantation and survival and ultimately increases litter size in mice. We further employed transcriptomic analysis to determine the characteristics of uterus, which found an enhanced uterine receptivity after L. vaginalis gavage. The plasma untargeted metabolomic analysis after L. vaginalis gavage in mice and targeted metabolomics analysis of in vitro cultured medium of L. vaginalis were used to evaluate the metabolic regulation of L. vaginalis and to reveal the underlying functional metabolites. Next, an increasing adhesion rate of endometrial-embryonic cells and an obvious increasing formation of pinopodes in cell surface of porcine endometrial epithelial cells were observed after treatments of L. vaginalis metabolites, especially galangin and daidzein. Also, the gene expression levels related to uterine receptivity were increased after treatments of L. vaginalis metabolites in porcine endometrial epithelial cells. Finally, we found that L. vaginalis or its metabolites supplementation during early gestation significantly increased the litter performance in sows.
CONCLUSIONS: Overall, intestinal microbial-host interactions can occur during early pregnancy and may be contribute to maternal metabolic changes and influence pregnancy outcomes in mammals. Our study provides insights of maternal intestinal L. vaginalis to enhance uterine receptivity and to benefit embryo/fetal survival through a gut-uterus axis, contributing to advanced concept and novel strategy to manipulate gut microbiota during early pregnancy, and in turn to improve embryo implantation and reduce embryo loss in sows. Video Abstract.
Additional Links: PMID-40533850
PubMed:
Citation:
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@article {pmid40533850,
year = {2025},
author = {Ye, Q and Hu, Y and Jiang, H and Luo, T and Han, L and Chen, Y and Chen, J and Ma, L and He, Z and Yan, X},
title = {Maternal intestinal L. vaginalis facilitates embryo implantation and survival through enhancing uterine receptivity in sows.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {145},
pmid = {40533850},
issn = {2049-2618},
support = {32202700//National Natural Science Foundation of China/ ; 31925037//National Natural Science Foundation of China/ ; 2022YFD1300405//National Key Research and Development Program of China/ ; 2022YFD1300405//National Key Research and Development Program of China/ ; 2022YFD1300405//National Key Research and Development Program of China/ ; 2022020801020232//Knowledge Innovation Program of Wuhan-Shuguang Project/ ; AML2023B06//National Key Laboratory of Agricultural Microbiology/ ; 2662023DKPY002//Fundamental Research Funds for the Central University/ ; },
mesh = {Animals ; Female ; *Embryo Implantation/physiology ; Swine ; *Gastrointestinal Microbiome/physiology ; Pregnancy ; Mice ; *Uterus/physiology ; RNA, Ribosomal, 16S/genetics ; Litter Size ; Metabolomics ; Fecal Microbiota Transplantation ; },
abstract = {BACKGROUND: The embryo implantation quality during early pregnancy is the predominant factor for embryo survival and litter performance in sows. Gut microbiota is demonstrated to show a correlation to pregnancy outcomes by participating in regulating maternal metabolism. However, the specific functional microbiota and its mechanical effects on regulating embryo implantation and survival remain unclear. The objective of this study was to clarify whether embryo implantation and litter performance were affected by maternal intestinal microbiota, and to identify specific microbial communities and its mechanism in regulating embryo implantation.
RESULTS: In this study, we first conducted 16S rRNA sequencing and metabolomic analysis revealing the intestinal microbiota and metabolism of 42 sows with different litter size to select the potential functional microbiota that may contribute to embryo survival. Then, we explored the effects of that microbiota on embryo implantation and litter performance through microbiota transplantation in mice and sows. We found that maternal intestinal L. vaginalis exhibits enrichment in sows with higher litter size, which could facilitate embryo implantation and survival and ultimately increases litter size in mice. We further employed transcriptomic analysis to determine the characteristics of uterus, which found an enhanced uterine receptivity after L. vaginalis gavage. The plasma untargeted metabolomic analysis after L. vaginalis gavage in mice and targeted metabolomics analysis of in vitro cultured medium of L. vaginalis were used to evaluate the metabolic regulation of L. vaginalis and to reveal the underlying functional metabolites. Next, an increasing adhesion rate of endometrial-embryonic cells and an obvious increasing formation of pinopodes in cell surface of porcine endometrial epithelial cells were observed after treatments of L. vaginalis metabolites, especially galangin and daidzein. Also, the gene expression levels related to uterine receptivity were increased after treatments of L. vaginalis metabolites in porcine endometrial epithelial cells. Finally, we found that L. vaginalis or its metabolites supplementation during early gestation significantly increased the litter performance in sows.
CONCLUSIONS: Overall, intestinal microbial-host interactions can occur during early pregnancy and may be contribute to maternal metabolic changes and influence pregnancy outcomes in mammals. Our study provides insights of maternal intestinal L. vaginalis to enhance uterine receptivity and to benefit embryo/fetal survival through a gut-uterus axis, contributing to advanced concept and novel strategy to manipulate gut microbiota during early pregnancy, and in turn to improve embryo implantation and reduce embryo loss in sows. Video Abstract.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Female
*Embryo Implantation/physiology
Swine
*Gastrointestinal Microbiome/physiology
Pregnancy
Mice
*Uterus/physiology
RNA, Ribosomal, 16S/genetics
Litter Size
Metabolomics
Fecal Microbiota Transplantation
RevDate: 2025-06-18
Transfer toxicity of polystyrene microplastics in vivo: Multi-organ crosstalk.
Environment international, 202:109604 pii:S0160-4120(25)00355-1 [Epub ahead of print].
The accumulation of microplastics (MPs) within the environment caused serious ecological and health problems. Nevertheless, its systemic toxicity to organisms and its mechanisms lack effective evidence. This study established a model of MP exposure through the gavage of polystyrene (PS)-MPs particles to maternal mice on days 1 to 21 of lactation. The results demonstrated that PS-MPs were distributed widely in maternal mice, occurring mainly in the feces, colon, liver and mammary glands. Further experiments revealed that the gut and blood-milk barriers were disrupted, and pathological injury and inflammatory reactions were observed in the liver, gut, and mammary glands. Metabolomic and metagenome analysis indicated abnormalities in hepatic bile acid metabolism and significant alterations in the gut microbiota after exposure to PS-MPs. These alterations led to increased disruption of the intestine-liver axis. Notably, with fecal microbiota transplantation and antibiotic experiments, we observed that elimination of the intestinal microbiota reduced tissue inflammation and improved gut and blood-milk barrier leakage. These findings demonstrated that PS-MPs exaggerated intestine-liver axis disorders by inducing colonic injury, intestinal ecological dysregulation and abnormal hepatic bile acid metabolism. Furthermore, PS-MPs translocated via the intestine-liver axis and exerted broader toxic effects on mammary tissue. Overall, our study uncovered the transfer toxicity of PS-MPs in mice, proposing the possibility of a gut-liver-mammary axis.
Additional Links: PMID-40532535
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PubMed:
Citation:
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@article {pmid40532535,
year = {2025},
author = {Wang, Z and He, Y and Luo, M and Liu, S and Hou, J and Cao, B and An, X},
title = {Transfer toxicity of polystyrene microplastics in vivo: Multi-organ crosstalk.},
journal = {Environment international},
volume = {202},
number = {},
pages = {109604},
doi = {10.1016/j.envint.2025.109604},
pmid = {40532535},
issn = {1873-6750},
abstract = {The accumulation of microplastics (MPs) within the environment caused serious ecological and health problems. Nevertheless, its systemic toxicity to organisms and its mechanisms lack effective evidence. This study established a model of MP exposure through the gavage of polystyrene (PS)-MPs particles to maternal mice on days 1 to 21 of lactation. The results demonstrated that PS-MPs were distributed widely in maternal mice, occurring mainly in the feces, colon, liver and mammary glands. Further experiments revealed that the gut and blood-milk barriers were disrupted, and pathological injury and inflammatory reactions were observed in the liver, gut, and mammary glands. Metabolomic and metagenome analysis indicated abnormalities in hepatic bile acid metabolism and significant alterations in the gut microbiota after exposure to PS-MPs. These alterations led to increased disruption of the intestine-liver axis. Notably, with fecal microbiota transplantation and antibiotic experiments, we observed that elimination of the intestinal microbiota reduced tissue inflammation and improved gut and blood-milk barrier leakage. These findings demonstrated that PS-MPs exaggerated intestine-liver axis disorders by inducing colonic injury, intestinal ecological dysregulation and abnormal hepatic bile acid metabolism. Furthermore, PS-MPs translocated via the intestine-liver axis and exerted broader toxic effects on mammary tissue. Overall, our study uncovered the transfer toxicity of PS-MPs in mice, proposing the possibility of a gut-liver-mammary axis.},
}
RevDate: 2025-06-18
Dynamic changes in intestinal microbiota mediate mechanical hyperalgesia in surgical menopause model: a potential mechanism of DRG neuroinflammation.
International immunopharmacology, 161:115098 pii:S1567-5769(25)01088-4 [Epub ahead of print].
The role of the intestinal microbiota in hyperalgesia in ovariectomized mice remains unclear. This study aimed to investigate pain behavior and dynamic changes in the intestinal microbiota and the levels of related metabolites in a model of surgical menopause and to verify the hypothesis that the intestinal microbiota mediates the occurrence and persistence of hyperalgesia through neuroinflammation. An ovariectomy (OVX) model was constructed to assess the intestinal microbiota composition, the levels of related metabolites, and inflammation levels in the spinal dorsal root ganglion (DRG). Fecal microbiota transplantation (FMT) was used to alter the intestinal microbiota, and its impact on pain-related behaviors and the level of inflammation in the DRG was evaluated. The mechanical pain threshold was significantly lower in the OVX group compared with the sham group at 4-8 w after surgery, and the thermal pain threshold was greater at 5 and 8 w after surgery. A decrease in the mechanical pain threshold was observed in the OVX group 5, and 7-9 weeks after FMT, indicating hyperalgesia. PCoA and OPLS-DA revealed differences in the composition of the microbiota and the abundance of related metabolites between the OVX and sham groups. Correlation analysis revealed an association between pain thresholds and the levels and metabolites of certain bacterial genera. The expression of C/EBPβ and IL-1β in the OVX group was greater than that in the sham group, and the expression of IL-6, IL-1β, and TRPV1 in the sham group was greater than that in the OVX group after FMT. In conclusion, the dynamic changes in the intestinal microbiota in female mice induced by surgical menopause result in hyperalgesia, possibly due to an increase in the severity of inflammation in the spinal DRG.
