@article {pmid39814666,
year = {2025},
author = {Shekhar, S and Schwarzer, M and Dhariwal, A and Petersen, FC},
title = {Nasal microbiota transplantation: a gateway to novel treatments.},
journal = {Trends in microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tim.2024.12.010},
pmid = {39814666},
issn = {1878-4380},
abstract = {Two recent studies have highlighted the potential of nasal microbiota transplantation (NMT) to treat chronic rhinosinusitis (CRS). Here we evaluate these findings and propose that lessons from fecal microbiota transplantation (FMT) could guide NMT development, with possible implications for combating antimicrobial resistance in respiratory infections.},
}

@article {pmid39813598,
year = {2025},
author = {Ren, M and Xia, Y and Pan, H and Zhou, X and Yu, M and Ji, F},
title = {Duodenal-jejunal bypass ameliorates MASLD in rats by regulating gut microbiota and bile acid metabolism through FXR pathways.},
journal = {Hepatology communications},
volume = {9},
number = {2},
pages = {},
pmid = {39813598},
issn = {2471-254X},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Receptors, Cytoplasmic and Nuclear/metabolism ; Rats ; *Bile Acids and Salts/metabolism ; *Duodenum/surgery/metabolism/microbiology ; Male ; *Fecal Microbiota Transplantation ; Jejunum/surgery/metabolism ; Rats, Sprague-Dawley ; Disease Models, Animal ; Fatty Liver/metabolism ; Anti-Bacterial Agents/pharmacology ; Diet, High-Fat ; Gastric Bypass ; Insulin Resistance ; },
abstract = {BACKGROUND: Although bariatric and metabolic surgical methods, including duodenal-jejunal bypass (DJB), were shown to improve metabolic dysfunction-associated steatotic liver disease (MASLD) in clinical trials and experimental rodent models, their underlying mechanisms remain unclear. The present study therefore evaluated the therapeutic effects and mechanisms of action of DJB in rats with MASLD.

METHODS: Rats with MASLD were randomly assigned to undergo DJB or sham surgery. Rats were orally administered a broad-spectrum antibiotic cocktail (Abx) or underwent fecal microbiota transplantation to assess the role of gut microbiota in DJB-induced improvement of MASLD. Gut microbiota were profiled by 16S rRNA gene sequencing and metagenomic sequencing, and bile acids (BAs) were analyzed by BA-targeted metabolomics.

RESULTS: DJB alleviated hepatic steatosis and insulin resistance in rats with diet-induced MASLD. Abx depletion of bacteria abrogated the ameliorating effects of DJB on MASLD. Fecal microbiota transplantation from rats that underwent DJB improved MASLD in high-fat diet-fed recipients by reshaping the gut microbiota, especially by significantly reducing the abundance of Clostridium. This, in turn, suppressed secondary BA biosynthesis and activated the hepatic BA receptor, farnesoid X receptor. Inhibition of farnesoid X receptor attenuated the ameliorative effects of post-DJB microbiota on MASLD.

CONCLUSIONS: DJB ameliorates MASLD by regulating gut microbiota and BA metabolism through hepatic farnesoid X receptor pathways.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Receptors, Cytoplasmic and Nuclear/metabolism
Rats
*Bile Acids and Salts/metabolism
*Duodenum/surgery/metabolism/microbiology
Male
*Fecal Microbiota Transplantation
Jejunum/surgery/metabolism
Rats, Sprague-Dawley
Disease Models, Animal
Fatty Liver/metabolism
Anti-Bacterial Agents/pharmacology
Diet, High-Fat
Gastric Bypass
Insulin Resistance

@article {pmid39812804,
year = {2025},
author = {Sobral, J and Empadinhas, N and Esteves, AR and Cardoso, SM},
title = {Impact of Nutrition on the Gut Microbiota: Implications for Parkinson's Disease.},
journal = {Nutrition reviews},
volume = {},
number = {},
pages = {},
doi = {10.1093/nutrit/nuae208},
pmid = {39812804},
issn = {1753-4887},
support = {//Portuguese national funds/ ; //FCT/ ; },
abstract = {Parkinson's disease (PD) is a multifactorial neurodegenerative disease that is characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta and by the anomalous accumulation of α-synuclein aggregates into Lewy bodies and Lewy neurites. Research suggests 2 distinct subtypes of PD: the brain-first subtype if the pathology arises from the brain and then spreads to the peripheral nervous system (PNS) and the body-first subtype, where the pathological process begins in the PNS and then spreads to the central nervous system. This review primarily focuses on the body-first subtype. The influence of the gut microbiota on the development of PD has been the subject of growing interest among researchers. It has been suggested that gut inflammation may be closely associated with pathogenesis in PD, therefore leading to the hypothesis that gut microbiota modulation could play a significant role in this process. Nutrition can influence gut health and alter the risk and progression of PD by altering inflammatory markers. This review provides an overview of recent research that correlates variations in gut microbiota composition between patients with PD and healthy individuals with the impact of certain nutrients and dietary patterns, including the Mediterranean diet, the Western diet, and the ketogenic diet. It explores how these diets influence gut microbiota composition and, consequently, the risk of PD. Last, it examines fecal transplantation and the use of prebiotics, probiotics, or synbiotics as potential therapeutic strategies to balance the gut microbiome, aiming to reduce the risk or delay the progression of PD.},
}

@article {pmid39812540,
year = {2025},
author = {Cerna, C and Vidal-Herrera, N and Silva-Olivares, F and Álvarez, D and González-Arancibia, C and Hidalgo, M and Aguirre, P and González-Urra, J and Astudillo-Guerrero, C and Jara, M and Porras, O and Cruz, G and Hodar, C and Llanos, P and Urrutia, P and Ibacache-Quiroga, C and Nevzorova, Y and Cubero, FJ and Fuenzalida, M and Thomas-Valdés, S and Jorquera, G},
title = {Fecal Microbiota Transplantation from Young-Trained Donors Improves Cognitive Function in Old Mice Through Modulation of the Gut-Brain Axis.},
journal = {Aging and disease},
volume = {},
number = {},
pages = {},
doi = {10.14336/AD.2024.1089},
pmid = {39812540},
issn = {2152-5250},
abstract = {The gut-brain axis is a bidirectional communication pathway that modulates cognitive function. A dysfunctional gut-brain axis has been associated with cognitive impairments during aging. Therefore, we propose evaluating whether modulation of the gut microbiota through fecal microbiota transplantation (FMT) from young-trained donors (YT) to middle-aged or aged mice could enhance brain function and cognition in old age. Twelve-month-old male mice received an initial FMT from YT (YT-Tr) or age-matched donors (Auto-Tr) following antibiotic treatment. Three months later, the mice received a second FMT as reinforcement. Additionally, 18-month-old mice received Auto-Tr, YT-Tr, or FMT from young sedentary donors (YS-Tr). Cognitive function was assessed using novel object recognition and object location memory tests. Long-term potentiation (LTP) in hippocampal brain slices was studied, while neuroinflammation and synaptic plasticity were analyzed in hippocampal samples via qPCR and immunoblot. Gut permeability was evaluated in ileum and colon sections, serum samples were analyzed for cytokine levels, and fecal samples were used to measure short-chain fatty acid (SCFA) levels and perform 16S rRNA gene sequencing. We observed that YT-Tr, whether performed in middle age or old age, improved cognitive function in aged mice. Recognition and spatial memory were significantly enhanced in YT-Tr mice compared to Auto-Tr and YS-Tr groups. Intact LTP was observed in YT-Tr mice at 18 months of age, whereas LTP was impaired in the Auto-Tr group. Neuroinflammation was reduced, and synaptic plasticity modulators such as PSD-95 and FNDC5/Irisin were upregulated in the hippocampus of YT-Tr mice compared to both YS-Tr and Auto-Tr groups. A significant reduction in ileal and colon permeability was detected in YT-Tr animals, along with elevated cecal levels of butyrate and valerate compared to Auto-Tr. Moreover, YT-Tr decreased pro-inflammatory factors and increased anti-inflammatory factors in the serum of aged mice. Beta diversity analysis revealed significant differences in microbial community composition between YT-Tr and Auto-Tr animals, with higher abundances of Akkermansia, Prevotellaceae_UCG-001, and Odoribacter in YT-Tr mice. In conclusion, our study demonstrates that FMT from young-trained donors improves cognitive function and synaptic plasticity by modulating gut permeability, inflammation, SCFA levels, and gut microbiota composition in aged mice.},
}

@article {pmid39812347,
year = {2025},
author = {Gustafson, KL and Rodriguez, TR and McAdams, ZL and Coghill, LM and Ericsson, AC and Franklin, CL},
title = {Failure of colonization following gut microbiota transfer exacerbates DSS-induced colitis.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2447815},
pmid = {39812347},
issn = {1949-0984},
support = {T32 GM008396/GM/NIGMS NIH HHS/United States ; T32 OD011126/OD/NIH HHS/United States ; U42 OD010918/OD/NIH HHS/United States ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Colitis/microbiology/chemically induced/pathology ; *Dextran Sulfate ; Mice ; *Disease Models, Animal ; *Mice, Inbred C57BL ; *Fecal Microbiota Transplantation ; Bacteria/classification/isolation & purification/genetics/metabolism ; Female ; Specific Pathogen-Free Organisms ; Feces/microbiology ; Inflammatory Bowel Diseases/microbiology ; Male ; },
abstract = {To study the impact of differing specific pathogen-free gut microbiomes (GMs) on a murine model of inflammatory bowel disease, selected GMs were transferred using embryo transfer (ET), cross-fostering (CF), and co-housing (CH). Prior work showed that the GM transfer method and the microbial composition of donor and recipient GMs can influence microbial colonization and disease phenotypes in dextran sodium sulfate-induced colitis. When a low richness GM was transferred to a recipient with a high richness GM via CH, the donor GM failed to successfully colonize, and a more severe disease phenotype resulted when compared to ET or CF, where colonization was successful. By comparing CH and gastric gavage for fecal material transfer, we isolated the microbial component of this effect and determined that differences in disease severity and survival were associated with microbial factors rather than the transfer method itself. Mice receiving a low richness GM via CH and gastric gavage exhibited greater disease severity and higher expression of pro-inflammatory immune mediators compared to those receiving a high richness GM. This study provides valuable insights into the role of GM composition and colonization in disease modulation.},
}

Animals
*Gastrointestinal Microbiome
*Colitis/microbiology/chemically induced/pathology
*Dextran Sulfate
Mice
*Disease Models, Animal
*Mice, Inbred C57BL
*Fecal Microbiota Transplantation
Bacteria/classification/isolation & purification/genetics/metabolism
Female
Specific Pathogen-Free Organisms
Feces/microbiology
Inflammatory Bowel Diseases/microbiology
Male

@article {pmid39812329,
year = {2025},
author = {Zhang, Y and Wang, A and Zhao, W and Qin, J and Zhang, Y and Liu, B and Yao, C and Long, J and Yuan, M and Yan, D},
title = {Microbial succinate promotes the response to metformin by upregulating secretory immunoglobulin a in intestinal immunity.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2450871},
pmid = {39812329},
issn = {1949-0984},
mesh = {*Metformin/pharmacology ; Animals ; *Immunoglobulin A, Secretory/metabolism ; Mice ; *Gastrointestinal Microbiome/drug effects ; Humans ; *Succinic Acid/metabolism ; Up-Regulation/drug effects ; Diabetes Mellitus, Type 2/immunology/drug therapy/metabolism/microbiology ; Bacteroides thetaiotaomicron/drug effects ; Intestines/immunology/microbiology/drug effects ; Male ; Fecal Microbiota Transplantation ; Female ; Hypoglycemic Agents/pharmacology ; Mice, Inbred C57BL ; Mice, Knockout ; },
abstract = {Metformin is the first-line pharmacotherapy for type 2 diabetes mellitus; however, many patients respond poorly to this drug in clinical practice. The potential involvement of microbiota-mediated intestinal immunity and related signals in metformin responsiveness has not been previously investigated. In this study, we successfully constructed a humanized mouse model by fecal transplantation of the gut microbiota from clinical metformin-treated - responders and non-responders, and reproduced the difference in clinical phenotypes of responsiveness to metformin. The abundance of Bacteroides thetaiotaomicron, considered a representative differential bacterium of metformin responsiveness, and the level of secretory immunoglobulin A (SIgA) in intestinal immunity increased significantly in responder recipient mice following metformin treatment. In contrast, no significant alterations in B. thetaiotaomicron and SIgA were observed in non-responder recipient mice. The study of IgA[-/-] mice confirmed that downregulated expression or deficiency of SIgA resulted in non-response to metformin, meaning that metformin was unable to improve dysfunctional glucose metabolism and reduce intestinal and adipose tissue inflammation, ultimately leading to systemic insulin resistance. Furthermore, supplementation with succinate, a microbial product of B. thetaiotaomicron, potentially reversed the non-response to metformin by inducing the production of SIgA. In conclusion, we demonstrated that upregulated SIgA, which could be regulated by succinate, was functionally involved in metformin response through its influence on immune cell-mediated inflammation and insulin resistance. Conversely, an inability to regulate SIgA may result in a lack of response to metformin.},
}

*Metformin/pharmacology
Animals
*Immunoglobulin A, Secretory/metabolism
Mice
*Gastrointestinal Microbiome/drug effects
Humans
*Succinic Acid/metabolism
Up-Regulation/drug effects
Diabetes Mellitus, Type 2/immunology/drug therapy/metabolism/microbiology
Bacteroides thetaiotaomicron/drug effects
Intestines/immunology/microbiology/drug effects
Male
Fecal Microbiota Transplantation
Female
Hypoglycemic Agents/pharmacology
Mice, Inbred C57BL
Mice, Knockout

@article {pmid39812000,
year = {2025},
author = {Zhao, H and Fu, X and Wang, Y and Shang, Z and Li, B and Zhou, L and Liu, Y and Liu, D and Yi, B},
title = {Therapeutic Potential of Vanillic Acid in Ulcerative Colitis Through Microbiota and Macrophage Modulation.},
journal = {Molecular nutrition & food research},
volume = {},
number = {},
pages = {e202400785},
doi = {10.1002/mnfr.202400785},
pmid = {39812000},
issn = {1613-4133},
support = {81760587//National Natural Science Foundation of China/ ; 81760731)//National Natural Science Foundation of China/ ; },
abstract = {This study investigated the protective effects of the dietary polyphenol vanillic acid (VA) on dextran sulfate sodium-induced acute ulcerative colitis (UC) in mice, focusing on its impact on the gut microbiota and inflammatory responses. VA was supplemented following dextran sulfate sodium administration, and key indicators, including body weight, disease activity index, colon length, spleen index, and inflammatory markers, were assessed. VA supplementation significantly alleviated UC symptoms, preserved intestinal barrier integrity, and reduced pro-inflammatory cytokine levels. Additionally, VA positively altered the gut microbiota composition, promoting beneficial bacteria such as Akkermansia muciniphila while suppressing the arachidonic acid metabolism pathway. Fecal microbiota transplantation confirmed that the VA-modified gut microbiota contributed to these protective effects. VA also facilitated macrophage polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype, further mitigating inflammation. These findings highlight the potential of VA as a natural dietary intervention for UC, emphasizing its role in regulating the gut microbiota and inflammatory pathways, which may have significant nutritional relevance in managing inflammatory bowel diseases.},
}

@article {pmid39816646,
year = {2023},
author = {Karukappadath, RM and Sirbu, D and Zaky, A},
title = {Drug-resistant bacteria in the critically ill: patterns and mechanisms of resistance and potential remedies.},
journal = {Frontiers in antibiotics},
volume = {2},
number = {},
pages = {1145190},
pmid = {39816646},
issn = {2813-2467},
abstract = {Antimicrobial resistance in the intensive care unit is an ongoing global healthcare concern associated with high mortality and morbidity rates and high healthcare costs. Select groups of bacterial pathogens express different mechanisms of antimicrobial resistance. Clinicians face challenges in managing patients with multidrug-resistant bacteria in the form of a limited pool of available antibiotics, slow and potentially inaccurate conventional diagnostic microbial modalities, mimicry of non-infective conditions with infective syndromes, and the confounding of the clinical picture of organ dysfunction associated with sepsis with postoperative surgical complications such as hemorrhage and fluid shifts. Potential remedies for antimicrobial resistance include specific surveillance, adequate and systematic antibiotic stewardship, use of pharmacokinetic and pharmacodynamic techniques of therapy, and antimicrobial monitoring and adequate employment of infection control policies. Novel techniques of combating antimicrobial resistance include the use of aerosolized antibiotics for lung infections, the restoration of gut microflora using fecal transplantation, and orally administered probiotics. Newer antibiotics are urgently needed as part of the armamentarium against multidrug-resistant bacteria. In this review we discuss mechanisms and patterns of microbial resistance in a select group of drug-resistant bacteria, and preventive and remedial measures for combating antibiotic resistance in the critically ill.},
}

@article {pmid39811933,
year = {2025},
author = {Zhang, L and Wang, K and Huang, L and Deng, B and Chen, C and Zhao, K and Wang, W},
title = {Ganoderic Acid A Alleviates Severe Acute Pancreatitis by Modulating Gut Homeostasis and Inhibiting TLR4-NLRP3 Signaling.},
journal = {Journal of agricultural and food chemistry},
volume = {73},
number = {2},
pages = {1563-1579},
pmid = {39811933},
issn = {1520-5118},
mesh = {Animals ; *Toll-Like Receptor 4/metabolism/genetics ; Mice ; *NLR Family, Pyrin Domain-Containing 3 Protein/metabolism/genetics ; *Signal Transduction/drug effects ; *Pancreatitis/drug therapy/metabolism/immunology ; Male ; *Mice, Inbred C57BL ; Humans ; *Gastrointestinal Microbiome/drug effects ; *Homeostasis/drug effects ; *Heptanoic Acids/pharmacology ; Mice, Knockout ; Pancreas/immunology/metabolism/drug effects ; Rats ; Lanosterol/analogs & derivatives ; },
abstract = {Background Severe acute pancreatitis (SAP) manifests as a critical state marked by acute abdominal symptoms, often associated with intestinal barrier dysfunction, exacerbating SAP retroactively. Ganoderic acid A (GAA) demonstrates anti-inflammatory properties in various inflammatory disorders. Nonetheless, its potential therapeutic impact on SAP and the underlying mechanisms remain unexplored. Methods In both wild-type and TLR4[-/-] mice, experimental SAP was induced using caerulein plus lipopolysaccharide. Caerulein injections were administered intraperitoneally following 7 days of intragastric GAA administration. Additionally, the potential mechanisms by which GAA ameliorates SAP were further investigated using fecal microbiota transplantation and TLR4-overexpressing IEC-6 cells. Results We observed that GAA treatment significantly ameliorated serum levels of amylase, lipase, and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) in SAP mice. Pretreatment with GAA mitigated pathological injuries and reduced M1 macrophage and neutrophil infiltration in pancreatic or ileal tissues. Additionally, GAA treatment down-regulated TLR4-MAPK/NF-κB signaling and NLRP3 inflammasome activation in the pancreatic and ileal tissues of SAP mice. The results further revealed that the gavage of GAA decreased bacterial translocation (Escherichia coli and EUB338), repaired intestinal barrier dysfunction (ZO-1, occludin, DAO, and FITC), increased lysozyme and MUC2 expression, and raised the levels of short-chain fatty acids. Analysis of the gut microbiome showed that the beneficial effects of GAA treatment were associated with improvements in pancreatitis-associated gut microbiota dysbiosis, characterized by notable increases in α-diversity and the abundance of probiotics such as Akkermansia, GCA-900066575, and Parvibacter. Fecal transplantation experiments further confirmed that GAA exerts protective effects by modulating intestinal flora. The protective role of GAA in intestinal and pancreatic injuries is mediated by the inhibition of TLR4 signaling, as further evidenced in TLR4-deficient mice and TLR4-overexpressed IEC-6 cells. The results of docking indicated that GAA interacts with TLR4 via a hydrophobic interaction. Conclusions The study demonstrates that GAA significantly alleviates SAP through its anti-inflammatory and antioxidant capacities, as well as by restoring intestinal homeostasis, thereby providing insights into novel treatments for SAP.},
}

Animals
*Toll-Like Receptor 4/metabolism/genetics
Mice
*NLR Family, Pyrin Domain-Containing 3 Protein/metabolism/genetics
*Signal Transduction/drug effects
*Pancreatitis/drug therapy/metabolism/immunology
Male
*Mice, Inbred C57BL
Humans
*Gastrointestinal Microbiome/drug effects
*Homeostasis/drug effects
*Heptanoic Acids/pharmacology
Mice, Knockout
Pancreas/immunology/metabolism/drug effects
Rats
Lanosterol/analogs & derivatives

@article {pmid39811913,
year = {2025},
author = {Ribeiro, G and Schellekens, H and Cuesta-Marti, C and Maneschy, I and Ismael, S and Cuevas-Sierra, A and Martínez, JA and Silvestre, MP and Marques, C and Moreira-Rosário, A and Faria, A and Moreno, LA and Calhau, C},
title = {A Menu for Microbes: Unraveling Appetite Regulation and Weight Dynamics Through the Microbiota-Brain Connection Across the Lifespan.},
journal = {American journal of physiology. Gastrointestinal and liver physiology},
volume = {},
number = {},
pages = {},
doi = {10.1152/ajpgi.00227.2024},
pmid = {39811913},
issn = {1522-1547},
support = {UIDB/4255/2020//Centro de Investigação em Tecnologias e Serviços de Saúde (CINTESIS)/ ; UIDP/4255/2020//Centro de Investigação em Tecnologias e Serviços de Saúde (CINTESIS)/ ; UIDP/04923/2020//Comprehensive Health Research Centre/ ; UIDB/04923/2020//Comprehensive Health Research Centre/ ; SFI/12/RC/2273 _P2//Science Foundation Ireland (SFI)/ ; TC20180025//Food for Health Ireland EI Technology Centre/ ; GOIPG/2023/4836//Irish Research Council (IrishResearch)/ ; CD22/00011//Ministerio de Ciencia e Innovación (MCIN)/ ; MV23/00115//Instituto Carlos III de Salud/ ; Y2020/6600//Comunidad de Madrid (Community of Madrid)/ ; 2020.06333.BD//Fundacao para a Ciencia e a Technologia/ ; },
abstract = {Appetite, as the internal drive for food intake, is often dysregulated in a broad spectrum of conditions associated with over- and under-nutrition across the lifespan. Appetite regulation is a complex, integrative process comprising psychological and behavioral events, peripheral and metabolic inputs, and central neurotransmitter and metabolic interactions. The microbiota-gut-brain axis has emerged as a critical mediator of multiple physiological processes, including energy metabolism, brain function, and behavior. Therefore, the role of the microbiota-gut-brain axis in appetite and obesity is receiving increased attention. Omics approaches such as genomics, epigenomics, transcriptomics, proteomics, and metabolomics in appetite and weight regulation offer new opportunities for featuring obesity phenotypes. Furthermore, gut microbiota-targeted approaches such as pre- pro- post- and synbiotic, personalized nutrition, and fecal microbiota transplantation are novel avenues for precision treatments. The aim of this narrative review is (1) to provide an overview of the role of the microbiota-gut-brain-axis in appetite regulation across the lifespan and (2) to discuss the potential of omics and gut microbiota-targeted approaches to deepen understanding of appetite regulation and obesity.},
}

@article {pmid39811513,
year = {2025},
author = {Wang, Y and Liu, J},
title = {Interplay between creeping fat and gut microbiota: A brand-new perspective on fecal microbiota transplantation in Crohn's disease.},
journal = {World journal of gastroenterology},
volume = {31},
number = {2},
pages = {100024},
pmid = {39811513},
issn = {2219-2840},
mesh = {*Crohn Disease/microbiology/therapy/immunology ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; Humans ; Animals ; *Dysbiosis ; Mice ; *Disease Models, Animal ; Mesentery ; Adipose Tissue ; Recurrence ; Permeability ; Treatment Outcome ; Intestinal Mucosa/microbiology ; },
abstract = {Inflammatory bowel disease, particularly Crohn's disease (CD), has been linked to modifications in mesenteric adipose tissue (MAT) and the phenomenon known as "creeping fat" (CrF). The presence of CrF is believed to serve as a predictor for early clinical recurrence following surgical intervention in patients with CD. Notably, the incorporation of the mesentery during ileocolic resection for CD has been correlated with a decrease in surgical recurrence, indicating the significant role of MAT in the pathogenesis of CD. While numerous studies have indicated that dysbiosis of the gut microbiota is a critical factor in the development of CD, the functional implications of translocated microbiota within the MAT of CD patients remain ambiguous. This manuscript commentary discusses a recent basic research conducted by Wu et al. In their study, intestinal bacteria from individuals were transplanted into CD model mice, revealing that fecal microbiota transplantation (FMT) from healthy donors alleviated CD symptoms, whereas FMT from CD patients exacerbated these symptoms. Importantly, FMT was found to affect intestinal permeability, barrier function, and the levels of proinflammatory factors and adipokines. Collectively, these findings suggest that targeting MAT and CrF may hold therapeutic potential for patients with CD. However, the study did not evaluate the composition of the intestinal microbiota of the donors or the subsequent alterations in the gut microbiota. Overall, the gut microbiota plays a crucial role in the histopathology of CD, and thus, targeting MAT and CrF may represent a promising avenue for treatment in this patient population.},
}

*Crohn Disease/microbiology/therapy/immunology
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
Humans
Animals
*Dysbiosis
Mice
*Disease Models, Animal
Mesentery
Adipose Tissue
Recurrence
Permeability
Treatment Outcome
Intestinal Mucosa/microbiology

@article {pmid39811502,
year = {2025},
author = {Qiao, T and Wen, XH},
title = {Exploring gut microbiota as a novel therapeutic target in Crohn's disease: Insights and emerging strategies.},
journal = {World journal of gastroenterology},
volume = {31},
number = {2},
pages = {100827},
pmid = {39811502},
issn = {2219-2840},
mesh = {*Crohn Disease/microbiology/therapy/immunology ; Humans ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation ; *Dysbiosis ; Enteral Nutrition/methods ; Disease Progression ; Animals ; },
abstract = {Extensive research has investigated the etiology of Crohn's disease (CD), encompassing genetic predisposition, lifestyle factors, and environmental triggers. Recently, the gut microbiome, recognized as the human body's second-largest gene pool, has garnered significant attention for its crucial role in the pathogenesis of CD. This paper investigates the mechanisms underlying CD, focusing on the role of 'creeping fat' in disease progression and exploring emerging therapeutic strategies, including fecal microbiota transplantation, enteral nutrition, and therapeutic diets. Creeping fat has been identified as a unique pathological feature of CD and has recently been found to be associated with dysbiosis of the gut microbiome. We characterize this dysbiotic state by identifying key microbiome-bacteria, fungi, viruses, and archaea, and their contributions to CD pathogenesis. Additionally, this paper reviews contemporary therapies, emphasizing the potential of biological therapies like fecal microbiota transplantation and dietary interventions. By elucidating the complex interactions between host-microbiome dynamics and CD pathology, this article aims to advance our understanding of the disease and guide the development of more effective therapeutic strategies for managing CD.},
}

*Crohn Disease/microbiology/therapy/immunology
Humans
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation
*Dysbiosis
Enteral Nutrition/methods
Disease Progression
Animals

@article {pmid39810863,
year = {2024},
author = {Uździcki, AW and Wawrzynowicz-Syczewska, M},
title = {Impact of liver transplantation on intestinal and systemic inflammation markers in patients with colitis ulcerosa concomitant with primary sclerosing cholangitis.},
journal = {Przeglad gastroenterologiczny},
volume = {16},
number = {4},
pages = {439-445},
pmid = {39810863},
issn = {1895-5770},
abstract = {INTRODUCTION: Primary sclerosing cholangitis (PSC) is an uncommon, chronic liver disease characterised by fibrosis and strictures of a bile ducts, causing cholestasis. In the long term it can lead to complete stenosis leading in turn to liver cirrhosis. In patients with severe form of the disease, the recommended treatment is liver transplantation. Because PSC frequently coexists with ulcerative colitis (UC), it is crucial to determine the effect of liver transplantation on the course of UC.