Additional Links: PMID-40532322
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PubMed:
Citation:
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@article {pmid40532322,
year = {2025},
author = {Zhao, Y and Gong, N and Wang, S and Yuan, Q and Chen, X and Li, B and Zhang, L and Li, W and Zhu, R and Zhang, J and Zhang, W},
title = {Dynamic changes in intestinal microbiota mediate mechanical hyperalgesia in surgical menopause model: a potential mechanism of DRG neuroinflammation.},
journal = {International immunopharmacology},
volume = {161},
number = {},
pages = {115098},
doi = {10.1016/j.intimp.2025.115098},
pmid = {40532322},
issn = {1878-1705},
abstract = {The role of the intestinal microbiota in hyperalgesia in ovariectomized mice remains unclear. This study aimed to investigate pain behavior and dynamic changes in the intestinal microbiota and the levels of related metabolites in a model of surgical menopause and to verify the hypothesis that the intestinal microbiota mediates the occurrence and persistence of hyperalgesia through neuroinflammation. An ovariectomy (OVX) model was constructed to assess the intestinal microbiota composition, the levels of related metabolites, and inflammation levels in the spinal dorsal root ganglion (DRG). Fecal microbiota transplantation (FMT) was used to alter the intestinal microbiota, and its impact on pain-related behaviors and the level of inflammation in the DRG was evaluated. The mechanical pain threshold was significantly lower in the OVX group compared with the sham group at 4-8 w after surgery, and the thermal pain threshold was greater at 5 and 8 w after surgery. A decrease in the mechanical pain threshold was observed in the OVX group 5, and 7-9 weeks after FMT, indicating hyperalgesia. PCoA and OPLS-DA revealed differences in the composition of the microbiota and the abundance of related metabolites between the OVX and sham groups. Correlation analysis revealed an association between pain thresholds and the levels and metabolites of certain bacterial genera. The expression of C/EBPβ and IL-1β in the OVX group was greater than that in the sham group, and the expression of IL-6, IL-1β, and TRPV1 in the sham group was greater than that in the OVX group after FMT. In conclusion, the dynamic changes in the intestinal microbiota in female mice induced by surgical menopause result in hyperalgesia, possibly due to an increase in the severity of inflammation in the spinal DRG.},
}
RevDate: 2025-06-18
Gastrointestinal health and nutritional strategies in autism spectrum disorder.
Journal of gastroenterology [Epub ahead of print].
Beyond the hallmark social and sensory difficulties in autism spectrum disorder (ASD), the comorbid gastrointestinal (GI) conditions and their potential link to the severity of core symptoms require clinical attention. Although evidence indicates that autistic children face a greater risk of GI disorders and require more intensive nutritional management compared to neurotypical peers, standard guidelines for managing GI symptoms in this population remain lacking. This review seeks to pinpoint critical considerations for the implementation of nutrition-based strategies aimed at addressing GI dysfunction in individuals with ASD. By emphasizing clinical translation and the mechanistic understanding of these strategies, it highlights the importance of restoring gut homeostasis as a pathway to improve functional independence and overall well-being. Furthermore, we outline priorities for clinical research aimed at developing evidence-based nutritional recommendations to support GI health in autistic individuals, emphasizing personalized and population-specific needs.
Additional Links: PMID-40531376
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Citation:
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@article {pmid40531376,
year = {2025},
author = {Wu, Y and Wong, OWH and Chen, S and Ng, SC and Su, Q and Chan, FKL},
title = {Gastrointestinal health and nutritional strategies in autism spectrum disorder.},
journal = {Journal of gastroenterology},
volume = {},
number = {},
pages = {},
pmid = {40531376},
issn = {1435-5922},
support = {R4030-22//Research Grants Council-Research Impact Fund/ ; NCI202346//New Cornerstone Science Foundation/ ; PF22-77807//Hong Kong PhD Fellowship Scheme (HKPFS) of the Research Grants Council of Hong Kong/ ; },
abstract = {Beyond the hallmark social and sensory difficulties in autism spectrum disorder (ASD), the comorbid gastrointestinal (GI) conditions and their potential link to the severity of core symptoms require clinical attention. Although evidence indicates that autistic children face a greater risk of GI disorders and require more intensive nutritional management compared to neurotypical peers, standard guidelines for managing GI symptoms in this population remain lacking. This review seeks to pinpoint critical considerations for the implementation of nutrition-based strategies aimed at addressing GI dysfunction in individuals with ASD. By emphasizing clinical translation and the mechanistic understanding of these strategies, it highlights the importance of restoring gut homeostasis as a pathway to improve functional independence and overall well-being. Furthermore, we outline priorities for clinical research aimed at developing evidence-based nutritional recommendations to support GI health in autistic individuals, emphasizing personalized and population-specific needs.},
}
RevDate: 2025-06-18
CmpDate: 2025-06-18
Donor-centric administration of the stool donor program is vital to its feasibility and patient safety.
Gut microbes, 17(1):2508950.
Human stool-based products composed of fecal microbiota are a new frontier of medical therapeutics development. The development of standardized manufacturing protocols of donor microbiota has transformed fecal microbiota transplantation (FMT) from a crude and rarely used procedure to a widely accepted and highly effective option for treatment Clostridioides difficile infections. There is also a growing interest in using microbiota transplant therapies for multiple other clinical indications. In this manuscript, we review the logistical challenges experienced by various stool banks and our own group in establishing and administering a stool donor program. Furthermore, we explore and highlight the multiple ethical considerations that are ultimately essential to product safety and efficacy and propose basic principles that are necessary to maintain stool donor program integrity.
Additional Links: PMID-40530459
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PubMed:
Citation:
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@article {pmid40530459,
year = {2025},
author = {Kabage, AJ and Haselhorst, PJ and Khoruts, A},
title = {Donor-centric administration of the stool donor program is vital to its feasibility and patient safety.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2508950},
doi = {10.1080/19490976.2025.2508950},
pmid = {40530459},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/ethics/adverse effects/standards ; *Clostridium Infections/therapy ; *Patient Safety ; *Feces/microbiology ; *Tissue Donors ; Gastrointestinal Microbiome ; Clostridioides difficile ; },
abstract = {Human stool-based products composed of fecal microbiota are a new frontier of medical therapeutics development. The development of standardized manufacturing protocols of donor microbiota has transformed fecal microbiota transplantation (FMT) from a crude and rarely used procedure to a widely accepted and highly effective option for treatment Clostridioides difficile infections. There is also a growing interest in using microbiota transplant therapies for multiple other clinical indications. In this manuscript, we review the logistical challenges experienced by various stool banks and our own group in establishing and administering a stool donor program. Furthermore, we explore and highlight the multiple ethical considerations that are ultimately essential to product safety and efficacy and propose basic principles that are necessary to maintain stool donor program integrity.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Fecal Microbiota Transplantation/methods/ethics/adverse effects/standards
*Clostridium Infections/therapy
*Patient Safety
*Feces/microbiology
*Tissue Donors
Gastrointestinal Microbiome
Clostridioides difficile
RevDate: 2025-06-18
Decoding the gut-sleep Nexus: a bibliometric mapping of gut microbiota and sleep disorders.
Frontiers in microbiology, 16:1598173.
BACKGROUND: An increasing number of studies have focused on the interaction between gut microbiota and sleep disorders. However, there is currently no bibliometric analysis of the literature on gut microbiota and sleep disorders. This study employs bibliometric methods to analyze the current research status and hotspots in the field of gut microbiota and sleep disorders, providing a reference for future research in this area.
METHODS: Articles related to gut microbiota and sleep disorders were retrieved from the WOS core database, covering the period from the database's inception to December 31, 2024. After rigorous screening, VOSviewer and CiteSpace were used to conduct analyses on quantity, collaboration networks, clustering, and citation bursts.
RESULTS: The number of articles on gut microbiota and sleep disorders has increased annually, with a significant surge after 2022. China has the highest number of publications, while the United States has the highest citation count. The institution with the most publications is Shanghai Jiao Tong University, and the institution with the most citations is Deakin University. The top 10 journals by publication volume are all ranked above Q2 in the JCR. The most cited article is "Gut microbiome diversity is associated with sleep physiology in humans" by Smith et al., published in PLOS ONE in 2019. The top 10 most frequent keywords are gut microbiota, sleep, depression, inflammation, chain fatty acids, anxiety, brain, oxidative stress, obesity, and health. The keyword cluster "obstructive sleep apnea" is a focal research direction, while fecal microbiota transplantation is a current research hotspot.
CONCLUSION: This study reveals the publication trends, collaboration relationships among countries, regions, and authors, and recent research hotspots in the field of gut microbiota and sleep disorders through bibliometric methods, providing an objective data reference for scientific research in this domain.
Additional Links: PMID-40529581
PubMed:
Citation:
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@article {pmid40529581,
year = {2025},
author = {Xu, D and Lu, Z and Li, Q and Cheng, Y and Yang, Z},
title = {Decoding the gut-sleep Nexus: a bibliometric mapping of gut microbiota and sleep disorders.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1598173},
pmid = {40529581},
issn = {1664-302X},
abstract = {BACKGROUND: An increasing number of studies have focused on the interaction between gut microbiota and sleep disorders. However, there is currently no bibliometric analysis of the literature on gut microbiota and sleep disorders. This study employs bibliometric methods to analyze the current research status and hotspots in the field of gut microbiota and sleep disorders, providing a reference for future research in this area.
METHODS: Articles related to gut microbiota and sleep disorders were retrieved from the WOS core database, covering the period from the database's inception to December 31, 2024. After rigorous screening, VOSviewer and CiteSpace were used to conduct analyses on quantity, collaboration networks, clustering, and citation bursts.
RESULTS: The number of articles on gut microbiota and sleep disorders has increased annually, with a significant surge after 2022. China has the highest number of publications, while the United States has the highest citation count. The institution with the most publications is Shanghai Jiao Tong University, and the institution with the most citations is Deakin University. The top 10 journals by publication volume are all ranked above Q2 in the JCR. The most cited article is "Gut microbiome diversity is associated with sleep physiology in humans" by Smith et al., published in PLOS ONE in 2019. The top 10 most frequent keywords are gut microbiota, sleep, depression, inflammation, chain fatty acids, anxiety, brain, oxidative stress, obesity, and health. The keyword cluster "obstructive sleep apnea" is a focal research direction, while fecal microbiota transplantation is a current research hotspot.
CONCLUSION: This study reveals the publication trends, collaboration relationships among countries, regions, and authors, and recent research hotspots in the field of gut microbiota and sleep disorders through bibliometric methods, providing an objective data reference for scientific research in this domain.},
}
RevDate: 2025-06-18
Research focus and trends of the association between gut microbiota and neuroinflammation.
Frontiers in microbiology, 16:1564717.
BACKGROUND: The interaction between the gut microbiota and neuroinflammation plays a crucial role in the pathogenesis of many diseases, particularly neurodegenerative diseases, and has become one of the focal points of research in recent years. Despite the large number of related studies, there is currently a lack of comprehensive analysis and prediction of these data to drive the field forward. This study aims to systematically analyze the clinical practices and research hotspots of the underlying mechanisms in this field using bibliometric and visualization methods, and to explore the future development pathways.
METHODS: CiteSpace, VOSviewer, GraphPad Prism and other software were used to analyze 1,404 studies on gut microbiota and neuroinflammation collected by the core of the Web of Science since 2000, to visually present the collaborative network between literatures, structure of authors and countries, co-occurrence of keywords, emerging reference literature, and research hotspots.
RESULTS: From 2000 to 2024, the number of related papers on this topic showed an overall upward trend, and the annual citation peaked in 2020, with significant contributions from China and the United States. Research focused on the relationship between gut microbiota and neuroinflammation, with a particular emphasis on investigating the mechanisms of the microbiota-gut-brain axis through both basic and clinical research. Treatment strategies include probiotic therapy, fecal microbiota transplantation and traditional Chinese medicine.
CONCLUSION: This study comprehensively reviews the research progress on the association between gut microbiota and neuroinflammation, and discusses the current research focus and frontier directions of this relationship, so as to provide reference for the development of this field.
Additional Links: PMID-40529577
PubMed:
Citation:
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@article {pmid40529577,
year = {2025},
author = {Wu, S and Chen, N and Wang, C and So, KF},
title = {Research focus and trends of the association between gut microbiota and neuroinflammation.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1564717},
pmid = {40529577},
issn = {1664-302X},
abstract = {BACKGROUND: The interaction between the gut microbiota and neuroinflammation plays a crucial role in the pathogenesis of many diseases, particularly neurodegenerative diseases, and has become one of the focal points of research in recent years. Despite the large number of related studies, there is currently a lack of comprehensive analysis and prediction of these data to drive the field forward. This study aims to systematically analyze the clinical practices and research hotspots of the underlying mechanisms in this field using bibliometric and visualization methods, and to explore the future development pathways.
METHODS: CiteSpace, VOSviewer, GraphPad Prism and other software were used to analyze 1,404 studies on gut microbiota and neuroinflammation collected by the core of the Web of Science since 2000, to visually present the collaborative network between literatures, structure of authors and countries, co-occurrence of keywords, emerging reference literature, and research hotspots.
RESULTS: From 2000 to 2024, the number of related papers on this topic showed an overall upward trend, and the annual citation peaked in 2020, with significant contributions from China and the United States. Research focused on the relationship between gut microbiota and neuroinflammation, with a particular emphasis on investigating the mechanisms of the microbiota-gut-brain axis through both basic and clinical research. Treatment strategies include probiotic therapy, fecal microbiota transplantation and traditional Chinese medicine.
CONCLUSION: This study comprehensively reviews the research progress on the association between gut microbiota and neuroinflammation, and discusses the current research focus and frontier directions of this relationship, so as to provide reference for the development of this field.},
}
RevDate: 2025-06-18
CmpDate: 2025-06-18
Microbiota and gastric cancer: from molecular mechanisms to therapeutic strategies.
Frontiers in cellular and infection microbiology, 15:1563061.
Gastric cancer, a prevalent malignancy globally, is influenced by various factors. The imbalance in the gut microbiome and the existence of particular intratumoural microbiota could have a strong connection with the onset and progression of gastric cancer. High-throughput sequencing technology and bioinformatics analysis have revealed a close correlation between abnormal abundance of specific microbial communities and the risk of gastric cancer. These microbial communities contribute to gastric cancer progression through mechanisms including increasing cellular genomic damage, inhibiting DNA repair, activating abnormal signaling pathways, exacerbating tumor hypoxia, and shaping a tumor immune-suppressive microenvironment. This significantly impacts the efficacy of gastric cancer treatments, including chemotherapy and immunotherapy. Probiotic, prebiotic, antibiotic, carrier-based, dietary interventions, fecal microbiota transplantation, and traditional Chinese medicine show potential applications in gastric cancer treatment. However, the molecular mechanisms regarding dysbiosis of microbiota, including gut microbiota, and intra-tumoral microbiota during the progression of gastric cancer, as well as the therapeutic efficacy of microbiota-related applications, still require extensive exploration through experiments.
Additional Links: PMID-40529304
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Citation:
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@article {pmid40529304,
year = {2025},
author = {Chen, Z and Jin, D and Hu, J and Guan, D and Bai, Q and Gou, Y},
title = {Microbiota and gastric cancer: from molecular mechanisms to therapeutic strategies.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1563061},
pmid = {40529304},
issn = {2235-2988},
mesh = {*Stomach Neoplasms/therapy/microbiology/pathology ; Humans ; *Gastrointestinal Microbiome ; Dysbiosis/complications/microbiology ; Tumor Microenvironment ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; },
abstract = {Gastric cancer, a prevalent malignancy globally, is influenced by various factors. The imbalance in the gut microbiome and the existence of particular intratumoural microbiota could have a strong connection with the onset and progression of gastric cancer. High-throughput sequencing technology and bioinformatics analysis have revealed a close correlation between abnormal abundance of specific microbial communities and the risk of gastric cancer. These microbial communities contribute to gastric cancer progression through mechanisms including increasing cellular genomic damage, inhibiting DNA repair, activating abnormal signaling pathways, exacerbating tumor hypoxia, and shaping a tumor immune-suppressive microenvironment. This significantly impacts the efficacy of gastric cancer treatments, including chemotherapy and immunotherapy. Probiotic, prebiotic, antibiotic, carrier-based, dietary interventions, fecal microbiota transplantation, and traditional Chinese medicine show potential applications in gastric cancer treatment. However, the molecular mechanisms regarding dysbiosis of microbiota, including gut microbiota, and intra-tumoral microbiota during the progression of gastric cancer, as well as the therapeutic efficacy of microbiota-related applications, still require extensive exploration through experiments.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Stomach Neoplasms/therapy/microbiology/pathology
Humans
*Gastrointestinal Microbiome
Dysbiosis/complications/microbiology
Tumor Microenvironment
Probiotics/therapeutic use
Fecal Microbiota Transplantation
RevDate: 2025-06-17
CmpDate: 2025-06-17
Fecal microbiota transplantation from patients into animals to establish human microbiota-associated animal models: a scoping review.
Journal of translational medicine, 23(1):662.
BACKGROUND: Fecal microbiota transplantation (FMT) from humans with specific medical conditions to animal models can demonstrate causality by inducing or exacerbating pathophenotypes, linking the gut microbiota to health outcomes.
METHODS: We conducted a scoping review searching MEDLINE, EMBASE, Scopus, and Web of Science through July 2024 to identify human noninfectious diseases studied using FMT in animal models, investigate FMT methodologies, and assess the feasibility of systematic reviews on the role of the microbiota in specific diseases.
RESULTS: From 605 reports of 489 studies, we found that inflammatory bowel diseases, irritable bowel syndrome, obesity, colorectal cancer, and depression were the most commonly studied, with cancer research focusing on immunotherapy non-responsiveness. In a random sample of studies, gastrointestinal outcomes were most frequently reported, with remarkably high rates (> 80%) of successful induction of disease-specific alterations for intestinal barrier function, gastrointestinal inflammation, circulating immune parameters, and fecal metabolites. Most studies used C57BL/6 mice and oral gavage administration, with recipients being either germ-free or antibiotic-pretreated. We created tables linking conditions with publications to facilitate future systematic reviews.
CONCLUSIONS: Although human-to-animal FMT studies cover diverse conditions, methodological heterogeneity and inconsistent reporting hinder comparability. Standardized protocols and guidelines are needed. For several conditions, sufficient literature exists to assess the role of the gut microbiota in human health through systematic reviews.
Additional Links: PMID-40528217
PubMed:
Citation:
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@article {pmid40528217,
year = {2025},
author = {Ruszkowski, J and Kachlik, Z and Walaszek, M and Storman, D and Podkowa, K and Garbarczuk, P and Jemioło, P and Łyzińska, W and Nowakowska, K and Grych, K and Dębska-Ślizień, AM},
title = {Fecal microbiota transplantation from patients into animals to establish human microbiota-associated animal models: a scoping review.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {662},
pmid = {40528217},
issn = {1479-5876},
support = {"Medical University of Gdansk Excellence Initiative- Research University" program//Gdański Uniwersytet Medyczny/ ; },
mesh = {Animals ; Humans ; Mice ; *Disease Models, Animal ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; },
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) from humans with specific medical conditions to animal models can demonstrate causality by inducing or exacerbating pathophenotypes, linking the gut microbiota to health outcomes.
METHODS: We conducted a scoping review searching MEDLINE, EMBASE, Scopus, and Web of Science through July 2024 to identify human noninfectious diseases studied using FMT in animal models, investigate FMT methodologies, and assess the feasibility of systematic reviews on the role of the microbiota in specific diseases.
RESULTS: From 605 reports of 489 studies, we found that inflammatory bowel diseases, irritable bowel syndrome, obesity, colorectal cancer, and depression were the most commonly studied, with cancer research focusing on immunotherapy non-responsiveness. In a random sample of studies, gastrointestinal outcomes were most frequently reported, with remarkably high rates (> 80%) of successful induction of disease-specific alterations for intestinal barrier function, gastrointestinal inflammation, circulating immune parameters, and fecal metabolites. Most studies used C57BL/6 mice and oral gavage administration, with recipients being either germ-free or antibiotic-pretreated. We created tables linking conditions with publications to facilitate future systematic reviews.