AIM: The aim was to determine the impact of liver transplantation on intestinal and systemic inflammation markers with UC concomitant with PSC (PSC-UC).

MATERIAL AND METHODS: Sixty-three patients with PSC-UC were enrolled, 25 of whom underwent liver transplantation (OLTx) due to PSC progression. Clinical symptoms, faecal calprotectin levels, C-reactive protein (CRP) serum concentration, erythrocyte sedimentation rate, and white blood cell count (WBC) were obtained.

RESULTS: Faecal calprotectin was significantly higher in the post-OLTx group. Mean calprotectin values were 163% higher - 474 ng/ml and 180 ng/ml (p = 0.024) in the post-OLTx group and in the PSC-UC group without the transplantation, respectively. Calprotectin levels exceeded the upper limit of normal (defined as 200 ng/l) in 66% of liver recipients and in 18% of non-transplanted patients (OR = 9.33, p = 0.011). In the post-OLTx group, also CRP concentration (11.01 mg/l vs. 6.54 mg/l, p = 0.30) and WBC (7.58 K/ml vs. 5.72 K/ml, p = 0.006) were higher than in the PSC-UC group without transplantation.

CONCLUSIONS: We found significantly higher inflammation markers in PSC-UC patients who underwent liver transplantation due to PSC. The effect was strongest in faecal calprotectin levels. In PSC-UC patients after liver transplantation, intensification of UC treatment may be needed, despite the lack of worsening of clinical symptoms.},
}

@article {pmid39809955,
year = {2025},
author = {Kumar, D and Bishnoi, M and Kondepudi, KK and Sharma, SS},
title = {Gut Microbiota-Based Interventions for Parkinson's Disease: Neuroprotective Mechanisms and Current Perspective.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {39809955},
issn = {1867-1314},
abstract = {Recent evidence links gut microbiota alterations to neurodegenerative disorders, including Parkinson's disease (PD). Replenishing the abnormal composition of gut microbiota through gut microbiota-based interventions "prebiotics, probiotics, synbiotics, postbiotics, and fecal microbiota transplantation (FMT)" has shown beneficial effects in PD. These interventions increase gut metabolites like short-chain fatty acids (SCFAs) and glucagon-like peptide-1 (GLP-1), which may protect dopaminergic neurons via the gut-brain axis. Neuroprotective effects of these interventions are mediated by several mechanisms, including the enhancement of neurotrophin and activation of the PI3K/AKT/mTOR signaling pathway, GLP-1-mediated gut-brain axis signaling, Nrf2/ARE pathway, and autophagy. Other pathways, such as free fatty acid receptor activation, synaptic plasticity improvement, and blood-brain and gut barrier integrity maintenance, also contribute to neuroprotection. Furthermore, the inhibition of the TLR4/NF-кB pathway, MAPK pathway, GSK-3β signaling pathway, miR-155-5p-mediated neuroinflammation, and ferroptosis could account for their protective effects. Clinical studies involving gut microbiota-based interventions have shown therapeutic benefits in PD patients, particularly in improving gastrointestinal dysfunction and some neurological symptoms. However, the effectiveness in alleviating motor symptoms remains mild. Large-scale clinical trials are still needed to confirm these findings. This review emphasizes the neuroprotective mechanisms of gut microbiota-based interventions in PD as supported by both preclinical and clinical studies.},
}

@article {pmid39806466,
year = {2025},
author = {Khemiri, H and Ben Fraj, I and Lorusso, A and Mekki, N and Mangone, I and Gdoura, M and Di Pasqual, A and Cammà, C and Di Lollo, V and Cherni, A and Touzi, H and Sadraoui, A and Meddeb, Z and Hogga, N and Ben Mustapha, I and Barbouche, MR and Ouederni, M and Triki, H and Haddad-Boubaker, S},
title = {SARS-CoV-2 excretion and genetic evolution in nasopharyngeal and stool samples from primary immunodeficiency and immunocompetent pediatric patients.},
journal = {Virology journal},
volume = {22},
number = {1},
pages = {9},
pmid = {39806466},
issn = {1743-422X},
mesh = {Humans ; *SARS-CoV-2/genetics/immunology ; *Feces/virology ; *Nasopharynx/virology ; *COVID-19/virology/immunology ; Child ; Male ; Female ; Child, Preschool ; *RNA, Viral/genetics ; *Virus Shedding ; Infant ; Phylogeny ; Evolution, Molecular ; Primary Immunodeficiency Diseases/genetics ; Adolescent ; Whole Genome Sequencing ; },
abstract = {BACKGROUND: Primary Immunodeficiency disorders (PID) can increase the risk of severe COVID-19 and prolonged infection. This study investigates the duration of SARS-CoV-2 excretion and the genetic evolution of the virus in pediatric PID patients as compared to immunocompetent (IC) patients.

MATERIALS AND METHODS: A total of 40 nasopharyngeal and 24 stool samples were obtained from five PID and ten IC children. RNA detection was performed using RT-qPCR, and whole-genome sequencing was conducted with the NexSeq 1000 platform. Data analysis used the nextflow/viralrecon pipeline. Hotspot amino acid frequencies were investigated using GraphPad Prism v10. Phylodynamic analysis was conducted with BEAST software.

RESULTS: In IC children, the viral excretion period lasted up to 14 days in nasopharyngeal swabs, with an average duration of 7 days, and ranged from 7 to 14 days in stool samples. In PID patients, the viral RNA was detected in nasopharyngeal for periods between 7 and 28 days, with an average duration of 15 days, and up to 28 days in stool samples. Two SARS-CoV-2 variants were detected in PID patients: Delta (AY.122) and Omicron (BA.1.1). Patients with antibody and combined deficiencies, exhibited the most prolonged shedding periods in both nasopharyngeal and stool samples and one patient presented complications and fatal outcome. Specific Hotspot amino acid changes were detected in PID: A2821V and R550H (ORF1ab).

CONCLUSION: Our findings underscore the prolonged excretion of SARS-CoV-2 RNA in patients with antibody and combined deficiencies. Thus, specialized care is essential for effectively managing PID patients.},
}

Humans
*SARS-CoV-2/genetics/immunology
*Feces/virology
*Nasopharynx/virology
*COVID-19/virology/immunology
Child
Male
Female
Child, Preschool
*RNA, Viral/genetics
*Virus Shedding
Infant
Phylogeny
Evolution, Molecular
Primary Immunodeficiency Diseases/genetics
Adolescent
Whole Genome Sequencing

@article {pmid39805780,
year = {2024},
author = {Ye, LJ and Xu, XF and Chen, SY and Zhang, H and Gan, YX and Meng, T and Ding, R and Li, J and Cao, G and Wang, KL},
title = {[Regulation of Bifidobacterium-short chain fatty acid metabolism and improvement of intestinal toxicity of vinegar-processed Euphorbiae Pekinensis Radix].},
journal = {Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica},
volume = {49},
number = {23},
pages = {6331-6341},
doi = {10.19540/j.cnki.cjcmm.20240912.301},
pmid = {39805780},
issn = {1001-5302},
mesh = {Mice ; Animals ; *Fatty Acids, Volatile/metabolism ; *Acetic Acid ; Humans ; Caco-2 Cells ; *Gastrointestinal Microbiome/drug effects ; *Drugs, Chinese Herbal/pharmacology/chemistry ; *Bifidobacterium/drug effects ; RAW 264.7 Cells ; Intestines/drug effects ; Male ; Intestinal Mucosa/metabolism/drug effects ; Feces/microbiology/chemistry ; },
abstract = {To explore the mechanism by which vinegar-processed Euphorbiae Pekinensis Radix regulates gut microbiota and reduces intestinal toxicity, this study aimed to identify key microbial communities related to vinegar-induced detoxification and verify their functions. Using a derivatization method, the study measured the content of short-chain fatty acids(SCFAs) in feces before and after vinegar-processing of Euphorbiae Pekinensis Radix. Combined with the results of previous gut microbiota sequencing, correlation analysis was used to identify key microbial communities related to SCFAs content. Through single-bacterium transplantation experiments, the role of key microbial communities in regulating SCFAs metabolism and alleviating the intestinal toxicity of Euphorbiae Pekinensis Radix was clarified. Fecal extracts were then added to a co-culture system of Caco-2 and RAW264.7 cells, and toxicity differences were evaluated using intestinal tight junction proteins and inflammatory factors as indicators. Additionally, the application of a SCFAs receptor blocker helped confirm the role of SCFAs in reducing intestinal toxicity during vinegar-processing of Euphorbiae Pekinensis Radix. The results of this study indicated that vinegar-processing of Euphorbiae Pekinensis Radix improved the decline in SCFAs content caused by the raw material. Correlation analysis revealed that Bifidobacterium was positively correlated with the levels of acetic acid, propionic acid, isobutyric acid, n-butyric acid, isovaleric acid, and n-valeric acid. RESULTS:: from single-bacterium transplantation experiments demonstrated that Bifidobacterium could mitigate the reduction in SCFAs content induced by raw Euphorbiae Pekinensis Radix, enhance the expression of tight junction proteins, and reduce intestinal inflammation. Similarly, cell experiment results confirmed that fecal extracts from Bifidobacterium-transplanted mice alleviated inflammation and increased the expression of tight junction proteins in intestinal epithelial cells. The use of the free fatty acid receptor-2 inhibitor GLPG0974 verified that this improvement effect was related to the SCFAs pathway. This study demonstrates that Bifidobacterium is the key microbial community responsible for reducing intestinal toxicity in vinegar-processed Euphorbiae Pekinensis Radix. Vinegar-processing increases the abundance of Bifidobacterium, elevates the intestinal SCFAs content, inhibits intestinal inflammation, and enhances the expression of tight junction proteins, thereby improving the intestinal toxicity of Euphorbiae Pekinensis Radix.},
}

Mice
Animals
*Fatty Acids, Volatile/metabolism
*Acetic Acid
Humans
Caco-2 Cells
*Gastrointestinal Microbiome/drug effects
*Drugs, Chinese Herbal/pharmacology/chemistry
*Bifidobacterium/drug effects
RAW 264.7 Cells
Intestines/drug effects
Male
Intestinal Mucosa/metabolism/drug effects
Feces/microbiology/chemistry

@article {pmid39804518,
year = {2025},
author = {Claytor, JD and Lin, DL and Magnaye, KM and Guerrero, YS and Langelier, CR and Lynch, SV and El-Nachef, N},
title = {Effect of Fecal Microbiota Transplant on Antibiotic Resistance Genes Among Patients with Chronic Pouchitis.},
journal = {Digestive diseases and sciences},
volume = {},
number = {},
pages = {},
pmid = {39804518},
issn = {1573-2568},
abstract = {BACKGROUND: Pouchitis is common among patients with ulcerative colitis (UC) who have had colectomy with ileal pouch-anal anastomosis. Antibiotics are first-line therapy for pouch inflammation, increasing the potential for gut colonization with multi-drug resistant organisms (MDRO). Fecal microbial transplant (FMT) is being studied in the treatment of pouchitis and in the eradication of MDRO. Prior work using aerobic antibiotic culture disks suggests that some patients with chronic pouchitis may regain fluoroquinolone sensitivity after FMT. However, gut MDRO include anaerobic, fastidious organisms that are difficult to culture using traditional methods.

AIM: We aimed to assess whether FMT reduced the abundance of antibiotic resistance genes (ARG) or affected resistome diversity, evenness, or richness in patients with chronic pouchitis.

METHODS: We collected clinical characteristics regarding infections and antibiotic exposures for 18 patients who had previously been enrolled in an observational study investigating FMT as a treatment for pouchitis. Twenty-six pre- and post-FMT stool samples were analyzed using FLASH (Finding Low Abundance Sequences by Hybridization), a CRISPR/Cas9-based shotgun metagenomic sequence enrichment technique that detects acquired and chromosomal bacterial ARGs. Wilcoxon rank sum tests were used to assess differences in clinical characteristics, ARG counts, resistome diversity and ARG richness, pre- and post-FMT.

RESULTS: All 13 of the patients with sufficient stool samples for analysis had recently received antibiotics for pouchitis prior to a single endoscopic FMT. Fecal microbiomes of all patients had evidence of multi-drug resistance genes and ESBL resistance genes at baseline; 62% encoded fluoroquinolone resistance genes. A numerical decrease in overall ARG counts was noted post-FMT, but no statistically significant differences were noted (P = 0.19). Richness and diversity were not significantly altered. Three patients developed infections during the 5-year follow-up period, none of which were associated with MDRO.

CONCLUSION: Antibiotic resistance genes are prevalent among antibiotic-exposed patients with chronic pouchitis. FMT led to a numerical decrease, but no statistically significant change in ARG, nor were there significant changes in the diversity, richness, or evenness of ARGs. Further investigations to improve FMT engraftment and to optimize FMT delivery in patients with inflammatory pouch disorders are warranted.},
}

@article {pmid39801363,
year = {2025},
author = {Chevalier, C and Tournier, BB and Marizzoni, M and Park, R and Paquis, A and Ceyzériat, K and Badina, AM and Lathuiliere, A and Saleri, S and Cillis, F and Cattaneo, A and Millet, P and Frisoni, GB},
title = {Fecal Microbiota Transplantation (FMT) From a Human at Low Risk for Alzheimer's Disease Improves Short-Term Recognition Memory and Increases Neuroinflammation in a 3xTg AD Mouse Model.},
journal = {Genes, brain, and behavior},
volume = {24},
number = {1},
pages = {e70012},
pmid = {39801363},
issn = {1601-183X},
support = {1216//Velux Stiftung/ ; },
mesh = {Animals ; *Fecal Microbiota Transplantation ; Mice ; *Alzheimer Disease/therapy/microbiology ; Humans ; Female ; *Gastrointestinal Microbiome ; Memory, Short-Term/physiology ; Neuroinflammatory Diseases/therapy/metabolism ; Disease Models, Animal ; Hippocampus/metabolism ; Aged ; },
abstract = {Human microbiota-associated murine models, using fecal microbiota transplantation (FMT) from human donors, help explore the microbiome's role in diseases like Alzheimer's disease (AD). This study examines how gut bacteria from donors with protective factors against AD influence behavior and brain pathology in an AD mouse model. Female 3xTgAD mice received weekly FMT for 2 months from (i) an 80-year-old AD patient (AD-FMT), (ii) a cognitively healthy 73-year-old with the protective APOEe2 allele (APOEe2-FMT), (iii) a 22-year-old healthy donor (Young-FMT), and (iv) untreated mice (Mice-FMT). Behavioral assessments included novel object recognition (NOR), Y-maze, open-field, and elevated plus maze tests; brain pathology (amyloid and tau), neuroinflammation (in situ autoradiography of the 18 kDa translocator protein in the hippocampus); and gut microbiota were analyzed. APOEe2-FMT improved short-term memory in the NOR test compared to AD-FMT, without significant changes in other behavioral tests. This was associated with increased neuroinflammation in the hippocampus, but no effect was detected on brain amyloidosis and tauopathy. Specific genera, such as Parabacteroides and Prevotellaceae_UGC001, were enriched in the APOEe2-FMT group and associated with neuroinflammation, while genera like Desulfovibrio were reduced and linked to decreased neuroinflammation. Gut microbiota from a donor with a protective factor against AD improved short-term memory and induced neuroinflammation in regions strategic to AD. The association of several genera with neuroinflammation in the APOEe2-FMT group suggests a collegial effect of the transplanted microbiome rather than a single-microbe driver effect. These data support an association between gut bacteria, glial cell activation, and cognitive function in AD.},
}

Animals
*Fecal Microbiota Transplantation
Mice
*Alzheimer Disease/therapy/microbiology
Humans
Female
*Gastrointestinal Microbiome
Memory, Short-Term/physiology
Neuroinflammatory Diseases/therapy/metabolism
Disease Models, Animal
Hippocampus/metabolism
Aged

@article {pmid39800714,
year = {2025},
author = {Sall, I and Foxall, R and Felth, L and Maret, S and Rosa, Z and Gaur, A and Calawa, J and Pavlik, N and Whistler, JL and Whistler, CA},
title = {Gut dysbiosis was inevitable, but tolerance was not: temporal responses of the murine microbiota that maintain its capacity for butyrate production correlate with sustained antinociception to chronic morphine.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2446423},
pmid = {39800714},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Morphine/administration & dosage ; *Dysbiosis/microbiology ; Mice ; *Butyrates/metabolism ; Male ; *Fecal Microbiota Transplantation ; *Drug Tolerance ; *Analgesics, Opioid/administration & dosage/metabolism ; *Mice, Inbred C57BL ; Bacteria/metabolism/classification/genetics/drug effects ; Probiotics/administration & dosage ; },
abstract = {The therapeutic benefits of opioids are compromised by the development of analgesic tolerance, which necessitates higher dosing for pain management thereby increasing the liability for drug dependence and addiction. Rodent models indicate opposing roles of the gut microbiota in tolerance: morphine-induced gut dysbiosis exacerbates tolerance, whereas probiotics ameliorate tolerance. Not all individuals develop tolerance, which could be influenced by differences in microbiota, and yet no study design has capitalized upon this natural variation. We leveraged natural behavioral variation in a murine model of voluntary oral morphine self-administration to elucidate the mechanisms by which microbiota influences tolerance. Although all mice shared similar morphine-driven microbiota changes that largely masked informative associations with variability in tolerance, our high-resolution temporal analyses revealed a divergence in the progression of dysbiosis that best explained sustained antinociception. Mice that did not develop tolerance maintained a higher capacity for production of the short-chain fatty acid (SCFA) butyrate known to bolster intestinal barriers and promote neuronal homeostasis. Both fecal microbial transplantation (FMT) from donor mice that did not develop tolerance and dietary butyrate supplementation significantly reduced the development of tolerance independently of suppression of systemic inflammation. These findings could inform immediate therapies to extend the analgesic efficacy of opioids.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Morphine/administration & dosage
*Dysbiosis/microbiology
Mice
*Butyrates/metabolism
Male
*Fecal Microbiota Transplantation
*Drug Tolerance
*Analgesics, Opioid/administration & dosage/metabolism
*Mice, Inbred C57BL
Bacteria/metabolism/classification/genetics/drug effects
Probiotics/administration & dosage

@article {pmid39800223,
year = {2025},
author = {Lista, S and Munafò, A and Caraci, F and Imbimbo, C and Emanuele, E and Minoretti, P and Pinto-Fraga, J and Merino-País, M and Crespo-Escobar, P and López-Ortiz, S and Monteleone, G and Imbimbo, BP and Santos-Lozano, A},
title = {Gut microbiota in Alzheimer's disease: Understanding molecular pathways and potential therapeutic perspectives.},
journal = {Ageing research reviews},
volume = {104},
number = {},
pages = {102659},
doi = {10.1016/j.arr.2025.102659},
pmid = {39800223},
issn = {1872-9649},
abstract = {Accumulating evidence suggests that gut microbiota (GM) plays a crucial role in Alzheimer's disease (AD) pathogenesis and progression. This narrative review explores the complex interplay between GM, the immune system, and the central nervous system in AD. We discuss mechanisms through which GM dysbiosis can compromise intestinal barrier integrity, enabling pro-inflammatory molecules and metabolites to enter systemic circulation and the brain, potentially contributing to AD hallmarks. Additionally, we examine other pathophysiological mechanisms by which GM may influence AD risk, including the production of short-chain fatty acids, secondary bile acids, and tryptophan metabolites. The role of the vagus nerve in gut-brain communication is also addressed. We highlight potential therapeutic implications of targeting GM in AD, focusing on antibiotics, probiotics, prebiotics, postbiotics, phytochemicals, and fecal microbiota transplantation. While preclinical studies showed promise, clinical evidence remains limited and inconsistent. We critically assess clinical trials, emphasizing challenges in translating GM-based therapies to AD patients. The reviewed evidence underscores the need for further research to elucidate precise molecular mechanisms linking GM to AD and determine whether GM dysbiosis is a contributing factor or consequence of AD pathology. Future studies should focus on large-scale clinical trials to validate GM-based interventions' efficacy and safety in AD.},
}

@article {pmid39800192,
year = {2025},
author = {Bajaj, JS and Fagan, A and Gavis, EA and Sterling, RK and Gallagher, ML and Lee, H and Matherly, SC and Siddiqui, MS and Bartels, A and Mousel, T and Davis, BC and Puri, P and Fuchs, M and Moutsoglou, DM and Thacker, LR and Sikaroodi, M and Gillevet, PM and Khoruts, A},
title = {Microbiota transplant for hepatic encephalopathy in cirrhosis: The THEMATIC trial.},
journal = {Journal of hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jhep.2024.12.047},
pmid = {39800192},
issn = {1600-0641},
abstract = {BACKGROUND: Preventing hepatic encephalopathy (HE) recurrence in cirrhosis, which is associated with an altered gut-liver-brain axis, is an unmet need. Fecal microbiota transplantation (FMT) is beneficial in phase-1 studies, but route and dose-related questions remain.

METHODS: We performed a phase-2 randomized, placebo-controlled, double-blind, clinical trial of capsule and enema FMT in cirrhosis and HE on lactulose and rifaximin. Subjects were randomized into 4 groups receiving 3 active and 0-placebo, 2 active and 1-placebo, 1 active and 2-placebo, or all 3-placebo doses. Each patient received two capsule and one enema FMT and were followed for six months.

PRIMARY OUTCOME: FMT-related serious adverse events/AEs using intention-to-treat analysis. Secondary outcomes were HE recurrence, all-cause hospitalizations, death, donor engraftment, and quality-of-life (QOL). FMT was from a vegan or omnivorous donor.

RESULTS: 60 patients (15/group) with similar baseline characteristics were enrolled.

PRIMARY OUTCOMES: FMT was safe without any FMT-related SAEs/ AEs.

SECONDARY OUTCOMES: Overall SAEs (p=0.96) or death (p=1.0) were similar. There were significant differences in HE recurrence between groups (p=0.035, Cramer's V=0.39). Post-hoc, recurrence was highest in all-placebo vs FMT [40% vs 9%, OR:0.15 (95% CI: 0.04, 0.64)]. Within FMT, HE-recurrence rates were similar regardless of route, doses, or donor type. QOL improved in FMT-recipient groups. Engraftment was highest in those with high pre-FMT Lachnospiraceae and lower in those whose HE recurred.

CONCLUSIONS: In a Phase 2 double-blind, placebo-controlled, randomized clinical trial in cirrhosis with HE on maximal therapy, FMT regardless of dose, route, or donor was safe without any FMT-related adverse events. On post-hoc analysis, groups differed on HE recurrence, which was highest in the placebo-only group and linked with lower baseline Lachnospiraceae and reduced donor engraftment.},
}

@article {pmid39798925,
year = {2025},
author = {Aleksandrova, RR and Nieuwenhuis, LM and Karmi, N and Zhang, S and Swarte, JC and Björk, JR and Gacesa, R and Blokzijl, H and Connelly, MA and Weersma, RK and Lisman, T and Festen, EAM and de Meijer, VE and , },
title = {Gut microbiome dysbiosis is not associated with portal vein thrombosis in patients with end-stage liver disease: a cross-sectional study.},
journal = {Journal of thrombosis and haemostasis : JTH},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jtha.2024.12.036},
pmid = {39798925},
issn = {1538-7836},
abstract = {BACKGROUND: Portal vein thrombosis (PVT) is a common complication in patients with end-stage liver disease (ESLD). The portal vein in ESLD patients is proposedly an inflammatory vascular bed due to translocation of endotoxins and cytokines from the gut. We hypothesized that a pro-inflammatory gut microbiome and elevated trimethylamine N-oxide (TMAO), a driver of thrombosis, may contribute to PVT development.

OBJECTIVES: We investigated whether gut microbiome diversity, bacterial species, metabolic pathways, and TMAO levels are associated with PVT in ESLD patients.

METHODS: Fecal samples, plasma samples and data from ESLD patients and healthy controls were collected through the TransplantLines Biobank and Cohort Study. PVT was defined as a thrombus in the portal vein within a year prior to or after fecal sample collection. Fecal samples were analyzed using Shotgun Metagenomic Sequencing, and TMAO levels were measured in plasma using a Vantera® Clinical Analyzer.

RESULTS: 102 ESLD patients, of which 23 with PVT, and 246 healthy controls were included. No significant difference in gut microbiome diversity was found between patients with PVT and without PVT (P=0.18). Both ESLD groups had significantly lower alpha-diversity compared with controls. Bacteroides fragilis and three Clostridiales species were increased in patients with PVT compared to without PVT. TMAO levels between the three groups were not significantly different.

CONCLUSION: We observed profound differences in gut microbiota between ESLD patients and controls, but minimal differences between ESLD patients with or without PVT. In our cohort, a gut-derived pro-inflammatory state was not associated with presence of PVT in ESLD patients.},
}

@article {pmid39797102,
year = {2024},
author = {Díez-Madueño, K and de la Cueva Dobao, P and Torres-Rojas, I and Fernández-Gosende, M and Hidalgo-Cantabrana, C and Coto-Segura, P},
title = {Gut Dysbiosis and Adult Atopic Dermatitis: A Systematic Review.},
journal = {Journal of clinical medicine},
volume = {14},
number = {1},
pages = {},
pmid = {39797102},
issn = {2077-0383},
abstract = {Background/Objectives: Research on the relationship between gut microbiota (GM) and atopic dermatitis (AD) has seen a growing interest in recent years. The aim of this systematic review was to determine whether differences exist between the GM of adults with AD and that of healthy adults (gut dysbiosis). Methods: We conducted a systematic review based on the PRISMA guidelines (Preferred Reporting Items for Systematic Reviews and Meta-Analyses). The search was performed using PubMed, EMBASE, and Web of Science. Observational and interventional studies were analyzed. Results: Although the studies showed heterogeneous results, some distinguishing characteristics were found in the intestinal microbial composition of adults with dermatitis. Even though no significant differences in diversity were found between healthy and affected adults, certain microorganisms, such as Bacteroidales, Enterobacteriaceae, and Clostridium (perfringens), were more characteristic of the fecal microbiota in adults with AD. Healthy individuals exhibited lower abundances of aerobic bacteria and higher abundances of short-chain fatty acid-producing species and polyamines. Clinical trials showed that the consumption of probiotics (Bifidobacterium and/or Lactobacillus), fecal microbiota transplants, and balneotherapy modified the fecal microbiota composition of participants and were associated with significant improvements in disease management. Conclusions: In anticipation of forthcoming clinical trials, it is essential to conduct meta-analyses that comprehensively evaluate the effectiveness and safety of interventions designed to modify intestinal flora in the context of AD. Preliminary evidence suggests that certain interventions may enhance adult AD management.},
}

@article {pmid39796717,
year = {2024},
author = {Kumari, S and Srilatha, M and Nagaraju, GP},
title = {Effect of Gut Dysbiosis on Onset of GI Cancers.},
journal = {Cancers},
volume = {17},
number = {1},
pages = {},
pmid = {39796717},
issn = {2072-6694},
abstract = {Dysbiosis in the gut microbiota plays a significant role in GI cancer development by influencing immune function and disrupting metabolic functions. Dysbiosis can drive carcinogenesis through pathways like immune dysregulation and the release of carcinogenic metabolites, and altered metabolism, genetic instability, and pro-inflammatory signalling, contributing to GI cancer initiation and progression. Helicobacter pylori infection and genotoxins released from dysbiosis, lifestyle and dietary habits are other factors that contribute to GI cancer development. Emerging diagnostic and therapeutic approaches show promise in colorectal cancer treatment, including the multitarget faecal immunochemical test (mtFIT), standard FIT, and faecal microbiota transplantation (FMT) combined with PD-1 inhibitors. We used search engine databases like PubMed, Scopus, and Web of Science. This review discusses the role of dysbiosis in GI cancer onset and explores strategies such as FMT, probiotics, and prebiotics to enhance the immune response and improve cancer therapy outcomes.},
}

@article {pmid39796536,
year = {2024},
author = {Cuffaro, F and Lamminpää, I and Niccolai, E and Amedei, A},
title = {Nutritional and Microbiota-Based Approaches in Amyotrophic Lateral Sclerosis: From Prevention to Treatment.},
journal = {Nutrients},
volume = {17},
number = {1},
pages = {},
pmid = {39796536},
issn = {2072-6643},
support = {PNRR-MAD-2022-12375798//Ministero della Salute/ ; PE0000006//Ministry of University and Research (MUR)/ ; },
mesh = {*Amyotrophic Lateral Sclerosis/therapy ; Humans ; *Gastrointestinal Microbiome ; *Dysbiosis/therapy ; Probiotics/therapeutic use ; Brain-Gut Axis/physiology ; Fecal Microbiota Transplantation ; Fatty Acids, Omega-3 ; Prebiotics/administration & dosage ; Oxidative Stress ; Nutritional Status ; Diet, Mediterranean ; Antioxidants ; },
abstract = {Metabolic alterations, including hypermetabolism, lipid imbalances, and glucose dysregulation, are pivotal contributors to the onset and progression of Amyotrophic Lateral Sclerosis (ALS). These changes exacerbate systemic energy deficits, heighten oxidative stress, and fuel neuroinflammation. Simultaneously, gastrointestinal dysfunction and gut microbiota (GM) dysbiosis intensify disease pathology by driving immune dysregulation, compromising the intestinal barrier, and altering gut-brain axis (GBA) signaling, and lastly advancing neurodegeneration. Therapeutic and preventive strategies focused on nutrition offer promising opportunities to address these interconnected pathophysiological mechanisms. Diets enriched with antioxidants, omega-3 fatty acids, and anti-inflammatory compounds-such as the Mediterranean diet-have shown potential in reducing oxidative stress and systemic inflammation. Additionally, microbiota-targeted approaches, including probiotics, prebiotics, postbiotics, and fecal microbiota transplantation, are emerging as innovative tools to restore microbial balance, strengthen gut integrity, and optimize GBA function. This review highlights the critical need for personalized strategies integrating immunonutrition and microbiota modulation to slow ALS progression, improve quality of life, and develop preventive measures for neurodegenerative and neuroinflammatory diseases. Future research should prioritize comprehensive dietary and microbiota-based interventions to uncover their therapeutic potential and establish evidence-based guidelines for managing ALS and related disorders.},
}

*Amyotrophic Lateral Sclerosis/therapy
Humans
*Gastrointestinal Microbiome
*Dysbiosis/therapy
Probiotics/therapeutic use
Brain-Gut Axis/physiology
Fecal Microbiota Transplantation
Fatty Acids, Omega-3
Prebiotics/administration & dosage
Oxidative Stress
Nutritional Status
Diet, Mediterranean
Antioxidants

@article {pmid39796390,
year = {2025},
author = {Yu, R and Zhang, H and Chen, R and Lin, Y and Xu, J and Fang, Z and Ru, Y and Fan, C and Wu, G},
title = {Fecal Microbiota Transplantation from Methionine-Restricted Diet Mouse Donors Improves Alzheimer's Learning and Memory Abilities Through Short-Chain Fatty Acids.},
journal = {Foods (Basel, Switzerland)},
volume = {14},
number = {1},
pages = {},
pmid = {39796390},
issn = {2304-8158},
support = {LQ22H260002//Natural Science Foundation of Zhejiang Province/ ; 82103836//National Natural Science Foundation of China/ ; },
abstract = {Alzheimer's disease (AD) is marked by impaired cognitive functions, particularly in learning and memory, owing to complex and diverse mechanisms. Methionine restriction (MR) has been found to exert a mitigating effect on brain oxidative stress to improve AD. However, the bidirectional crosstalk between the gut and brain through which MR enhances learning and memory in AD, as well as the effects of fecal microbiota transplantation (FMT) from MR mice on AD mice, remains underexplored. In this study, APP/PS1 double transgenic AD mice were used and an FMT experiment was conducted. 16S rRNA gene sequencing, targeted metabolomics, and microbial metabolite short-chain fatty acids (SCFAs) of feces samples were analyzed. The results showed that MR reversed the reduction in SCFAs induced by AD, and further activated the free fatty acid receptors, FFAR2 and FFAR3, as well as the transport protein MCT1, thereby signaling to the brain to mitigate inflammation and enhance the learning and memory capabilities. Furthermore, the FMT experiment from methionine-restricted diet mouse donors showed that mice receiving FMT ameliorated Alzheimer's learning and memory ability through SCFAs. This study offers novel non-pharmaceutical intervention strategies for AD prevention.},
}

@article {pmid39795549,
year = {2024},
author = {Tsuji, K and Uchida, N and Nakanoh, H and Fukushima, K and Haraguchi, S and Kitamura, S and Wada, J},
title = {The Gut-Kidney Axis in Chronic Kidney Diseases.},
journal = {Diagnostics (Basel, Switzerland)},
volume = {15},
number = {1},
pages = {},
pmid = {39795549},
issn = {2075-4418},
support = {24K11411//the Japanese Society for the Promotion of Science (JSPS)/Grant-in-Aid for Young Scientists/ ; },
abstract = {The gut-kidney axis represents the complex interactions between the gut microbiota and kidney, which significantly impact the progression of chronic kidney disease (CKD) and overall patient health. In CKD patients, imbalances in the gut microbiota promote the production of uremic toxins, such as indoxyl sulfate and p-cresyl sulfate, which impair renal function and contribute to systemic inflammation. Mechanisms like endotoxemia, immune activation and oxidative stress worsen renal damage by activating pro-inflammatory and oxidative pathways. Insights into these mechanisms highlight the impact of gut-derived metabolites, bacterial translocation, and immune response changes on kidney health, suggesting new potential approaches for CKD treatment. Clinical applications, such as dietary interventions, prebiotics, probiotics and fecal microbiota transplantation, are promising in adjusting the gut microbiota to alleviate CKD symptoms and slow disease progression. Current research highlights the clinical relevance of the gut-kidney axis, but further study is essential to clarify these mechanisms' diagnostic biomarkers and optimize therapeutic interventions. This review emphasizes the importance of an integrated approach to CKD management, focusing on the gut microbiota as a therapeutic target to limit kidney injury.},
}

@article {pmid39736240,
year = {2025},
author = {Qiu, M and Geng, H and Zou, C and Zhao, X and Zhao, C and Xie, J and Wang, J and Zhang, N and Hu, Y and Fu, Y and Wang, J and Hu, X},
title = {Intestinal inflammation exacerbates endometritis through succinate production by gut microbiota and SUCNR1-mediated proinflammatory response.},
journal = {International immunopharmacology},
volume = {146},
number = {},
pages = {113919},
doi = {10.1016/j.intimp.2024.113919},
pmid = {39736240},
issn = {1878-1705},
mesh = {Animals ; Female ; *Gastrointestinal Microbiome ; *Endometritis/microbiology/immunology/pathology/metabolism ; *Succinic Acid/metabolism ; Mice ; *Lipopolysaccharides/immunology ; *Mice, Inbred C57BL ; Dysbiosis/immunology ; Receptors, G-Protein-Coupled/metabolism/genetics ; Dextran Sulfate ; Uterus/pathology/immunology/microbiology/metabolism ; Inflammation/immunology ; Disease Models, Animal ; Intestines/immunology/microbiology/pathology ; Fecal Microbiota Transplantation ; Humans ; },
abstract = {Endometritis poses higher health risks to women. Clinical practice has found that gastrointestinal dysfunction is more likely to lead to the occurrence of endometritis. However, the mechanism is unclear. This study explored the influence and mechanism of DSS-induced intestinal inflammation on endometritis. Our findings demonstrate that DSS-induced intestinal inflammation can worsen LPS-induced endometritis in mice, and this effect is dependent on the gut microbiota, as depleting the gut microbiota eliminates this protective effect. Similarly, FMT from DSS-treated mice to recipient mice exacerbates LPS-induced endometritis. In addition, treatment of DSS disrupted an imbalance of succinate-producing and succinate-consuming bacteria and increased the levels of succinate in the gut and uterine tissues. Furthermore, treatment with succinate aggravates LPS-induced endometritis by activating the succinate receptor 1 (SUCNR1), evidenced by inhibition of the activation of SUCNR1 reversed the inflammatory response in uterine tissues induced by succinate during endometritis induced by LPS. Collectively, the results suggested that dysbiosis of the gut microbiota exacerbates LPS-induced endometritis by production and migration of succinate from gut to uterine tissues via the gut-uterus axis, then activates the SUCNR1. This identifies gut-derived succinate as a novel target for treating endometritis, and it indicates that targeting the gut microbiota and its metabolism could be a potential strategy for intervention in endometritis.},
}

Animals
Female
*Gastrointestinal Microbiome
*Endometritis/microbiology/immunology/pathology/metabolism
*Succinic Acid/metabolism
Mice
*Lipopolysaccharides/immunology
*Mice, Inbred C57BL
Dysbiosis/immunology
Receptors, G-Protein-Coupled/metabolism/genetics
Dextran Sulfate
Uterus/pathology/immunology/microbiology/metabolism
Inflammation/immunology
Disease Models, Animal
Intestines/immunology/microbiology/pathology
Fecal Microbiota Transplantation
Humans

@article {pmid39792405,
year = {2024},
author = {Guo, Z and He, M and Shao, L and Li, Y and Xiang, X and Wang, Q},
title = {The role of fecal microbiota transplantation in the treatment of acute graft-versus-host disease.},
journal = {Journal of cancer research and therapeutics},
volume = {20},
number = {7},
pages = {1964-1973},
doi = {10.4103/jcrt.jcrt_33_24},
pmid = {39792405},
issn = {1998-4138},
mesh = {Humans ; *Graft vs Host Disease/therapy/etiology/microbiology ; *Fecal Microbiota Transplantation/methods ; *Hematopoietic Stem Cell Transplantation/adverse effects/methods ; *Gastrointestinal Microbiome ; Transplantation, Homologous/methods ; Acute Disease ; Treatment Outcome ; },
abstract = {Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is one of the most important methods for treating a wide range of hematologic malignancies and bone marrow failure diseases. However, graft-versus-host disease (GVHD), a major complication associated with this method, can seriously affect the survival and quality of life of patients. Acute GVHD (aGVHD) occurs within 100 days after transplantation, and gastrointestinal aGVHD (GI-aGVHD) is one of the leading causes of nonrecurrent death after allo-HSCT. In recent years, fecal microbiota transplantation (FMT) has been attempted as an emerging treatment method for various diseases, including aGVHD after HSCT. Studies have shown encouraging preliminary clinical results after the application of FMT in aGVHD, particularly steroid-resistant aGVHD. Additionally, several studies have demonstrated that the gut microbiota plays an important immunomodulatory role in the pathogenesis of GVHD. Consensus guidelines recommend FMT as a secondary option for the treatment of aGVHD. This article aims to review FMT treatment for GI-aGVHD after allo-HSCT.},
}

Humans
*Graft vs Host Disease/therapy/etiology/microbiology
*Fecal Microbiota Transplantation/methods
*Hematopoietic Stem Cell Transplantation/adverse effects/methods
*Gastrointestinal Microbiome
Transplantation, Homologous/methods
Acute Disease
Treatment Outcome

@article {pmid39791180,
year = {2025},
author = {Shakya, R and Sivakumar, PM and Prabhakar, PK},
title = {Gut Microbiota and Diabetes: Pioneering New Treatment Frontiers.},
journal = {Endocrine, metabolic & immune disorders drug targets},
volume = {},
number = {},
pages = {},
doi = {10.2174/0118715303342579241119155225},
pmid = {39791180},
issn = {2212-3873},
abstract = {Diabetes Mellitus (DM) is a complex metabolic disorder characterized by chronic hyperglycemia and poses significant global health challenges. Conventional treatments, such as insulin therapy and lifestyle modifications, have shown limited efficacy in addressing the multifactorial nature of DM. Emerging evidence suggests that gut microbiota, a diverse community of microorganisms critical for metabolism and immune function, plays a pivotal role in metabolic health. Dysbiosis, an imbalance in gut microbiota composition, has been linked to insulin resistance, obesity, and DM. Gut microbiota influences glucose metabolism through mechanisms, including short-chain fatty acid production, gut permeability regulation, and immune system interactions, indicating a bidirectional relationship between microbial health and metabolism. Clinical and experimental studies demonstrate that modulating gut microbiota through dietary interventions (prebiotics, probiotics, synbiotics) improves glycemic control and insulin sensitivity in DM patients. Fecal Microbiota Transplantation (FMT) has also shown promise in restoring healthy gut microbiota and alleviating DM-related metabolic disturbances. However, challenges remain, including the need for personalized treatments due to individual microbiota variability and the unknown long-term effects of these interventions. Future research should focus on elucidating the mechanisms by which gut microbiota influences metabolism and refining personalized approaches to enhance DM management.},
}

@article {pmid39791141,
year = {2025},
author = {Li, X and Sun, B and Qin, Y and Yue, F and Lü, X},
title = {Amelioration of Obesity-Related Disorders in High-Fat Diet-Fed C57BL/6 Mice Following Fecal Microbiota Transplantation From DL-Norvaline-Dosed Mice.},
journal = {Molecular nutrition & food research},
volume = {},
number = {},
pages = {e202400577},
doi = {10.1002/mnfr.202400577},
pmid = {39791141},
issn = {1613-4133},
support = {2023-ZDLNY-35//Shaanxi Province Science and Technology Plan Project/ ; 2022A02006//Major Scientific and Technological Special Project of Xinjiang Uygur Autonomous Region/ ; },
abstract = {Fecal microbiota transplantation (FMT) could significantly alter the recipient's gut bacteria composition and attenuate obesity and obesity-related metabolic syndromes. DL-norvaline is a nonproteinogenic amino acid and possesses anti-obesity potential. However, the specific mechanisms by which gut microbiota might mediate beneficial effects of DL-norvaline have not been completely elucidated. In this study, DL-norvaline-mediated FMT upregulated the beneficial bacteria (Clostridia_UCG_014, Christensenellales, Bacilli, Ileibacterium, Dubosiella, Lactobacillus, Muribaculaceae, and Bacteroidaceae) and downregulated the harmful bacteria (Tuzzerella and Marinifilaceae), further intestinal inflammation, oxidative stress, and intestinal barrier were alleviated as well as short chain fatty acids levels were increased, thus alleviating glucose and insulin metabolism, improving biochemical indexes and energy metabolism and decreasing body weight gain and tissue weight. However, heat-inactivated FMT did not demonstrate any of those improvements in obese mice. Notably, both DL-norvaline-mediated FMT and heat-inactivated FMT increased Bacteroidaceae and Muribaculaceae, this being a signature of alterations to the gut microbiota marker caused by DL-norvaline. Therefore, the beneficial effects of DL-norvaline were transmissible via FMT. This study highlighted the pivotal involvement of the gut microbiota in the development of obesity and provided a novel insight into the underlying mechanisms of FMT, thereby potentially enhancing the efficacy and refinement of FMT utilization.},
}

@article {pmid39791120,
year = {2024},
author = {Huang, H and Yang, Y and Wang, X and Wen, B and Yang, X and Zhong, W and Wang, Q and He, F and Li, J},
title = {Gut virome dysbiosis impairs antitumor immunity and reduces 5-fluorouracil treatment efficacy for colorectal cancer.},
journal = {Frontiers in oncology},
volume = {14},
number = {},
pages = {1501981},
pmid = {39791120},
issn = {2234-943X},
abstract = {INTRODUCTION: Despite the established influence of gut bacteria, the role of the gut virome in modulating colorectal cancer (CRC) patient chemotherapy response remains poorly understood. In this study, we investigated the impact of antiviral (AV) drug-induced gut virome dysbiosis on the efficacy of 5-FU in CRC treatment.

METHODS: Using a subcutaneous CRC mouse model, we assessed tumor growth and immune responses following AV treatment, fecal microbiota transplantation (FMT), and 5-FU administration.

RESULTS: AV therapy reduced the abundance of gut DNA and RNA viruses, leading to accelerated tumor growth, shortened survival, and diminished chemotherapy efficacy. FMT restored the gut virome, improving tumor suppression and extending the survival of 5-FU-treated mice. Metagenomic sequencing revealed significant changes in virome composition, AV treatment expanded Kahnovirus, Petivirales, and Enterogokushovirus, whereas FMT enriched Peduovirus STYP1, Mahlunavirus rarus, and Jouyvirus ev207. AV treatment reduced the number of dendritic cells and CD8+ T cells in peripheral blood and tumor tissues, impairing antitumor immunity, FMT reversed these deficiencies. To further investigate the underlying mechanisms, we examined the TLR3-IRF3-IFN-β pathway, essential for recognizing viral RNA and triggering immune responses. AV treatment downregulated this pathway, impairing immune cell recruitment and reducing chemotherapy efficacy, while activation of TLR3 with Poly(I:C) restored pathway function and enhanced the effectiveness of 5-FU.

DISCUSSION: These findings suggest the importance of maintaining gut virome integrity or activating TLR3 as adjunct strategies to enhance chemotherapy outcomes in CRC patients.},
}

@article {pmid39791110,
year = {2025},
author = {Høyer, KL and Dahl Baunwall, SM and Kornum, DS and Klinge, MW and Drewes, AM and Yderstræde, KB and Thingholm, LB and Mortensen, MS and Mikkelsen, S and Erikstrup, C and Hvas, CL and Krogh, K},
title = {Faecal microbiota transplantation for patients with diabetes type 1 and severe gastrointestinal neuropathy (FADIGAS): a randomised, double-blinded, placebo-controlled trial.},
journal = {EClinicalMedicine},
volume = {79},
number = {},
pages = {103000},
pmid = {39791110},
issn = {2589-5370},
abstract = {BACKGROUND: Diabetic gastroenteropathy is associated with nausea, vomiting, bloating, pain, constipation, and diarrhoea. Current therapies are scarce. We tested faecal microbiota transplantation (FMT) for patients with type 1 diabetes and gastroenteropathy.

METHODS: In a randomised, double-blinded, placebo-controlled pilot trial, adults with type 1 diabetes and moderate-to-severe gastrointestinal symptoms were randomised (1:1) to encapsulated FMT or placebo. Each patient received around 25 capsules containing 50 g of faeces, administered in a single dose. The placebo capsules contained glycerol, saline and food colouring. All patients received FMT as a second intervention. The primary endpoint was number of adverse events of severity grade 2 or more assessed by the Common Terminology Criteria for Adverse Events during the week following the first intervention. Secondary endpoints included gastrointestinal symptoms and quality of life assessed four weeks after treatment. Public trial registration, ClinicalTrials.govNCT04749030.

FINDINGS: We randomised 20 patients to FMT or placebo. Following this intervention, 26 adverse events of grade 2 or more occurred. Four patients in the FMT group reported seven adverse events, and five patients in the placebo group reported 19, with no differences between the groups. The most frequent adverse events were diarrhoea, bloating, and abdominal pain. No serious adverse events were related to the treatment. Patients who received FMT reduced their median Gastrointestinal Symptom Rating Scale-Irritable Bowel Syndrome score from 58 (IQR 54-65) to 35 (32-48), whereas patients receiving placebo reduced their score from 64 (55-70) to 56 (50-77) (p = 0.01). The Irritable Bowel Syndrome Impact Scale score improved from 108 (101-123) to 140 (124-161) with FMT and 77 (53-129) to 92 (54-142) with placebo (p = 0.02). The Patient Assessment of Gastrointestinal Symptom Severity Index declined from a median of 42 (28-47) to 25 (14-31) after FMT and 47 (31-69) to 41 (36-64) after placebo (p = 0.03).

INTERPRETATION: FMT was safe and improved clinical outcomes for patients with type 1 diabetes suffering from bowel symptoms.

FUNDING: Steno Collaborative Grant.},
}

@article {pmid39788762,
year = {2025},
author = {Augustijn, QJJ and Grefhorst, A and de Groen, P and Wortelboer, K and Seegers, JFM and Gül, IS and Suenaert, P and Verheij, J and de Vos, WM and Herrema, H and Nieuwdorp, M and Holleboom, AG},
title = {Randomised double-blind placebo-controlled trial protocol to evaluate the therapeutic efficacy of lyophilised faecal microbiota capsules amended with next-generation beneficial bacteria in individuals with metabolic dysfunction-associated steatohepatitis.},
journal = {BMJ open},
volume = {15},
number = {1},
pages = {e088290},
doi = {10.1136/bmjopen-2024-088290},
pmid = {39788762},
issn = {2044-6055},
mesh = {Humans ; Double-Blind Method ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome ; Adult ; Male ; Randomized Controlled Trials as Topic ; Capsules ; Female ; Middle Aged ; Fatty Liver/therapy ; Feces/microbiology ; Freeze Drying ; },
abstract = {BACKGROUND: The spectrum of metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent, affecting 30% of the world's population, with a significant risk of hepatic and cardiometabolic complications. Different stages of MASLD are accompanied by distinct gut microbial profiles, and several microbial components have been implicated in MASLD pathophysiology. Indeed, earlier studies demonstrated that hepatic necroinflammation was reduced in individuals with MASLD after allogenic faecal microbiota transplantation (FMT) from healthy donors on a vegan diet. Here, we further investigate the therapeutic potential of gut microbiome modulation using a syntrophic combination of next-generation beneficial bacteria with FMT in individuals with advanced MASLD.

METHODS AND ANALYSIS: This trial is a randomised, double-blind, placebo-controlled study investigating the therapeutic potential of lyophilised faecal microbiota capsules (LFMCs) in individuals with metabolic dysfunction-associated steatohepatitis. In this study, 48 participants will be randomised 1:1 to receive either healthy vegan donor LFMCs or placebo for 24 weeks. In addition, all participants will be supplemented with a set of next-generation beneficial bacteria, including Anaerobutyricum soehngenii, pasteurised Akkermansia muciniphila and Bifidobacterium animalis subsp. lactis, as well as fructo-oligosaccharides. A liver biopsy will be performed at baseline and at the end of the trial. In addition, participants will be assessed through MRI, FibroScan, blood tests, faecal samples and continuous glucose monitoring. The first participant was enrolled on 25 April 2023.

ETHICS AND DISSEMINATION: Ethical approval was obtained from the Medical Ethics Committee of the University Medical Centre of Amsterdam. The results of this study will be disseminated through peer-reviewed journals.

TRIAL REGISTRATION NUMBER: The trial is registered on clinicaltrials.gov (NCT05821010).},
}

Humans
Double-Blind Method
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome
Adult
Male
Randomized Controlled Trials as Topic
Capsules
Female
Middle Aged
Fatty Liver/therapy
Feces/microbiology
Freeze Drying

@article {pmid39788096,
year = {2025},
author = {Wang, W and Pi, Z and Yu, Y and Zhang, F},
title = {The butterfly effect of the strain richness influences the efficacy of microbiota transplantation.},
journal = {Cell host & microbe},
volume = {33},
number = {1},
pages = {3-5},
doi = {10.1016/j.chom.2024.12.010},
pmid = {39788096},
issn = {1934-6069},
mesh = {*Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; Humans ; Animals ; Feces/microbiology ; Bacteria/classification ; },
abstract = {Strain-level variation in the gut microbiome modulates its impact on host health. Recently in Nature, Chen-Liaw et al. propose that strain richness is a crucial element in the gut ecosystem, thus influencing efficacy of fecal microbiota transplantation, and provide a theoretical foundation for optimizing microbiota-based treatments and developing microbiota medicine.},
}

*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
Humans
Animals
Feces/microbiology
Bacteria/classification

@article {pmid39787138,
year = {2025},
author = {Luo, Y and Zhou, S and Zhang, X and Lin, Y and Liu, J and Cheng, W and Zeng, Y},
title = {The role of the microbiota and metabolites in the treatment of pulmonary fibrosis with UC-MSCs: Integrating fecal metabolomics and 16S rDNA analysis.},
journal = {PloS one},
volume = {20},
number = {1},
pages = {e0313989},
pmid = {39787138},
issn = {1932-6203},
mesh = {Animals ; Mice ; *Pulmonary Fibrosis/therapy/metabolism/pathology/microbiology ; *Metabolomics/methods ; *Feces/microbiology ; *RNA, Ribosomal, 16S/genetics ; Mesenchymal Stem Cell Transplantation/methods ; Mesenchymal Stem Cells/metabolism ; Gastrointestinal Microbiome ; Male ; DNA, Ribosomal/genetics ; Mice, Inbred C57BL ; Disease Models, Animal ; Lung/pathology/metabolism/microbiology ; Bleomycin ; Microbiota ; Cytokines/metabolism ; },
abstract = {INTRODUCTION: Pulmonary fibrosis (PF) is a chronic and irreversible interstitial lung disease characterized by a lack of effective therapies. Mesenchymal stem cells (MSCs) have garnered significant interest in the realm of lung regeneration due to their abundant availability, ease of isolation, and capacity for expansion. The objective of our study was to investigate the potential therapeutic role of umbilical cord-derived MSCs (UC-MSCs) in the management of PF, with a focus on the alterations in the gut microbiota and its metabolites during the use of UC-MSCs for the treatment of pulmonary fibrosis, as well as the possible mechanisms involved.

METHODS: Bleomycin injection was utilized to establish a mouse model of lung fibrosis, followed by the application of 16S rDNA sequencing and LC-MS/MS metabolomics to explore the underlying mechanism of UC-MSC treatment for lung fibrosis. Seventy-five mice were allocated into five groups, namely Control, Model, and low/medium/high dose of UC-MSCs groups, and survival metrics, lung morphology, and the levels of the inflammatory cytokines TNF-α, IL-1β, IL-6, and TGF-β1 were subsequently evaluated. Fecal samples from six mice in each of the Control group, Model group, and UC-MSCs-M groups were collected randomly for 16S rDNA sequencing to analyze the gut microbiota and nontargeted metabolomics.

RESULTS: In comparison to IPF model mice, the three treatment groups exhibited increased survival rates, restored alveolar morphology, and reduced levels of the inflammatory cytokines TNF-α, IL-1β, IL-6, and TGF-β1, confirming the anti-inflammatory properties of UC-MSCs in IPF treatment. The findings from the 16S rDNA assay indicate that UC-MSCs treatment effectively lower α-diversity induced such as Chao 1 and ACE, as well as β-diversity, leading to a decrease in microbiota abundance. The findings from the metabolomics analysis revealed that the metabolites exhibiting notable variances were primarily composed of Lipids and lipid-like molecules, Organoheterocyclic compounds, Organic acids and derivatives, and Benzenoids, indicating the potential of UC-MSCs to exert antifibrotic effects via these metabolic pathways.