CONCLUSIONS: Although human-to-animal FMT studies cover diverse conditions, methodological heterogeneity and inconsistent reporting hinder comparability. Standardized protocols and guidelines are needed. For several conditions, sufficient literature exists to assess the role of the gut microbiota in human health through systematic reviews.},
}
MeSH Terms:
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Animals
Humans
Mice
*Disease Models, Animal
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
RevDate: 2025-06-17
CmpDate: 2025-06-17
Common mechanisms of Gut microbe-based strategies for the treatment of intestine-related diseases: based on multi-target interactions with the intestinal barrier.
Cell communication and signaling : CCS, 23(1):288.
The concurrent occurrence and exacerbation of multiple diseases, including geriatric diseases and chronic diseases, impose a heavy burden on human health and medical expenses. Clarifying the common mechanisms of related multifarious diseases and developing preventive and therapeutic strategies with synergistic effects for multiple diseases are of great significance in alleviating the burden on the medical system and reducing patients' burden of drug metabolism. Recent studies have revealed that gut microbiota disorders and intestinal barrier damage, which consequently cause metabolic and immunological disorders, may be a common pathological basis underlying various intestinal-related diseases. In this review, we focus on the intestinal barrier function, summarizing the multi-target interactions and common mechanisms involved in diseases related to the gut such as ulcerative colitis, colorectal cancer, and type 2 diabetes. We identified gut microbe-based strategies, including probiotics, prebiotics, synbiotics, postbiotics, as well as potential targets in faecal microbiota transplant and berberine. The common mechanisms and key targets in the treatment of these diseases mainly include increasing the abundance of beneficial genera Bifidobacterium and Lactobacillus, increasing the levels of Short Chain Fatty Acids, restoring the intestinal mechanical barrier, and suppressing gut inflammation infiltration. We aim to provide a crucial basis and direction for the development of novel drugs with therapeutic effects for multiple diseases, thereby alleviating the patients' burden of medication and enhancing the efficacy of treatment.
Additional Links: PMID-40528179
PubMed:
Citation:
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@article {pmid40528179,
year = {2025},
author = {Chen, K and Wang, H and Yang, Y and Tang, C and Sun, X and Zhou, J and Liu, S and Li, Q and Zhao, L and Gao, Z},
title = {Common mechanisms of Gut microbe-based strategies for the treatment of intestine-related diseases: based on multi-target interactions with the intestinal barrier.},
journal = {Cell communication and signaling : CCS},
volume = {23},
number = {1},
pages = {288},
pmid = {40528179},
issn = {1478-811X},
support = {82274343//National Natural Science Foundation of China/ ; 82405302//National Natural Science Foundation of China/ ; ZR2024QH032//Shandong Provincial Natural Science Foundation/ ; 24-4-4-zrjj-111-jch//Qingdao Natural Science Foundation/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; Animals ; *Intestinal Mucosa/microbiology/metabolism ; Probiotics/therapeutic use ; *Intestinal Diseases/microbiology/therapy ; Fecal Microbiota Transplantation ; },
abstract = {The concurrent occurrence and exacerbation of multiple diseases, including geriatric diseases and chronic diseases, impose a heavy burden on human health and medical expenses. Clarifying the common mechanisms of related multifarious diseases and developing preventive and therapeutic strategies with synergistic effects for multiple diseases are of great significance in alleviating the burden on the medical system and reducing patients' burden of drug metabolism. Recent studies have revealed that gut microbiota disorders and intestinal barrier damage, which consequently cause metabolic and immunological disorders, may be a common pathological basis underlying various intestinal-related diseases. In this review, we focus on the intestinal barrier function, summarizing the multi-target interactions and common mechanisms involved in diseases related to the gut such as ulcerative colitis, colorectal cancer, and type 2 diabetes. We identified gut microbe-based strategies, including probiotics, prebiotics, synbiotics, postbiotics, as well as potential targets in faecal microbiota transplant and berberine. The common mechanisms and key targets in the treatment of these diseases mainly include increasing the abundance of beneficial genera Bifidobacterium and Lactobacillus, increasing the levels of Short Chain Fatty Acids, restoring the intestinal mechanical barrier, and suppressing gut inflammation infiltration. We aim to provide a crucial basis and direction for the development of novel drugs with therapeutic effects for multiple diseases, thereby alleviating the patients' burden of medication and enhancing the efficacy of treatment.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome
Animals
*Intestinal Mucosa/microbiology/metabolism
Probiotics/therapeutic use
*Intestinal Diseases/microbiology/therapy
Fecal Microbiota Transplantation
RevDate: 2025-06-17
Multi-omics approaches to explore the therapeutic mechanism for ginsenoside Rg1 against MASLD.
Biochemical and biophysical research communications, 776:152161 pii:S0006-291X(25)00876-9 [Epub ahead of print].
Ginsenoside Rg1 (G-Rg1), a traditional Chinese medicine, alleviates metabolic dysfunction-associated steatotic liver disease (MASLD). However, the mechanism by which G-Rg1 improves metabolic disorders in MASLD by regulating the gut microbiota remains ambiguous. We constructed a diet-induced murine MASLD model and employed 16S rRNA sequencing and non-targeted metabolomic analysis to investigate the mechanism of G-Rg1 in treating MASLD, focusing on its regulatory effect on the gut microbiota. Our results revealed that G-Rg1 significantly increased the 5-hydroxyindoleacetic acid levels and activated the aryl hydrocarbon receptor (AHR) by enhancing intestinal permeability, modulating the gut microbiota composition, and influencing tryptophan metabolism. Therefore, G-Rg1 improved immune function and reduced liver inflammation and lipid deposition in the MASLD mouse model. In contrast, the effect of G-Rg1 was impaired upon removal of the gut microbiota. Furthermore, fecal microbiota transplantation in G-Rg1-treated mice improved MASLD. These finding s suggest that regulating the gut microbiota may play an important role in G-Rg1's ability to protect against MASLD. G-Rg1 may exert its anti-MASLD effects through the gut microbiota, tryptophan metabolism, AHR activation, and interleukin-22 signaling, offering a novel approach for G-Rg1-mediated MASLD treatment.
Additional Links: PMID-40527176
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PubMed:
Citation:
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@article {pmid40527176,
year = {2025},
author = {Wang, Z and Wang, Y and Zhang, J and Yin, K and Luo, H and Huang, W},
title = {Multi-omics approaches to explore the therapeutic mechanism for ginsenoside Rg1 against MASLD.},
journal = {Biochemical and biophysical research communications},
volume = {776},
number = {},
pages = {152161},
doi = {10.1016/j.bbrc.2025.152161},
pmid = {40527176},
issn = {1090-2104},
abstract = {Ginsenoside Rg1 (G-Rg1), a traditional Chinese medicine, alleviates metabolic dysfunction-associated steatotic liver disease (MASLD). However, the mechanism by which G-Rg1 improves metabolic disorders in MASLD by regulating the gut microbiota remains ambiguous. We constructed a diet-induced murine MASLD model and employed 16S rRNA sequencing and non-targeted metabolomic analysis to investigate the mechanism of G-Rg1 in treating MASLD, focusing on its regulatory effect on the gut microbiota. Our results revealed that G-Rg1 significantly increased the 5-hydroxyindoleacetic acid levels and activated the aryl hydrocarbon receptor (AHR) by enhancing intestinal permeability, modulating the gut microbiota composition, and influencing tryptophan metabolism. Therefore, G-Rg1 improved immune function and reduced liver inflammation and lipid deposition in the MASLD mouse model. In contrast, the effect of G-Rg1 was impaired upon removal of the gut microbiota. Furthermore, fecal microbiota transplantation in G-Rg1-treated mice improved MASLD. These finding s suggest that regulating the gut microbiota may play an important role in G-Rg1's ability to protect against MASLD. G-Rg1 may exert its anti-MASLD effects through the gut microbiota, tryptophan metabolism, AHR activation, and interleukin-22 signaling, offering a novel approach for G-Rg1-mediated MASLD treatment.},
}
RevDate: 2025-06-16
Fecal Microbiota Transplantation Versus Vancomycin for Primary Clostridioides difficile Infection : A Randomized Controlled Trial.
Annals of internal medicine [Epub ahead of print].
BACKGROUND: Fecal microbiota transplantation (FMT) is recommended for recurrent Clostridioides difficile infection (CDI), but its role in primary CDI is unclear.
OBJECTIVE: To investigate the efficacy and safety of FMT in primary CDI.
DESIGN: Randomized, open-label, noninferiority, multicenter trial. (ClinicalTrials.gov: NCT03796650).
SETTING: Hospitals and primary care facilities in Norway.
PATIENTS: Adults with CDI (C difficile toxin in stool and ≥3 loose stools daily) and no previous CDI within 365 days before enrollment.
INTERVENTION: FMT without antibiotic pretreatment versus oral vancomycin, 125 mg 4 times daily for 10 days.
MEASUREMENTS: The primary end point was clinical cure (firm stools or <3 bowel movements daily) at day 14 and no disease recurrence within 60 days with the assigned treatment alone.
RESULTS: Of 104 randomly assigned patients, 100 received FMT or the first dose of vancomycin and were eligible for analysis. Clinical cure and no disease recurrence within 60 days without additional treatment was observed in 34 of 51 patients (66.7%) with FMT versus 30 of 49 (61.2%) with vancomycin (difference, 5.4 percentage points [95.2% CI, -13.5 to 24.4 percentage points]; P for noninferiority < 0.001, rejecting the hypothesis that response to FMT is 25 percentage points lower than response to vancomycin). Eleven patients in the FMT group and 4 in the vancomycin group had additional C difficile treatment. Clinical cure at day 14 and no recurrence with or without additional treatment was observed in 40 of 51 patients (78.4%) with FMT and 30 of 49 (61.2%) with vancomycin (difference, 17.2 percentage points [95.2% CI, -0.7 to 35.1 percentage points]). No significant differences in adverse events were observed between groups.
LIMITATIONS: Open-label design and reliance on clinical end points.
CONCLUSION: FMT may be considered as first-line therapy in primary CDI.
PRIMARY FUNDING SOURCE: South-East Norway Health Trust.