CONCLUSION: Umbilical cord-derived mesenchymal stem cells (UC-MSCs) ameliorate bleomycin-induced pulmonary fibrosis symptoms in mice by exerting anti-inflammatory effects and mitigating pulmonary fibrosis through the modulation of gut microbiota disorders and their metabolism. These findings offer novel insights into the potential mechanisms and clinical utility of stem cell therapy for pulmonary fibrosis.},
}

Animals
Mice
*Pulmonary Fibrosis/therapy/metabolism/pathology/microbiology
*Metabolomics/methods
*Feces/microbiology
*RNA, Ribosomal, 16S/genetics
Mesenchymal Stem Cell Transplantation/methods
Mesenchymal Stem Cells/metabolism
Gastrointestinal Microbiome
Male
DNA, Ribosomal/genetics
Mice, Inbred C57BL
Disease Models, Animal
Lung/pathology/metabolism/microbiology
Bleomycin
Microbiota
Cytokines/metabolism

@article {pmid39786379,
year = {2024},
author = {Yang, Q and Zhu, Y and Jian, X and Qiu, Y and Zhu, Y and Zhao, L and He, Y and An, G and Qiu, L and Guo, J and He, N and Abudumijiti, H and Hu, C and Chen, X and Huang, S and Feng, X and Li, X and Liu, J and Xu, Y and Zhou, W},
title = {Targeting Enterobacter cloacae attenuates osteolysis by reducing ammonium in multiple myeloma.},
journal = {Blood},
volume = {},
number = {},
pages = {},
doi = {10.1182/blood.2024025694},
pmid = {39786379},
issn = {1528-0020},
abstract = {Multiple myeloma (MM)-induced bone disease affects not only patients' quality of life but also their overall survival. Our previous work demonstrated that the gut microbiome plays a crucial role in MM progression and drug resistance. However, the role of altered gut microbiota in MM bone disease remains unclear. In this study, we show that intestinal E. cloacae is significantly enriched in MM patients with osteolysis. Through fecal microbial transplantation and single bacterial colonization experiments in a 5TGM1 MM mouse model, we found that intestinal colonization of E. cloacae promotes osteolysis by increasing circulating ammonium levels. Elevated ammonium promotes osteoclastogenesis by increasing Trap protein levels in osteoclast precursors and by acetylating and stabilizing CCL3 protein in MM cells. Inhibition of ammonium synthesis, using E. cloacae with a deleted dcd gene, along with probiotic supplementation, alleviated osteolysis in MM. Overall, our work suggests that E. cloacae promotes osteolysis in MM by synthesizing ammonium. This establishes a novel mechanism and potential intervention strategy for managing MM with osteolysis.},
}

@article {pmid39780269,
year = {2025},
author = {Li, X and Ding, Q and Wan, X and Wu, Q and Ye, S and Lou, Y},
title = {Fecal microbiota transplantation attenuates Alzheimer's disease symptoms in APP/PS1 transgenic mice via inhibition of the TLR4-MyD88-NF-κB signaling pathway-mediated inflammation.},
journal = {Behavioral and brain functions : BBF},
volume = {21},
number = {1},
pages = {2},
pmid = {39780269},
issn = {1744-9081},
support = {Grant No. Y20220029//Health Project of the Science and Technology Department of Wenzhou/ ; 231104408302408//Industry-university Cooperative education program of Ministry of Education/ ; First Class, Category A//the Key Discipline of Zhejiang Province in Medical Technology/ ; },
mesh = {Animals ; *Fecal Microbiota Transplantation/methods ; *Myeloid Differentiation Factor 88/metabolism ; Mice ; *Alzheimer Disease/therapy/microbiology ; *Mice, Transgenic ; *Toll-Like Receptor 4/metabolism ; *NF-kappa B/metabolism ; *Signal Transduction/physiology ; *Presenilin-1/genetics ; Amyloid beta-Protein Precursor/genetics ; Gastrointestinal Microbiome/physiology ; Inflammation/therapy/metabolism ; Male ; Disease Models, Animal ; Mice, Inbred C57BL ; },
abstract = {Alzheimer's disease (AD) is a prevalent and progressive neurodegenerative disorder that is the leading cause of dementia. The underlying mechanisms of AD have not yet been completely explored. Neuroinflammation, an inflammatory response mediated by certain mediators, has been exhibited to play a crucial role in the pathogenesis of AD. Additionally, disruption of the gut microbiota has been found to be associated with AD, and fecal microbiota transplantation (FMT) has emerged as a potential therapeutic approach. However, the precise mechanism of FMT in the treatment of AD remains elusive. In this study, FMT was performed by transplanting fecal microbiota from healthy wild-type mice into APP/PS1 mice (APPswe, PSEN1dE9) to assess the effectiveness of FMT in mitigating AD-associated inflammation and to reveal its precise mechanism of action. The results demonstrated that FMT treatment improved cognitive function and reduced the expression levels of inflammatory factors by regulating the TLR4/MyD88/NF-κB signaling pathway in mice, which was accompanied by the restoration of gut microbial dysbiosis. These findings suggest that FMT has the potential to ameliorate AD symptoms and delay the disease progression in APP/PS1 mice.},
}

Animals
*Fecal Microbiota Transplantation/methods
*Myeloid Differentiation Factor 88/metabolism
Mice
*Alzheimer Disease/therapy/microbiology
*Mice, Transgenic
*Toll-Like Receptor 4/metabolism
*NF-kappa B/metabolism
*Signal Transduction/physiology
*Presenilin-1/genetics
Amyloid beta-Protein Precursor/genetics
Gastrointestinal Microbiome/physiology
Inflammation/therapy/metabolism
Male
Disease Models, Animal
Mice, Inbred C57BL

@article {pmid39779925,
year = {2025},
author = {He, X and Hu, M and Xu, Y and Xia, F and Tan, Y and Wang, Y and Xiang, H and Wu, H and Ji, T and Xu, Q and Wang, L and Huang, Z and Sun, M and Wan, Y and Cui, P and Liang, S and Pan, Y and Xiao, S and He, Y and Song, R and Yan, J and Quan, X and Wei, Y and Hong, C and Liao, W and Li, F and El-Omar, E and Chen, J and Qi, X and Gao, J and Zhou, H},
title = {The gut-brain axis underlying hepatic encephalopathy in liver cirrhosis.},
journal = {Nature medicine},
volume = {},
number = {},
pages = {},
pmid = {39779925},
issn = {1546-170X},
support = {82372305//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {Up to 50-70% of patients with liver cirrhosis develop hepatic encephalopathy (HE), which is closely related to gut microbiota dysbiosis, with an unclear mechanism. Here, by constructing gut-brain modules to assess bacterial neurotoxins from metagenomic datasets, we found that phenylalanine decarboxylase (PDC) genes, mainly from Ruminococcus gnavus, increased approximately tenfold in patients with cirrhosis and higher in patients with HE. Cirrhotic, not healthy, mice colonized with R. gnavus showed brain phenylethylamine (PEA) accumulation, along with memory impairment, symmetrical tremors and cortex-specific neuron loss, typically found in patients with HE. This accumulation of PEA was primarily driven by decreased monoamine oxidase-B activity in both the liver and serum due to cirrhosis. Targeting PDC or PEA reversed the neurological symptoms induced by R. gnavus. Furthermore, fecal microbiota transplantation from patients with HE to germ-free cirrhotic mice replicated these symptoms and further corroborated the efficacy of targeting PDC or PEA. Clinically, high baseline PEA levels were linked to a sevenfold increased risk of HE after intrahepatic portosystemic shunt procedures. Our findings expand the understanding of the gut-liver-brain axis and identify a promising therapeutic and predictive target for HE.},
}

@article {pmid39779878,
year = {2025},
author = {Keskey, RC and Xiao, J and Hyoju, S and Lam, A and Kim, D and Sidebottom, AM and Zaborin, A and Dijkstra, A and Meltzer, R and Thakur, A and Zhang, K and Chen, HJ and Beloborodova, NV and Pautova, AK and Wolfe, K and Patel, B and Thewissen, R and Zaborina, O and Alverdy, JC},
title = {Enterobactin inhibits microbiota-dependent activation of AhR to promote bacterial sepsis in mice.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {39779878},
issn = {2058-5276},
support = {R01GMO62344-22//U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS)/ ; },
abstract = {Sepsis is a major cause of morbidity and mortality, but our understanding of the mechanisms underlying survival or susceptibility is limited. Here, as pathogens often subvert host defence mechanisms, we hypothesized that this might influence the outcome of sepsis. We used microbiota analysis, faecal microbiota transplantation, antibiotic treatment and caecal metabolite analysis to show that gut-microbiota-derived tryptophan metabolites including indoles increased host survival in a mouse model of Serratia marcescens sepsis. Infection in macrophage-specific aryl hydrocarbon receptor (AhR) knockout mice revealed that AhR activation induced transcriptional reprogramming in macrophages and increased bacterial clearance and host survival. However, culture supernatants from multiple bacterial pathogens inhibited AhR activation in vitro. We showed that the secreted siderophore, enterobactin, inhibited AhR activation in vitro and increased sepsis mortality in vivo. By contrast, oral or systemic tryptophan supplementation increased survival. These findings show that sepsis survival depends upon the interplay between pathogen inhibition and the activation of AhR by a microbiota-derived metabolite.},
}

@article {pmid39779854,
year = {2025},
author = {Won, TH and Arifuzzaman, M and Parkhurst, CN and Miranda, IC and Zhang, B and Hu, E and Kashyap, S and Letourneau, J and Jin, WB and Fu, Y and Guzior, DV and , and Quinn, RA and Guo, CJ and David, LA and Artis, D and Schroeder, FC},
title = {Host metabolism balances microbial regulation of bile acid signalling.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {39779854},
issn = {1476-4687},
abstract = {Metabolites derived from the intestinal microbiota, including bile acids (BA), extensively modulate vertebrate physiology, including development[1], metabolism[2-4], immune responses[5-7] and cognitive function[8]. However, to what extent host responses balance the physiological effects of microbiota-derived metabolites remains unclear[9,10]. Here, using untargeted metabolomics of mouse tissues, we identified a family of BA-methylcysteamine (BA-MCY) conjugates that are abundant in the intestine and dependent on vanin 1 (VNN1), a pantetheinase highly expressed in intestinal tissues. This host-dependent MCY conjugation inverts BA function in the hepatobiliary system. Whereas microbiota-derived free BAs function as agonists of the farnesoid X receptor (FXR) and negatively regulate BA production, BA-MCYs act as potent antagonists of FXR and promote expression of BA biosynthesis genes in vivo. Supplementation with stable-isotope-labelled BA-MCY increased BA production in an FXR-dependent manner, and BA-MCY supplementation in a mouse model of hypercholesteraemia decreased lipid accumulation in the liver, consistent with BA-MCYs acting as intestinal FXR antagonists. The levels of BA-MCY were reduced in microbiota-deficient mice and restored by transplantation of human faecal microbiota. Dietary intervention with inulin fibre further increased levels of both free BAs and BA-MCY levels, indicating that BA-MCY production by the host is regulated by levels of microbiota-derived free BAs. We further show that diverse BA-MCYs are also present in human serum. Together, our results indicate that BA-MCY conjugation by the host balances host-dependent and microbiota-dependent metabolic pathways that regulate FXR-dependent physiology.},
}

@article {pmid39779737,
year = {2025},
author = {Corcione, S and Ferrocino, I and Lupia, T and Busca, A and Bianco, G and Dellacasa, C and Giaccone, L and Brunello, L and Butera, S and Costa, C and Bruno, B and De Rosa, FG},
title = {Influence of ESBL colonization status on gut microbiota composition during allogenic hematopoietic stem cell transplantation.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {1275},
pmid = {39779737},
issn = {2045-2322},
support = {Project no. PE00000007, INF-ACT//EU funding within the MUR PNRR Extended Partnership initiative on Emerging Infectious Diseases/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; *Hematopoietic Stem Cell Transplantation/adverse effects ; Male ; Female ; Middle Aged ; Adult ; Prospective Studies ; Pilot Projects ; *beta-Lactamases/metabolism ; *Transplantation, Homologous/adverse effects ; Aged ; Feces/microbiology ; Italy ; Anti-Bacterial Agents/therapeutic use/pharmacology ; },
abstract = {After allogeneic HSCT (allo-HSCT), the diversity of the intestinal microbiota significantly decreases. The changes can be rapid and are thought to be caused by chemotherapy, antibiotics, or intestinal inflammation. Most patients are exposed to prophylactic and therapeutic antibiotics during neutropenia and several patients are colonized by ESBL bacteria. We investigated the changes in gut microbiota composition in allo-HSCT, aiming at investigating if the acquisition of ESBL colonization may affect gut microbiome diversity during allo-HSCT. This was a single-center prospective pilot study. All patients consecutively admitted to the Haematological Unit of the City of Health and Science, Molinette Hospital in Turin, Italy, and undergoing allo-HSCT between August 2017 to August 2020 were enrolled in the study. Microbiome analysis on fecal samples were collected every 7 days from hospital admission to discharge and until 1 year after HSCT. 48 patients were enrolled in the study. At baseline 14 patients (29.16%) were colonized by MDR bacteria, mostly extended-spectrum beta-lactamase (ESBL)-producing gram negatives (N = 11; 78.57%). During allo-HSCT, one patient had a positive rectal swab for a carbapenemase-producing Klebsiella pneumoniae and eight patients lost the colonization during the hospital stay. Microbiota composition was compared between patients colonized by ESBL at baseline and non-colonized patients. Patients colonized by ESBL had a greater abundances of Bifidobacterium, Blautia, Clostridium, Coprococcus, L-Ruminococcus Mogibacteriaceae, Peptostreptococceae and Oscillospira, while non-colonized ESBL patients had a greater abundance of Actinomycetales, Staphylococcus and Sutterella. Moreover, microbiota composition of colonized by ESBL that retained colonization after HSCT showed an increased in abundances of Akkermansia, Dialister, Erysipelotrichaceae and Methanobrevibacter when compared with patients that become negative at rectal swabs. From a clinical perspective, the evolution of this prospective pilot study will be to investigate markers of gut barrier functions, SCFA productions and to correlate the predictivity of these parameters with risk of invasive infections and clinical outcomes in allo-HSCT population.},
}

Humans
*Gastrointestinal Microbiome/drug effects
*Hematopoietic Stem Cell Transplantation/adverse effects
Male
Female
Middle Aged
Adult
Prospective Studies
Pilot Projects
*beta-Lactamases/metabolism
*Transplantation, Homologous/adverse effects
Aged
Feces/microbiology
Italy
Anti-Bacterial Agents/therapeutic use/pharmacology

@article {pmid39778887,
year = {2025},
author = {Pérez-Accino, J and Salavati, M and Glendinning, L and Salavati Schmitz, S},
title = {Effect of a single rectal fecal microbiota transplantation on clinical severity and fecal microbial communities in dogs with chronic inflammatory enteropathy.},
journal = {Journal of veterinary internal medicine},
volume = {39},
number = {1},
pages = {e17264},
pmid = {39778887},
issn = {1939-1676},
support = {//Fiona and Ian Russel Fund/ ; },
mesh = {Animals ; Dogs ; *Dog Diseases/therapy/microbiology ; *Fecal Microbiota Transplantation/veterinary ; *Feces/microbiology ; Male ; Female ; Inflammatory Bowel Diseases/veterinary/therapy/microbiology ; RNA, Ribosomal, 16S/genetics ; Gastrointestinal Microbiome ; Chronic Disease ; },
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) has been advocated as a treatment for chronic enteropathy (CE) in dogs. However, so far only short-term clinical effects have been reported whereas the effect on the microbiota remains unexplored.

HYPOTHESIS/OBJECTIVES: Assess if a single FMT enema can lead to clinical improvement in dogs with CE when accompanied by presumed favorable microbiota changes. The effect of glycerol as a cryopreservative when storing FMT preparations also was assessed.

ANIMALS: Seven dogs with CE that received FMTs from 2 healthy donor dogs.

MATERIALS AND METHODS: Six dogs received a single FMT, 1 dog received 3 consecutive FMTs. Canine chronic enteropathy clinical activity index (CCECAI) and fecal samples were obtained before (Day 0), and 7, 30 and 90 days after FMT. Samples were stored with and without 10% glycerol. Sequencing of microbiota (16S rRNA, Illumina) was performed and compared by accepted analysis pipelines.

RESULTS: Median CCECAI before FMT was 8 (range, 5-14), decreased to a median of 3 (range, 1-12) within 1 week and a median of 1 (range, 0-12) by Day 30 (P < .01), with an average duration of response of approximately 10 weeks. Significant variation in the donors' microbiota composition was observed across different donations. Recipient microbiota composition or diversity did not change over time. Glycerol addition was associated with a difference in microbiota composition (P ≤ .001).

A single FMT can be considered an appropriate treatment in dogs with CE, but consistent microbiota changes were not observed.},
}

Animals
Dogs
*Dog Diseases/therapy/microbiology
*Fecal Microbiota Transplantation/veterinary
*Feces/microbiology
Male
Female
Inflammatory Bowel Diseases/veterinary/therapy/microbiology
RNA, Ribosomal, 16S/genetics
Gastrointestinal Microbiome
Chronic Disease

@article {pmid39778639,
year = {2025},
author = {Chen, C and Wang, J and Cheng, M and Xie, H and Li, W and Zhang, C},
title = {Muribaculum intestinale-derived 3-hydroxybutyric acid from Heterophyllin B attenuated pulmonary fibrosis through IDO1-mediated ferroptosis.},
journal = {Pharmacological research},
volume = {212},
number = {},
pages = {107587},
doi = {10.1016/j.phrs.2025.107587},
pmid = {39778639},
issn = {1096-1186},
abstract = {Pulmonary fibrosis (PF) is a fatal disease with increasing incidence, poor prognosis, and unclear pathogenesis. Our previous research demonstrated the beneficial effects of the natural cyclopeptide Heterophyllin B (HB) in PF. However, the precise mechanism by which HB exerts its effects in PF remains unclear. Our study revealed HB's beneficial effects in alleviating PF symptoms and restoring the intestinal mucosal barrier. Subsequently, the microbiota-dependent antifibrotic efficacy of HB was verified using various delivery routes, antibiotic treatments, and faecal microbiota transplantation. Functionally, 16S rRNA sequencing, untargeted metabolomics, and co-incubation experiments revealed that the antifibrotic efficacy of HB was primarily contingent on the enrichment of Muribaculum intestinale and its metabolite, 3-hydroxybutyric acid. Mechanistically, indoleamine 2,3- dioxygenase 1 (IDO1)-mediated ferroptosis was identified as a pivotal process in initiating PF, and the anti-fibrotic efficacy of HB relies on suppressing IDO1-mediated ferroptosis. Conversely, IDO1 deficiency alleviated the symptoms of bleomycin-induced PF and ferroptosis in mice. Coincidentally, both IDO1 overexpression and ferroptosis were observed in the pulmonary tissue of patients with idiopathic PF. Collectively, this study revealed that HB alleviates PF by eliminating intestinal microecology and metabolism and highlights the feasibility of targeting IDO1 for PF treatment.},
}

@article {pmid39777251,
year = {2025},
author = {Quaglio, AE and Magro, DO and Imbrizi, M and De Oliveira, EC and Di Stasi, LC and Sassaki, LY},
title = {Creeping fat and gut microbiota in Crohn's disease.},
journal = {World journal of gastroenterology},
volume = {31},
number = {1},
pages = {102042},
pmid = {39777251},
issn = {2219-2840},
mesh = {*Crohn Disease/microbiology/immunology/therapy ; Humans ; *Gastrointestinal Microbiome/physiology/immunology ; *Dysbiosis/immunology ; *Fecal Microbiota Transplantation ; *Intra-Abdominal Fat/immunology ; *Probiotics/therapeutic use ; *Disease Progression ; Prebiotics/administration & dosage ; Fibrosis ; Animals ; Mesentery ; },
abstract = {In this article, we explored the role of adipose tissue, especially mesenteric adipose tissue and creeping fat, and its association with the gut microbiota in the pathophysiology and progression of Crohn's disease (CD). CD is a form of inflammatory bowel disease characterized by chronic inflammation of the gastrointestinal tract, influenced by genetic predisposition, gut microbiota dysbiosis, and environmental factors. Gut microbiota plays a crucial role in modulating immune response and intestinal inflammation and is associated with the onset and progression of CD. Further, visceral adipose tissue, particularly creeping fat, a mesenteric adipose tissue characterized by hypertrophy and fibrosis, has been implicated in CD pathogenesis, inflammation, and fibrosis. The bacteria from the gut microbiota may translocate into mesenteric adipose tissue, contributing to the formation of creeping fat and influencing CD progression. Although creeping fat may be a protective barrier against bacterial invasion, its expansion can damage adjacent tissues, leading to complications. Modulating gut microbiota through interventions such as fecal microbiota transplantation, probiotics, and prebiotics has shown potential in managing CD. However, more research is needed to clarify the mechanisms linking gut dysbiosis, creeping fat, and CD progression and develop targeted therapies for microbiota modulation and fat-related complications in patients with CD.},
}

*Crohn Disease/microbiology/immunology/therapy
Humans
*Gastrointestinal Microbiome/physiology/immunology
*Dysbiosis/immunology
*Fecal Microbiota Transplantation
*Intra-Abdominal Fat/immunology
*Probiotics/therapeutic use
*Disease Progression
Prebiotics/administration & dosage
Fibrosis
Animals
Mesentery

@article {pmid39777148,
year = {2024},
author = {An, Y and He, L and Xu, X and Piao, M and Wang, B and Liu, T and Cao, H},
title = {Gut microbiota in post-acute COVID-19 syndrome: not the end of the story.},
journal = {Frontiers in microbiology},
volume = {15},
number = {},
pages = {1500890},
pmid = {39777148},
issn = {1664-302X},
abstract = {The coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has led to major global health concern. However, the focus on immediate effects was assumed as the tip of iceberg due to the symptoms following acute infection, which was defined as post-acute COVID-19 syndrome (PACS). Gut microbiota alterations even after disease resolution and the gastrointestinal symptoms are the key features of PACS. Gut microbiota and derived metabolites disorders may play a crucial role in inflammatory and immune response after SARS-CoV-2 infection through the gut-lung axis. Diet is one of the modifiable factors closely related to gut microbiota and COVID-19. In this review, we described the reciprocal crosstalk between gut and lung, highlighting the participation of diet and gut microbiota in and after COVID-19 by destroying the gut barrier, perturbing the metabolism and regulating the immune system. Therefore, bolstering beneficial species by dietary supplements, probiotics or prebiotics and fecal microbiota transplantation (FMT) may be a novel avenue for COVID-19 and PACS prevention. This review provides a better understanding of the association between gut microbiota and the long-term consequences of COVID-19, which indicates modulating gut dysbiosis may be a potentiality for addressing this multifaceted condition.},
}

@article {pmid39776845,
year = {2024},
author = {Zhuang, L and You, Y and Zeng, S and Yu, Z and Wang, H and Chen, M and Wen, W},
title = {Fecal microbiota transplantation in severe pneumonia: a case report on overcoming pan-drug resistant Klebsiella pneumoniae infection.},
journal = {Frontiers in medicine},
volume = {11},
number = {},
pages = {1451751},
pmid = {39776845},
issn = {2296-858X},
abstract = {OBJECTIVE: To evaluate the therapeutic potential of fecal microbiota transplantation (FMT) in treating severe pneumonia patients with concurrent pan-drug resistant Klebsiella pneumoniae infection.

METHODS: A case report of a 95-year-old female patient with severe pneumonia, complicated by pan-resistant bacterial infections, is presented. The patient was diagnosed with severe pneumonia caused by COVID-19, along with co-infections of Staphylococcus hominis, Enterococcus faecalis, Candida tropicalis, Pseudomonas aeruginosa, ESBL-producing pan-drug resistant Klebsiella pneumoniae and pan-resistant Acinetobacter baumannii. During hospitalization, the patient underwent comprehensive treatments, including antimicrobials, mechanical ventilation, and fiberoptic bronchoscopic alveolar lavage. FMT was administered following the failure of conventional treatments to resolve recurrent diarrhea, increased sputum production, and persistent pan-drug resistant Klebsiella pneumoniae infection.

RESULTS: Post-FMT, the patient exhibited significant clinical improvement, including reduced sputum production, cessation of diarrhea, and the normalization of respiratory symptoms. Gut microbiota analysis revealed that FMT enhanced the abundance of beneficial microbiota and suppressed Klebsiella pneumoniae, and the patient was successfully discharged after 133 days of hospitalization.

CONCLUSION: FMT emerged as a pivotal intervention in the management of this severe pneumonia case, suggesting its efficacy in restoring gut microbiota balance and aiding recovery from multi-drug-resistant infections. This case underscores the potential of FMT as a therapeutic option in severe pulmonary infections, especially in the context of antibiotic resistance in severe pneumonia patients.},
}

@article {pmid39776440,
year = {2024},
author = {Fang, L and Ning, J},
title = {Recent advances in gut microbiota and thyroid disease: pathogenesis and therapeutics in autoimmune, neoplastic, and nodular conditions.},
journal = {Frontiers in cellular and infection microbiology},
volume = {14},
number = {},
pages = {1465928},
pmid = {39776440},
issn = {2235-2988},
mesh = {*Gastrointestinal Microbiome ; Humans ; *Probiotics/therapeutic use ; *Thyroid Diseases/therapy/microbiology ; *Fecal Microbiota Transplantation ; Animals ; Bacteria/classification/metabolism ; Neoplasms/therapy/microbiology ; Dysbiosis/therapy/microbiology ; },
abstract = {This review synthesizes key findings from the past five years of experimental literature, elucidating the gut microbiome's significant influence on the pathogenesis of thyroid diseases. A pronounced shift in the gut microbiota composition has been consistently observed, with a significant reduction in bacteria such as Bifidobacterium, Bacillaceae, Megamonas, and Clostridium, and a notable increase in bacteria, including Bacteroides, Proteobacteria, Actinobacteria, Desulfobacterota, and Klebsiella. These alterations are implicated in the development and progression of thyroid diseases by impacting metabolic pathways including bile acid and cytokine production, including a decrease in short-chain fatty acids (SCFAs) that are crucial for immune regulation and thyroid hormone homeostasis. The review also highlights the therapeutic implications of probiotics in managing thyroid conditions. Evidence suggests that probiotic adjunct therapy can modulate the gut microbiota, leading to improvements in thyroid function and patient outcomes. The use of specific probiotic strains, such as Lactiplantibacillus plantarum 299v and Bifidobacterium longum, has demonstrated potential in enhancing the effects of traditional treatments and possibly restoring a balanced gut microbiota. Notably, fecal microbiota transplantation (FMT) has emerged as a promising intervention in Graves' Disease (GD), demonstrating the potential to recalibrate the gut microbiota, thereby influencing neurotransmitters and trace elements via the gut-brain and gut-thyroid axes. The integration of microbiome-based therapies with traditional treatments is anticipated to usher in a new era of personalized thyroid disease management, offering a more nuanced approach to patient care. By integrating this body of work, the review offers an innovative perspective on the gut microbiome's broad impact on thyroid diseases and the therapeutic applications of probiotics.},
}

*Gastrointestinal Microbiome
Humans
*Probiotics/therapeutic use
*Thyroid Diseases/therapy/microbiology
*Fecal Microbiota Transplantation
Animals
Bacteria/classification/metabolism
Neoplasms/therapy/microbiology
Dysbiosis/therapy/microbiology

@article {pmid39775925,
year = {2025},
author = {Bloem, MN and Baaleman, DF and Thapar, N and Roberts, SE and Koppen, IJN and Benninga, MA},
title = {Prevalence of functional defecation disorders in European children: A systematic review and meta-analysis.},
journal = {Journal of pediatric gastroenterology and nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1002/jpn3.12437},
pmid = {39775925},
issn = {1536-4801},
support = {//None/ ; },
abstract = {OBJECTIVES: Functional defecation disorders (FDDs) are common among children worldwide. The prevalence of these disorders has not been clearly described in Europe. This study performed a systematic review and meta-analysis on the prevalence of FDD in European children and assessed geographical, age, and sex distribution and associated factors.

METHODS: PubMed, Embase, Psycinfo, Cochrane Library, and Cinahl were searched from 1999 to July 2023. Included studies were (1) prospective or cross-sectional studies of European population-based samples; (2) reporting the prevalence of infant dyschezia (ID) according to Rome II, III, or IV criteria or functional constipation (FC) or functional non-retentive fecal incontinence (FNRFI) according to Rome III or IV criteria; (3) aged 0-18 years; and (4) published in English, Dutch or Spanish. PRISMA guidelines for extracting data and assessing data quality were followed.

RESULTS: Twenty-eight studies were included. Pooled prevalence was 6.9% (95% confidence interval [CI]: 3.1%-11.9%) for ID in infants 0-12 months (9 studies, n = 5611), 8.17% (95% CI: 6.33%-10.22%) for FC in children <4 years (25 studies, n = 35,189), 11.39% (95% CI: 9.34%-14.11%) for FC in children 4-18 years, and 0.24% (95% CI: 0.07%-0.49%) for FNRFI in children 4-18 years (7 studies, n = 16,873). No sex predominance was found for FC. FC prevalence did not differ significantly when diagnosed according to Rome III versus IV. FC prevalence differed between countries, with greatest rates in Italy, Germany, and Spain. No meta-analysis could be performed on other factors associated with FDD.

CONCLUSIONS: FDD is common in European children. Future longitudinal studies are needed to provide better insight into associated factors in pathogenesis.},
}

@article {pmid39775370,
year = {2025},
author = {Lai, Y and Qiu, R and Zhou, J and Ren, L and Qu, Y and Zhang, G},
title = {Fecal Microbiota Transplantation Alleviates Airway Inflammation in Asthmatic Rats by Increasing the Level of Short-Chain Fatty Acids in the Intestine.},
journal = {Inflammation},
volume = {},
number = {},
pages = {},
pmid = {39775370},
issn = {1573-2576},
support = {(No. 2021JJ30513, No. 2017JJ3245)//Natural Science Foundation of Hunan Province/ ; No. 20B444//Education Department of Hunan Province/ ; (No. 81603705)//National Natural Science Foundation of China/ ; (No. 2017M612567)//Postdoctoral Science Foundation of China/ ; (2024XJZA008)//Hunan University of Chinese Medicine research project/ ; },
abstract = {Asthma is a prevalent chronic inflammatory disorder of the respiratory tract that not only manifests with respiratory symptoms but also often involves intestinal flora disorders and gastrointestinal dysfunction. Recent studies have confirmed the close relationship between the gut and lungs, known as the "gut-lung axis" theory. Fecal microbiota transplantation (FMT), a method for restoring normal intestinal flora, has shown promise in treating common gastrointestinal diseases. The "gut-lung axis" theory suggests that FMT may have significant therapeutic potential for asthma. In this study, we established an Ovalbumin (OVA)-induced rat model of asthma to investigate the protective effect of FMT on airway inflammation and the restoration of intestinal short-chain fatty acids (SCFAs), aiming to explore its underlying mechanism. Rats in the Control group underwent fecal treatment via gavage (Control-FMT, C-FMT group), while rats in the Asthma group underwent fecal treatment via gavage after asthma induction (Asthma-FMT, A-FMT group). Following a two-week period of continuous intragastric administration, various measurements were conducted to assess pulmonary function, peripheral blood neutrophil, lymphocyte, and eosinophil content, lung tissue pathology, and collagen fiber deposition in the lungs. Additionally, neutrophil and eosinophil content in bronchoalveolar lavage fluid (BALF), expression levels of Interleukin-4 (IL-4), IL-5, IL-13, IL-17, IL-33, leukotrienes (LT), thymic stromal lymphopoietin (TSLP), prostaglandin D2 (PGD2) protein and mRNA in lung tissue, and SCFAs content in stool were evaluated. In the C-FMT group, lung function significantly improved, inflammatory cell content in peripheral blood and BALF decreased, lung tissue pathology and collagen fiber deposition significantly improved, the protein and mRNA levels of lung inflammatory factors IL-4, IL-5, IL-13, IL-17, IL-33, LT, TSLP, PGD2 were significantly decreased, and SCFAs such as acetate (C2), propionate (C3), butyrate (C4), isobutyric acid (I-C4), valeric acid (C5), and isovaleric acid (I-C5) content in stool significantly increased. However, the indexes in the A-FMT group did not show significant recovery, and the treatment effect on asthma symptoms in rats was inferior to that in the C-FMT group. Asthma induced intestinal flora disorders in rats, and FMT treatment improved the inflammatory response in asthmatic rat models and corrected their intestinal SCFAs disorders. Encouraging the recovery of intestinal SCFAs may play a significant role, and beneficial bacteria present in feces may improve asthma symptoms by promoting the remodeling of intestinal flora. This experiment provides further scientific evidence supporting the "gut-lung axis" theory.},
}

@article {pmid39773995,
year = {2024},
author = {Mullish, BH and Innes, AJ and Roberts, LA and Anim-Burton, S and Webber, L and Johnson, NA and Ghani, R and Farshi, P and Khan, AB and Kinsella, F and Kottaridis, P and Krishnamurthy, P and Nicholson, E and Palanicawandar, R and Wheeler, G and Davies, F and Marchesi, JR and Pavlů, J},
title = {Intestinal Microbiota Transplant Prior to Allogeneic Stem Cell Transplant (MAST) trial: study protocol for a multicentre, double-blinded, placebo-controlled, phase IIa trial.},
journal = {BMJ open},
volume = {14},
number = {12},
pages = {e093120},
doi = {10.1136/bmjopen-2024-093120},
pmid = {39773995},
issn = {2044-6055},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Hematopoietic Stem Cell Transplantation ; Double-Blind Method ; *Transplantation, Homologous ; Multicenter Studies as Topic ; Clinical Trials, Phase II as Topic ; Adult ; Randomized Controlled Trials as Topic ; Transplantation Conditioning/methods ; Fecal Microbiota Transplantation/methods ; Hematologic Neoplasms/therapy ; Female ; Male ; },
abstract = {INTRODUCTION: Lower diversity of the gut microbiome prior to allogeneic haematopoietic cell transplantation (HCT) correlates with reduced survival after the intervention. Most patients undergoing HCT for a haematological malignancy have previously received intensive chemotherapy, resulting in prolonged neutropenic episodes requiring broad-spectrum antibiotics; use of these has been linked to reduced microbiome diversity. Intestinal microbiota transplant (IMT) is a novel treatment approach that restores this diversity. We hypothesised that IMT performed prior to initiation of HCT conditioning restores microbiome diversity during the early stages of HCT, leading to decreased frequency of complications and improved outcomes of HCT.

METHODS AND ANALYSIS: 50 adult patients receiving allogeneic HCT will be recruited into this phase IIa trial and randomised 1:1 to receive capsulised IMT or matched placebo shortly prior to initiation of HCT conditioning and followed for up to 12 months. The primary outcome will be to assess the increase in alpha diversity between pre-IMT and that measured at ~42 days after IMT administration (day +28 of HCT), comparing the difference between patients receiving IMT compared with placebo. Secondary outcomes will include tolerability, the dynamics of gut microbiome diversity metrics and taxonomy over all time points assessed, as well as clinical outcomes (including burden of invasive infections, days of fever, admission to intensive care, development of graft-vs-host disease and mortality).

ETHICS AND DISSEMINATION: This study was approved by a UK Research Ethics Committee (REC reference: 23/NE/0105). Dissemination of results will be in concert with patient and public involvement group input and is expected to be primarily via abstract presentation at conferences and manuscripts in peer-reviewed journals.

TRIAL REGISTRATION NUMBERS: NCT6355583; EudraCT: 2022-003617-10.},
}

Humans
*Gastrointestinal Microbiome
*Hematopoietic Stem Cell Transplantation
Double-Blind Method
*Transplantation, Homologous
Multicenter Studies as Topic
Clinical Trials, Phase II as Topic
Adult
Randomized Controlled Trials as Topic
Transplantation Conditioning/methods
Fecal Microbiota Transplantation/methods
Hematologic Neoplasms/therapy
Female
Male

@article {pmid39773319,
year = {2025},
author = {Prince, N and Peralta Marzal, LN and Roussin, L and Monnoye, M and Philippe, C and Maximin, E and Ahmed, S and Salenius, K and Lin, J and Autio, R and Adolfs, Y and Pasterkamp, RJ and Garssen, J and Naudon, L and Rabot, S and Kraneveld, AD and Perez-Pardo, P},
title = {Mouse strain-specific responses along the gut-brain axis upon fecal microbiota transplantation from children with autism.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2447822},
doi = {10.1080/19490976.2024.2447822},
pmid = {39773319},
issn = {1949-0984},
mesh = {Animals ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; Humans ; Mice ; Male ; *Mice, Inbred C57BL ; *Brain-Gut Axis/physiology ; *Mice, Inbred BALB C ; Child ; Autism Spectrum Disorder/microbiology ; Dysbiosis/microbiology ; Feces/microbiology ; Disease Models, Animal ; Autistic Disorder/microbiology/physiopathology ; Female ; Social Behavior ; Species Specificity ; Bacteria/classification/isolation & purification/genetics/metabolism ; },
abstract = {Several factors are linked to the pathophysiology of autism spectrum disorders (ASD); however, the molecular mechanisms of the condition remain unknown. As intestinal problems and gut microbiota dysbiosis are associated with ASD development and severity, recent studies have focused on elucidating the microbiota-gut-brain axis' involvement. This study aims to explore mechanisms through which gut microbiota might influence ASD. Briefly, we depleted the microbiota of conventional male BALB/cAnNCrl (Balb/c) and C57BL/6J (BL/6) mice prior to human fecal microbiota transplantation (hFMT) with samples from children with ASD or their neurotypical siblings. We found mouse strain-specific responses to ASD hFMT. Notably, Balb/c mice exhibit decreased exploratory and social behavior, and show evidence of intestinal, systemic, and central inflammation accompanied with metabolic shifts. BL/6 mice show less changes after hFMT. Our results reveal that gut microbiota alone induce changes in ASD-like behavior, and highlight the importance of mouse strain selection when investigating multifactorial conditions like ASD.},
}

Animals
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
Humans
Mice
Male
*Mice, Inbred C57BL
*Brain-Gut Axis/physiology
*Mice, Inbred BALB C
Child
Autism Spectrum Disorder/microbiology
Dysbiosis/microbiology
Feces/microbiology
Disease Models, Animal
Autistic Disorder/microbiology/physiopathology
Female
Social Behavior
Species Specificity
Bacteria/classification/isolation & purification/genetics/metabolism

@article {pmid39772953,
year = {2025},
author = {Teigen, LM and Hoeg, A and Zehra, H and Shah, P and Johnson, R and Hutchison, K and Kocher, M and Lin, AW and Johnson, AJ and Vaughn, BP},
title = {Nutritional optimization of fecal microbiota transplantation in humans: a scoping review.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2446378},
doi = {10.1080/19490976.2024.2446378},
pmid = {39772953},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome ; *Diet ; Clostridium Infections/therapy/microbiology ; Feces/microbiology ; Dietary Supplements ; },
abstract = {Diet constitutes a major source of nutrient flow to the gut microbes. As such, it can be used to help shape the gut microbiome. Fecal microbiota transplantation (FMT) is an increasingly promising therapy in disease states beyond recurrent Clostridioides difficile infection, but diet is largely overlooked for its potential to help optimize this therapy. Therefore, the aim of this scoping review is to present the literature landscape that captures pre- and post-FMT dietary intake in humans, identify research gaps, and provide recommendations for future research. A comprehensive search strategy was developed and searches were run in five databases. Studies were included if they discussed adults who underwent FMT for any recognized treatment indication and had dietary intake as a study objective, this search encompassed studies with interventions that included foods and dietary supplements. The initial screening identified a total of 7721 articles, of which 18 met the inclusion criteria for this review. Studies were heterogeneous, but taken together, they introduce a framework that defines important nutritional considerations for both donors and FMT recipients in the period around FMT dosing. This framework is summarized with this review and highlights the opportunities available to develop FMT-based precision nutrition strategies to optimize its clinical efficacy.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome
*Diet
Clostridium Infections/therapy/microbiology
Feces/microbiology
Dietary Supplements

@article {pmid39772388,
year = {2025},
author = {Wouters, S and Moors, H and Verslegers, M and Leys, N and Malhotra-Kumar, S and Kumar-Singh, S and Mysara, M},
title = {Protocol for fecal microbiota transplantation: A microaerophilic approach for mice housed in a specific pathogen-free facility.},
journal = {STAR protocols},
volume = {6},
number = {1},
pages = {103517},
doi = {10.1016/j.xpro.2024.103517},
pmid = {39772388},
issn = {2666-1667},
abstract = {Recently, studies have emerged exploring the potential application of fecal microbiota transplantation (FMT) in pre-clinical settings. Here, we present a protocol for FMT for mice housed in a specific pathogen-free (SPF) facility. We describe steps for sample collection, microaerophilic processing of freshly collected fecal pellets, and administration through oral gavage. We then detail procedures for the engraftment of the bacterial community. This protocol focuses on age- and gender-matched, healthy donor mice using a mobile and cost-effective alternative to an anoxic cabinet.},
}

@article {pmid39771031,
year = {2024},
author = {Olga, B and Boicean, A and Fleacă, SR and Blanca, G and Florin, S and Corina, RF and Iulian, RF and Adelaida, S and Sabrina, B and Dura, H and Corina, P and Cristian, A and Onisor, DM},
title = {Importance of Fecal Microbiota Transplantation and Molecular Regulation as Therapeutic Strategies in Inflammatory Bowel Diseases.},
journal = {Nutrients},
volume = {16},
number = {24},
pages = {},
doi = {10.3390/nu16244411},
pmid = {39771031},
issn = {2072-6643},
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Inflammatory Bowel Diseases/therapy/microbiology/immunology ; *MicroRNAs/metabolism ; *Gastrointestinal Microbiome ; Gene Expression Regulation ; Animals ; Intestinal Mucosa/microbiology/metabolism/immunology ; },
abstract = {Noncoding RNAs, particularly microRNAs (miRNAs) and small interfering RNAs (siRNAs), have emerged as key players in the pathogenesis and therapeutic strategies for inflammatory bowel disease (IBD). MiRNAs, small endogenous RNA molecules that silence target mRNAs to regulate gene expression, are closely linked to immune responses and inflammatory pathways in IBD. Notably, miR-21, miR-146a, and miR-155 are consistently upregulated in IBD, influencing immune cell modulation, cytokine production, and the intestinal epithelial barrier. These miRNAs serve as biomarkers for disease progression and severity, as well as therapeutic targets for controlling inflammation. This comprehensive review highlights the intricate interplay between the gut microbiota, fecal microbiota transplantation (FMT), and miRNA regulation. It concludes that microbiota and FMT influence miRNA activity, presenting a promising avenue for personalized IBD treatment.},
}

Humans
*Fecal Microbiota Transplantation
*Inflammatory Bowel Diseases/therapy/microbiology/immunology
*MicroRNAs/metabolism
*Gastrointestinal Microbiome
Gene Expression Regulation
Animals
Intestinal Mucosa/microbiology/metabolism/immunology

@article {pmid39771027,
year = {2024},
author = {Gruenbaum, BF and Merchant, KS and Zlotnik, A and Boyko, M},
title = {Gut Microbiome Modulation of Glutamate Dynamics: Implications for Brain Health and Neurotoxicity.},
journal = {Nutrients},
volume = {16},
number = {24},
pages = {},
doi = {10.3390/nu16244405},
pmid = {39771027},
issn = {2072-6643},
mesh = {*Gastrointestinal Microbiome/physiology ; Humans ; *Glutamic Acid/metabolism ; *Brain-Gut Axis/physiology ; *Brain/metabolism ; Animals ; Fecal Microbiota Transplantation ; Blood-Brain Barrier/metabolism ; Neurotoxicity Syndromes/etiology/metabolism ; Depression/metabolism/microbiology ; },
abstract = {The gut-brain axis plays an integral role in maintaining overall health, with growing evidence suggesting its impact on the development of various neuropsychiatric disorders, including depression. This review explores the complex relationship between gut microbiota and glutamate (Glu) regulation, highlighting its effect on brain health, particularly in the context of depression following certain neurological insults. We discuss how microbial populations can either facilitate or limit Glu uptake, influencing its bioavailability and predisposing to neuroinflammation and neurotoxicity. Additionally, we examine the role of gut metabolites and their influence on the blood-brain barrier and neurotransmitter systems involved in mood regulation. The therapeutic potential of microbiome-targeted interventions, such as fecal microbiota transplantation, is also highlighted. While much research has explored the role of Glu in major depressive disorders and other neurological diseases, the contribution of gut microbiota in post-neurological depression remains underexplored. Future research should focus on explaining the mechanisms linking the gut microbiota to neuropsychiatric outcomes, particularly in conditions such as post-stroke depression, post-traumatic brain-injury depression, and epilepsy-associated depression. Systematic reviews and human clinical studies are needed to establish causal relationships and assess the efficacy of microbiome-targeted therapies in improving the neuropsychiatric sequalae after neurological insults.},
}

*Gastrointestinal Microbiome/physiology
Humans
*Glutamic Acid/metabolism
*Brain-Gut Axis/physiology
*Brain/metabolism
Animals
Fecal Microbiota Transplantation
Blood-Brain Barrier/metabolism
Neurotoxicity Syndromes/etiology/metabolism
Depression/metabolism/microbiology

@article {pmid39770958,
year = {2024},
author = {Puca, P and Del Gaudio, A and Becherucci, G and Sacchetti, F and Sofo, L and Lopetuso, LR and Papa, A and Cammarota, G and Scaldaferri, F},
title = {Diet and Microbiota Modulation for Chronic Pouchitis: Evidence, Challenges, and Opportunities.},
journal = {Nutrients},
volume = {16},
number = {24},
pages = {},
doi = {10.3390/nu16244337},
pmid = {39770958},
issn = {2072-6643},
mesh = {*Pouchitis/therapy/microbiology ; Humans ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation ; Chronic Disease ; *Probiotics/therapeutic use ; *Prebiotics/administration & dosage ; Colitis, Ulcerative/microbiology/therapy ; Proctocolectomy, Restorative/adverse effects ; Diet/methods ; Diet, Mediterranean ; },
abstract = {Chronic pouchitis occurs in about 50% of patients undergoing a restorative proctocolectomy for ulcerative colitis. This affection represents a significant therapeutic challenge, particularly for symptomatic patients who do not respond to antibiotic treatments and biologic therapies. Several dietary approaches, including low FODMAP diets and the Mediterranean diet, have shown promising results in improving symptoms and disease burden. The rationale for dietary intervention lies in the reduction in inflammation and modulation of gut microbiota. However, conflicting results and methodological heterogeneity jeopardize the transition of these approaches from the field of research to clinical practice. Together with a nutritional approach, innovative methods of microbiota modulation, including probiotics and fecal microbiota transplantation, are emerging as safe and effective strategies in managing chronic pouchitis. This narrative review analyzes recent advancements in nutritional therapies and microbiota modulation as innovative and complementary approaches for managing chronic pouchitis. After examining microbiota modulation strategies, specifically the effectiveness of probiotics, prebiotics, and fecal microbiota transplantation in restoring microbial diversity and their potential role in alleviating symptoms, the review assesses the available clinical evidence concerning dietary interventions and their impact on gut microbiota. A comprehensive understanding of interventions aimed at modulating the microbiota is crucial for enhancing the effectiveness of conventional therapies. Such strategies may lead to significant improvements in patients' quality of life and their perception of the disease. However, the variability in microbiota composition, the use of restrictive diets, and the lack of standardized methods for evaluating these interventions remain significant challenges. Future research is essential to improve our understanding of the underlying mechanisms and optimize clinical application.},
}

*Pouchitis/therapy/microbiology
Humans
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation
Chronic Disease
*Probiotics/therapeutic use
*Prebiotics/administration & dosage
Colitis, Ulcerative/microbiology/therapy
Proctocolectomy, Restorative/adverse effects
Diet/methods
Diet, Mediterranean

@article {pmid39770742,
year = {2024},
author = {Park, SH and Lee, JH and Lee, S and Shin, J and Cha, B and Hong, JT and Kwon, KS},
title = {Factors for Treatment Failure After Fecal Microbiota Transplantation in Clostridioides difficile Infection.},
journal = {Microorganisms},
volume = {12},
number = {12},
pages = {},
doi = {10.3390/microorganisms12122539},
pmid = {39770742},
issn = {2076-2607},
support = {2023AR05//Seoul Clinical Laboratories/ ; },
abstract = {Recently, fecal microbiota transplantation (FMT) has been introduced as an effective treatment option for Clostridioides difficile infection (CDI). However, the risk factors associated with FMT treatment failure have not been well demonstrated. Therefore, we aimed to investigate the risk factors of treatment failure or recurrence after FMT for CDI. This retrospective study included 124 patients with CDI who underwent FMT at Inha University Hospital between November 2017 and August 2021 and were followed up for 8 weeks after FMT for symptoms of CDI. FMT failure was defined as diarrhea recurrence or a positive stool test. We assessed the risk factors for treatment failure, including comorbidities, antibiotic use pre- and post-FMT, and the number of CDI episodes before FMT. Ninety-three patients (75%) experienced symptom improvement <7 days after FMT, while treatment failure occurred in 40 patients (32.3%). Multivariate analysis revealed that males had a lower symptom improvement rate <7 days after FMT (p = 0.049). Patients using antibiotics after FMT showed a higher rate of recurrence or treatment failure in <8 weeks (p = 0.032). Patients requiring antibiotics after FMT should be considered at higher risk of treatment failure. Careful antibiotic stewardship, particularly minimizing non-essential antibiotic use before and after FMT, may significantly enhance treatment outcomes. Further large-scale prospective studies are warranted to confirm these findings and develop targeted antibiotic management protocols for improving the efficacy of FMT in CDI treatment.},
}

@article {pmid39770703,
year = {2024},
author = {Islam, MZ and Jozipovic, D and Lopez, PA and Krych, L and Correia, BSB and Bertram, HC and Hansen, AK and Hansen, CHF},
title = {Wild-Mouse-Derived Gut Microbiome Transplantation in Laboratory Mice Partly Alleviates House-Dust-Mite-Induced Allergic Airway Inflammation.},
journal = {Microorganisms},
volume = {12},
number = {12},
pages = {},
doi = {10.3390/microorganisms12122499},
pmid = {39770703},
issn = {2076-2607},
support = {R288-2018-1123//Lundbeck Foundation/ ; N/A//Sigrid Rigmor Morans Mindefond/ ; },
abstract = {Laboratory mice are instrumental for preclinical research but there are serious concerns that the use of a clean standardized environment for specific-pathogen-free (SPF) mice results in poor bench-to-bedside translation due to their immature immune system. The aim of the present study was to test the importance of the gut microbiota in wild vs. SPF mice for evaluating host immune responses in a house-dust-mite-induced allergic airway inflammation model without the influence of pathogens. The wild mouse microbiome reduced histopathological changes and TNF-α in the lungs and serum when transplanted to microbiota-depleted mice compared to mice transplanted with the microbiome from SPF mice. Moreover, the colonic gene expression of Gata3 was significantly lower in the wild microbiome-associated mice, whereas Muc1 was more highly expressed in both the ileum and colon. Intestinal microbiome and metabolomic analyses revealed distinct profiles associated with the wild-derived microbiome. The wild-mouse microbiome thus partly reduced sensitivity to house-dust-mite-induced allergic airway inflammation compared to the SPF mouse microbiome, and preclinical studies using this model should consider using both 'dirty' rewilded and SPF mice for testing new therapeutic compounds due to the significant effects of their respective microbiomes and derived metabolites on host immune responses.},
}

@article {pmid39770634,
year = {2024},
author = {Chun, M and Tun, KM and Vongsavath, T and Verma, R and Batra, K and Limsui, D and Jenkins, E},
title = {Fecal Microbiota Transplantation for Chronic Pouchitis: A Systematic Review and Meta-Analysis.},
journal = {Microorganisms},
volume = {12},
number = {12},
pages = {},
doi = {10.3390/microorganisms12122430},
pmid = {39770634},
issn = {2076-2607},
abstract = {Pouchitis is a common complication after ileal-pouch anal anastomosis in patients with medically refractory ulcerative colitis. There has been a lack of high-level evidence focusing on the safety and efficacy outcomes of fecal microbiota transplantation (FMT). We aim to evaluate outcomes and complications of fecal microbiota transplantation (FMT) for chronic pouchitis. Databases were systematically searched to retrieve English-only, original studies, published from inception to 31 March 2024, investigating chronic pouchitis only. Primary outcomes included overall remission, clinical response, remission, relapse, and complications. Seven studies with 94 patients were included. The pooled overall remission rate was 15% (95% CI: 0-29%, p < 0.001), the clinical response rate was 33% (95% CI: 19-46%, p = 0.14), the clinical remission rate was 14% (95% CI: 19-46%, p < 0.001), and the clinical relapse rate was 36% (95% CI: 16-55%, p = 0.11). The pooled proportion of patients with mild adverse events after FMT treatment was 39% (95% CI: 6-71%, p < 0.001). No severe adverse events or deaths were reported. Although FMT is an effective treatment for chronic pouchitis, there is still a high rate of mild adverse events. High-level evidence for FMT is still sparse, limiting recommendations for clinical use.},
}

@article {pmid39767682,
year = {2024},
author = {Farhadi Rad, H and Tahmasebi, H and Javani, S and Hemati, M and Zakerhamidi, D and Hosseini, M and Alibabaei, F and Banihashemian, SZ and Oksenych, V and Eslami, M},
title = {Microbiota and Cytokine Modulation: Innovations in Enhancing Anticancer Immunity and Personalized Cancer Therapies.},
journal = {Biomedicines},
volume = {12},
number = {12},
pages = {},
doi = {10.3390/biomedicines12122776},
pmid = {39767682},
issn = {2227-9059},
abstract = {The gut microbiota plays a crucial role in modulating anticancer immunity, significantly impacting the effectiveness of various cancer therapies, including immunotherapy, chemotherapy, and radiotherapy. Its impact on the development of cancer is complex; certain bacteria, like Fusobacterium nucleatum and Bacteroides fragilis, can stimulate the growth of tumors by causing immunological evasion and inflammation, while advantageous strains, like Faecalibaculum rodentium, have the ability to suppress tumors by modifying immune responses. Cytokine activity and immune system regulation are intimately related. Cytokines including TGF-β, IL-6, and IL-10 promote tumor development by inhibiting efficient immune surveillance. The gut microbiome exhibits a delicate balance between pro- and anti-tumorigenic factors, as evidenced by the enhancement of anti-tumor immunity by cytokines such as IL-12 and IFN-γ. Improved immunotherapy responses are linked to a diverse microbiota, which is correlated with higher tumor infiltration and cytotoxic T-cell activation. Because microbial metabolites, especially short-chain fatty acids, affect cytokine expression and immune cell activation inside the tumor microenvironment, this link highlights the need to maintain microbial balance for optimal treatment effects. Additionally, through stimulating T-cell activation, bacteria like Lactobacillus rhamnosus and Bifidobacterium bifidum increase cytokine production and improve the efficacy of immune checkpoint inhibitors (ICIs). An option for overcoming ICI resistance is fecal microbiota transplantation (FMT), since research suggests that it improves melanoma outcomes by increasing CD8+ T-cell activation. This complex interaction provides an opportunity for novel cancer therapies by highlighting the possibility of microbiome modification as a therapeutic approach in personalized oncology approaches.},
}

@article {pmid39767577,
year = {2024},
author = {Munteanu, C and Onose, G and Rotariu, M and Poștaru, M and Turnea, M and Galaction, AI},
title = {Role of Microbiota-Derived Hydrogen Sulfide (H2S) in Modulating the Gut-Brain Axis: Implications for Alzheimer's and Parkinson's Disease Pathogenesis.},
journal = {Biomedicines},
volume = {12},
number = {12},
pages = {},
doi = {10.3390/biomedicines12122670},
pmid = {39767577},
issn = {2227-9059},
support = {CNFIS - FDI - 2024 - F - 0099//Supporting the institutional capacity for research and innovation through transdisciplinary biotechnologies (InovBiotech)/ ; },
abstract = {Microbiota-derived hydrogen sulfide (H2S) plays a crucial role in modulating the gut-brain axis, with significant implications for neurodegenerative diseases such as Alzheimer's and Parkinson's. H2S is produced by sulfate-reducing bacteria in the gut and acts as a critical signaling molecule influencing brain health via various pathways, including regulating inflammation, oxidative stress, and immune responses. H2S maintains gut barrier integrity at physiological levels and prevents systemic inflammation, which could impact neuroinflammation. However, as H2S has a dual role or a Janus face, excessive H2S production, often resulting from gut dysbiosis, can compromise the intestinal barrier and exacerbate neurodegenerative processes by promoting neuroinflammation and glial cell dysfunction. This imbalance is linked to the early pathogenesis of Alzheimer's and Parkinson's diseases, where the overproduction of H2S exacerbates beta-amyloid deposition, tau hyperphosphorylation, and alpha-synuclein aggregation, driving neuroinflammatory responses and neuronal damage. Targeting gut microbiota to restore H2S homeostasis through dietary interventions, probiotics, prebiotics, and fecal microbiota transplantation presents a promising therapeutic approach. By rebalancing the microbiota-derived H2S, these strategies may mitigate neurodegeneration and offer novel treatments for Alzheimer's and Parkinson's diseases, underscoring the critical role of the gut-brain axis in maintaining central nervous system health.},
}