Additional Links: PMID-40523286
Publisher:
PubMed:
Citation:
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@article {pmid40523286,
year = {2025},
author = {Juul, FE and Bretthauer, M and Johnsen, PH and Samy, F and Tonby, K and Berdal, JE and Hoff, DAL and Ofstad, EH and Abraham, A and Seip, B and Wiig, H and Rognstad, ØB and Glad, IF and Valeur, J and Nissen-Lie, AE and Ness-Jensen, E and Lund, KMA and Skjevling, LK and Hanevik, K and Skudal, H and Melsom, EJ and Boyar, R and Cooper, TJ and Ranheim, TE and Riise, EM and Adami, HO and Kalager, M and Løberg, M and Garborg, KK},
title = {Fecal Microbiota Transplantation Versus Vancomycin for Primary Clostridioides difficile Infection : A Randomized Controlled Trial.},
journal = {Annals of internal medicine},
volume = {},
number = {},
pages = {},
doi = {10.7326/ANNALS-24-03285},
pmid = {40523286},
issn = {1539-3704},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) is recommended for recurrent Clostridioides difficile infection (CDI), but its role in primary CDI is unclear.
OBJECTIVE: To investigate the efficacy and safety of FMT in primary CDI.
DESIGN: Randomized, open-label, noninferiority, multicenter trial. (ClinicalTrials.gov: NCT03796650).
SETTING: Hospitals and primary care facilities in Norway.
PATIENTS: Adults with CDI (C difficile toxin in stool and ≥3 loose stools daily) and no previous CDI within 365 days before enrollment.
INTERVENTION: FMT without antibiotic pretreatment versus oral vancomycin, 125 mg 4 times daily for 10 days.
MEASUREMENTS: The primary end point was clinical cure (firm stools or <3 bowel movements daily) at day 14 and no disease recurrence within 60 days with the assigned treatment alone.
RESULTS: Of 104 randomly assigned patients, 100 received FMT or the first dose of vancomycin and were eligible for analysis. Clinical cure and no disease recurrence within 60 days without additional treatment was observed in 34 of 51 patients (66.7%) with FMT versus 30 of 49 (61.2%) with vancomycin (difference, 5.4 percentage points [95.2% CI, -13.5 to 24.4 percentage points]; P for noninferiority < 0.001, rejecting the hypothesis that response to FMT is 25 percentage points lower than response to vancomycin). Eleven patients in the FMT group and 4 in the vancomycin group had additional C difficile treatment. Clinical cure at day 14 and no recurrence with or without additional treatment was observed in 40 of 51 patients (78.4%) with FMT and 30 of 49 (61.2%) with vancomycin (difference, 17.2 percentage points [95.2% CI, -0.7 to 35.1 percentage points]). No significant differences in adverse events were observed between groups.
LIMITATIONS: Open-label design and reliance on clinical end points.
CONCLUSION: FMT may be considered as first-line therapy in primary CDI.
PRIMARY FUNDING SOURCE: South-East Norway Health Trust.},
}
RevDate: 2025-06-16
Microplastics Change the Food Utilization of Filter-Feeding Fish via Gut Microbiota.
Environmental science & technology [Epub ahead of print].
Microplastics (MPs) are ubiquitous in aquatic environments, while their effects on filter-feeding fish are poorly understood. This study aims to explore how MPs change the feeding of planktivorous silver carp. After exposure to MPs, the utilization efficiency of zooplankton by carp increased from 28.45% to 38.63-40.20%, while that of phytoplankton decreased from 50.64% to 40.47-43.32%. MPs did not cause changes in the phytoplankton and zooplankton communities that carp consumed but altered its gut microbiota, leading to increased abundance of genes encoding proteases but decreased carbohydrase genes. Gut metabolomics further showed corresponding metabolic changes especially with increased levels of l-tyrosine, citrulline, succinic acid, and propionic acid, which are significantly correlated with the isotopic signatures of carp utilizing zooplankton. Germ-free zebrafish transplanted with feces of MPs-exposed carp showed metabolic changes like those of carp, verifying that the gut microbiota mediated the effects induced by MPs, while silver carp transplanted with feces of MPs-exposed carp exhibited increased protease activity and enhanced zooplankton utilization efficiency, confirming that MPs could alter its food utilization via gut microbiota. Our findings fill a knowledge gap regarding the ecological risk of MPs to the feeding of planktivorous fish, with potential cascading effects on aquatic ecosystems.
Additional Links: PMID-40522165
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PubMed:
Citation:
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@article {pmid40522165,
year = {2025},
author = {Huang, JN and Wen, B and Wang, ZN and Gao, JZ and Chen, ZZ},
title = {Microplastics Change the Food Utilization of Filter-Feeding Fish via Gut Microbiota.},
journal = {Environmental science & technology},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.est.5c02067},
pmid = {40522165},
issn = {1520-5851},
abstract = {Microplastics (MPs) are ubiquitous in aquatic environments, while their effects on filter-feeding fish are poorly understood. This study aims to explore how MPs change the feeding of planktivorous silver carp. After exposure to MPs, the utilization efficiency of zooplankton by carp increased from 28.45% to 38.63-40.20%, while that of phytoplankton decreased from 50.64% to 40.47-43.32%. MPs did not cause changes in the phytoplankton and zooplankton communities that carp consumed but altered its gut microbiota, leading to increased abundance of genes encoding proteases but decreased carbohydrase genes. Gut metabolomics further showed corresponding metabolic changes especially with increased levels of l-tyrosine, citrulline, succinic acid, and propionic acid, which are significantly correlated with the isotopic signatures of carp utilizing zooplankton. Germ-free zebrafish transplanted with feces of MPs-exposed carp showed metabolic changes like those of carp, verifying that the gut microbiota mediated the effects induced by MPs, while silver carp transplanted with feces of MPs-exposed carp exhibited increased protease activity and enhanced zooplankton utilization efficiency, confirming that MPs could alter its food utilization via gut microbiota. Our findings fill a knowledge gap regarding the ecological risk of MPs to the feeding of planktivorous fish, with potential cascading effects on aquatic ecosystems.},
}
RevDate: 2025-06-16
The gut virome in association with the bacteriome in gastrointestinal diseases and beyond: roles, mechanisms, and clinical applications.
Precision clinical medicine, 8(2):pbaf010.
The gut virome, an essential component of the intestinal microbiome, constitutes ∼0.1% of the total microbial biomass but contains a far greater number of particles than bacteria, with phages making up 90%-95% of this virome. This review systematically examines the developmental patterns of the gut virome, focusing on factors influencing its composition, including diet, environment, host genetics, and immunity. Additionally, it explores the gut virome's associations with various diseases, its interactions with gut bacteria and the immune system, and its emerging clinical applications.
Additional Links: PMID-40520768
PubMed:
Citation:
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@article {pmid40520768,
year = {2025},
author = {Feng, Z and Burgermeister, E and Philips, A and Zuo, T and Wen, W},
title = {The gut virome in association with the bacteriome in gastrointestinal diseases and beyond: roles, mechanisms, and clinical applications.},
journal = {Precision clinical medicine},
volume = {8},
number = {2},
pages = {pbaf010},
pmid = {40520768},
issn = {2516-1571},
abstract = {The gut virome, an essential component of the intestinal microbiome, constitutes ∼0.1% of the total microbial biomass but contains a far greater number of particles than bacteria, with phages making up 90%-95% of this virome. This review systematically examines the developmental patterns of the gut virome, focusing on factors influencing its composition, including diet, environment, host genetics, and immunity. Additionally, it explores the gut virome's associations with various diseases, its interactions with gut bacteria and the immune system, and its emerging clinical applications.},
}
RevDate: 2025-06-16
CmpDate: 2025-06-16
Gut-brain-liver axis in growth hormone deficiency: role of microbiota-derived short-chain fatty acids in ethnic variability and therapeutic development.
Frontiers in public health, 13:1541654.
Growth hormone deficiency (GHD) is a pediatric endocrine disorder characterized by dysregulated growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis activity and gut microbiota imbalance. Emerging evidence highlights the gut-brain-liver axis as a critical modulator of growth, with microbiota-derived short-chain fatty acids (SCFAs) playing dual roles in GH suppression and IGF-1 enhancement. This review synthesizes preclinical and clinical data to address ethnic variability in microbiota composition and therapeutic challenges. Key findings reveal that Chinese GHD cohorts exhibit reduced Bifidobacterium and fecal butyrate, whereas Spanish cohorts show minimal differences, potentially due to dietary fiber intake (e.g., Prevotella-enriched diets in Asia) or methodological variations in microbiota sequencing. Mechanistically, propionate (>500 μM) inhibits pituitary GH synthesis via GPR41/43-cAMP signaling, while butyrate enhances hepatic IGF-1 through GPR109A-mediated IL-6 secretion and osteoblastic histone deacetylase (HDAC) inhibition. Interventions such as probiotics (e.g., Lactobacillus plantarum increased IGF-1 by 1.2-1.8-fold in murine models) and high-fiber diets demonstrate preclinical efficacy but face clinical barriers, including poor adherence (<30%) and limited GHD-specific trials. Fecal microbiota transplantation (FMT) shows hormonal restoration in animal models but induces gastrointestinal adverse effects (22% bloating, 15% diarrhea) in humans. Multi-omics approaches are proposed to identify biomarkers (e.g., low butyrate + elevated trimethylamine N-oxide). These approaches also aim to optimize precision therapies, such as nanoparticle-delivered SCFAs. This review underscores the need for multicenter randomized controlled trials to validate synbiotics or engineered microbial consortia, bridging mechanistic insights into the microbiota-SCFA-endocrine axis with clinical translation for GHD management.