@article {pmid39766423,
year = {2024},
author = {Menezes, AA and Shah, ZA},
title = {A Review of the Consequences of Gut Microbiota in Neurodegenerative Disorders and Aging.},
journal = {Brain sciences},
volume = {14},
number = {12},
pages = {},
doi = {10.3390/brainsci14121224},
pmid = {39766423},
issn = {2076-3425},
support = {R01NS112642/NS/NINDS NIH HHS/United States ; },
abstract = {Age-associated alterations in the brain lead to cognitive deterioration and neurodegenerative disorders (NDDs). This review with a particular focus on Alzheimer's disease (AD), emphasizes the burgeoning significance of the gut microbiota (GMB) in neuroinflammation and its impact on the gut-brain axis (GBA), a communication conduit between the gut and the central nervous system (CNS). Changes in the gut microbiome, including diminished microbial diversity and the prevalence of pro-inflammatory bacteria, are associated with AD pathogenesis. Promising therapies, such as fecal microbiota transplantation (FMT), probiotics, and prebiotics, may restore gut health and enhance cognitive performance. Clinical data remain insufficient, necessitating further research to elucidate causes, enhance therapy, and consider individual variances. This integrative approach may yield innovative therapies aimed at the GMB to improve cognitive function and brain health in older people.},
}

@article {pmid39766170,
year = {2024},
author = {Ciernikova, S and Sevcikova, A and Novisedlakova, M and Mego, M},
title = {Insights into the Relationship Between the Gut Microbiome and Immune Checkpoint Inhibitors in Solid Tumors.},
journal = {Cancers},
volume = {16},
number = {24},
pages = {},
doi = {10.3390/cancers16244271},
pmid = {39766170},
issn = {2072-6694},
support = {1/0071/24//Scientific Grant Agency of the Ministry of Education, Science, Research and Sport of the Slovak Republic and Slovak Academy of Sciences (VEGA)/ ; 2/0069/22//Scientific Grant Agency of the Ministry of Education, Science, Research and Sport of the Slovak Republic and Slovak Academy of Sciences (VEGA)/ ; },
abstract = {Immunotherapy with immune checkpoint inhibitors represents a revolutionary approach to the treatment of solid tumors, including malignant melanoma, lung cancer, and gastrointestinal malignancies. Anti-CTLA-4 and anti-PD-1/PDL-1 therapies provide prolonged survival for cancer patients, but their efficacy and safety are highly variable. This review focuses on the crucial role of the gut microbiome in modulating the efficacy and toxicity of immune checkpoint blockade. Studies suggest that the composition of the gut microbiome may influence the response to immunotherapy, with specific bacterial strains able to promote an anti-tumor immune response. On the other hand, dysbiosis may increase the risk of adverse effects, such as immune-mediated colitis. Interventions aimed at modulating the microbiome, including the use of probiotics, prebiotics, fecal microbial transplantation, or dietary modifications, represent promising strategies to increase treatment efficacy and reduce toxicity. The combination of immunotherapy with the microbiome-based strategy opens up new possibilities for personalized treatment. In addition, factors such as physical activity and nutritional supplementation may indirectly influence the gut ecosystem and consequently improve treatment outcomes in refractory patients, leading to enhanced patient responses and prolonged survival.},
}

@article {pmid39766032,
year = {2024},
author = {Altrawy, A and Khalifa, MM and Abdelmaksoud, A and Khaled, Y and Saleh, ZM and Sobhy, H and Abdel-Ghany, S and Alqosaibi, A and Al-Muhanna, A and Almulhim, J and El-Hashash, A and Sabit, H and Arneth, B},
title = {Metabolites in the Dance: Deciphering Gut-Microbiota-Mediated Metabolic Reprogramming of the Breast Tumor Microenvironment.},
journal = {Cancers},
volume = {16},
number = {24},
pages = {},
doi = {10.3390/cancers16244132},
pmid = {39766032},
issn = {2072-6694},
abstract = {Breast cancer (BC), a major cause of death among women worldwide, has traditionally been linked to genetic and environmental factors. However, emerging research highlights the gut microbiome's significant role in shaping BC development, progression, and treatment outcomes. This review explores the intricate relationship between the gut microbiota and the breast tumor microenvironment, emphasizing how these microbes influence immune responses, inflammation, and metabolic pathways. Certain bacterial species in the gut either contribute to or hinder BC progression by producing metabolites that affect hormone metabolism, immune system pathways, and cellular signaling. An imbalance in gut bacteria, known as dysbiosis, has been associated with a heightened risk of BC, with metabolites like short-chain fatty acids (SCFAs) and enzymes such as β-glucuronidase playing key roles in this process. Additionally, the gut microbiota can impact the effectiveness of chemotherapy, as certain bacteria can degrade drugs like gemcitabine and irinotecan, leading to reduced treatment efficacy. Understanding the complex interactions between gut bacteria and BC may pave the way for innovative treatment approaches, including personalized microbiome-targeted therapies, such as probiotics and fecal microbiota transplants, offering new hope for more effective prevention, diagnosis, and treatment of BC.},
}

@article {pmid39765038,
year = {2024},
author = {Wang, C and Peng, M and Gao, Z and Fu, F and Li, G and Su, D and Huang, L and Guo, J and Shan, Y},
title = {Citrus aurantium 'Changshan-huyou' physiological premature fruit drop: A promising prebiotic to tackle obesity.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {136},
number = {},
pages = {156347},
doi = {10.1016/j.phymed.2024.156347},
pmid = {39765038},
issn = {1618-095X},
abstract = {BACKGROUND: Presently, the mitigation and governance of obesity have surfaced as significant public health dilemmas on a global scale. A wealth of studies indicated that the host gut microbiota is instrumental in regulating the interplay between high-fat diet (HFD) intake and the pathogenesis of obesity. Physiological premature fruit drop, a major byproduct of citrus, is rich in a variety of bioactive constituents, yet its potential has remained underutilized for an extended period.

PURPOSE: The objective of this investigation is to examine the chemical constituents of Citrus aurantium'Changshan-huyou' premature fruit drop (HYFD) and investigate its anti-obesity effects, elucidating its potential pathways.

METHODS: Volatile compounds and flavonoids in HYFD were analyzed using chromatographic and mass spectrometric techniques. Furthermore, this study utilized biochemical assays and histopathological examinations to evaluate the effects of HYFD on HFD-fed mice. The impact of HYFD on the gut microbiota of the mice was examined through 16S rRNA gene sequencing, and fecal microbiota transplantation was employed to validate the role of the gut microbial community in host obesity prevention. Concurrently, transcriptome was employed to identify differentially expressed genes, providing further insights into the molecular mechanisms through which HYFD manifests its anti-obesity effects.

RESULTS: Our findings demonstrated that HYFD supplementation significantly alleviated adiposity and ameliorated the dysbiosis of gut microbiota in HFD-induced mice. HYFD rectified the HFD-induced gut microbiota dysregulation, enhanced the presence of beneficial microbial taxa linked to lipid metabolism, including Parabacteroides and Alistipes, and elevated concentrations of the anti-obesity short-chain fatty acids, comprising caproic acid and isocaproic acid. Additionally, transcriptomic analyses confirmed that HYFD prevented obesity in mice by enhancing fatty acid catabolism via the activation of the AMPK/PPARα/CPT1a signaling pathway.

CONCLUSION: Our results provided novel insights into the mechanism of citrus physiological premature fruit drop and its potential role in preventing obesity, while sparking greater interest in leveraging more biomass waste.},
}

@article {pmid39764653,
year = {2024},
author = {Mao, Y and Huang, Y and Zhang, W and Liang, H and Liu, F and Luo, Q and Xu, C and Qin, Y and Liu, J and Tang, S and Liu, H and Ge, X},
title = {FMT reduces systemic inflammatory response in severe acute pancreatitis by increasing the abundance of intestinal Bifidobacteria and fecal bacteria.},
journal = {Biomolecules & biomedicine},
volume = {},
number = {},
pages = {},
doi = {10.17305/bb.2024.11445},
pmid = {39764653},
issn = {2831-090X},
abstract = {Severe acute pancreatitis (SAP) is one of the leading causes of hospital admissions for gastrointestinal diseases, with a rising incidence worldwide. Intestinal microbiota dysbiosis caused by SAP exacerbates systemic inflammatory response syndrome and organ dysfunction. Fecal microbiota transplantation (FMT) has emerged as a promising therapeutic option for gastrointestinal diseases. In this study, fecal samples from healthy, control, and FMT-treated groups were analyzed using 16S rRNA sequencing to assess microbiome abundance and diversity. Composition and functional prediction analyses were conducted to explore the mechanisms underlying FMT in SAP. FMT significantly improved clinical parameters in SAP patients, including leukocyte count, C-reactive protein (CRP), neutrophil granulocyte count, lactate dehydrogenase (LDH), and calcitonin (P < 0.05). Organ failure rates significantly increased in the control group but decreased in the FMT group after treatment (P < 0.05). Fecal microbiota sequencing revealed that FMT significantly upregulated the abundance of Bifidobacterium longum among all SAP patients (P < 0.05). Receiver operating characteristic (ROC) curve analysis indicated that Bifidobacterium longum might play a critical role in the efficacy of FMT, with an area under the curve (AUC) value of 0.84. Additionally, there was a negative correlation between Bifidobacterium longum abundance and procalcitonin (PCT) levels, as well as a negative correlation between Escherichia coli abundance and both CT and Ca values (P < 0.05). The relative abundances of Bifidobacterium longum and Escherichia coli were significantly higher in the FMT group compared to the Bifidobacterium triple viable group (P < 0.05). In conclusion, this research supports FMT as a safe and effective intervention for treating SAP patients.},
}

@article {pmid39764615,
year = {2025},
author = {Harris, SC and Bajaj, JS},
title = {Interaction of the Gut-Liver-Brain Axis and the sterolbiome with sexual dysfunction in patients with cirrhosis.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2446390},
doi = {10.1080/19490976.2024.2446390},
pmid = {39764615},
issn = {1949-0984},
mesh = {Humans ; *Liver Cirrhosis/complications/metabolism ; *Gastrointestinal Microbiome ; *Brain-Gut Axis/physiology ; *Sexual Dysfunction, Physiological/metabolism/etiology/physiopathology ; *Liver/metabolism ; Sterols/metabolism ; Brain/metabolism ; Gonadal Steroid Hormones/metabolism ; Animals ; Quality of Life ; },
abstract = {There is a complex interplay between the gut microbes, liver, and central nervous system, a gut-liver-brain axis, where the brain impacts intestinal and hepatic function while the gut and liver can impact cognition and mental status. Dysregulation of this axis can be seen in numerous diseases. Hepatic encephalopathy, a consequence of cirrhosis, is perhaps the best studied perturbation of this system. However, patients with cirrhosis have been shown to have increased incidence of other disorders of mental health which may be otherwise less clinically identifiable. Sexual dysfunction affects a large proportion of patients with cirrhosis and is associated with decreased quality of life. Screening for sexual dysfunction in patients with cirrhosis is often overlooked, and even when identified, treatment options are limited, particularly in patients with advanced liver disease. The mechanism by which patients with cirrhosis develop sexual dysfunction is multifactorial, but a key driver of this clinical manifestation is alterations in circulating sex hormones. In patients with cirrhosis, low serum sex hormones have been shown to be associated with higher mortality regardless of MELD score. The gut microbiome has been shown to have an immense metabolic capacity to metabolize steroid hormones. This "sterolbiome" has already been implicated in other disease processes and has been linked to low circulating sex hormones, suggesting a new mechanism by which sex hormones may be altered in disease states where the gut-liver-brain axis is disrupted. The aim of this review is to cover sex hormone changes and sexual dysfunction in cirrhosis, examine the gut microbiome and its metabolic capacity, particularly for steroid hormones, and consider how microbial changes using fecal microbiota transplant could modulate sexual dysfunction.},
}

Humans
*Liver Cirrhosis/complications/metabolism
*Gastrointestinal Microbiome
*Brain-Gut Axis/physiology
*Sexual Dysfunction, Physiological/metabolism/etiology/physiopathology
*Liver/metabolism
Sterols/metabolism
Brain/metabolism
Gonadal Steroid Hormones/metabolism
Animals
Quality of Life

@article {pmid39764447,
year = {2024},
author = {Wang, J and Zhuang, P and Lin, B and Zheng, J and Li, H and Tang, W and Ye, W and Chen, X and Zheng, M},
title = {Comparative analysis of gut microbiota in metabolic syndrome and obese children from Southeastern China.},
journal = {Frontiers in microbiology},
volume = {15},
number = {},
pages = {1503302},
pmid = {39764447},
issn = {1664-302X},
abstract = {The prevalence of childhood obesity is rising globally, with some obese children progressing to develop metabolic syndrome (MS). However, the specific differences between these groups remain unclear. To investigate the differences in gut microbiota, we conducted physiological and biochemical assessments, alongside 16S rRNA sequencing, in a cohort of 32 children from Southeastern China, which included 4 normal-weight children, 5 with mild obesity, 9 with moderate obesity, 9 with severe obesity, and 5 with metabolic syndrome. Our results indicated that waist circumference, serum triglycerides, total cholesterol, non-HDL levels, and the prevalence of fatty liver were significantly elevated in both obese and MS children compared to their normal-weight peers, with the MS group exhibiting more pronounced abnormalities. Conversely, HDL levels showed a contrasting trend. Additionally, alpha diversity of gut microbiota increased with weight, while beta diversity analysis revealed significant compositional differences between children with MS and those who were normal weight or obese. At the class and genus levels, we found that the relative abundance of c_Gammaproteobacteria increased with weight, whereas c_Bacteroidia and g_Bacteroides decreased. Notably, g_Faecalibacterium was significantly less abundant in the MS group compared to the other cohorts. LEfSe and functional analyses identified distinct gut microbiota and functional differences between children with MS and those with normal weight or obesity. Furthermore, gavage experiments in mice showed that gut microbiota from obese and MS subjects significantly increased serum triglycerides and cholesterol levels, leading to hepatocellular damage. In contrast, fecal gavage from normal-weight individuals into obese model mice significantly reduced serum triglycerides and the number of degenerative liver cells, as well as the extent of fat accumulation. These findings provide critical insights into the understanding and management of obesity and metabolic syndrome in pediatric populations.},
}

@article {pmid39762283,
year = {2025},
author = {Feng, C and Wu, Y and Zhang, X and Wang, S and Wang, J and Yang, H},
title = {Maternal milk fat globule membrane enriched gut L. murinus and circulating SCFAs to improve placental efficiency and fetal development in intrauterine growth restricted mice model.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2449095},
doi = {10.1080/19490976.2024.2449095},
pmid = {39762283},
issn = {1949-0984},
mesh = {Animals ; Female ; Pregnancy ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Placenta/metabolism ; *Fetal Growth Retardation/metabolism ; *Glycoproteins/metabolism ; *Fatty Acids, Volatile/metabolism ; *Lipid Droplets/metabolism ; *Glycolipids/metabolism ; *Fetal Development/drug effects ; *Disease Models, Animal ; Lactobacillus ; Mice, Inbred C57BL ; Fecal Microbiota Transplantation ; },
abstract = {Intrauterine growth restriction (IUGR) caused by placental dysfunctions leads to fetal growth defects. Maternal microbiome and its metabolites have been reported to promote placental development. Milk fat globule membrane (MFGM) is known for its diverse bioactive functions, while the effects of gestational MFGM supplementation on the maternal gut microbiota, placental efficiency, and fetal development remained unclear. In this study, low protein diet-induced IUGR decreased the litter birth weight, fetal birth weight, and the fetal/placental ratio in pregnant mice, while gestational MFGM supplementation restored these impairments. Meanwhile, MFGM supplementation during gestation enriched intestinal Lactobacillus murinus (L. murinus) and increased luminal and circulating short chain fatty acids (SCFAs) in IUGR pregnant mice, which improved placental efficiency and fetal development due to an enhanced antioxidant capacity and a decreased inflammation. In addition, fecal microbiota transplantation (FMT) with MFGM-derived microbiota reprinted the promoted phenotypes of maternal litter characteristics, gut L. murinus enrichment, placental efficiency, and fetal gut development in MFGM-fed pregnant mice, which were also recapitulated by exogenous administration with L. murinus or SCFAs cocktail. Mechanically, MFGM, MFGM-derived microbiota, L. murinus, or SCFAs cocktail activated IUGR-induced depressive phosphorylation of PI3K-Akt signaling in the placenta. Moreover, in vitro placental cells cultivation under amino acid shortage model (AAS) or oxygen-glucose shortage model (OGS) was used to validate that MFGM-derived key microbial and circulating SCFAs cocktails can alleviate placental oxidative stress and inflammation via activating PI3K/Akt signaling. Taken together, gestational MFGM supplementation enriched intestinal L. murinus and circulating SCFAs of IUGR pregnant mice, thereby improving placental efficiency, fetal growth, and intestinal functions of IUGR fetus. Our findings will provide theoretical support for the application of MFGM in the maternal-placental-fetal nutrition to address pregnancy malnutrition-induced IUGR.},
}

Animals
Female
Pregnancy
*Gastrointestinal Microbiome/drug effects
Mice
*Placenta/metabolism
*Fetal Growth Retardation/metabolism
*Glycoproteins/metabolism
*Fatty Acids, Volatile/metabolism
*Lipid Droplets/metabolism
*Glycolipids/metabolism
*Fetal Development/drug effects
*Disease Models, Animal
Lactobacillus
Mice, Inbred C57BL
Fecal Microbiota Transplantation

@article {pmid39762111,
year = {2025},
author = {Al-Shakhshir, S and Quraishi, MN and Mullish, B and Patel, A and Vince, A and Rowe, A and Homer, V and Jackson, N and Gyimah, D and Shabir, S and Manzoor, S and Cooney, R and Alrubaiy, L and Quince, C and van Schaik, W and Hares, M and Beggs, AD and Efstathiou, E and Rimmer, P and Weston, C and Iqbal, T and Trivedi, PJ},
title = {FAecal micRobiota transplantation in primary sclerosinG chOlangitis (FARGO): study protocol for a randomised, multicentre, phase IIa, placebo-controlled trial.},
journal = {BMJ open},
volume = {15},
number = {1},
pages = {e095392},
doi = {10.1136/bmjopen-2024-095392},
pmid = {39762111},
issn = {2044-6055},
mesh = {Adult ; Female ; Humans ; Male ; *Cholangitis, Sclerosing/therapy ; Clinical Trials, Phase II as Topic ; *Fecal Microbiota Transplantation/methods ; Gastrointestinal Microbiome ; Inflammatory Bowel Diseases/therapy/microbiology ; Multicenter Studies as Topic ; Randomized Controlled Trials as Topic ; Treatment Outcome ; },
abstract = {INTRODUCTION: Primary sclerosing cholangitis (PSC) is the classical hepatobiliary manifestation of inflammatory bowel disease (IBD). The strong association between gut and liver inflammation has driven several pathogenic hypotheses to which the intestinal microbiome is proposed to contribute. Pilot studies of faecal microbiota transplantation (FMT) in PSC and IBD are demonstrated to be safe and associated with increased gut bacterial diversity. However, the longevity of such changes and the impact on markers of disease activity and disease progression have not been studied. The aim of this clinical trial is to determine the effects of repeated FMT as a treatment for PSC-IBD.

METHODS AND ANALYSIS: FAecal micRobiota transplantation in primary sclerosinG chOlangitis (FARGO) is a phase IIa randomised placebo-controlled trial to assess the efficacy and safety of repeated colonic administration of FMT in patients with non-cirrhotic PSC-IBD. Fifty-eight patients will be recruited from six sites across England and randomised in a 1:1 ratio between active FMT or FMT placebo arms. FMT will be manufactured by the University of Birmingham Microbiome Treatment Centre, using stool collected from rigorously screened healthy donors. A total of 8 weekly treatments will be delivered; the first through colonoscopic administration (week 1) and the remaining seven via once-weekly enema (up to week 8). Participants will then be followed on a 12-weekly basis until week 48 from the first treatment visit. The primary efficacy outcome will be to determine the effect of FMT on serum alkaline phosphatase values over time (end of study at 48 weeks). Key secondary outcomes will be to evaluate the impact of FMT on other liver biochemical parameters, PSC risk scores, circulating and imaging markers of liver fibrosis, health-related quality of life measures, IBD activity and the incidence of PSC-related clinical events. Key translational objectives will be to identify mucosal metagenomic, metatranscriptomic, metabolomic and immunological pathways associated with the administration of FMT.

ETHICS AND DISSEMINATION: The protocol was approved by the South Central-Hampshire B Research Ethics Committee (REC 23/SC/0147). Participants will be required to provide written informed consent. The results of this trial will be disseminated through national and international presentations and peer-reviewed publications.

TRIAL REGISTRATION NUMBER: The trial was registered at ClinicalTrials.gov on 23 February 2024 (NCT06286709). Weblink: Study Details | FAecal Microbiota Transplantation in primaRy sclerosinG chOlangitis | ClinicalTrials.gov.},
}

Adult
Female
Humans
Male
*Cholangitis, Sclerosing/therapy
Clinical Trials, Phase II as Topic
*Fecal Microbiota Transplantation/methods
Gastrointestinal Microbiome
Inflammatory Bowel Diseases/therapy/microbiology
Multicenter Studies as Topic
Randomized Controlled Trials as Topic
Treatment Outcome

@article {pmid39761011,
year = {2024},
author = {Jain, V and Dalby, MJ and Alexander, EC and Burford, C and Acford-Palmer, H and Serghiou, IR and Teng, NMY and Kiu, R and Gerasimidis, K and Zafeiropoulou, K and Logan, M and Verma, A and Davenport, M and Hall, LJ and Dhawan, A},
title = {Association of gut microbiota and gut metabolites and adverse outcomes in biliary atresia: A longitudinal prospective study.},
journal = {Hepatology communications},
volume = {8},
number = {11},
pages = {},
pmid = {39761011},
issn = {2471-254X},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Biliary Atresia/surgery/microbiology/metabolism ; *Feces/microbiology ; Male ; Female ; Prospective Studies ; Infant ; Longitudinal Studies ; Portoenterostomy, Hepatic ; RNA, Ribosomal, 16S/genetics ; Enterococcus ; Case-Control Studies ; Infant, Newborn ; Bifidobacterium/isolation & purification ; },
abstract = {BACKGROUND: The Kasai portoenterostomy (KPE) aims to re-establish bile flow in biliary atresia (BA); however, BA remains the commonest indication for liver transplantation in pediatrics. Gut microbiota-host interplay is increasingly associated with outcomes in chronic liver disease. This study characterized fecal microbiota and fatty acid metabolites in BA.

METHODS: Fecal samples were prospectively collected in newly diagnosed BA infants (n = 55) before and after KPE. Age-matched healthy control (n = 19) and cholestatic control (n = 21) fecal samples were collected. Fecal 16S rRNA gene amplicon sequencing for gut microbiota and gas chromatography for fecal fatty acids was performed.

RESULTS: Increased abundance of Enterococcus in pre-KPE BA and cholestatic control infants, compared to healthy infants, was demonstrated. At the early post-KPE time points, increased alpha diversity was revealed in BA versus healthy cohorts. A lower relative abundance of Bifidobacterium and increased Enterococcus, Clostridium, Fusobacterium, and Pseudomonas was seen in infants with BA. Fecal acetate was reduced, and fecal butyrate and propionate were elevated in early post-KPE BA infants. Higher post-KPE alpha diversity was associated with nonfavorable clinical outcomes (6-month jaundice and liver transplantation). A higher relative abundance of post-KPE Streptococcus and Fusobacterium and a lower relative abundance of Dorea, Blautia, and Oscillospira were associated with nonfavorable clinical outcomes. Blautia inversely correlated to liver disease severity, and Bifidobacterium inversely correlated to fibrosis biomarkers. Bifidobacterium abundance was significantly lower in infants experiencing cholangitis within 6 months after KPE.

CONCLUSIONS: Increased diversity, enrichment of pathogenic, and depletion of beneficial microbiota early post-KPE are all factors associated with nonfavorable BA outcomes. Manipulation of gut microbiota in the early postsurgical period could provide therapeutic potential.},
}

Humans
*Gastrointestinal Microbiome
*Biliary Atresia/surgery/microbiology/metabolism
*Feces/microbiology
Male
Female
Prospective Studies
Infant
Longitudinal Studies
Portoenterostomy, Hepatic
RNA, Ribosomal, 16S/genetics
Enterococcus
Case-Control Studies
Infant, Newborn
Bifidobacterium/isolation & purification

@article {pmid39760535,
year = {2025},
author = {Saha, S and Schnabl, B},
title = {Modulating the microbiome in chronic liver diseases- current evidence on the role of fecal microbiota transplantation.},
journal = {Expert review of gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1080/17474124.2025.2450707},
pmid = {39760535},
issn = {1747-4132},
abstract = {INTRODUCTION: The gut microbiota has a complex relationship with the human host and is key to maintaining health. Disruption of the healthy diverse gut microbial milieu plays an important role in the pathogenesis of several diseases including Clostridioides difficile infection (CDI), inflammatory bowel disease, irritable bowel syndrome, alcohol-related liver disease and metabolic-dysfunction associated steatotic liver disease (MASLD). Fecal microbiota transplantation (FMT) is highly effective in treating CDI, though its utility in other diseases is still being explored.

AREAS COVERED: In this narrative review, we explore the role of gut microbiota in liver diseases, focusing on key changes in the microbial composition and function. We summarize current evidence on the role of FMT, identifying gaps in current research and outlining future directions for investigation. We comprehensively searched PubMed through 15 October 2024 to identify relevant studies.

EXPERT OPINION: While data from available studies shows promise, more research is necessary before we can use FMT for liver diseases. Key areas that require further study are- determining the optimal FMT regimen for each disease, establishing efficacy and safety with larger clinical trials, ensuring safe and equitable access to the FMT product and mechanistic insights into the reasons for success or failure of FMT.},
}

@article {pmid39759692,
year = {2024},
author = {Muzaffer, M and Masarath, A and Mohammed, F},
title = {Biliary Atresia: A Case Report.},
journal = {Cureus},
volume = {16},
number = {12},
pages = {e75087},
pmid = {39759692},
issn = {2168-8184},
abstract = {Biliary atresia (BA) is a serious hepatobiliary disorder that occurs due to progressive inflammation and scarring obstruction in the bile ducts, posing a threat to life. This condition usually appears in infants, and timely identification is fundamental for a better prognosis. If left untreated, individuals will inevitably experience liver damage and mortality. This case report describes a nine-month-old female infant presenting with jaundice, icteric sclera, yellowish skin, acholic feces, and hepatomegaly. Elevated liver enzymes and a hepatobiliary iminodiacetic acid (HIDA) scan confirmed BA. Histopathological examination revealed fibrosis, cholestatic disease, and an atretic gallbladder. A modified Kasai portoenterostomy (KPE) with Roux-en-Y jejunojejunostomy was performed, and the infant was discharged with supportive care. However, seven months post-Kasai portoenterostomy, the infant presented with persistent jaundice and progressive deterioration of liver function, indicative of a failed Kasai procedure. Consequently, she was scheduled to undergo liver transplantation (LT) as a definitive treatment. BA is a rare disorder that is observed across nearly all ethnic groups, though the incidence rates vary significantly. This case highlights the efficacy of liver transplantation in treating failed Kasai procedures and demonstrates the potential for enhanced outcomes in infants with end-stage liver disease.},
}

@article {pmid39758967,
year = {2025},
author = {Thorndal, C and Kragsnaes, MS and Nilsson, AC and Holm, DK and dePont Christensen, R and Ellingsen, T and Kjeldsen, J and Bjørsum-Meyer, T},
title = {Safety and efficacy of faecal microbiota transplantation in patients with acute uncomplicated diverticulitis: study protocol for a randomised placebo-controlled trial.},
journal = {Therapeutic advances in gastroenterology},
volume = {18},
number = {},
pages = {17562848241309868},
pmid = {39758967},
issn = {1756-283X},
abstract = {BACKGROUND: Little is known about the involvement of gut microbiota in the disease course of diverticulitis and the potential benefits of manipulating the gut milieu. We propose to conduct a randomised placebo-controlled feasibility trial of faecal microbiota transplantation (FMT) given as capsules to patients with acute uncomplicated diverticulitis.