Additional Links: PMID-40520290
PubMed:
Citation:
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@article {pmid40520290,
year = {2025},
author = {Meng, D and Kong, W and Cheng, S and Liu, H and Huang, C},
title = {Gut-brain-liver axis in growth hormone deficiency: role of microbiota-derived short-chain fatty acids in ethnic variability and therapeutic development.},
journal = {Frontiers in public health},
volume = {13},
number = {},
pages = {1541654},
pmid = {40520290},
issn = {2296-2565},
mesh = {Humans ; *Fatty Acids, Volatile/metabolism ; *Gastrointestinal Microbiome/physiology ; *Liver/metabolism ; *Human Growth Hormone/deficiency ; Animals ; *Brain/metabolism ; },
abstract = {Growth hormone deficiency (GHD) is a pediatric endocrine disorder characterized by dysregulated growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis activity and gut microbiota imbalance. Emerging evidence highlights the gut-brain-liver axis as a critical modulator of growth, with microbiota-derived short-chain fatty acids (SCFAs) playing dual roles in GH suppression and IGF-1 enhancement. This review synthesizes preclinical and clinical data to address ethnic variability in microbiota composition and therapeutic challenges. Key findings reveal that Chinese GHD cohorts exhibit reduced Bifidobacterium and fecal butyrate, whereas Spanish cohorts show minimal differences, potentially due to dietary fiber intake (e.g., Prevotella-enriched diets in Asia) or methodological variations in microbiota sequencing. Mechanistically, propionate (>500 μM) inhibits pituitary GH synthesis via GPR41/43-cAMP signaling, while butyrate enhances hepatic IGF-1 through GPR109A-mediated IL-6 secretion and osteoblastic histone deacetylase (HDAC) inhibition. Interventions such as probiotics (e.g., Lactobacillus plantarum increased IGF-1 by 1.2-1.8-fold in murine models) and high-fiber diets demonstrate preclinical efficacy but face clinical barriers, including poor adherence (<30%) and limited GHD-specific trials. Fecal microbiota transplantation (FMT) shows hormonal restoration in animal models but induces gastrointestinal adverse effects (22% bloating, 15% diarrhea) in humans. Multi-omics approaches are proposed to identify biomarkers (e.g., low butyrate + elevated trimethylamine N-oxide). These approaches also aim to optimize precision therapies, such as nanoparticle-delivered SCFAs. This review underscores the need for multicenter randomized controlled trials to validate synbiotics or engineered microbial consortia, bridging mechanistic insights into the microbiota-SCFA-endocrine axis with clinical translation for GHD management.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Fatty Acids, Volatile/metabolism
*Gastrointestinal Microbiome/physiology
*Liver/metabolism
*Human Growth Hormone/deficiency
Animals
*Brain/metabolism
RevDate: 2025-06-16
Fecal or bacterial transplantation in mice transfer environment-induced brain plasticity and associated behavioral changes.
Frontiers in physiology, 16:1572854.
INTRODUCTION: Recent studies have shown that lifestyle factors, including diet and environmental stimuli, significantly alter the composition of gut microbiota and the metabolites they produce. Specifically, housing mice in an enriched environment (EE) enhances the production of short-chain fatty acids, which in part mediate the effects of EE on brain plasticity. In this study, we tested the hypothesis that the gut microbial composition of EE-exposed mice could be transplanted into mice housed in a standard environment (SE) to replicate the environmental effects on behavior, gene expression and neurogenesis.
METHODS: To test this hypothesis, we transplanted either a specific bacterial mixture or fecal material from EE-housed mice into SE-housed mice.
RESULTS: Our data show that both bacterial and fecal transplants reduce anxiety-like behaviors in mice. Additionally, we observed increased expression of hippocampal neurotrophins and enhanced neurogenesis.
DISCUSSION: These findings support the idea that gut microbiota influence brain functions, including anxiety-like behavior. Further research is necessary to clarify the underlying mechanisms. Moreover, the results suggest that fecal material transplantation (FMT) from individuals with healthy lifestyles may represent a promising strategy for the treatment of mood disorders.
Additional Links: PMID-40519780
PubMed:
Citation:
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@article {pmid40519780,
year = {2025},
author = {Marrocco, F and Khan, R and Reccagni, A and Lin, X and Delli Carpini, M and Iebba, V and D'Alessandro, G and Limatola, C},
title = {Fecal or bacterial transplantation in mice transfer environment-induced brain plasticity and associated behavioral changes.},
journal = {Frontiers in physiology},
volume = {16},
number = {},
pages = {1572854},
pmid = {40519780},
issn = {1664-042X},
abstract = {INTRODUCTION: Recent studies have shown that lifestyle factors, including diet and environmental stimuli, significantly alter the composition of gut microbiota and the metabolites they produce. Specifically, housing mice in an enriched environment (EE) enhances the production of short-chain fatty acids, which in part mediate the effects of EE on brain plasticity. In this study, we tested the hypothesis that the gut microbial composition of EE-exposed mice could be transplanted into mice housed in a standard environment (SE) to replicate the environmental effects on behavior, gene expression and neurogenesis.
METHODS: To test this hypothesis, we transplanted either a specific bacterial mixture or fecal material from EE-housed mice into SE-housed mice.
RESULTS: Our data show that both bacterial and fecal transplants reduce anxiety-like behaviors in mice. Additionally, we observed increased expression of hippocampal neurotrophins and enhanced neurogenesis.
DISCUSSION: These findings support the idea that gut microbiota influence brain functions, including anxiety-like behavior. Further research is necessary to clarify the underlying mechanisms. Moreover, the results suggest that fecal material transplantation (FMT) from individuals with healthy lifestyles may represent a promising strategy for the treatment of mood disorders.},
}
RevDate: 2025-06-16
Unlocking therapeutic potential of amlexanox in MASH with insights into bile acid metabolism and microbiome.
Npj gut and liver, 2:.
Metabolic dysfunction-associated steatohepatitis (MASH) has become a global health issue associated with obesity and diabetes. It is becoming a leading cause of end-stage liver diseases such as cirrhosis and hepatocellular carcinoma (HCC). Despite its increasing prevalence, effective pharmacotherapies for MASH remain limited, underscoring the urgent need for novel interventions. Amlexanox, an inhibitor of noncanonical IκB kinases, has demonstrated potential in restoring insulin sensitivity and glucose homeostasis in obese mice and human patients, as shown in our earlier studies. Here, we aimed to assess the therapeutic potential of amlexanox in dyslipidemia-associated diseases, particularly MASH and HCC, and to elucidate the underlying mechanism. We employed GAN diet-fed Ldlr [-/-] mice, which simultaneously develop obesity, MASH, and atherosclerosis, to recapitulate human metabolic syndrome and associated complications. Amlexanox was administrated orally to these mice after disease onset to examine its therapeutic efficacy. Our study demonstrates that even a low dose of amlexanox significantly reversed MASH and nearly completely prevented the progression from MASH to HCC. Both phenotypic and transcriptomic studies revealed that amlexanox markedly improved MASH-related dyslipidemia, hepatic steatosis, inflammation, liver injury, and hepatic fibrosis. Furthermore, multi-omics analysis revealed that amlexanox enhances hepatic bile acid synthesis and promotes fecal bile acid excretion. Notably, amlexanox reprogrammed gut microbiota, robustly increasing the abundance of Akkermansia muciniphila, a probiotic known to improve metabolic dysfunction. These findings uncover the multifaceted therapeutic potential of amlexanox in treating MASH and atherosclerosis by targeting bile acid metabolism, gut microbiota, hepatic inflammation, and fibrosis. Our study highlights amlexanox as a promising candidate for clinical applications.
Additional Links: PMID-40519640
PubMed:
Citation:
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@article {pmid40519640,
year = {2025},
author = {You, W and Ji, J and Wen, D and Wang, C and Sun, X and Zhao, P},
title = {Unlocking therapeutic potential of amlexanox in MASH with insights into bile acid metabolism and microbiome.},
journal = {Npj gut and liver},
volume = {2},
number = {},
pages = {},
pmid = {40519640},
issn = {3004-9806},
abstract = {Metabolic dysfunction-associated steatohepatitis (MASH) has become a global health issue associated with obesity and diabetes. It is becoming a leading cause of end-stage liver diseases such as cirrhosis and hepatocellular carcinoma (HCC). Despite its increasing prevalence, effective pharmacotherapies for MASH remain limited, underscoring the urgent need for novel interventions. Amlexanox, an inhibitor of noncanonical IκB kinases, has demonstrated potential in restoring insulin sensitivity and glucose homeostasis in obese mice and human patients, as shown in our earlier studies. Here, we aimed to assess the therapeutic potential of amlexanox in dyslipidemia-associated diseases, particularly MASH and HCC, and to elucidate the underlying mechanism. We employed GAN diet-fed Ldlr [-/-] mice, which simultaneously develop obesity, MASH, and atherosclerosis, to recapitulate human metabolic syndrome and associated complications. Amlexanox was administrated orally to these mice after disease onset to examine its therapeutic efficacy. Our study demonstrates that even a low dose of amlexanox significantly reversed MASH and nearly completely prevented the progression from MASH to HCC. Both phenotypic and transcriptomic studies revealed that amlexanox markedly improved MASH-related dyslipidemia, hepatic steatosis, inflammation, liver injury, and hepatic fibrosis. Furthermore, multi-omics analysis revealed that amlexanox enhances hepatic bile acid synthesis and promotes fecal bile acid excretion. Notably, amlexanox reprogrammed gut microbiota, robustly increasing the abundance of Akkermansia muciniphila, a probiotic known to improve metabolic dysfunction. These findings uncover the multifaceted therapeutic potential of amlexanox in treating MASH and atherosclerosis by targeting bile acid metabolism, gut microbiota, hepatic inflammation, and fibrosis. Our study highlights amlexanox as a promising candidate for clinical applications.},
}
RevDate: 2025-06-16
Effects of maternal rumen microbiota on the development of the microbial communities in the gastrointestinal tracts of neonatal sika deer.
Journal of animal science and technology, 67(3):619-635.
This study investigated whether the microbial assemblages in the gastrointestinal tracts (GITs) of sika deer calves can be manipulated by maternal rumen microbiota transplantation (MRMT). The results suggest that MRMT had no significant effect on the growth of calves but markedly lowered the duration of diarrhea and increased rumen fermentation in sika deer calves. Sequencing analysis of 16S rRNA gene amplicons revealed that MRMT increased the ability of some microbial taxa to colonize the GIT or enabled the colonization of others, which caused the ruminal microbial communities in sika deer calves to shift such that they resembled those of their mothers and promoted the temporal development of gut microbial diversity in deer calves. Moreover, after inoculation, 7 inoculum-dominant taxa (Butyrivibrio, Tenericutes, RFP12, SR1, Verrucomicrobia, Verruco_5, and WCHB1_41) and one inoculum-dominant taxon (Butyrivibrio) were significantly enriched in the rumen and feces of the sika deer calves, respectively. These data suggest that MRMT may be an effective approach for promoting microbial establishment in the GIT and preventing diarrhea in sika deer calves.
Additional Links: PMID-40519616
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Citation:
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@article {pmid40519616,
year = {2025},
author = {Zhang, Y and Liang, S and Choi, S and Li, G},
title = {Effects of maternal rumen microbiota on the development of the microbial communities in the gastrointestinal tracts of neonatal sika deer.},
journal = {Journal of animal science and technology},
volume = {67},
number = {3},
pages = {619-635},
pmid = {40519616},
issn = {2055-0391},
abstract = {This study investigated whether the microbial assemblages in the gastrointestinal tracts (GITs) of sika deer calves can be manipulated by maternal rumen microbiota transplantation (MRMT). The results suggest that MRMT had no significant effect on the growth of calves but markedly lowered the duration of diarrhea and increased rumen fermentation in sika deer calves. Sequencing analysis of 16S rRNA gene amplicons revealed that MRMT increased the ability of some microbial taxa to colonize the GIT or enabled the colonization of others, which caused the ruminal microbial communities in sika deer calves to shift such that they resembled those of their mothers and promoted the temporal development of gut microbial diversity in deer calves. Moreover, after inoculation, 7 inoculum-dominant taxa (Butyrivibrio, Tenericutes, RFP12, SR1, Verrucomicrobia, Verruco_5, and WCHB1_41) and one inoculum-dominant taxon (Butyrivibrio) were significantly enriched in the rumen and feces of the sika deer calves, respectively. These data suggest that MRMT may be an effective approach for promoting microbial establishment in the GIT and preventing diarrhea in sika deer calves.},
}
RevDate: 2025-06-16
The Lasting Imprint of Antibiotics on Gut Microbiota: Exploring Long-Term Consequences and Therapeutic Interventions.
Cureus, 17(5):e84114.
The widespread use of antibiotics has significantly impacted gut microbiota, often leading to long-term dysbiosis with profound health consequences. Antibiotics not only target pathogenic bacteria but also disrupt beneficial microbial communities, reducing diversity and increasing susceptibility to metabolic disorders, immune dysfunction, and opportunistic infections like Clostridioides difficile. The antibiotic-induced microbiota alterations can persist for weeks or even months post-treatment, contributing to ongoing health challenges. Restorative strategies, including probiotics, prebiotics, fecal microbiota transplantation, and dietary modifications, offer potential solutions to mitigate these effects. A balanced approach to antibiotic use, coupled with targeted interventions, is essential to preserving gut microbial health and minimizing long-term complications. Further research is needed to optimize therapeutic strategies and enhance patient outcomes. So, this editorial aims to examine the long-term consequences of antibiotic-induced gut microbiota disruption, highlight clinical and subclinical implications, and evaluate emerging therapeutic interventions aimed at microbiota restoration.
Additional Links: PMID-40519460
PubMed:
Citation:
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@article {pmid40519460,
year = {2025},
author = {Suvvari, TK and Vallurupalli, V and Koneru, KS and Ingawale, S and Yegurla, RR},
title = {The Lasting Imprint of Antibiotics on Gut Microbiota: Exploring Long-Term Consequences and Therapeutic Interventions.},
journal = {Cureus},
volume = {17},
number = {5},
pages = {e84114},
pmid = {40519460},
issn = {2168-8184},
abstract = {The widespread use of antibiotics has significantly impacted gut microbiota, often leading to long-term dysbiosis with profound health consequences. Antibiotics not only target pathogenic bacteria but also disrupt beneficial microbial communities, reducing diversity and increasing susceptibility to metabolic disorders, immune dysfunction, and opportunistic infections like Clostridioides difficile. The antibiotic-induced microbiota alterations can persist for weeks or even months post-treatment, contributing to ongoing health challenges. Restorative strategies, including probiotics, prebiotics, fecal microbiota transplantation, and dietary modifications, offer potential solutions to mitigate these effects. A balanced approach to antibiotic use, coupled with targeted interventions, is essential to preserving gut microbial health and minimizing long-term complications. Further research is needed to optimize therapeutic strategies and enhance patient outcomes. So, this editorial aims to examine the long-term consequences of antibiotic-induced gut microbiota disruption, highlight clinical and subclinical implications, and evaluate emerging therapeutic interventions aimed at microbiota restoration.},
}
RevDate: 2025-06-15
CmpDate: 2025-06-16
Anxiety-like behavior during protracted morphine withdrawal is driven by gut microbial dysbiosis and attenuated with probiotic treatment.
Gut microbes, 17(1):2517838.
The development of anxiety during protracted opioid withdrawal heightens the risk of relapse into the cycle of addiction. Understanding the mechanisms driving anxiety during opioid withdrawal could facilitate the development of therapeutics to prevent negative affect and promote continued abstinence. Our lab has previously established the gut microbiome as a driver of various side effects of opioid use, including analgesic tolerance and somatic withdrawal symptoms. We therefore hypothesized that the gut microbiome contributes to the development of anxiety-like behavior during protracted opioid withdrawal. In this study, we first established a mouse model of protracted morphine withdrawal, characterized by anxiety-like behavior and gut microbial dysbiosis. Next, we used fecal microbiota transplantation (FMT) to show that gut dysbiosis alone is sufficient to induce anxiety-like behavior. We further demonstrated that probiotic therapy during morphine withdrawal attenuated the onset of anxiety-like behavior, highlighting its therapeutic potential. Lastly, we examined transcriptional changes in the amygdala of morphine-withdrawn mice treated with probiotics to explore mechanisms by which the gut-brain axis mediates anxiety-like behavior. Our results support the use of probiotics as a promising therapeutic strategy to prevent gut dysbiosis and associated anxiety during opioid withdrawal, with potential implications for improving treatment outcomes in opioid recovery programs.
Additional Links: PMID-40518557
Publisher:
PubMed:
Citation:
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@article {pmid40518557,
year = {2025},
author = {Oppenheimer, M and Tao, J and Moidunny, S and Roy, S},
title = {Anxiety-like behavior during protracted morphine withdrawal is driven by gut microbial dysbiosis and attenuated with probiotic treatment.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2517838},
doi = {10.1080/19490976.2025.2517838},
pmid = {40518557},
issn = {1949-0984},
mesh = {Animals ; *Probiotics/administration & dosage/therapeutic use ; *Dysbiosis/microbiology ; *Gastrointestinal Microbiome/drug effects ; *Substance Withdrawal Syndrome/microbiology/psychology ; Mice ; *Anxiety/microbiology/etiology ; *Morphine/adverse effects ; Male ; Mice, Inbred C57BL ; Fecal Microbiota Transplantation ; Disease Models, Animal ; Behavior, Animal ; Morphine Dependence ; },
abstract = {The development of anxiety during protracted opioid withdrawal heightens the risk of relapse into the cycle of addiction. Understanding the mechanisms driving anxiety during opioid withdrawal could facilitate the development of therapeutics to prevent negative affect and promote continued abstinence. Our lab has previously established the gut microbiome as a driver of various side effects of opioid use, including analgesic tolerance and somatic withdrawal symptoms. We therefore hypothesized that the gut microbiome contributes to the development of anxiety-like behavior during protracted opioid withdrawal. In this study, we first established a mouse model of protracted morphine withdrawal, characterized by anxiety-like behavior and gut microbial dysbiosis. Next, we used fecal microbiota transplantation (FMT) to show that gut dysbiosis alone is sufficient to induce anxiety-like behavior. We further demonstrated that probiotic therapy during morphine withdrawal attenuated the onset of anxiety-like behavior, highlighting its therapeutic potential. Lastly, we examined transcriptional changes in the amygdala of morphine-withdrawn mice treated with probiotics to explore mechanisms by which the gut-brain axis mediates anxiety-like behavior. Our results support the use of probiotics as a promising therapeutic strategy to prevent gut dysbiosis and associated anxiety during opioid withdrawal, with potential implications for improving treatment outcomes in opioid recovery programs.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Probiotics/administration & dosage/therapeutic use
*Dysbiosis/microbiology
*Gastrointestinal Microbiome/drug effects
*Substance Withdrawal Syndrome/microbiology/psychology
Mice
*Anxiety/microbiology/etiology
*Morphine/adverse effects
Male
Mice, Inbred C57BL
Fecal Microbiota Transplantation
Disease Models, Animal
Behavior, Animal
Morphine Dependence
RevDate: 2025-06-15
Sorafenib induces intestinal toxicity by disturbing gut microbiota and activating the LPS/TLR4/NF-κB signaling pathway in mice.
Toxicology pii:S0300-483X(25)00179-9 [Epub ahead of print].
Sorafenib is a multitargeted tyrosine kinase inhibitor approved by the FDA as a standard first-line therapy for advanced hepatocellular carcinoma. Nevertheless, the high incidence rate of gastrointestinal (GI) adverse effects substantially limits its clinical application. The molecular mechanisms underlying the GI damage remain poorly understood. In this study, we explored the critical role of gut microbiota in sorafenib-induced intestinal toxicity using a mouse model and proposed a potential therapeutic intervention strategy. Sorafenib administration caused intestinal pathological damage, systemic inflammation, and oxidative stress in mice. Antibiotic (ABX) treatment and fecal microbiota transplantation (FMT) experiments demonstrated that the GI toxicity induced by sorafenib was mediated by the gut microbiota. 16S rRNA sequencing analysis revealed that sorafenib dramatically disturbed gut microbial homeostasis, leading to an increased abundance of Gram-negative bacteria and upregulated biosynthesis of lipopolysaccharide (LPS). Intestinal transcriptomic sequencing further indicated that sorafenib induced Gram-negative bacterial-derived LPS leakage via the compromised intestinal barrier and exacerbated inflammation via TLR4/NF-κB pathway activation. Notably, the TLR4-specific inhibitor TAK-242 effectively attenuated sorafenib-induced intestinal damage. Taken together, our study unveils a novel mechanism by which sorafenib exacerbates intestinal injury through gut microbiota dysbiosis and LPS/TLR4/NF-κB signaling pathway, while proposing TAK-242 as a promising therapeutic strategy. This study underscores the critical role of the gut microbiota in sorafenib-induced intestinal damage and offers new avenues for clinical intervention.