OBJECTIVES: The objective is primarily to investigate the feasibility of clinical safety, explore efficacy associated with FMT in this patient population, and examine changes in patient-reported quality of life and the composition and function of the gut microbiota.

DESIGN: Study protocol for a randomised placebo-controlled trial.

METHODS AND ANALYSIS: Participants with acute, uncomplicated diverticulitis, as confirmed by computed tomography (CT) scan, will be recruited from Odense University Hospital (Denmark) and randomly assigned to either the intervention group or the control group. The intervention group will consist of 20 patients who receive encapsulated FMT. The control group will also consist of 20 patients, receiving placebo capsules. Primary safety endpoint: Patient safety is monitored by (a) the number of re-admissions and (b) the number of adverse events within 3 months of FMT/placebo; Primary efficacy endpoint: Reduction in the proportion of patients treated with antibiotics within 3 months following FMT/placebo; Secondary outcome: Change from baseline to 3 months in the GI-QLI questionnaire. Results will be analysed using an intention-to-treat approach. Adverse events or unintended consequences will be reported.

ETHICS AND DISCUSSION: This is the first study to investigate the safety and efficacy of FMT in patients with acute uncomplicated diverticulitis. The project has the potential to broaden the knowledge and literature on the role of the intestinal microbiota in diverticulitis, and we believe it will elevate our understanding of cause and effect.

TRIAL REGISTRATION: Informed consent is obtained from all participants. The study is approved by the regional ethics committee (ref. S-20230023) and the Danish Data Protection Agency (ref. 24/2435). The trial was registered on clinicaltrials.gov (NCT06254625) on 10th February 2024.},
}

@article {pmid39758313,
year = {2024},
author = {Liu, B and Zhang, Z and Zhao, J and Li, X and Wang, Y and Liu, L and Qiao, W and Chen, L},
title = {Lactiplantibacillus plantarum HM-P2 influences gestational gut microbiome and microbial metabolism.},
journal = {Frontiers in nutrition},
volume = {11},
number = {},
pages = {1489359},
pmid = {39758313},
issn = {2296-861X},
abstract = {INTRODUCTION: Human milk-derived probiotics are beneficial bacteria that provide gestational health benefits, for both pregnant women and their offspring. The study aims to investigate whether the administration of human milk-derived probiotic L. plantarum HM-P2 could effectively influence gestational health.

METHODS: The gestational humanized microbiome model was built by fecal microbiome transplant from gestational women into germ-free (GF) mice.

RESULTS: HM-P2 was successfully planted and increased the top crypt depth of the colon, and microbes such as L. reuteri, Anaerofilum sp. An201, and Gemmiger were up-regulated in the HM-P2 group throughout gestation. HM-P2 significantly promoted the contents of intestinal caproic acid, bile acids, and tryptophan catabolites such as serotonin. Gut microbes were associated with these bile acids and tryptophans.

DISCUSSION: HM-P2 could modulate the microbial community and microbial metabolites in gestational humanized GF mice. This probiotic strain could be a potential gestational dietary supplement with health benefits.},
}

@article {pmid39757809,
year = {2025},
author = {Huang, ST and Hu, YH and Gao, YC and Zhou, DD and Chen, MY and Wang, L and Song, JY and Zhou, HH and Zhang, W and Huang, WH},
title = {Hypoglycemic Effect of Ginsenoside Compound K Mediated by N-Acetylserotonin Derived From Gut Microbiota.},
journal = {Phytotherapy research : PTR},
volume = {},
number = {},
pages = {},
doi = {10.1002/ptr.8385},
pmid = {39757809},
issn = {1099-1573},
support = {82074000//National Natural Science Foundation of China/ ; 82073945//National Natural Science Foundation of China/ ; 81874329//National Natural Science Foundation of China/ ; 2023YFC3405200//National Key Research and Development Program of China/ ; 2021YFA1301200//National Key Research and Development Program of China/ ; 2024JJ5585//Hunan Provincial Natural Science Foundation of China/ ; 2023SK2083//Scientific Research Project of Furong Laboratory of Central South University/ ; },
abstract = {Ginsenoside compound K (GCK) has been proved to have great hypoglycemic effect pertinent to gut microbiota. However, the improvement of high-fat-diet (HFD)-induced type 2 diabetes (T2D) as well as the mechanism of GCK mediated by gut microbiota is not well-known. This study aimed to investigate the hypoglycemic effects and mechanism of GCK on a HFD-induced diabetic mouse model. HFD-induced pseudo-germ free (GF) T2D mice model and fecal microbiota transplantation (FMT) experiments were performed to clarify the role of gut microbiota in the hypoglycemic effect of GCK. Differential metabolites were screened by untargeted metabolomics analysis and their functions were verified by suppling to T2D mice. The level of glucagon-like peptide-1 (GLP-1) in plasma was detected by ELISA analysis to explore the potential hypoglycemic mechanism of GCK. The results showed GCK alleviated metabolic disorders and altered gut microbiota in HFD-induced diabetic mice, which was transmitted to pseudo-GF diabetic mice via FMT experiment to reproduce the hypoglycemic effect. Non-targeted metabolites analysis on cecal content samples indicated that N-acetylserotonin (NAS) was markedly increased after GCK treatment. Moreover, gavage with NAS improved insulin sensitivity and increased the secretion of GLP-1 in HFD mice. Our study showed that GCK had hypoglycemic effect through modifying gut microbiota profiling.},
}

@article {pmid39757609,
year = {2024},
author = {Bhat, MM and Hussain, MS and Bisht, AS and Agrawal, M and Sultana, A and Khurrana, N and Kumar, R},
title = {Frontiers in Pulmonary Hypertension: A Comprehensive Insight of Etiological Advances.},
journal = {Current reviews in clinical and experimental pharmacology},
volume = {},
number = {},
pages = {},
doi = {10.2174/0127724328325178241210174545},
pmid = {39757609},
issn = {2772-4336},
abstract = {Pulmonary hypertension (PH) is a severe, progressive disorder characterized by elevated pulmonary arterial pressure, leading to right ventricular failure and increased mortality. Despite advancements in management, the median survival for PH patients remains 5-7 years, with an inhospital mortality rate of approximately 6%. The core pathological feature of PH is pulmonary vascular remodeling (PVR), a multifactorial process involving endothelial dysfunction, inflammation, and aberrant immune responses. While current therapies target endothelial dysfunction, they fall short of preventing PVR or halting disease progression. Emerging research highlights the potential of immune-inflammatory pathways, oxygen-sensing mechanisms, and gut microbiota modulation as therapeutic targets. Integrating nutritional strategies, probiotics, and fecal microbiota transplantation (FMT) as adjunctive therapies also shows promise. These factors may collectively influence PVR, offering novel insights into therapeutic avenues for PH management in the future.},
}

@article {pmid39756658,
year = {2025},
author = {Chen, Q and Liu, F and Zhang, G and Qu, Q and Chen, Y and Li, M and Huang, Q and Fu, H and Zhu, X and He, Y and Huang, X and Zhang, X},
title = {Progesterone Regulates Gut Microbiota Mediating Bone Marrow MSCs Injury in ITP Patients during Pregnancy.},
journal = {Journal of thrombosis and haemostasis : JTH},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jtha.2024.12.027},
pmid = {39756658},
issn = {1538-7836},
abstract = {BACKGROUND: Immune thrombocytopenia during pregnancy (PITP) is the most common cause of platelet reduction in early and mid-pregnancy. However, the pathogenesis of PITP is still unclear.

OBJECTIVES: To determine the characteristics of bone marrow mesenchymal stem cells (BM-MSCs) in PITP patients and to explore the associations between metabolites, the gut microbiota, and BM-MSCs in PITP.

METHODS: The characteristics of BM-MSCs were detected through in vitro and in vivo experiments. Non-targeted metabolomics was used to screen metabolites. The features of the gut microbiota were analyzed by 16S rDNA sequencing. PITP and a fecal microbiota transplantation (FMT) mouse model were established to explore the associations between metabolites, the gut microbiota, and BM-MSCs.

RESULTS: BM-MSCs from PITP patients had significant senescence and apoptosis, as well as impaired immunoregulatory function. Metabolomic analysis indicated that progesterone was the most significant specific metabolite in PITP patients. In vivo studies showed that progesterone mediated the MSCs injury. Further analysis of the gut microbiota and FMT experiments revealed that progesterone mediated BM-MSCs injury by regulating the the composition of the gut microbiota in the PITP. RNA-seq analysis of BM-MSCs from FMT mice revealed abnormal expression of genes related to cell aging and the NOD-like receptor signaling pathway.

CONCLUSION: In conclusion, BM-MSCs in the PITP were significantly impaired, which was associated with increased progesterone and changes in the gut microbiota regulated by progesterone. Intervening with the gut microbiota may become a new treatment for PITP.},
}

@article {pmid39754054,
year = {2025},
author = {Azhar Ud Din, M and Lin, Y and Lyu, C and Yi, C and Fang, A and Mao, F},
title = {Advancing therapeutic strategies for graft-versus-host disease by targeting gut microbiome dynamics in allogeneic hematopoietic stem cell transplantation: current evidence and future directions.},
journal = {Molecular medicine (Cambridge, Mass.)},
volume = {31},
number = {1},
pages = {2},
pmid = {39754054},
issn = {1528-3658},
mesh = {*Graft vs Host Disease/etiology/microbiology ; Humans ; *Hematopoietic Stem Cell Transplantation/adverse effects ; *Gastrointestinal Microbiome ; *Transplantation, Homologous ; Animals ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; },
abstract = {Hematopoietic stem cell transplantation (HSCT) is a highly effective therapy for malignant blood illnesses that pose a high risk, as well as diseases that are at risk due to other variables, such as genetics. However, the prevalence of graft-versus-host disease (GVHD) has impeded its widespread use. Ensuring the stability of microbial varieties and associated metabolites is crucial for supporting metabolic processes, preventing pathogen intrusion, and modulating the immune system. Consequently, it significantly affects the overall well-being and susceptibility of the host to disease. Patients undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT) may experience a disruption in the balance between the immune system and gut bacteria when treated with medicines and foreign cells. This can lead to secondary intestinal inflammation and GVHD. Thus, GM is both a reliable indicator of post-transplant mortality and a means of enhancing GVHD prevention and treatment after allo-HSCT. This can be achieved through various strategies, including nutritional support, probiotics, selective use of antibiotics, and fecal microbiota transplantation (FMT) to target gut microbes. This review examines research advancements and the practical use of intestinal bacteria in GVHD following allo-HSCT. These findings may offer novel insights into the prevention and treatment of GVHD after allo-HSCT.},
}

*Graft vs Host Disease/etiology/microbiology
Humans
*Hematopoietic Stem Cell Transplantation/adverse effects
*Gastrointestinal Microbiome
*Transplantation, Homologous
Animals
Fecal Microbiota Transplantation
Probiotics/therapeutic use

@article {pmid39747695,
year = {2025},
author = {Wang, X and Fang, Y and Liang, W and Cai, Y and Wong, CC and Wang, J and Wang, N and Lau, HC and Jiao, Y and Zhou, X and Ye, L and Mo, M and Yang, T and Fan, M and Song, L and Zhou, H and Zhao, Q and Chu, ES and Liang, M and Liu, W and Liu, X and Zhang, S and Shang, H and Wei, H and Li, X and Xu, L and Liao, B and Sung, JJY and Kuang, M and Yu, J},
title = {Gut-liver translocation of pathogen Klebsiella pneumoniae promotes hepatocellular carcinoma in mice.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {39747695},
issn = {2058-5276},
support = {82173191//National Science Foundation of China | National Natural Science Foundation of China-Yunnan Joint Fund (NSFC-Yunnan Joint Fund)/ ; },
abstract = {Hepatocellular carcinoma (HCC) is accompanied by an altered gut microbiota but whether the latter contributes to carcinogenesis is unclear. Here we show that faecal microbiota transplantation (FMT) using stool samples from patients with HCC spontaneously initiate liver inflammation, fibrosis and dysplasia in wild-type mice, and accelerate disease progression in a mouse model of HCC. We find that HCC-FMT results in gut barrier injury and translocation of live bacteria to the liver. Metagenomic analyses and bacterial culture of liver tissues reveal enrichment of the gut pathogen Klebsiella pneumoniae in patients with HCC and mice transplanted with the HCC microbiota. Moreover, K. pneumoniae monocolonization recapitulates the effect of HCC-FMT in promoting liver inflammation and hepatocarcinogenesis. Mechanistically, K. pneumoniae surface protein PBP1B interacts with and activates TLR4 on HCC cells, leading to increased cell proliferation and activation of oncogenic signalling. Targeting gut colonization using K. oxytoca or TLR4 inhibition represses K. pneumoniae-induced HCC progression. These findings indicate a role for an altered gut microbiota in hepatocarcinogenesis.},
}

@article {pmid39746875,
year = {2025},
author = {Faith, JJ},
title = {Assessing live microbial therapeutic transmission.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2447836},
doi = {10.1080/19490976.2024.2447836},
pmid = {39746875},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Clostridium Infections/microbiology/therapy/drug therapy ; *Clostridioides difficile/drug effects/physiology/genetics ; *Gastrointestinal Microbiome ; Feces/microbiology ; Animals ; },
abstract = {The development of fecal microbiota transplantation and defined live biotherapeutic products for the treatment of human disease has been an empirically driven process yielding a notable success of approved drugs for the treatment of recurrent Clostridioides difficile infection. Assessing the potential of this therapeutic modality in other indications with mixed clinical results would benefit from consistent quantitative frameworks to characterize drug potency and composition and to assess the impact of dose and composition on the frequency and duration of strain engraftment. Monitoring these drug properties and engraftment outcomes would help identify minimally sufficient sets of microbial strains to treat disease and provide insights into the intersection between microbial function and host physiology. Broad and correct usage of strain detection methods is essential to this advancement. This article describes strain detection approaches, where they are best applied, what data they require, and clinical trial designs that are best suited to their application.},
}

Humans
*Fecal Microbiota Transplantation
*Clostridium Infections/microbiology/therapy/drug therapy
*Clostridioides difficile/drug effects/physiology/genetics
*Gastrointestinal Microbiome
Feces/microbiology
Animals

@article {pmid39746695,
year = {2024},
author = {He, H and Zhang, JP and Wei, ZJ and Lu, Y and Zhao, YL and Sun, RJ},
title = {[Role of human herpesvirus infection in refractory gastrointestinal graft-versus-host-disease after hematopoietic stem cell transplantation and the diagnosis and treatment thereof].},
journal = {Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi},
volume = {45},
number = {11},
pages = {1016-1021},
doi = {10.3760/cma.j.cn121090-20240906-00339},
pmid = {39746695},
issn = {0253-2727},
mesh = {Humans ; *Hematopoietic Stem Cell Transplantation/adverse effects ; Male ; Female ; Adult ; Middle Aged ; *Graft vs Host Disease/diagnosis/etiology ; Retrospective Studies ; Adolescent ; Young Adult ; Child ; Child, Preschool ; Infant ; Herpesviridae Infections/diagnosis ; Transplantation, Homologous ; Cytomegalovirus/isolation & purification ; Herpesvirus 6, Human/isolation & purification ; },
abstract = {Objective: This study aimed to investigate the role of human herpesvirus (HHV) infection in refractory intestinal graft-versus-host disease (GI-GVHD) after hematopoietic stem cell transplantation (HSCT) and its diagnosis and treatment. Methods: This study retrospectively analyzed patients presenting with refractory GI-GVHD after allogeneic HSCT (allo-HSCT) with concomitant colonoscopy and mucosal biopsy at Lu Daopei Hospital, Yanda, Hebei, from March 2022 to July 2024. Human herpesvirus 6 (HHV6), HHV7, cytomegalovirus (CMV), and Epstein-Barr virus (EBV) detection with the RQ-PCR method. The intestinal mucosa was pathologically assessed and immunohistochemistry was utilized to detect the CMV early antigen, CMV late antigen, and EBV by in situ hybridization. Results: This study included 42 patients, consisting of 25 males and 17 females with a median age of 26 (1-59) years. All were histopathologically diagnosed as GI-GVHD. Among them, 34 (81.0%) cases had combined viral enteritis, with 52.4% positive for EBV, 38.1% positive for HHV6, 26.2% positive for CMV, and 14.3% positive for HHV7. Further, 17 (40.5%) cases had mixed viral infections, including 5 EBV+ HHV6, 3 CMV+HHV6, 3 CMV+EBV, 2 CMV+EBV+HHV6, 2 EBV+HHV6+HHV7, 1 EBV+HHV7, and 1 HHV6 + HHV7 cases. Furthermore, 17 (40.5%) had a single viral infection, including 9 EBV, 3 CMV, 3 HHV6, and 2 HHV7 cases. Moreover, 17 (40.5%) patients exhibited a positive histopathological viral test, including 7 (16.6%) CMV-positive and 12 (28.5%) EBV-positive cases. The same positive virus was detected in the feces of all 34 patients with positive tissue homogenate virus, and the positive rate of the same virus in the blood was 17.6%. Tissue homogenized virus testing was utilized as the diagnostic criterion for enterocolitis: blood tests for CMV, EBV, HHV6, and HHV7 demonstrated a sensitivity of 45.4%, 4.5%, 6.3%, and 0%, and specificity of 90.3%, 95%, 100%, and 110%, respectively. Additionally, fecal tests for CMV, EBV, HHV6, and HHV7 demonstrated a sensitivity and specificity of 100%. Treatment based on etiology caused ORR and CR rates for diarrhea of 76.1% (32/42) and 66.6% (28/42), respectively. The median follow-up of 42 patients was 13 (1 - 49) months, and 28 patients survived, with an expected 2-year survival rate of 61.9%. Conclusion: In addition to GVHD itself, intestinal human herpesvirus infection is one of the reasons for the refractory nature of GI-GVHD. Viral testing in blood and tissues reveals significant segregation, and the possibility of comorbid viral enteritis cannot be excluded even if a patient with GI-GVHD tests negative for blood viruses.},
}

Humans
*Hematopoietic Stem Cell Transplantation/adverse effects
Male
Female
Adult
Middle Aged
*Graft vs Host Disease/diagnosis/etiology
Retrospective Studies
Adolescent
Young Adult
Child
Child, Preschool
Infant
Herpesviridae Infections/diagnosis
Transplantation, Homologous
Cytomegalovirus/isolation & purification
Herpesvirus 6, Human/isolation & purification

@article {pmid39744736,
year = {2024},
author = {Jeyaraman, N and Jeyaraman, M and Dhanpal, P and Ramasubramanian, S and Ragavanandam, L and Muthu, S and Santos, GS and da Fonseca, LF and Lana, JF},
title = {Gut microbiome and orthopaedic health: Bridging the divide between digestion and bone integrity.},
journal = {World journal of orthopedics},
volume = {15},
number = {12},
pages = {1135-1145},
pmid = {39744736},
issn = {2218-5836},
abstract = {The gut microbiome, a complex ecosystem of microorganisms in the digestive tract, has emerged as a critical factor in human health, influencing metabolic, immune, and neurological functions. This review explores the connection between the gut microbiome and orthopedic health, examining how gut microbes impact bone density, joint integrity, and skeletal health. It highlights mechanisms linking gut dysbiosis to inflammation in conditions such as rheumatoid arthritis and osteoarthritis, suggesting microbiome modulation as a potential therapeutic strategy. Key findings include the microbiome's role in bone metabolism through hormone regulation and production of short-chain fatty acids, crucial for mineral absorption. The review also considers the effects of diet, probiotics, and fecal microbiota transplantation on gut microbiome composition and their implications for orthopedic health. While promising, challenges in translating microbiome research into clinical practice persist, necessitating further exploration and ethical consideration of microbiome-based therapies. This interdisciplinary research aims to link digestive health with musculoskeletal integrity, offering new insights into the prevention and management of bone and joint diseases.},
}

@article {pmid39744230,
year = {2025},
author = {Singh, A and Chandrasekar, SV and Valappil, VT and Scaria, J and Ranjan, A},
title = {Tumor immunomodulation by nanoparticle and focused ultrasound alters gut microbiome in a sexually dimorphic manner.},
journal = {Theranostics},
volume = {15},
number = {1},
pages = {216-232},
pmid = {39744230},
issn = {1838-7640},
mesh = {Animals ; Female ; Male ; *Gastrointestinal Microbiome/immunology ; Mice ; *Nanoparticles/administration & dosage ; *Immunomodulation ; Calreticulin/metabolism ; Cell Line, Tumor ; Immunogenic Cell Death/drug effects ; Mice, Inbred C57BL ; Mouth Neoplasms/immunology/microbiology/therapy ; Sex Characteristics ; Cytokines/metabolism ; },
abstract = {Background: Local immunomodulation with nanoparticles (NPs) and focused ultrasound (FUS) is recognized for triggering anti-tumor immunity. However, the impact of these tumor immunomodulations on sex-specific microbiome diversity at distant sites and their correlation with therapeutic effectiveness remains unknown. Here, we conducted local intratumoral therapy using immunogenic cell death-enhancing Calreticulin-Nanoparticles (CRT-NPs) and FUS in male and female mice. We identified immune-related microbiome populations, aiming to translate our findings into clinical applications. Methods: CRT-NPs were synthesized by loading CRT-delivering plasmids into cationic liposomes. Local tumor therapy was performed using CRT-NP and FUS-based histotripsy (HT) on poorly immunogenic Mouse Oral Squamous Cell Carcinoma (MOC2) in the flank regions of male and female mice. Fecal samples were collected and analyzed before and three weeks post-treatment. The microbiome features were then correlated with immune cell dynamics within tumors and systemic cytokine responses to identify prognostic biomarkers in both male and female subjects. Results: Intratumorally administered CRT-NP induced tumor remission and immune cell activation in both male and female mice, whereas HT was ineffective in males and showed efficacy only in females. Turicibacter and Peptococcus inversely correlated with tumor growth, while Enterorhabdus, Subdologranulum, Desulfovibrio, and Aldercreutzia-Asaccharobacter showed direct correlations with tumor growth. HT induced higher levels of Turicibacter in MOC2-bearing females, while males displayed increased Enterorhabdus and Streptococcus populations. Independent of sex, treatments promoting CD4+ T helper cells, functional CD8+ T cells, and total macrophage infiltration correlated with higher levels of Gastrophilales, Romboutsia, Turicibacter, and Peptococcus. Alternatively, Enterorhabdus, Desulfovibrio, Streptococcus, and Staphylococcus corresponded to poor treatment outcomes in both sexes. Conclusion: An enhanced abundance of Enterorhabdus, Desulfovibrio, Streptococcus, and Staphylococcus in response to immunomodulatory therapies could serve as predictive biomarkers in a sex-independent manner. These findings could also be potentially extended to the realm of personalized interventions through fecal transplantations to reverse immunosuppressive phenotypes in males and improve patient outcomes.},
}

Animals
Female
Male
*Gastrointestinal Microbiome/immunology
Mice
*Nanoparticles/administration & dosage
*Immunomodulation
Calreticulin/metabolism
Cell Line, Tumor
Immunogenic Cell Death/drug effects
Mice, Inbred C57BL
Mouth Neoplasms/immunology/microbiology/therapy
Sex Characteristics
Cytokines/metabolism

@article {pmid39741383,
year = {2024},
author = {van Rheenen, PF and Kolho, KL and Russell, RK and Aloi, M and Deganello, A and Hussey, S and Junge, N and De Laffolie, J and Deneau, MR and Fitzpatrick, E and Griffiths, AM and Hojsak, I and Nicastro, E and Nita, A and Pakarinen, M and Ricciuto, A and de Ridder, L and Sonzogni, A and Tenca, A and Samyn, M and Indolfi, G},
title = {Primary sclerosing cholangitis in children with inflammatory bowel disease: An ESPGHAN position paper from the Hepatology Committee and the IBD Porto group.},
journal = {Journal of pediatric gastroenterology and nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1002/jpn3.12378},
pmid = {39741383},
issn = {1536-4801},
support = {//European Society for Paediatric Gastroenterology Hepatology and Nutrition/ ; },
abstract = {OBJECTIVE: We aimed to provide an evidence-supported approach to diagnose, monitor, and treat children with inflammatory bowel disease (IBD) and primary sclerosing cholangitis (PSC).

METHODS: The core group formulated seven PICO-structured clinical questions. A systematic literature search from inception to December 2022 was conducted by a medical librarian using MEDLINE and EMBASE. Core messages from the literature were phrased as position statements and then circulated to a sounding board composed of international experts in pediatric gastroenterology and hepatology, histopathology, adult gastroenterology and hepatology, radiology, and surgery. Statements reaching at least 80% agreement were considered as final. The other statements were refined and then subjected to a second online vote or rejection.

RESULTS: Regular screening for gamma-glutamyltransferase (GGT) is essential for detecting possible biliary disease in children with IBD. MR cholangiopancreatography is the radiological modality of choice for establishing the diagnosis of PSC. Liver biopsy is relevant in the evaluation of small duct PSC or autoimmune hepatitis. Children who do not have known IBD at the time of PSC diagnosis should undergo initial screening with fecal calprotectin for asymptomatic colitis, and then at least once yearly thereafter. Children with a cholestatic liver enzyme profile can be considered for treatment with ursodeoxycholic acid and can continue if there is a meaningful reduction or normalization in GGT. Oral vancomycin may have a beneficial effect on GGT and intestinal inflammation, but judicious use is recommended due to the lack of long-term studies. Children with PSC-IBD combined with convincing features of autoimmune hepatitis may benefit from corticosteroids and antimetabolites.