Additional Links: PMID-40518001
Publisher:
PubMed:
Citation:
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@article {pmid40518001,
year = {2025},
author = {Xu, Y and Mo, Y and Zhou, W and Qin, M and Li, M and Yin, G and Yu, H and Chen, Y and Du, H and Jin, Y and Huang, H and Ma, C and Xia, J and Li, H and Xie, Z and Wang, P and Hong, Y},
title = {Sorafenib induces intestinal toxicity by disturbing gut microbiota and activating the LPS/TLR4/NF-κB signaling pathway in mice.},
journal = {Toxicology},
volume = {},
number = {},
pages = {154220},
doi = {10.1016/j.tox.2025.154220},
pmid = {40518001},
issn = {1879-3185},
abstract = {Sorafenib is a multitargeted tyrosine kinase inhibitor approved by the FDA as a standard first-line therapy for advanced hepatocellular carcinoma. Nevertheless, the high incidence rate of gastrointestinal (GI) adverse effects substantially limits its clinical application. The molecular mechanisms underlying the GI damage remain poorly understood. In this study, we explored the critical role of gut microbiota in sorafenib-induced intestinal toxicity using a mouse model and proposed a potential therapeutic intervention strategy. Sorafenib administration caused intestinal pathological damage, systemic inflammation, and oxidative stress in mice. Antibiotic (ABX) treatment and fecal microbiota transplantation (FMT) experiments demonstrated that the GI toxicity induced by sorafenib was mediated by the gut microbiota. 16S rRNA sequencing analysis revealed that sorafenib dramatically disturbed gut microbial homeostasis, leading to an increased abundance of Gram-negative bacteria and upregulated biosynthesis of lipopolysaccharide (LPS). Intestinal transcriptomic sequencing further indicated that sorafenib induced Gram-negative bacterial-derived LPS leakage via the compromised intestinal barrier and exacerbated inflammation via TLR4/NF-κB pathway activation. Notably, the TLR4-specific inhibitor TAK-242 effectively attenuated sorafenib-induced intestinal damage. Taken together, our study unveils a novel mechanism by which sorafenib exacerbates intestinal injury through gut microbiota dysbiosis and LPS/TLR4/NF-κB signaling pathway, while proposing TAK-242 as a promising therapeutic strategy. This study underscores the critical role of the gut microbiota in sorafenib-induced intestinal damage and offers new avenues for clinical intervention.},
}
RevDate: 2025-06-15
Nutrient Acquisition of Gut Microbiota: Implications for Tumor Immunity.
Seminars in cancer biology pii:S1044-579X(25)00085-9 [Epub ahead of print].
The gut microbiota is essential in colorectal cancer (CRC) development, progression, and therapeutic responsiveness through its metabolic acquisitions and immunomodulatory functions. The composition of gut microbiota is shaped by habitat filters such as oxygen availability, dietary components, and host-derived factors, which influence both bacterial colonization and metabolic strategies. Furthermore, microbial metabolism of carbohydrates, proteins, and lipids produces metabolites, including short-chain fatty acids (SCFAs), polyamines, ammonia, hydrogen sulfide, and secondary bile acids (BAs). These microbial metabolites can either support anti-tumor immune surveillance or promote tumorigenesis depending on their type, concentration, and the host context. Consequently, interventions such as high-fiber diets, prebiotic and probiotic supplementation, and fecal microbiota transplantation (FMT) have emerged as promising strategies to reshape the gut ecosystem and improve CRC treatment efficacy. This review summarizes current insights into microbial nutrient metabolism, discusses the immune-regulatory effects of key microbial metabolites, and explores microbiota-targeted strategies for enhancing antitumor efficacy. Understanding these interactions offers new therapeutic opportunities for cancer prevention and treatment.
Additional Links: PMID-40517921
Publisher:
PubMed:
Citation:
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@article {pmid40517921,
year = {2025},
author = {Wang, Y and Huang, J and Tong, H and Jiang, Y and Jiang, Y and Ma, X},
title = {Nutrient Acquisition of Gut Microbiota: Implications for Tumor Immunity.},
journal = {Seminars in cancer biology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.semcancer.2025.06.003},
pmid = {40517921},
issn = {1096-3650},
abstract = {The gut microbiota is essential in colorectal cancer (CRC) development, progression, and therapeutic responsiveness through its metabolic acquisitions and immunomodulatory functions. The composition of gut microbiota is shaped by habitat filters such as oxygen availability, dietary components, and host-derived factors, which influence both bacterial colonization and metabolic strategies. Furthermore, microbial metabolism of carbohydrates, proteins, and lipids produces metabolites, including short-chain fatty acids (SCFAs), polyamines, ammonia, hydrogen sulfide, and secondary bile acids (BAs). These microbial metabolites can either support anti-tumor immune surveillance or promote tumorigenesis depending on their type, concentration, and the host context. Consequently, interventions such as high-fiber diets, prebiotic and probiotic supplementation, and fecal microbiota transplantation (FMT) have emerged as promising strategies to reshape the gut ecosystem and improve CRC treatment efficacy. This review summarizes current insights into microbial nutrient metabolism, discusses the immune-regulatory effects of key microbial metabolites, and explores microbiota-targeted strategies for enhancing antitumor efficacy. Understanding these interactions offers new therapeutic opportunities for cancer prevention and treatment.},
}
RevDate: 2025-06-15
Fecal microbiota transplantation alleviates female offspring's ovarian inflammation in arsenic and fluoride co-exposed rats through the PI3K/ Akt /NF-κB pathway.
Ecotoxicology and environmental safety, 301:118508 pii:S0147-6513(25)00853-X [Epub ahead of print].
Numerous studies have shown that exposure to arsenic (As) or fluoride(F) can damage the reproductive system, but limited evidence exists regarding the combined toxicity and pathogenesis of As and F co-exposure in female reproduction. Moreover, the role of gut microbiota in mediating such toxicity remains unclear. This study investigated the effects of As and F co-exposure on ovarian development and the potential protective role of fecal microbiota transplantation (FMT). We established an animal model of ovarian injury induced via co-exposure to NaAsO2 and NaF from birth to postnatal day 120(PND120) and introduced FMT from PND60. Co-exposure reduced serum levels of estradiol(E2) and luteinizing hormone (LH), along with morphological alterations in ovarian tissue. Meanwhile, the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/nuclear transcription factor-κB (NF-κB) pathway, a known mediator of inflammation-related ovarian dysfunction, was significantly upregulated. Interestingly, with prolonged exposure, the inflammatory indicators (Akt, IL-1β, IL-6, TNF-α) on PND120 were significantly higher than those on PND60. Notably, FMT alleviated ovarian inflammation, potentially by improving colonic barrier function, thereby indirectly mitigating ovarian damage. Taken together, this study reveals that NaAsO2 and NaF co-exposure induces progressive ovarian inflammation via the PI3K/Akt/NF-κB pathway, and that FMT may offer protective effects. Our findings provide new insights into the environmental risks to female reproductive health.
Additional Links: PMID-40517506
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid40517506,
year = {2025},
author = {Li, Y and Yue, D and Zhao, Y and Liu, P and Li, M and Chen, J and Yan, X and Fan, L and Song, G and Tian, X and Lv, Y and Zhao, Q and Qiu, Y and Yan, X},
title = {Fecal microbiota transplantation alleviates female offspring's ovarian inflammation in arsenic and fluoride co-exposed rats through the PI3K/ Akt /NF-κB pathway.},
journal = {Ecotoxicology and environmental safety},
volume = {301},
number = {},
pages = {118508},
doi = {10.1016/j.ecoenv.2025.118508},
pmid = {40517506},
issn = {1090-2414},
abstract = {Numerous studies have shown that exposure to arsenic (As) or fluoride(F) can damage the reproductive system, but limited evidence exists regarding the combined toxicity and pathogenesis of As and F co-exposure in female reproduction. Moreover, the role of gut microbiota in mediating such toxicity remains unclear. This study investigated the effects of As and F co-exposure on ovarian development and the potential protective role of fecal microbiota transplantation (FMT). We established an animal model of ovarian injury induced via co-exposure to NaAsO2 and NaF from birth to postnatal day 120(PND120) and introduced FMT from PND60. Co-exposure reduced serum levels of estradiol(E2) and luteinizing hormone (LH), along with morphological alterations in ovarian tissue. Meanwhile, the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/nuclear transcription factor-κB (NF-κB) pathway, a known mediator of inflammation-related ovarian dysfunction, was significantly upregulated. Interestingly, with prolonged exposure, the inflammatory indicators (Akt, IL-1β, IL-6, TNF-α) on PND120 were significantly higher than those on PND60. Notably, FMT alleviated ovarian inflammation, potentially by improving colonic barrier function, thereby indirectly mitigating ovarian damage. Taken together, this study reveals that NaAsO2 and NaF co-exposure induces progressive ovarian inflammation via the PI3K/Akt/NF-κB pathway, and that FMT may offer protective effects. Our findings provide new insights into the environmental risks to female reproductive health.},
}
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ESP Quick Facts
ESP Origins
In the early 1990's, Robert Robbins was a faculty member at Johns Hopkins, where he directed the informatics core of GDB — the human gene-mapping database of the international human genome project. To share papers with colleagues around the world, he set up a small paper-sharing section on his personal web page. This small project evolved into The Electronic Scholarly Publishing Project.
ESP Support
In 1995, Robbins became the VP/IT of the Fred Hutchinson Cancer Research Center in Seattle, WA. Soon after arriving in Seattle, Robbins secured funding, through the ELSI component of the US Human Genome Project, to create the original ESP.ORG web site, with the formal goal of providing free, world-wide access to the literature of classical genetics.
ESP Rationale
Although the methods of molecular biology can seem almost magical to the uninitiated, the original techniques of classical genetics are readily appreciated by one and all: cross individuals that differ in some inherited trait, collect all of the progeny, score their attributes, and propose mechanisms to explain the patterns of inheritance observed.
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In reading the early works of classical genetics, one is drawn, almost inexorably, into ever more complex models, until molecular explanations begin to seem both necessary and natural. At that point, the tools for understanding genome research are at hand. Assisting readers reach this point was the original goal of The Electronic Scholarly Publishing Project.
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Usage of the site grew rapidly and has remained high. Faculty began to use the site for their assigned readings. Other on-line publishers, ranging from The New York Times to Nature referenced ESP materials in their own publications. Nobel laureates (e.g., Joshua Lederberg) regularly used the site and even wrote to suggest changes and improvements.
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When the site began, no journals were making their early content available in digital format. As a result, ESP was obliged to digitize classic literature before it could be made available. For many important papers — such as Mendel's original paper or the first genetic map — ESP had to produce entirely new typeset versions of the works, if they were to be available in a high-quality format.
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With the development of methods for adding typeset side notes to PDF files, the ESP project now plans to add annotated versions of some classical papers to its holdings. We also plan to add new reference and pedagogical material. We have already started providing regularly updated, comprehensive bibliographies to the ESP.ORG site.
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Dinosaur tail, complete with feathers, found preserved in amber.
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Mysterious fast radio burst (FRB) detected in the distant universe.
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