CONCLUSIONS: We present state-of-the-art guidance on the diagnostic criteria, follow-up strategies, and therapeutic strategies and point out research gaps in children and adolescents with PSC-IBD.},
}

@article {pmid39739648,
year = {2024},
author = {Lei, J and Lv, L and Zhong, L and Xu, F and Su, W and Chen, Y and Wu, Z and He, S and Chen, Y},
title = {The Gut Microbiota Affects Anti-TNF Responsiveness by Activating the NAD[+] Salvage Pathway in Ulcerative Colitis.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e2413128},
doi = {10.1002/advs.202413128},
pmid = {39739648},
issn = {2198-3844},
support = {82100548//National Natural Science Foundation of China/ ; CSTB2022NSCQ-MSX0094//Natural Science Foundation of Chongqing Municipality/ ; },
abstract = {Approximately 50% of the patients with ulcerative colitis (UC) are primarily nonresponsive to anti-tumor necrosis factor (TNF) therapy or lose their responsiveness over time. The gut microbiota plays an important role in the resistance of UC to anti-TNF therapy; however, the underlying mechanism remains unknown. Here, it is found that the transplantation of gut fecal microbiota from patients with UC alters the diversity of the gut microbiota in dextran sulfate sodium-induced colitis mice and may affect the therapeutic responsiveness of mice to infliximab. Furthermore, the abundances of Romboutsia and Fusobacterium increase in the tissues of patients with UC who do not respond to anti-TNF therapy. Differentially abundant metabolites are mainly enriched in nicotinate and nicotinamide metabolism in NCM460 cells after Fusobacterium nucleatum infection. Mechanistically, F. nucleatum promotes the nicotinamide adenine dinucleotide (NAD[+]) salvage pathway by upregulating NAMPT expression, which subsequently leads to the activation of the p38 mitogen-activated protein kinase (MAPK) signaling pathway and promotes the secretion of inflammatory factors, ultimately inhibiting the therapeutic response to anti-TNF drugs. These findings demonstrate that the gut microbiota can influence the response to anti-TNF therapy in patients with UC and highlight the therapeutic potential of targeting F. nucleatum and its associated pathways for preventing and treating drug resistance in UC.},
}

@article {pmid39738016,
year = {2024},
author = {Li, Z and Gu, M and Zaparte, A and Fu, X and Mahen, K and Mrdjen, M and Li, XS and Yang, Z and Ma, J and Thoudam, T and Chandler, K and Hesler, M and Heathers, L and Gorse, K and Van, TT and Wong, D and Gibson, AM and Wang, Z and Taylor, CM and Quijada, P and Makarewich, CA and Hazen, SL and Liangpunsakul, S and Brown, JM and Lefer, DJ and Welsh, DA and Sharp, TE},
title = {Alcohol-induced gut microbial reorganization and associated overproduction of phenylacetylglutamine promotes cardiovascular disease.},
journal = {Nature communications},
volume = {15},
number = {1},
pages = {10788},
pmid = {39738016},
issn = {2041-1723},
support = {R01 AA029984/AA/NIAAA NIH HHS/United States ; P50 AA024333/AA/NIAAA NIH HHS/United States ; UH2 AA026226/AA/NIAAA NIH HHS/United States ; P60 AA009803/AA/NIAAA NIH HHS/United States ; R21 AA027199/AA/NIAAA NIH HHS/United States ; U01 AA026917/AA/NIAAA NIH HHS/United States ; UH3 AA026903/AA/NIAAA NIH HHS/United States ; R01AA030312//U.S. Department of Health & Human Services | NIH | National Institute on Alcohol Abuse and Alcoholism (NIAAA)/ ; T32 AR065972/AR/NIAMS NIH HHS/United States ; T32 HL069766/HL/NHLBI NIH HHS/United States ; R25 HL145817/HL/NHLBI NIH HHS/United States ; HL160569//U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI)/ ; HL171221//U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI)/ ; P01 HL147823/HL/NHLBI NIH HHS/United States ; R01 HL103866/HL/NHLBI NIH HHS/United States ; R01 HL167831/HL/NHLBI NIH HHS/United States ; P01 HL147823/HL/NHLBI NIH HHS/United States ; R01 HL146098/HL/NHLBI NIH HHS/United States ; R01 HL146514/HL/NHLBI NIH HHS/United States ; R01 HL151398/HL/NHLBI NIH HHS/United States ; NSF 2018936//National Science Foundation (NSF)/ ; RF1 NS133812/NS/NINDS NIH HHS/United States ; P20 GM103424/GM/NIGMS NIH HHS/United States ; U54 GM104940/GM/NIGMS NIH HHS/United States ; U24 DK1132746//U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases)/ ; R01 DK130227/DK/NIDDK NIH HHS/United States ; R01 DK120679/DK/NIDDK NIH HHS/United States ; KC2210163//U.S. Department of Defense (United States Department of Defense)/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Male ; *Glutamine/metabolism/analogs & derivatives ; *Cardiovascular Diseases/metabolism/microbiology/etiology ; Mice ; Humans ; Mice, Inbred C57BL ; Myocytes, Cardiac/metabolism/drug effects ; Ethanol/pharmacology/metabolism ; Oxidative Stress/drug effects ; Fecal Microbiota Transplantation ; Alcoholism/metabolism ; Disease Models, Animal ; Female ; Glutamates/metabolism ; Endothelial Cells/metabolism/drug effects ; Middle Aged ; },
abstract = {The mechanism(s) underlying gut microbial metabolite (GMM) contribution towards alcohol-mediated cardiovascular disease (CVD) is unknown. Herein we observe elevation in circulating phenylacetylglutamine (PAGln), a known CVD-associated GMM, in individuals living with alcohol use disorder. In a male murine binge-on-chronic alcohol model, we confirm gut microbial reorganization, elevation in PAGln levels, and the presence of cardiovascular pathophysiology. Fecal microbiota transplantation from pair-/alcohol-fed mice into naïve male mice demonstrates the transmissibility of PAGln production and the CVD phenotype. Independent of alcohol exposure, pharmacological-mediated increases in PAGln elicits direct cardiac and vascular dysfunction. PAGln induced hypercontractility and altered calcium cycling in isolated cardiomyocytes providing evidence of improper relaxation which corresponds to elevated filling pressures observed in vivo. Furthermore, PAGln directly induces vascular endothelial cell activation through induction of oxidative stress leading to endothelial cell dysfunction. We thus reveal that the alcohol-induced microbial reorganization and resultant GMM elevation, specifically PAGln, directly contributes to CVD.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Male
*Glutamine/metabolism/analogs & derivatives
*Cardiovascular Diseases/metabolism/microbiology/etiology
Mice
Humans
Mice, Inbred C57BL
Myocytes, Cardiac/metabolism/drug effects
Ethanol/pharmacology/metabolism
Oxidative Stress/drug effects
Fecal Microbiota Transplantation
Alcoholism/metabolism
Disease Models, Animal
Female
Glutamates/metabolism
Endothelial Cells/metabolism/drug effects
Middle Aged

@article {pmid39736988,
year = {2024},
author = {Wang, F and Wang, Z and Qu, L},
title = {The changes of intestinal flora and metabolites in atopic dermatitis mice.},
journal = {Frontiers in microbiology},
volume = {15},
number = {},
pages = {1462491},
pmid = {39736988},
issn = {1664-302X},
abstract = {INTRODUCTION: Atopic dermatitis (AD) is an allergic disease caused by various factors that can affect an individual's appearance and cause psychological stress. Therefore, it is necessary to investigate the underlying mechanisms and develop effective treatment strategies. The gut microbiota and bacterial metabolism play crucial roles in human diseases. However, their specific role in AD remains unclear.

METHODS: In this study, we established a mouse model of AD and found that 2,4-dinitrofluorobenzene disrupted the skin barrier in mice. The species composition of intestinal bacteria was then analyzed by fecal 16s rRNA sequencing. The metabolic level of mice was analyzed by untargeted and targeted metabolomics in stool.

RESULTS: The levels of filaggrin and aquaporin 3 proteins in the model mice and total superoxide dismutase, catalase and malondialdehyde levels were significantly altered. Additionally, inflammatory factors such as tumor necrosis factor-alpha showed a significant increase. Using 16S rRNA gene sequencing, we identified 270 bacterial species with altered abundances of Ruminococcaceae and Bifidobacteriaceae. The untargeted metabolomic analysis detected 1,299 metabolites. Targeted analysis of free fatty acids revealed 49 metabolites with notable increases in linoleic and linolenic acid levels. Fecal bacterial transplantation experiments have demonstrated that oxidative stress, inflammation, and skin barrier damage were alleviated after transplantation.

DISCUSSION: These findings suggested that the metabolite linoleic acid negatively correlated with Ruminococcaceae and Bifidobacteriaceae may influence AD development. Perturbations in the intestinal bacteria and flora contributed to the development of AD, and the mouse model could serve as a valuable tool for further investigation of therapeutic approaches for managing ADS.},
}

@article {pmid39736924,
year = {2025},
author = {Yuan, C},
title = {Molecular mechanisms and therapeutic strategies of gut microbiota modulation in Sarcopenia (Review).},
journal = {Oncology letters},
volume = {29},
number = {3},
pages = {104},
pmid = {39736924},
issn = {1792-1082},
abstract = {Sarcopenia is an age-related disease that is characterized by a decline in muscle mass and function with significant epidemiological and clinical implications. In recent years, gut microbiota has gained attention as an important regulatory factor in human health. To the best of our knowledge, this is the first study to introduce the definition and epidemiological background of sarcopenia and analyze the potential impact of the gut microbiota on muscle metabolism and growth, including aspects such as gut microbiota metabolites, muscle protein synthesis and energy metabolism. Additionally, this article summarizes the current research progress in gut microbiota interventions for the treatment of sarcopenia, such as probiotics, prebiotics and fecal microbiota transplantation and discusses future research directions and potential therapeutic strategies.},
}

@article {pmid39735707,
year = {2024},
author = {Chu, C and Behera, TR and Huang, Y and Qiu, W and Chen, J and Shen, Q},
title = {Research progress of gut microbiome and diabetic nephropathy.},
journal = {Frontiers in medicine},
volume = {11},
number = {},
pages = {1490314},
pmid = {39735707},
issn = {2296-858X},
abstract = {Diabetic nephropathy is an important complication of diabetic microvascular injury, and it is also an important cause of end-stage renal disease. Its high prevalence and disability rate significantly impacts patients' quality of life while imposing substantial social and economic burdens. Gut microbiota affects host metabolism, multiple organ functions, and regulates host health throughout the life cycle. With the rapid development of technology, researchers have found that gut microbiota is closely related to the progression of diabetic kidney disease. This review explores the role of gut microbiome in diabetic nephropathy summarizing proposed mechanisms of progression and focusing on microbial metabolites, intestinal barrier disruption, inflammation, filtration barrier damage and renal fibrosis. This review also examines the mechanism and limitations of current treatments, including drugs, fecal microbiota transplantation, and lifestyle changes, offering new perspectives on prevention and treatment.},
}

@article {pmid39735647,
year = {2024},
author = {Wang, H and Li, S and Zhang, L and Zhang, N},
title = {The role of fecal microbiota transplantation in type 2 diabetes mellitus treatment.},
journal = {Frontiers in endocrinology},
volume = {15},
number = {},
pages = {1469165},
pmid = {39735647},
issn = {1664-2392},
mesh = {*Fecal Microbiota Transplantation/methods ; Humans ; *Diabetes Mellitus, Type 2/therapy/microbiology ; *Gastrointestinal Microbiome ; Animals ; },
abstract = {In contemporary microbial research, the exploration of interactions between microorganisms and multicellular hosts constitutes a burgeoning field. The gut microbiota is increasingly acknowledged as a pivotal contributor to various disorders within the endocrine system, encompassing conditions such as diabetes and thyroid diseases. A surge in research activities has been witnessed in recent years, elucidating the intricate interplay between the gut microbiota and disorders of the endocrine system. Simultaneously, fecal microbiota transplantation (FMT) has emerged as a focal point, garnering substantial attention in both biomedical and clinical spheres. Research endeavors have uncovered the remarkable therapeutic efficacy of FMT across diverse diseases, with particular emphasis on its application in addressing type 2 diabetes mellitus (T2DM) and associated com-plications. Consequently, this manuscript accentuates the intimate connection between the gut microbiota and disorders within the endocrine system, with a specific focus on exploring the potential of FMT as an intervention in the therapeutic landscape of T2DM and its complications. Furthermore, the article scrutinizes concerns inherent in treatment modalities centered around the gut microbiota, proposing viable solutions to address these issues.},
}

*Fecal Microbiota Transplantation/methods
Humans
*Diabetes Mellitus, Type 2/therapy/microbiology
*Gastrointestinal Microbiome
Animals

@article {pmid39735273,
year = {2024},
author = {Patnaik, S and Durairajan, SSK and Singh, AK and Krishnamoorthi, S and Iyaswamy, A and Mandavi, SP and Jeewon, R and Williams, LL},
title = {Role of Candida species in pathogenesis, immune regulation, and prognostic tools for managing ulcerative colitis and Crohn's disease.},
journal = {World journal of gastroenterology},
volume = {30},
number = {48},
pages = {5212-5220},
pmid = {39735273},
issn = {2219-2840},
mesh = {Humans ; *Crohn Disease/immunology/microbiology/therapy ; *Gastrointestinal Microbiome/immunology ; *Colitis, Ulcerative/microbiology/immunology/diagnosis/therapy ; *Dysbiosis/immunology/microbiology ; Prognosis ; Candida albicans/immunology/pathogenicity/isolation & purification ; Immunity, Mucosal ; Candida/immunology/pathogenicity/isolation & purification ; Candidiasis/immunology/microbiology/diagnosis ; Host-Pathogen Interactions ; Intestinal Mucosa/microbiology/immunology ; },
abstract = {The gut microbiome plays a key role in the pathogenesis and disease activity of inflammatory bowel disease (IBD). While research has focused on the bacterial microbiome, recent studies have shifted towards host genetics and host-fungal interactions. The mycobiota is a vital component of the gastrointestinal microbial community and plays a significant role in immune regulation. Among fungi, Candida species, particularly Candida albicans (C. albicans), have been extensively studied due to their dual role as gut commensals and invasive pathogens. Recent findings indicate that various strains of C. albicans exhibit considerable differences in virulence factors, impacting IBD's pathophysiology. Intestinal fungal dysbiosis and antifungal mucosal immunity may be associated to IBD, especially Crohn's disease (CD). This article discusses intestinal fungal dysbiosis and antifungal immunity in healthy individuals and CD patients. It discusses factors influencing the mycobiome's role in IBD pathogenesis and highlights significant contributions from the scientific community aimed at enhancing understanding of the mycobiome and encouraging further research and targeted intervention studies on specific fungal populations. Our article also provided insights into a recent study by Wu et al in the World Journal of Gastroenterology regarding the role of the gut microbiota in the pathogenesis of CD.},
}

Humans
*Crohn Disease/immunology/microbiology/therapy
*Gastrointestinal Microbiome/immunology
*Colitis, Ulcerative/microbiology/immunology/diagnosis/therapy
*Dysbiosis/immunology/microbiology
Prognosis
Candida albicans/immunology/pathogenicity/isolation & purification
Immunity, Mucosal
Candida/immunology/pathogenicity/isolation & purification
Candidiasis/immunology/microbiology/diagnosis
Host-Pathogen Interactions
Intestinal Mucosa/microbiology/immunology

@article {pmid39735176,
year = {2025},
author = {Bhatia, Z and Kumar, S and Seshadri, S},
title = {Fecal microbiota transplantation as a potential therapeutic approach to improve impaired glucose tolerance via gut microbiota modulation in rat model.},
journal = {Journal of diabetes and metabolic disorders},
volume = {24},
number = {1},
pages = {28},
pmid = {39735176},
issn = {2251-6581},
abstract = {OBJECTIVES: To investigate the impact of diet-induced gut microbiota alterations on type 2 diabetes and assess the therapeutic potential of Fecal Microbiota Transplantation (FMT) in restoring a balanced gut microenvironment.

METHODS: To induce type 2 diabetes, rats were fed a high-sugar high-fat diet (HSFD) for 90 days. After diabetes induction, animals were divided into an HSFD control group, a metformin group (100 mg/kg), and an FMT group (100 mg/kg), receiving treatment for an additional 90 days. Fasting blood glucose levels, glucose tolerance, serum markers (HbA1C, free fatty acids, lipopolysaccharides, pro-inflammatory and anti-inflammatory cytokines), and gut microbiota profiles via cecal metagenome sequencing were analyzed post-treatment.

RESULTS: FMT effectively restored gut microbiota composition to a profile similar to healthy controls, rebalancing the Firmicutes/Bacteroidetes ratio and increasing beneficial taxa, including Prevotella ruminicola, Akkermansia muciniphila, Roseburia, and Faecalibacterium prausnitzii. These microbial shifts corresponded with significant metabolic improvements: FMT reduced inflammatory markers (LPS and FFA), lowered HbA1c, and improved glucose tolerance. Enhanced gut barrier integrity observed in FMT-treated animals likely contributed to reduced endotoxemia and systemic inflammation, distinguishing FMT's metabolic effects from those of metformin. Notably, FMT addressed the dysbiosis associated with HSFD, promoting microbial resilience and mitigating the metabolic disruptions linked to type 2 diabetes.

CONCLUSION: These findings underscore the potential of FMT as a targeted therapeutic approach to modulate gut microbiota composition and mitigate metabolic dysregulation induced by high sugar high fat diet.},
}

@article {pmid39733842,
year = {2024},
author = {Mamun, AA and Geng, P and Wang, S and Shao, C and Xiao, J},
title = {IUPHAR review: Targeted therapies of signaling pathways based on the gut microbiome in autism spectrum disorders: Mechanistic and therapeutic applications.},
journal = {Pharmacological research},
volume = {211},
number = {},
pages = {107559},
doi = {10.1016/j.phrs.2024.107559},
pmid = {39733842},
issn = {1096-1186},
abstract = {Autism spectrum disorders (ASD) are complex neurodevelopmental disorders characterized by impairments in social interaction, communication and repetitive activities. Gut microbiota significantly influences behavior and neurodevelopment by regulating the gut-brain axis. This review explores gut microbiota-influenced treatments for ASD, focusing on their therapeutic applications and mechanistic insights. In addition, this review discusses the interactions between gut microbiota and the immune, metabolic and neuroendocrine systems, focusing on crucial microbial metabolites including short-chain fatty acids (SCFAs) and several neurotransmitters. Furthermore, the review explores various therapy methods including fecal microbiota transplantation, dietary modifications, probiotics and prebiotics and evaluates their safety and efficacy in reducing ASD symptoms. The discussion shows the potential of customized microbiome-based therapeutics and the integration of multi-omics methods to understand the underlying mechanisms. Moreover, the review explores the intricate relationship between gut microbiota and ASD, aiming to develop innovative therapies that utilize the gut microbiome to improve the clinical outcomes of ASD patients. Microbial metabolites such as neurotransmitter precursors, tryptophan metabolites and SCFAs affect brain development and behavior. Symptoms of ASD are linked to changes in these metabolites. Dysbiosis in the gut microbiome may impact neuroinflammatory processes linked to autism, negatively affecting immune signaling pathways. Research indicates that probiotics and prebiotics can improve gut microbiota and alleviate symptoms in ASD patients. Fecal microbiota transplantation may also improve behavioral symptoms and restore gut microbiota balance. The review emphasizes the need for further research on gut microbiota modification as a potential therapeutic approach for ASD, highlighting its potential in clinical settings.},
}

@article {pmid39733798,
year = {2024},
author = {Luo, Y and Li, M and Luo, D and Tang, B},
title = {Gut Microbiota: An Important Participant in Childhood Obesity.},
journal = {Advances in nutrition (Bethesda, Md.)},
volume = {},
number = {},
pages = {100362},
doi = {10.1016/j.advnut.2024.100362},
pmid = {39733798},
issn = {2156-5376},
abstract = {Increasing prevalence of childhood obesity has emerged as a critical global public health concern. Recent studies have challenged the previous belief that obesity was solely a result of excessive caloric intake. Alterations in early-life gut microbiota can contribute to childhood obesity through their influence on nutrient absorption and metabolism, initiation of inflammatory responses, and regulation of gut-brain communication. The gut microbiota is increasingly acknowledged to play a crucial role in human health, as certain beneficial bacteria have been scientifically proven to possess the capacity to reduce body fat content and enhance intestinal barrier function, and their metabolic products to exhibit anti-inflammatory effect. Examples of such microbes include bifidobacteria, Akkermansia muciniphila, and Lactobacillus reuteri. In contrast, an increase in Enterobacteriaceae and Propionate-producing bacteria (Prevotellaceae and Veillonellaceae) has been implicated in the induction of low-grade systemic inflammation and disturbances in lipid metabolism, which can predispose individuals to obesity. Studies have demonstrated that modulating the gut microbiota through diet, lifestyle changes, prebiotics, probiotics, or fecal microbiota transplantation may contribute to gut homeostasis and the management of obesity and its associated comorbidities. This review elucidates the impact of alterations in gut microbiota composition during early-life on childhood obesity and explores the mechanisms by which gut microbiota contributes to the pathogenesis of obesity, and specifically focuses on recent advances in utilizing short-chain fatty acids for regulating gut microbiota and ameliorating obesity. Additionally, it discusses the therapeutic strategies for childhood obesity from the perspective of gut microbiota, aiming to provide a theoretical foundation for interventions targeting pediatric obesity based on gut microbiota. Statement of Significance: We provide a summary of the factors, mechanisms, and therapeutic strategies pertaining to the impact of gut microbiota alterations on childhood obesity, with particularly emphasis recent advancements in leveraging short-chain fatty acids for modulating gut microbiota composition and ameliorating obesity-related concerns.},
}

@article {pmid39732757,
year = {2024},
author = {Jasiński, M and Biliński, J and Maciejewska, M and Ostrowska, K and Rusicka-Krzewska, P and Konarski, W and Podsiadły, E and Snarski, E and Basak, GW},
title = {Impact of gut colonization by antibiotic-resistant bacteria on the outcomes of autologous stem cell transplantation in multiple myeloma.},
journal = {Scientific reports},
volume = {14},
number = {1},
pages = {31221},
pmid = {39732757},
issn = {2045-2322},
mesh = {Humans ; *Multiple Myeloma/therapy/microbiology ; Male ; Middle Aged ; Female ; *Transplantation, Autologous ; Aged ; Retrospective Studies ; *Gastrointestinal Microbiome ; Adult ; *Hematopoietic Stem Cell Transplantation/adverse effects ; Anti-Bacterial Agents/therapeutic use/pharmacology ; Drug Resistance, Bacterial ; Treatment Outcome ; },
abstract = {Patients undergoing autologous stem cell transplantation (auto-SCT) face elevated risks of infections. Additionally, patients colonized in the gastrointestinal tract with antibiotic-resistant bacteria (ARB) are at higher risk of infection with ARB and other infections. Therefore, patients colonized with ARB before auto-SCT should present with an exceptionally high incidence of infections. According to current literature, ARB colonization is the surrogate marker for dysbiosis, which is known to be associated with a diagnosis of multiple myeloma (MM). Given that, this retrospective study aimed to assess the influence of ARB colonization on infection rates, hematopoiesis regeneration, mucositis, overall survival, and progression-free survival following auto-SCT in MM. Data from 138 MM patients undergoing 141 auto-SCT were analyzed, with 15% showing ARB colonization. Among colonized patients, ESBL-producing gram-negative rods predominated. Patients with gut ARB colonization had significantly higher infection rates than non-colonized individuals (52 vs. 26%, P = 0.02), particularly bloodstream infections (43% vs. 14%, P = 0.004). Colonized patients also tended to exhibit shorter survival rates although there was no statistical significance (1-year and 2-year OS; non-colonized vs. colonized; 97 and 92% vs. 90 and 86%; p = 0.054). Based on our results, gut colonization before auto-SCT negatively affects treatment outcomes.},
}

Humans
*Multiple Myeloma/therapy/microbiology
Male
Middle Aged
Female
*Transplantation, Autologous
Aged
Retrospective Studies
*Gastrointestinal Microbiome
Adult
*Hematopoietic Stem Cell Transplantation/adverse effects
Anti-Bacterial Agents/therapeutic use/pharmacology
Drug Resistance, Bacterial
Treatment Outcome

@article {pmid39732731,
year = {2024},
author = {Lu, Y and Huangfu, S and Ma, C and Ding, Y and Zhang, Y and Zhou, C and Liao, L and Li, M and You, J and Chen, Y and Wang, D and Chen, A and Jiang, B},
title = {Exosomes derived from umbilical cord mesenchymal stem cells promote healing of complex perianal fistulas in rats.},
journal = {Stem cell research & therapy},
volume = {15},
number = {1},
pages = {414},
pmid = {39732731},
issn = {1757-6512},
support = {BE2022674//General Program of Jiangsu Province Social Development-oriented Special Fund Project/ ; No. 82004365//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Exosomes/metabolism ; Rats ; *Mesenchymal Stem Cells/metabolism/cytology ; *Wound Healing ; *Rats, Sprague-Dawley ; *Umbilical Cord/cytology ; *Rectal Fistula/therapy/metabolism ; Humans ; Signal Transduction ; Transforming Growth Factor beta/metabolism ; Disease Models, Animal ; Male ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism/genetics ; Mesenchymal Stem Cell Transplantation/methods ; },
abstract = {BACKGROUND: Complex perianal fistulas, challenging to treat and prone to recurrence, often require surgical intervention that may cause fecal incontinence and lower quality of life due to large surgical wounds and potential sphincter damage. Human umbilical cord-derived MSCs (hUC-MSCs) and their exosomes (hUCMSCs-Exo) may promote wound healing.

METHODS: This study assessed the efficacy, mechanisms, and safety of these exosomes in treating complex perianal fistulas in SD rats. We established a rat model, divided rats with fistulas into the control and the exosome groups. We assessed treatment efficacy through ultrasound, clinical observations, and histopathological analysis. We also evaluated the activation of the HIF-1α/TGF-β/Smad signaling pathway via PCR and Western blot and assessed serological markers for HIF-1α and inflammatory indices through ELISA. We analyzed gut microbiota and the systemic metabolic environment via untargeted metabolomics.

RESULTS: The hUCMSCs-Exo effectively promoted healing of wound, regulated the immune balance enhanced collagen synthesis and angiogenesis in the perianal fistulas model of rats, and regulated the gut microbiota and metabolomic profiles. Results of PCR and Western blot analyses indicated that the exosomes activated HIF-1α/TGF-β/Smad signaling pathways. To the dosages tested, the 10ug/100ul concentration (medium dose) was found to be the most effective to the treatment of complex perianal fistulas.

CONCLUSIONS: The hUCMSCs-Exo significantly promoted the healing of wound in perianal fistulas of rats and demonstrated higher safety. The underlying mechanism facilitating the healing process was likely associated with the activation of the HIF-1α/TGF-β/Smad signaling pathway.},
}

Animals
*Exosomes/metabolism
Rats
*Mesenchymal Stem Cells/metabolism/cytology
*Wound Healing
*Rats, Sprague-Dawley
*Umbilical Cord/cytology
*Rectal Fistula/therapy/metabolism
Humans
Signal Transduction
Transforming Growth Factor beta/metabolism
Disease Models, Animal
Male
Hypoxia-Inducible Factor 1, alpha Subunit/metabolism/genetics
Mesenchymal Stem Cell Transplantation/methods

@article {pmid39732352,
year = {2024},
author = {Kamath, S and Sokolenko, E and Collins, K and Chan, NSL and Mills, N and Clark, SR and Marques, FZ and Joyce, P},
title = {IUPHAR themed review: The gut microbiome in schizophrenia.},
journal = {Pharmacological research},
volume = {211},
number = {},
pages = {107561},
doi = {10.1016/j.phrs.2024.107561},
pmid = {39732352},
issn = {1096-1186},
abstract = {Gut microbial dysbiosis or altered gut microbial consortium, in schizophrenia suggests a pathogenic role through the gut-brain axis, influencing neuroinflammatory and neurotransmitter pathways critical to psychotic, affective, and cognitive symptoms. Paradoxically, conventional psychotropic interventions may exacerbate this dysbiosis, with antipsychotics, particularly olanzapine, demonstrating profound effects on microbial architecture through disruption of bacterial phyla ratios, diminished taxonomic diversity, and attenuated short-chain fatty acid synthesis. To address these challenges, novel therapeutic strategies targeting the gut microbiome, encompassing probiotic supplementation, prebiotic compounds, faecal microbiota transplantation, and rationalised co-pharmacotherapy, show promise in attenuating antipsychotic-induced metabolic disruptions while enhancing therapeutic efficacy. Harnessing such insights, precision medicine approaches promise to transform antipsychotic prescribing practices by identifying patients at risk of metabolic side effects based on their microbial profiles. This IUPHAR review collates the current literature landscape of the gut-brain axis and its intricate relationship with schizophrenia while advocating for integrating microbiome assessments and therapeutic management. Such a fundamental shift in proposing microbiome-informed psychotropic prescriptions to optimise therapeutic efficacy and reduce adverse metabolic impacts would align antipsychotic treatments with microbiome safety, prioritising 'gut-neutral' or gut-favourable drugs to safeguard long-term patient outcomes in schizophrenia therapy.},
}

@article {pmid39731142,
year = {2024},
author = {Yang, Y and Wang, L and Zhuang, T and Xu, T and Ji, M and Wang, Q},
title = {Washed microbiota transplantation stopped recurrent sepsis in a patient with myelofibrosis: a case report.},
journal = {Gut pathogens},
volume = {16},
number = {1},
pages = {78},
pmid = {39731142},
issn = {1757-4749},
abstract = {BACKGROUND: Sepsis represents the most prevalent infectious complication and the primary cause of mortality in myeloproliferative neoplasms (MPN). The risk of sepsis and the difficulty of treatment are significantly increased in MPN patients due to the need for immunomodulators and antibiotics.

CASE PRESENTATION: On June 9, 2023, a 69-year-old male was admitted to the hospital. Following a battery of tests, the diagnosis of sepsis due to Escherichia coli was ultimately established. The patient was administered amoxicillin clavulanate potassium intravenously. In light of the patient's recurrent sepsis and the likelihood that the source of infection is the intestinal tract, we advised that the patient undergo washed microbiota transplantation (WMT) via a colonic transendoscopic enteral tube (TET).

CONCLUSIONS: WMT as the new method of fecal microbiota transplantation (FMT) successfully cured the recurrent sepsis in this case, indicating the novel option for challenging the refractory or serious infections.},
}